<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Glucose/fructose/phosphoric acid and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sojourn and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hepatitis A and B vaccine and explain in detail? [/INST] Combined hepatitis A and B vaccine, is used to provide protection against hepatitis A and hepatitis B. It is given by injection into muscle.It is used in areas where hepatitis A and B are endemic, for travelers, people with hepatitis C or chronic liver disease, and those at high risk of sexually transmitted diseases.The combined vaccine is as safe and protective as if given as separate hepatitis A and B vaccines. It is generally well-tolerated. Common side effects are mild and include redness and pain at the injection site, where a small lump may appear. Feeling faint or tired, or a headache may occur. Other side effects include numbness, tingling, rash, bruising, abnormal bleeding such as from the nose or gums, weak muscle or pain </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Epoetin alfa and explain in detail? [/INST] Epoetin alfa is a human erythropoietin produced in cell culture using recombinant DNA technology. Authorised by the European Medicines Agency on 28 August 2007, it stimulates erythropoiesis (increasing red blood cell levels) and is used to treat anemia, commonly associated with chronic kidney failure and cancer chemotherapy.
Epoetin is manufactured and marketed by Amgen under the brand name Epogen. Johnson & Johnson subsidiary Janssen Biotech (formerly Ortho Biotech Products, LP), sells the same drug under the name Procrit, pursuant to a product license agreement. The average cost per  patient in the U.S. was $8,447 in 2009.  Darbepoetin alfa (rINN)  is a glycosylation analog of erythropoietin containing two additional N-linked carbohydrate chains, also manufactured and marketed by Amgen, with a brand name of Aranesp. The Food and Drug Administration (FDA) warnings and safety precautions for Procrit, Epogen and Aranesp are identical.
For several years, epoetin alfa has accounted for the single greatest drug expenditure paid by the U.S. Medicare system; in 2010, the program paid $2 billion for the drug. Raising hemoglobin levels has been found in some studies to be associated with higher risks of thrombotic events, strokes and death.It is on the World Health Organizations List of Essential Medicines.

Medical uses
Erythropoietin is available as a therapeutic agent produced by recombinant DNA technology in mammalian cell culture. It is used in treating anemia resulting from chronic kidney disease and myelodysplasia, from the treatment of cancer (chemotherapy and radiation).

Anemia caused by kidney disease
For people who require dialysis or have chronic kidney disease, iron should be given with erythropoietin, depending on some laboratory parameters such as ferritin and transferrin saturation. Dialysis patients in the U.S. are most often given Epogen; other brands of epoetin may be used in other countries.Erythropoietin is also used to treat anemia in people with chronic kidney disease who are not on dialysis (those in Stage 3 or 4 disease and those living with a kidney transplant). There are two types of erythropoietin for people with anemia due to chronic kidney disease (not on dialysis).

Anemia caused by cancer
In March 2008, a panel of advisers for the U.S. Food and Drug Administration (FDA) supported keeping erythropoiesis-stimulating agents (ESAs) produced by Amgen and Johnson & Johnson on the market for use in cancer patients. The FDA has focused its concern on study results from some clinical trials showing an increased risk of death and tumor growth in chemotherapy patients taking the anti-anemia drugs.

Anemia in critically ill people
Erythropoietin is used to treat people with anemia resulting from critical illness.
In a randomized controlled trial, erythropoietin was shown to not change the number of blood transfusions required by critically ill patients. A surprising finding in this study was a small mortality reduction in patients receiving erythropoietin. This result was statistically significant after 29 days but not at 140 days. The mortality difference was most marked in patients admitted to the ICU for trauma. The authors provide several hypotheses for potential etiologies of this reduced mortality, but, given the known increase in thrombosis and increased benefit in trauma patients as well as marginal nonsignificant benefit (adjusted hazard ratio of 0.9) in surgery patients, it could be speculated that some of the benefit might be secondary to the procoagulant effect of erythropoietin.  Regardless, this study suggests further research may be necessary to see which critical care patients, if any, might benefit from administration of erythropoietin. Any benefit of erythropoietin use must be weighed against the increased likelihood of thrombosis, which has been demonstrated in numerous trials.

Neurological diseases
Erythropoietin has been hypothesized to be beneficial in treating certain neurological diseases such as schizophrenia and stroke. Some research has suggested that erythropoietin improves the survival rate in children with cerebral malaria, which is caused by the malaria parasites blockage of blood vessels in the brain. However, the possibility that erythropoietin may be neuroprotective is inconsistent with the poor transport of the chemical into the brain and the low levels of erythropoietin receptors expressed on neuronal cells.
Psychiatric diseases
Randomized clinical control trials have shown promising results of EPO in improving cognition which is often intractable with the current treatment of mood disorders and schizophrenia.These domains include speed of complex cognitive processing across attention,memory and executive function.

Preterm infants
Infants born early often require transfusions with red blood cells and have low levels of erythropoietin. Erythropoietin has been studied as a treatment option to reduce anemia in preterm infants. Treating infants less than 8 days with erythropoietin old may slightly reduce the need for red blood cell transfusions, but increases the risk of retinopathy. Due to the limited clinical benefit and increased risk of retinopathy, early or late erythropoietin treatment is not recommended for preterm infants.

Adverse effects
Epoetin alfa is generally well tolerated. Common side effects include high blood pressure, headache, disabling cluster migraine (resistant to remedies), joint pain, and clotting at the injection site. Rare cases of stinging at the injection site, skin rash, and flu-like symptoms (joint and muscle pain) have occurred within a few hours following administration. More serious side effects, including allergic reactions, seizures and thrombotic events (e.g., heart attacks, strokes, and pulmonary embolism) rarely occur. Chronic self-administration of the drug has been shown to cause increases in blood hemoglobin and hematocrit to abnormally high levels, resulting in dyspnea and abdominal pain.Erythropoietin is associated with an increased risk of adverse cardiovascular complications in patients with kidney disease if it is used to target an increase of hemoglobin levels above 13.0 g/dl.Early treatment (before an infant is 8 days old) with erythropoietin correlated with an increase in the risk of retinopathy of prematurity in premature and anemic infants, raising concern that the angiogenic actions of erythropoietin may exacerbate retinopathy. Since anemia itself increases the risk of retinopathy, the correlation with erythropoietin treatment may be incidental.

Safety advisories in anemic cancer patients
Amgen sent a "dear doctor" letter in January 2007 that highlighted results from a recent anemia of cancer trial, and warned doctors to consider use in that off-label indication with caution.Amgen advised the U.S. Food and Drug Administration (FDA) regarding the results of the DAHANCA 10 clinical trial </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Thioridazine and explain in detail? [/INST] Thioridazine (Mellaril or Melleril) is a first generation antipsychotic drug belonging to the phenothiazine drug group and was previously widely used in the treatment of schizophrenia and psychosis. The branded product was withdrawn worldwide in 2005 because it caused severe cardiac arrhythmias. However, generic versions are still available in the US.

Indications
Thioridazine was voluntarily discontinued by its manufacturer, Novartis, worldwide because it caused severe cardiac arrhythmias.Its primary use in medicine was the treatment of schizophrenia. It was also tried with some success as a treatment for various psychiatric symptoms seen in people with dementia, but chronic use of thioridazine and other anti-psychotics in people with dementia is not recommended.

Side effects
For further information see: Phenothiazine
Thioridazine prolongs the QTc interval in a dose-dependent manner. It produces significantly less extrapyramidal side effects than most first-generation antipsychotics, likely due to its potent anticholinergic effect. Its use, along with the use of other typical antipsychotics, has been associated with degenerative retinopathies(specifically retinitis pigmentosa). It has a higher propensity for causing anticholinergic side effects coupled with a lower propensity for causing extrapyramidal side effects and sedation than chlorpromazine, but also has a higher incidence of hypotension and cardiotoxicity. It is also known to possess a relatively high liability for causing orthostatic hypotension compared to other antipsychotics. Similarly to other first-generation antipsychotics it has a relatively high liability for causing prolactin elevation. It is moderate risk for causing weight gain. As with all antipsychotics thioridazine has been linked to cases of tardive dyskinesia (an often permanent neurological disorder characterised by slow, repetitive, purposeless and involuntary movements, most often of the facial muscles, that is usually brought on by years of continued treatment with antipsychotics, especially the first-generation (or typical) antipsychotics such as thioridazine) and neuroleptic malignant syndrome (a potentially fatal complication of antipsychotic treatment). Blood dyscrasias such as agranulocytosis, leukopenia and neutropenia are possible with thioridazine treatment. Thioridazine is also associated with abnormal retinal pigmentation after many years of use.
Thioridazine has been correlated to rare instances of clinically apparent acute cholestatic liver injury.

Pharmacology
Thioridazine has the following binding profile:
Note: The Binding affinities given are towards cloned human receptors unless otherwise specified
Acronyms used
HB – Human brain receptor
RC – Cloned rat receptor
ND – No data

Metabolism
Thioridazine is a racemic compound with two enantiomers, both of which are metabolized, according to Eap et al., by CYP2D6 into (S)- and (R)-thioridazine-2-sulfoxide, better known as mesoridazine, and into (S)- and (R)-thioridazine-5-sulfoxide. Mesoridazine is in turn metabolized into sulforidazine. Thioridazine is an inhibitor of CYP1A2 and CYP3A4.

History
The manufacturer Novartis/Sandoz/Wander of the brands of thioridazine, Mellaril in the US and Canada and Melleril in Europe, discontinued the drug worldwide in June 2005.

Antibiotic activity
Thioridazine is known to kill extensively drug-resistant tuberculosis and to make methicillin-resistant Staphylococcus aureus sensitive to β-lactam antibiotics. A possible mechanism of action for the drugs antibiotic activity is via the inhibition of bacterial secretion pumps. The β-lactam antibiotic resistance is due to the secretion β-lactamase a protein that destroys antibiotics. If the bacteria cannot secrete the β-lactamase, then the antibiotic will be effective. The drug has been successfully used in the treatment of granulomatous amoebic encephalitis in conjunction with more conventional amoebicidal medications.

References
Further reading
Dean L (2017) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hydrogen peroxide - urea and explain in detail? [/INST] Hydrogen peroxide - urea (also called Hyperol, artizone, urea hydrogen peroxide, and UHP) is a solid composed of equal amounts of hydrogen peroxide and urea. This compound is a white crystalline solid which dissolves in water to give free hydrogen peroxide. Hydrogen peroxide - urea contains solid and water-free hydrogen peroxide, which offers a higher stability and better controllability than liquid hydrogen peroxide when used as an oxidizing agent. Often called carbamide peroxide in the dental office, it is used as a source of hydrogen peroxide for bleaching, disinfection, and oxidation.

Production
For the preparation of the complex, urea is dissolved in 30% hydrogen peroxide (molar ratio 2:3) at temperatures below 60 °C. upon cooling this solution, hydrogen peroxide - urea precipitates in the form of small platelets.Determination of the hydrogen peroxide content by titration with potassium permanganate solution gives a value of 35.4% which corresponds to 97.8% of the theoretical maximum value. The remaining impurity consists of urea.
Akin to water of crystallization, hydrogen peroxide cocrystallizes with urea with the stoichiometry of 1:1. The compound is simply produced (on a scale of several hundred tonnes a year) by the dissolution of urea in excess concentrated hydrogen peroxide solution, followed by crystallization. The laboratory synthesis is analogous.

Structure and properties
The solid state structure of this adduct has been determined by neutron diffraction.Hydrogen peroxide-urea is a readily water-soluble, odorless, crystalline solid, which is available as white powder or colorless needles or platelets. Upon dissolving in various solvents, the 1:1 complex dissociates back to urea and hydrogen peroxide. So just like hydrogen peroxide, the (erroneously) so-called adduct is an oxidizer but the release at room temperature in the presence of catalysts proceeds in a controlled manner </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Resinol and explain in detail? [/INST] Resinol is a skin protectant and topical analgesic that is made by ResiCal Inc. from Orchard Park, New York.  It is an over-the-counter drug that can currently be purchased in 1.25 or 3.3 ounce (35 or 94 g) jars by contacting a local pharmacys drug wholesaler to order the item or on the Internet.

History
Resinol was developed by Dr. Merville Hamilton Carter (1857-1939) in his private practice as treatment for his patients in Baltimore, Maryland during the late 19th century.  In 1895, Carter, along with his brother Allan L. Carter and his cousin Henry Stier Dulaney founded the Resinol Chemical Company and began to mass-produce the ointment and other medical products.  After over forty years of selling Resinol, the company had John H. Buffham & Co. as an outlet in Great Britain and was a successful global distributor.  Henry LeRoy Carter Sr., the son of Dr. Carter, began running the company after the deaths of his father and other staff members.  The companys sales began to decline in the 1940s, and after the death of Henry LeRoy Carter Sr. in 1951, his son Henry LeRoy Carter Jr. took the place of his father and grandfather as president of the Resinol Chemical Company.  At that time, the company focused more on soap manufacturing, but continued to sell Resinol.  For the rest of the 20th century, Resinols popularity continued to dwindle. It was purchased by ResiCal Inc. in 2002, which at the time was headed by D </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Lanthanum and explain in detail? [/INST] Lanthanum is a chemical element with the symbol La and atomic number 57. It is a soft, ductile, silvery-white metal that tarnishes slowly when exposed to air. It is the eponym of the lanthanide series, a group of 15 similar elements between lanthanum and lutetium in the periodic table, of which lanthanum is the first and the prototype. Lanthanum is traditionally counted among the rare earth elements. Like most other rare earth elements, the usual oxidation state is +3. Lanthanum has no biological role in humans but is essential to some bacteria. It is not particularly toxic to humans but does show some antimicrobial activity.
Lanthanum usually occurs together with cerium and the other rare earth elements. Lanthanum was first found by the Swedish chemist Carl Gustaf Mosander in 1839 as an impurity in cerium nitrate – hence the name lanthanum, from the Ancient Greek λανθάνειν (lanthanein), meaning to lie hidden. Although it is classified as a rare earth element, lanthanum is the 28th most abundant element in the Earths crust, almost three times as abundant as lead. In minerals such as monazite and bastnäsite, lanthanum composes about a quarter of the lanthanide content. It is extracted from those minerals by a process of such complexity that pure lanthanum metal was not isolated until 1923.
Lanthanum compounds have numerous applications as catalysts, additives in glass, carbon arc lamps for studio lights and projectors, ignition elements in lighters and torches, electron cathodes, scintillators, gas tungsten arc welding electrodes, and other things. Lanthanum carbonate is used as a phosphate binder in cases of high levels of phosphate in the blood seen with kidney failure.

Characteristics
Physical
Lanthanum is the first element and prototype of the lanthanide series. In the periodic table, it appears to the right of the alkaline earth metal barium and to the left of the lanthanide cerium. Its placement has been disputed, but most who study the matter along with a 2021 IUPAC provisional report consider lanthanum to be best placed as the first of the f-block elements. The 57 electrons of a lanthanum atom are arranged in the configuration [Xe]5d16s2, with three valence electrons outside the noble gas core. In chemical reactions, lanthanum almost always gives up these three valence electrons from the 5d and 6s subshells to form the +3 oxidation state, achieving the stable configuration of the preceding noble gas xenon. Some lanthanum(II) compounds are also known, but they are much less stable.Among the lanthanides, lanthanum is exceptional as it has no 4f electrons as a single gas-phase atom. Thus it is only very weakly paramagnetic, unlike the strongly paramagnetic later lanthanides (with the exceptions of the last two, ytterbium and lutetium, where the 4f shell is completely full). However, the 4f shell of lanthanum can become partially occupied in chemical environments and participate in chemical bonding. For example, the melting points of the trivalent lanthanides (all but europium and ytterbium) are related to the extent of hybridisation of the 6s, 5d, and 4f electrons (lowering with increasing 4f involvement), and lanthanum has the second-lowest melting point among them: 920 °C. (Europium and ytterbium have lower melting points because they delocalise about two electrons per atom rather than three.) This chemical availability of f orbitals justifies lanthanums placement in the f-block despite its anomalous ground-state configuration (which is merely the result of strong interelectronic repulsion making it less profitable to occupy the 4f shell, as it is small and close to the core electrons).The lanthanides become harder as the series is traversed: as expected, lanthanum is a soft metal. Lanthanum has a relatively high resistivity of 615 nΩm at room temperature; in comparison, the value for the good conductor aluminium is only 26.50 nΩm. Lanthanum is the least volatile of the lanthanides. Like most of the lanthanides, lanthanum has a hexagonal crystal structure at room temperature. At 310 °C, lanthanum changes to a face-centered cubic structure, and at 865 °C, it changes to a body-centered cubic structure.

Chemical
As expected from periodic trends, lanthanum has the largest atomic radius of the lanthanides. Hence, it is the most reactive among them, tarnishing quite rapidly in air, turning completely dark after several hours and can readily burn to form lanthanum(III) oxide, La2O3, which is almost as basic as calcium oxide. A centimeter-sized sample of lanthanum will corrode completely in a year as its oxide spalls off like iron rust, instead of forming a protective oxide coating like aluminium, scandium, yttrium, and lutetium. Lanthanum reacts with the halogens at room temperature to form the trihalides, and upon warming will form binary compounds with the nonmetals nitrogen, carbon, sulfur, phosphorus, boron, selenium, silicon and arsenic. Lanthanum reacts slowly with water to form lanthanum(III) hydroxide, La(OH)3. In dilute sulfuric acid, lanthanum readily forms the aquated tripositive ion [La(H2O)9]3+: this is colorless in aqueous solution since La3+ has no d or f electrons. Lanthanum is the strongest and hardest base among the rare earth elements, which is again expected from its being the largest of them.Some lanthanum(II) compounds are also known, but they are much less stable. Therefore, in officially naming compounds of lanthanum its oxidation number always is to be mentioned.

Isotopes
Naturally occurring lanthanum is made up of two isotopes, the stable 139La and the primordial long-lived radioisotope 138La. 139La is by far the most abundant, making up 99.910% of natural lanthanum: it is produced in the s-process (slow neutron capture, which occurs in low- to medium-mass stars) and the r-process (rapid neutron capture, which occurs in core-collapse supernovae). It is the only stable isotope of lanthanum. The very rare isotope 138La is one of the few primordial odd–odd nuclei, with a long half-life of 1.05×1011 years. It is one of the proton-rich p-nuclei which cannot be produced in the s- or r-processes. 138La, along with the even rarer 180mTa, is produced in the ν-process, where neutrinos interact with stable nuclei. All other lanthanum isotopes are synthetic: with the exception of 137La with a half-life of about 60,000 years, all of them have half-lives less than a day, and most have half-lives less than a minute. The isotopes 139La and 140La occur as fission products of uranium.

Compounds
Lanthanum oxide is a white solid that can be prepared by direct reaction of its constituent elements. Due to the large size of the La3+ ion, La2O3 adopts a hexagonal 7-coordinate structure that changes to the 6-coordinate structure of scandium oxide (Sc2O3) and yttrium oxide (Y2O3) at high temperature. When it reacts with water, lanthanum hydroxide is formed: a lot of heat is evolved in the reaction and a hissing sound is heard. Lanthanum hydroxide will react with atmospheric carbon dioxide to form the basic carbonate.Lanthanum fluoride is insoluble in water and can be used as a qualitative test for the presence of La3+. The heavier halides are all very soluble deliquescent compounds. The anhydrous halides are produced by direct reaction of their elements, as heating the hydrates causes hydrolysis: for example, heating hydrated LaCl3 produces LaOCl.Lanthanum reacts exothermically with hydrogen to produce the dihydride LaH2, a black, pyrophoric, brittle, conducting compound with the calcium fluoride structure. This is a non-stoichiometric compound, and further absorption of hydrogen is possible, with a concomitant loss of electrical conductivity, until the more salt-like LaH3 is reached. Like LaI2 and LaI, LaH2 is probably an electride compound.Due to the large ionic radius and great electropositivity of La3+, there is not much covalent contribution to its bonding and hence it has a limited coordination chemistry, like yttrium and the other lanthanides. Lanthanum oxalate does not dissolve very much in alkali-metal oxalate solutions, and [La(acac)3(H2O)2] decomposes around 500 °C. Oxygen is the most common donor atom in lanthanum complexes, which are mostly ionic and often have high coordination numbers over 6: 8 is the most characteristic, forming square antiprismatic and dodecadeltahedral structures. These high-coordinate species, reaching up to coordination number 12 with the use of chelating ligands such as in La2(SO4)3·9H2O, often have a low degree of symmetry because of stereo-chemical factors.Lanthanum chemistry tends not to involve π bonding due to the electron configuration of the element: thus its organometallic chemistry is quite limited. The best characterized organolanthanum compounds are the cyclopentadienyl complex La(C5H5)3, which is produced by reacting anhydrous LaCl3 with NaC5H5 in tetrahydrofuran, and its methyl-substituted derivatives.

History
In 1751, the Swedish mineralogist Axel Fredrik Cronstedt discovered a heavy mineral from the mine at Bastnäs, later named cerite. Thirty years later, the fifteen-year-old Wilhelm Hisinger, from the family owning the mine, sent a sample of it to Carl Scheele, who did not find any new elements within. In 1803, after Hisinger had become an ironmaster, he returned to the mineral with Jöns Jacob Berzelius and isolated a new oxide which they named ceria after the dwarf planet Ceres, which had been discovered two years earlier. Ceria was simultaneously independently isolated in Germany by Martin Heinrich Klaproth. Between 1839 and 1843, ceria was shown to be a mixture of oxides by the Swedish surgeon and chemist Carl Gustaf Mosander, who lived in the same house as Berzelius: he separated out two other oxides which he named lanthana and didymia. He partially decomposed a sample of cerium nitrate by roasting it in air and then treating the resulting oxide with dilute nitric acid. That same year, Axel Erdmann, a student also at the Karolinska Institute, discovered lanthanum in a new mineral from Låven island located in a Norwegian fjord.
Finally, Mosander explained his delay, saying that he had extracted a second element from cerium, and this he called didymium. Although he didnt realise it, didymium too was a mixture, and in 1885 it was separated into praseodymium and neodymium.
Since lanthanums properties differed only slightly from those of cerium, and occurred along with it in its salts, he named it from the Ancient Greek λανθάνειν [lanthanein] (lit. to lie hidden). Relatively pure lanthanum metal was first isolated in 1923.

Occurrence and production
Lanthanum is the third-most abundant of all the lanthanides, making up 39 mg/kg of the Earths crust, behind neodymium at 41.5 mg/kg and cerium at 66.5 mg/kg. It is almost three times as abundant as lead in the Earths crust. Despite being among the so-called "rare earth metals", lanthanum is thus not rare at all, but it is historically so named because it is rarer than "common earths" such as lime and magnesia, and historically only a few deposits were known. Lanthanum is considered a rare earth metal because the process to mine it is difficult, time-consuming, and expensive. Lanthanum is rarely the dominant lanthanide found in the rare earth minerals, and in their chemical formulae it is usually preceded by cerium. Rare examples of La-dominant minerals are monazite-(La) and lanthanite-(La).

The La3+ ion is similarly sized to the early lanthanides of the cerium group (those up to samarium and europium) that immediately follow in the periodic table, and hence it tends to occur along with them in phosphate, silicate and carbonate minerals, such as monazite (MIIIPO4) and bastnäsite (MIIICO3F), where M refers to all the rare earth metals except scandium and the radioactive promethium (mostly Ce, La, and Y). Bastnäsite is usually lacking in thorium and the heavy lanthanides, and the purification of the light lanthanides from it is less involved. The ore, after being crushed and ground, is first treated with hot concentrated sulfuric acid, evolving carbon dioxide, hydrogen fluoride, and silicon tetrafluoride: the product is then dried and leached with water, leaving the early lanthanide ions, including lanthanum, in solution.The procedure for monazite, which usually contains all the rare earths as well as thorium, is more involved. Monazite, because of its magnetic properties, can be separated by repeated electromagnetic separation. After separation, it is treated with hot concentrated sulfuric acid to produce water-soluble sulfates of rare earths. The acidic filtrates are partially neutralized with sodium hydroxide to pH 3–4. Thorium precipitates out of solution as hydroxide and is removed. After that, the solution is treated with ammonium oxalate to convert rare earths to their insoluble oxalates. The oxalates are converted to oxides by annealing. The oxides are dissolved in nitric acid that excludes one of the main components, cerium, whose oxide is insoluble in HNO3. Lanthanum is separated as a double salt with ammonium nitrate by crystallization. This salt is relatively less soluble than other rare earth double salts and therefore stays in the residue. Care must be taken when handling some of the residues as they contain 228Ra, the daughter of 232Th, which is a strong gamma emitter. Lanthanum is relatively easy to extract as it has only one neighbouring lanthanide, cerium, which can be removed by making use of its ability to be oxidised to the +4 state; thereafter, lanthanum may be separated out by the historical method of fractional crystallization of La(NO3)3·2NH4NO3·4H2O, or by ion-exchange techniques when higher purity is desired.Lanthanum metal is obtained from its oxide by heating it with ammonium chloride or fluoride and hydrofluoric acid at 300-400 °C to produce the chloride or fluoride:
La2O3 + 6 NH4Cl → 2 LaCl3 + 6 NH3 + 3 H2OThis is followed by reduction with alkali or alkaline earth metals in vacuum or argon atmosphere:
LaCl3 + 3 Li → La + 3 LiClAlso, pure lanthanum can be produced by electrolysis of molten mixture of anhydrous LaCl3 and NaCl or KCl at elevated temperatures.

Applications
The first historical application of lanthanum was in gas lantern mantles. Carl Auer von Welsbach used a mixture of lanthanum oxide and zirconium oxide, which he called Actinophor and patented in 1886. The original mantles gave a green-tinted light and were not very successful, and his first company, which established a factory in Atzgersdorf in 1887, failed in 1889.Modern uses of lanthanum include:

One material used for anodic material of nickel-metal hydride batteries is La(Ni3.6Mn0.4Al0.3Co0.7). Due to high cost to extract the other lanthanides, a mischmetal with more than 50% of lanthanum is used instead of pure lanthanum. The compound is an intermetallic component of the AB5 type. NiMH batteries can be found in many models of the Toyota Prius sold in the US.  These larger nickel-metal hydride batteries require massive quantities of lanthanum for the production. The 2008 Toyota Prius NiMH battery requires 10 to 15 kilograms (22 to 33 lb) of lanthanum. As engineers push the technology to increase fuel efficiency, twice that amount of lanthanum could be required per vehicle.
Hydrogen sponge alloys can contain lanthanum. These alloys are capable of storing up to 400 times their own volume of hydrogen gas in a reversible adsorption process. Heat energy is released every time they do so; therefore these alloys have possibilities in energy conservation systems.
Mischmetal, a pyrophoric alloy used in lighter flints, contains 25% to 45% lanthanum.
Lanthanum oxide and the boride are used in electronic vacuum tubes as hot cathode materials with strong emissivity of electrons. Crystals of LaB6 are used in high-brightness, extended-life, thermionic electron emission sources for electron microscopes and Hall-effect thrusters.
Lanthanum trifluoride (LaF3) is an essential component of a heavy fluoride glass named ZBLAN. This glass has superior transmittance in the infrared range and is therefore used for fiber-optical communication systems.
Cerium-doped lanthanum bromide and lanthanum chloride are the recent inorganic scintillators, which have a combination of high light yield, best energy resolution, and fast response. Their high yield converts into superior energy resolution; moreover, the light output is very stable and quite high over a very wide range of temperatures, making it particularly attractive for high-temperature applications. These scintillators are already widely used commercially in detectors of neutrons or gamma rays.
Carbon arc lamps use a mixture of rare earth elements to improve the light quality. This application, especially by the motion picture industry for studio lighting and projection, consumed about 25% of the rare-earth compounds produced until the phase out of carbon arc lamps.
Lanthanum(III) oxide (La2O3) improves the alkali resistance of glass and is used in making special optical glasses, such as infrared-absorbing glass, as well as camera and telescope lenses, because of the high refractive index and low dispersion of rare-earth glasses. Lanthanum oxide is also used as a grain-growth additive during the liquid-phase sintering of silicon nitride and zirconium diboride.
Small amounts of lanthanum added to steel improves its malleability, resistance to impact, and ductility, whereas addition of lanthanum to molybdenum decreases its hardness and sensitivity to temperature variations.
Small amounts of lanthanum are present in many pool products to remove the phosphates that feed algae.
Lanthanum oxide additive to tungsten is used in gas tungsten arc welding electrodes, as a substitute for radioactive thorium.
Various compounds of lanthanum and other rare-earth elements (oxides, chlorides, etc.) are components of various catalysis, such as petroleum cracking catalysts.
Lanthanum-barium radiometric dating is used to estimate age of rocks and ores, though the technique has limited popularity.
Lanthanum carbonate was approved as a medication (Fosrenol, Shire Pharmaceuticals) to absorb excess phosphate in cases of hyperphosphatemia seen in end-stage kidney disease.
Lanthanum fluoride is used in phosphor lamp coatings. Mixed with europium fluoride, it is also applied in the crystal membrane of fluoride ion-selective electrodes.
Like horseradish peroxidase, lanthanum is used as an electron-dense tracer in molecular biology.
Lanthanum-modified bentonite (or phoslock) is used to remove phosphates from water in lake treatments.
Lanthanum telluride (La3Te4) is considered to be applied in the field of radioisotope power system (nuclear power plant) due to its significant conversion capabilities. The transmuted elements and isotopes in the segment will not react with the material itself, thus presenting no harm to the safety of the power plant.  Though iodine, which can be generated during transmutation, is suspected to react with La3Te4 segment, the quantity of iodine is small enough to possess threat to the power system.

Biological role
Lanthanum has no known biological role in humans. The element is very poorly absorbed after oral administration and when injected its elimination is very slow. Lanthanum carbonate (Fosrenol) was approved as a phosphate binder to absorb excess phosphate in cases of end stage renal disease.While lanthanum has pharmacological effects on several receptors and ion channels, its specificity for the GABA receptor is unique among trivalent cations. Lanthanum acts at the same modulatory site on the GABA receptor as zinc, a known negative allosteric modulator. The lanthanum cation La3+ is a positive allosteric modulator at native and recombinant GABA receptors, increasing open channel time and decreasing desensitization in a subunit configuration dependent manner.Lanthanum is an essential cofactor for the methanol dehydrogenase of the methanotrophic bacterium Methylacidiphilum fumariolicum SolV, although the great chemical similarity of the lanthanides means that it may be substituted with cerium, praseodymium, or neodymium without ill effects, and with the smaller samarium, europium, or gadolinium giving no side effects other than slower growth.

Precautions
Lanthanum has a low to moderate level of toxicity and should be handled with care. The injection of lanthanum solutions produces hyperglycemia, low blood pressure, degeneration of the spleen and hepatic alterations. The application in carbon arc light led to the exposure of people to rare earth element oxides and fluorides, which sometimes led to pneumoconiosis. As the La3+ ion is similar in size to the Ca2+ ion, it is sometimes used as an easily traced substitute for the latter in medical studies. Lanthanum, like the other lanthanides, is known to affect human metabolism, lowering cholesterol levels, blood pressure, appetite, and risk of blood coagulation. When injected into the brain, it acts as a painkiller, similarly to morphine and other opiates, though the mechanism behind this is still unknown.

Prices
The price for a (metric) ton [1000 kg] of Lanthanum oxide 99% (FOB China in USD/Mt) is given by the Institute of Rare Earths Elements and Strategic Metals as below $2,000 for most of the period from early 2001 to September 2010 (at $10,000 in the short term in 2008); it rose steeply to $140,000 in mid-2011 and fell back just as rapidly to $38,000 by early 2012. The average price for the last six months (March to August 2022) is given by the Institute as follows: Lanthanum Oxide - 99.9%min FOB China - 1305 EUR/mt and for Lanthanum Metal - 99%min FOB China - 3784 EUR/mt.

See also
| CASNo_Ref =  Y
| CASNo = 7439-91-0
| UNII_Ref =  Y
| UNII = 6I3K30563S

References
Bibliography
Greenwood, Norman N.; Earnshaw, Alan (1984). Chemistry of the Elements. Oxford: Pergamon Press. ISBN 978-0-08-022057-4.

Further reading
The Industrial Chemistry of the Lanthanons, Yttrium, Thorium and Uranium, by R </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Colestipol and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sodium nitrite/sodium thiosulfate and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cyclopentolate and explain in detail? [/INST] Cyclopentolate is a muscarinic antagonist. It is commonly used as an eye drop during pediatric eye examinations to dilate the eye (mydriatic) and prevent the eye from focusing/accommodating (cycloplegic).  Cyclopentolate or atropine can also be administered to reverse muscarinic and central nervous system effects of indirect cholinomimetic (anti-AChase) administration.
It is on the World Health Organizations List of Essential Medicines.After instillation of cyclopentolate, pupil dilation (mydriasis) typically lasts up to 24 hours, while paralysis of the ciliary muscle (cycloplegia) typically lasts 6-24 hours. During this time, patients may be more light sensitive than normal and may notice close objects blurred (and possibly distant objects blurred, depending on the patients visual system).  Cyclopentolate is often chosen as a milder, shorter-lasting, cycloplegic alternative to atropine, another cycloplegic agent which lasts much longer.  Tropicamide is an even shorter-lasting cycloplegic than cyclopentolate, but is less reliable for finding latent hyperopia.  Cyclopentolate drops act rapidly to dilate the pupil.The side and adverse effects of cyclopentolate are similar to the side and adverse effects of other anticholinergic medications. Because of that, extra caution should be taken when prescribing cyclopentolate to patients who are already taking other anticholinergic drugs. A possible ocular (eye-related) side effect is increase in pressure inside the eye, which is of particular concern when there is a predisposition toward or a presence of glaucoma. Other ocular side effects can include burning sensations, discomfort with bright light (photophobia), blurred vision, irritation, inflammation of the eye mucous membranes (conjunctivitis), inflammation of the cornea of the eye (keratitis), and other issues. Nonocular (not eye-related) side and adverse effects can include neuropsychiatric symptoms like subtle concentration and memory problems, subtle decision-making problems, drowsiness, and more pronounced disorientation to time and place, confusion, disturbances of speech and movement, hyperactivity, restlessness, and seizures. Temporary psychosis can develop that includes hallucinations, particularly when higher doses are used in children or older adults on other anticholinergic medications. Patients with dementia of the Alzheimers type can experience worsening of their dementia symptoms. Additional side and adverse effects can include skin flushing, skin rashes, gastrointestinal problems, increased heart beat (tachycardia), increased body temperature (hyperpyrexia), blood vessel dilation, urinary retention, dry mouth and reduced sweating, and reduced bronchial secretions. Severe poisoning with cyclopentolate may result in coma, paralysis of breathing, and death. Cyclopentolate derivatives can be used as an antidote for organophosphate poisoning.Lethality of cyclopentolate has been studied in rodents </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Piperacillin and explain in detail? [/INST] Piperacillin is a broad-spectrum β-lactam antibiotic of the ureidopenicillin class. The chemical structure of piperacillin and other ureidopenicillins incorporates a polar side chain that enhances penetration into Gram-negative bacteria and reduces susceptibility to cleavage by Gram-negative beta lactamase enzymes. These properties confer activity against the important hospital pathogen Pseudomonas aeruginosa. Thus piperacillin is sometimes referred to as an "anti-pseudomonal penicillin".
When used alone, piperacillin lacks strong activity against the Gram-positive pathogens such as Staphylococcus aureus, as the beta-lactam ring is hydrolyzed by the bacterias beta-lactamase.It was patented in 1974 and approved for medical use in 1981. Piperacillin is most commonly used in combination with the beta-lactamase inhibitor tazobactam (piperacillin/tazobactam), which enhances piperacillins effectiveness by inhibiting many beta lactamases to which it is susceptible. However, the co-administration of tazobactam does not confer activity against MRSA, as penicillin (and most other beta lactams) do not avidly bind to the penicillin-binding proteins of this pathogen. The World Health Organization classifies piperacillin as critically important for human medicine.

Medical uses
Piperacillin is used almost exclusively in combination with the beta lactamase inhibitor tazobactam for the treatment of serious, hospital-acquired infections. This combination is among the most widely used drug therapies in United States non-federal hospitals, accounting for $388M in spending in spite of being a low-cost generic drug.Piperacillin-tazobactam is recommended as part of a three-drug regimen for the treatment of hospital-acquired pneumonia suspected as being due to infection by multi-drug resistant pathogens. It is also one of several antibacterial drugs recommended for the treatment of infections known to be caused by anaerobic Gram-negative rods.Piperacillin-tazobactam is recommended by the National Institute for Health and Care Excellence as initial empiric treatment for people with suspected neutropenic sepsis.Piperacillin is used to treat patients diagnosed with various internal infections such as abdominal, bacteremia, gynecological, respiratory, and urinary, mainly caused by Pseudomonas aeruginosa and other infectious bacteria. They are primarily used in current and former neutropenic patients, and patients with biliary tract infections. Other uses include applications in surgical infection prophylaxis; in biliary surgery, a single dose of piperacillin is administered intravenously to inhibit the development of acute cholangitis and prevent wound infections. The combination of piperacillin and an aminoglycoside is commonly used to treat severe infections, but due to the incompatibilities in drug interaction, they are administered separately.

Pneumonia
The piperacillin-tazobactam (piptaz) antibiotic commonly used with an aminoglycoside retains similar levels of drug safety and efficacy as other antibiotic combinations such as ceftazidime with the aminoglycoside tobramycin in the treatment of patients with hospital acquired pneumonia. In a clinical comparison primarily targeting patients not initially placed in intensive care units, piperacillin-tazobactam was found to produce higher clinical and microbiological rates of success. By contrast, the drug efficacy of ceftazidime and piperacillin-tazobactam resulted in similar response rates (61.5% and 63.9 respectively) when tobramycin was added into both groups. Identical evaluations are shown when compared to the imipenem and tobramycin combination, where the administration of piperacillin-tazobactam on patients (especially those under mechanical ventilation) was only consisted of a slightly higher response rate.

Administration
Piperacillin is not absorbed orally, and must therefore be given by intravenous or intramuscular injection. It has been shown that the bactericidal actions of the drug do not increase with concentrations of piperacillin higher than 4-6 x MIC, which means that the drug is concentration-independent in terms of its actions. Piperacillin has instead shown to offer higher bactericidal activity when its concentration remains above the MIC for longer periods of time (50% time>MIC showing the highest activity). This higher activity present in continuous dosing has not been directly linked to clinical outcomes, but however does show promise of lowering possibility of resistance and decreasing mortality.Extending the time of piperacillin-tazobactam infusion allows the drugs to maintain the necessary concentrations needed within the body to prevent bacterial growth, enhancing bactericidal activity. The studies supporting this theory generally administered ~3.375g of piperacillin-tazobactam every 8 hours during a 4-hour infusion, while for organisms with higher minimum inhibitory concentrations, ~4.5g of piperacillin-tazobactam was administered every 6 hours during a 3-hour infusion.The recommended doses provided by the BNFC for infants with hospital-acquired infections are 90 mg/kg every 8 hours for infants, a maximum of 4.5g every 6 hours for children, and 4.5g every 8 hours for children aged 12 and above. A dosage of 90 mg/kg every 6 hours is suggested for infants and children diagnosed with neutropenia.

Adverse effects
Common side effects associated with the administration of piperacillin-tazobactam include:
Gastrointestinal: constipation, diarrhea, nausea, vomiting
Dermatologic: erythema, pain, phlebitis, rash
Neurologic: headaches, insomniaProlonged periods of piperacillin-tazobactam therapy have been associated with the potential development of hematologic adversities such as leukopenia (16.3%), neutropenia (10%), and eosinophilia (10%) in adult patients. The combination of piperacillin-tazobactam with other antibiotics was found to be a major risk factor for leukopenia as well. Additionally, the chances of developing these illnesses increases in younger patients with fewer conditions, prolonging their time to recover.Other cases of adverse effects include instances of renal dysfunction, hepatitis, hyperactivity, anemia, abnormalities in coagulation, and hypokalemia. Allergic reactions can be induced from the side chains of β-lactam antibiotics such as amoxicillin, or antibodies surrounding the nucleus of penicillin.

Interactions
The combination of piperacillin and tazobactam, commonly branded as Zosyn, improves their overall bactericidal activity as amino-benzylpenicillins and ureidopencillins work synergistically with β-lactamase inhibitors. Concurrent use or unregulated dosages of piperacillin results in increasing levels of piperacillin within the body, prolonging neuromuscular transmission blockages created by non-depolarizing muscle relaxants, and disruptions in urine tests for glucose. Some compounds that may interfere with the bactericidal activity of piperacillin include chloramphenicol, macrolides, and sulfonamides.
Following two studies conducted in 1986 and 2006, piperacillin was found to inhibit the removal of methotrexate in animal kidneys. Furthermore, in the presence of piperacillin-tazobactam, the decay time for methotrexate triples in comparison to the normal half-life, leaving the patient exposed to cytotoxic effects produced by the chemical agent. While penicillin antibiotics generally work synergistically with aminoglycosides by enhancing their penetration of bacterial membranes, they can also work adversely by inactivating them. A reformulation of ethylenediaminetetraacetic acid and piperacillin-tazobactam has produced results showing an increase in their affinity with amikacin and gentamicin in vitro, enabling the process of simultaneous Y-site infusion to occur. However, tobramycin was found to be incompatible as a combination through Y-site infusion.

Pharmacology
Piperacillin irreversibly binds to the enzyme penicillin-binding proteins, inhibiting the biosynthesis of bacterial cell walls.

Mechanism of action
As a β-lactam antibiotic, piperacillin inhibits penicillin-binding proteins, preventing the spread of bacteria and infections. Responsible for catalyzing the cross-linkage between peptidoglycan strands that protect the bacterial cell from osmotic rupture, penicillin-binding proteins are unique to bacterial organisms, where every known bacteria with a peptidoglycan cell wall consists of homologous sub-families. By sharing a similar stereochemistry with the substrates that bind to penicillin-binding proteins, piperacillin is able to bind to serine residues found at the active site of the enzyme through the formation of a covalent complex, preventing other substrates from binding. Moreover, this leads to the release of autolysins that break down the bacterias cell wall.Some β-lactamase enzymes also consist of residue at their active site, enabling them to hydrolyze the β-lactam ring found within these antibiotics. However, this hydrolytic activity is inhibited when piperacillin works in conjunction with tazobactam. Tazobactam binds to these enzymes to form a stable acyl-enzyme complex; similar to one formed during the hydrolysis of the β-lactam ring. Thus, protecting piperacillin from hydrolysis.The inclusion of a β-lactamase inhibitor does not always increase drug efficacy. Some bacteria may produce certain types of β-lactamase such as AmpC, which are intrinsically resistant to tazobactam.

Mechanisms of resistance
A major mechanism of resistance against piperacillin-tazobactam is Gram-negative bacteria producing β-lactamases. Other currently known mechanisms include mutations in the active site of penicillin-binding proteins, changes in membrane efflux, or bacteria permeability. Some enzymes, such as extended-spectrum β-lactamase (ESBL) have evolved from narrow-spectrum β-lactamases due to genetic mutations, increasing their capabilities to hydrolyze much broader spectrum penicillin. Due to prior conflicting reports on the drugs affinity with ESBL-producing bacteria, piperacillin-tazobactam treatment for such is not recommended. Antibiotic resistance occurs sporadically, conferred by the continuous use of piperacillin-tazobactam in situations where it may prove to be ineffective, leading to cases where plasmid-mediated β-lactamases are being produced in bacteria that do not naturally produce it.Some Gram-positive bacteria penicillin-binding proteins such as Enterococcus faecium (PBP-5) or Staphylococcus aureus (PBP-2a) are intrinsically antibiotic resistant, consisting of relatively low affinity with piperacillin and therefore high resistance to piperacillin-tazobactam. Furthermore, mutations in penicillin-binding proteins cause fluctuations in piperacillin affinity, whereas Streptococcus pneumoniae (PBP-2b) autolytic response is significantly reduced due to decreased affinity with piperacillin. Although membrane permeability changes are less common as a mechanism of resistance, studies investigating Klebsiella pneumoniae have reported a correlation between decreased permeability of piperacillin and increased SHV-1 β-lactamase production.

Pharmacokinetics
Piperacillin is generally available in their stable form as crystallized potassium or sodium salt, quickly losing bactericidal activity upon dissolution due to their short half-lives. As the gastrointestinal tract does not absorb piperacillin and tazobactam, they are dissolved in a solution before being administered to a patient, through parenteral means. Excreted through renal mechanisms like glomerular or tubular filtration as a component of urine, uncontrolled dosages of the drug can cause renal dysfunction and competitive inhibition of excretion, delaying piperacillin-tazobactam excretion, and endangering patients to drug exposure.

Although the distribution of the drug remained the same, the half-life for elimination increased by three to five folds for patients diagnosed with renal dysfunction. Measured by creatinine clearance (CrCl), patients with less than 30ml/min of clearance had significantly reduced levels of piperacillin/tazobactam excretion, measuring down to 35% of the initial dosage, while the area under the curve (AUC) for piperacillin increased by about three folds for those with less than 20ml/min. A reduced dosage or alteration in the interval of administration is recommended for patients lying under 40ml/min of CrCl, depending on the severity of dysfunction.
Renal is the main pathway for drug elimination for both tazobactam and piperacillin in the body. While there are other non-renal means of drug elimination like Hepatobiliary excretion, they occur less frequently. A substantial amount (~80%) of piperacillin found in urine when excreted through glomerular and tubular filtration is unmetabolized. Tazobactam renal elimination may be significantly reduced through piperacillin interaction, dropping from 63.7% to 56.8% of the administered dose over a 24-hour period. Piperacillin may be actively diffused through filtration into the biliary tract during renal clearing, indicated by a generally higher concentration of piperacillin than tazobactam in the bile. The metabolites that make up the remaining percentage in the excreted urine are composed of M1 (inactive) and N-desethyl-piperacillin (active), formed from the division of β-lactam rings of both tazobactam and piperacillin respectively.Due to the hydrophilic nature of piperacillin-tazobactam, a volume distribution of ~15 L amounting to various sites (tissues) is desired, as hydrophilic compounds are not able to pass through plasma membranes as easily as hydrophobic compounds. Concentrations often in the range of 90 MIC or above are located in specific areas including the gallbladder, lung, muscle, and skin, making up 16 - 85% of the plasma concentrations. The concentration of piperacillin-tazobactam is especially lower in fatty tissue, making up less than 10% of the plasma concentrations.

Pharmacodynamics
Compared to concentration dependent bactericidal antibiotics like aminoglycosides and fluoroquinolones, the antibacterial activity of β-lactam antibiotics are generally more time dependent. Unlike the former, when piperacillin-tazobactam concentrations exceed minimum inhibitory concentrations (MIC) of a pathogen by five folds, the exponential relationship between concentration and activity begins to level off. Otherwise, piperacillin-tazobactam bactericidal efficacy is shown to consist of a strong association with the duration of time the concentration exceeds minimum inhibitory concentrations (T>MIC). When the T>MIC in the serum equates to 60 - 70% of the frequency for drug administration (dosing interval), maximal activity is achieved against Gram-negative bacteria, while for Gram-positive bacteria it occurs at around 40 - 50%.Within a 24-hour period in one clinical study, a T>MIC surpassing 60% was found for piperacillin-susceptible bacteria including Escherichia coli, Klebsiella pneumoniae and Staphylococcus aureus in two dosing regimes (4.5g every 8 hours and 3.375g every 8 hours).The evidence for this was obtained through Monte Carlo experiments procured by a special program (OPTAMA), where for several different scenarios (e.g </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Dapagliflozin/metformin and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Imiquimod and explain in detail? [/INST] Imiquimod, sold under the brand name Aldara among others, is a medication that acts as an immune response modifier that is used to treat genital warts, superficial basal cell carcinoma, and actinic keratosis. Scientists at 3Ms pharmaceuticals division discovered the drug and 3M obtained the first FDA approval in 1997. As of 2015, imiquimod is generic and is available worldwide under many brands.

Medical uses
Imiquimod is a patient-applied cream prescribed to treat genital warts, Bowens disease (squamous cell carcinoma in situ), and, secondary to surgery, for basal cell carcinoma, as well as actinic keratosis.Imiquimod 5% cream is indicated for the topical treatment of:

external genital and perianal warts (condylomata acuminata) in adults;
small superficial basal-cell carcinomas (sBCCs) in adults;
clinically typical, non-hyperkeratotic, non-hypertrophic actinic keratoses (AKs) on the face or scalp in immunocompetent adults when size or number of lesions limit the efficacy and / or acceptability of cryotherapy and other topical treatment options are contraindicated or less appropriate.Imiquimod 3.75% cream is indicated for the topical treatment of clinically typical, non-hyperkeratotic, non-hypertrophic, visible or palpable actinic keratosis of the full face or balding scalp in immunocompetent adults when other topical treatment options are contraindicated or less appropriate.

Side effects
Side effects include local inflammatory reactions, such as blisters, a burning sensation, skin redness, dry skin, itching, skin breakdown, skin crusting or scabbing, skin drainage, skin flaking or scaling, skin ulceration, sores, swelling, as well as systemic reactions, such as fever, "flu-like" symptoms, headache, and tiredness.People who have had an organ transplant and are taking immune-suppressing drugs should not use imiquimod.

Mechanism of action
Imiquimod yields profound antitumoral activity by acting on several immunological levels synergistically. Imiquimod stimulates the innate immune system by activating toll-like receptor 7 (TLR7), commonly involved in pathogen recognition. Cells activated by imiquimod via TLR-7 secrete cytokines (primarily interferon-α (IFN-α), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)). There is evidence that imiquimod, when applied to skin, can lead to the activation of Langerhans cells, which subsequently migrate to local lymph nodes to activate the adaptive immune system </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hydrea and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Propylthiouracil and explain in detail? [/INST] Propylthiouracil (PTU) is a medication used to treat hyperthyroidism. This includes hyperthyroidism due to  Graves disease and toxic multinodular goiter. In a thyrotoxic crisis it is generally more effective than methimazole. Otherwise it is typically only used when methimazole, surgery, and radioactive iodine is not possible. It is taken by mouth.Common side effects include itchiness, hair loss, parotid swelling, vomiting, muscle pains, numbness, and headache. Other severe side effects include liver problems and low blood cell counts. Use during pregnancy may harm the baby. Propylthiouracil is in the antithyroid family of medications. It works by decreasing the amount of thyroid hormone produced by the thyroid gland and blocking the conversion of thyroxine (T4) to triiodothyronine (T3).Propylthiouracil came into medical use in the 1940s. It is on the World Health Organizations List of Essential Medicines.

Side effects
Propylthiouracil is generally well tolerated, with side effects occurring in one of every 100 patients. The most common side effects are related to the skin and include rash, itching, hives, abnormal hair loss, and skin pigmentation. Other common side effects are swelling, nausea, vomiting, heartburn, loss of taste, joint or muscle aches, numbness and headache, allergic reactions, and hair whitening.Its notable side effects include a risk of agranulocytosis and aplastic anemia. On 3 June 2009, the FDA published an alert "notifying healthcare professionals of the risk of serious liver injury, including liver failure and death, with the use of propylthiouracil." As a result, propylthiouracil is no longer recommended in non-pregnant adults and in children as the front line antithyroid medication.One possible side effect is agranulocytosis, a decrease of white blood cells in the blood. Symptoms and signs of agranulocytosis include infectious lesions of the throat, the gastrointestinal tract, and skin with an overall feeling of illness and fever. A decrease in blood platelets (thrombocytopenia) also may occur. Since platelets are important for the clotting of blood, thrombocytopenia may lead to problems with excessive bleeding. Side effects are suspected and the drug is sometimes discontinued if the patient complains of recurrent episodes of sore throat.
Another life-threatening side effect is sudden, severe, fulminant liver failure resulting in death or the need for a liver transplantation, which occurs in up to 1 in 10,000 people taking propylthiouracil. Unlike agranulocytosis which most commonly occurs in the first three months of therapy, this side effect may occur at any time during treatment.

Pregnancy
Propylthiouracil is classified as Drug Class D in pregnancy.  Class D signifies there is positive evidence of human fetal risk. The maternal benefit may outweigh fetal risk in life-threatening situations. PTU is preferred over methimazole (which is also a class D) only in the first trimester of pregnancy and in women who may become pregnant because of the increased risk of teratogenicity of methimazole during critical organogenesis. In the second and third trimester, this risk is diminished and methimazole is preferred to avoid the risk of liver complications from PTU in the mother.The primary effect on the fetus from transplacental passage of PTU is the production of a mild hypothyroidism when the drug is used close to term.  This usually resolves within a few days without treatment.  The hypothyroid state may be observed as a goiter in the newborn, and is the result of increased levels of fetal pituitary thyrotropin.  The incidence of fetal goiter after PTU treatment in reported cases is approximately 12%.

Mechanism of action
Thyroid
PTU inhibits the enzyme thyroperoxidase, which normally acts in thyroid hormone synthesis by oxidizing the anion iodide (I−) to iodine (I0), facilitating iodines addition to tyrosine residues on the hormone precursor thyroglobulin.  This is one of the essential steps in the formation of thyroxine (T4).PTU does not inhibit the action of the sodium-dependent iodide transporter located on follicular cells basolateral membranes. Inhibition of this step requires competitive inhibitors, such as perchlorate and thiocyanate.

T3/T4 target tissues
PTU also acts by inhibiting the enzyme 5-deiodinase (tetraiodothyronine 5 deiodinase), which converts T4 to the more active form T3. (This is in contrast to methimazole, which shares propylthiouracils central mechanism, but not its peripheral one.)
It is important to recognize that these enzymes only work on the conjugated tyrosine molecules of T3 and T4: a completely different enzyme family is responsible for the deiodinase activity of iodized single tyrosine molecules within the thyroid follicular cells </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Anthrax vaccines and explain in detail? [/INST] Anthrax vaccines are vaccines to prevent the livestock and human disease anthrax, caused by the bacterium Bacillus anthracis.They have had a prominent place in the history of medicine, from Pasteurs pioneering 19th-century work with cattle (the first effective bacterial vaccine and the second effective vaccine ever) to the controversial late 20th century use of a modern product to protect American troops against the use of anthrax in biological warfare. Human anthrax vaccines were developed by the Soviet Union in the late 1930s and in the US and UK in the 1950s. The current vaccine approved by the U.S. Food and Drug Administration (FDA) was formulated in the 1960s.
Currently administered human anthrax vaccines include acellular (USA, UK) and live spore (Russia) varieties. All currently used anthrax vaccines show considerable local and general reactogenicity (erythema, induration, soreness, fever) and serious adverse reactions occur in about 1% of recipients. New third-generation vaccines being researched include recombinant live vaccines and recombinant sub-unit vaccines.

Pasteurs vaccine
In the 1870s, the French chemist Louis Pasteur (1822–1895) applied his previous method of immunising chickens against chicken cholera to anthrax, which affected cattle, and thereby aroused widespread interest in combating other diseases with the same approach. In May 1881, Pasteur performed a famous public experiment at Pouilly-le-Fort to demonstrate his concept of vaccination. He prepared two groups of 25 sheep, one goat and several cows. The animals of one group were twice injected, with an interval of 15 days, with an anthrax vaccine prepared by Pasteur; a control group was left unvaccinated. Thirty days after the first injection, both groups were injected with a culture of live anthrax bacteria. All the animals in the non-vaccinated group died, while all of the animals in the vaccinated group survived. The public reception was sensational.
Pasteur publicly claimed he had made the anthrax vaccine by exposing the bacilli to oxygen. His laboratory notebooks, now in the Bibliothèque Nationale in Paris, in fact show Pasteur used the method of rival Jean-Joseph-Henri Toussaint (1847–1890), a Toulouse veterinary surgeon, to create the anthrax vaccine. This method used the oxidizing agent potassium dichromate. Pasteurs oxygen method did eventually produce a vaccine but only after he had been awarded a patent on the production of an anthrax vaccine.
The notion of a weak form of a disease causing immunity to the virulent version was not new; this had been known for a long time for smallpox. Inoculation with smallpox (variolation) was known to result in far less scarring, and greatly reduced mortality, in comparison with the naturally acquired disease. The English physician Edward Jenner (1749–1823) had also discovered (1796) the process of vaccination by using cowpox to give cross-immunity to smallpox and by Pasteurs time this had generally replaced the use of actual smallpox material in inoculation. The difference between smallpox vaccination and anthrax or chicken cholera vaccination was that the weakened form of the latter two disease organisms had been "generated artificially", so a naturally weak form of the disease organism did not need to be found. This discovery revolutionized work in infectious diseases and Pasteur gave these artificially weakened diseases the generic name "vaccines", in honor of Jenners groundbreaking discovery. In 1885, Pasteur produced his celebrated first vaccine for rabies by growing the virus in rabbits and then weakening it by drying the affected nerve tissue.
In 1995, the centennial of Pasteurs death, The New York Times ran an article titled "Pasteurs Deception". After having thoroughly read Pasteurs lab notes, the science historian Gerald L. Geison declared Pasteur had given a misleading account of the preparation of the anthrax vaccine used in the experiment at Pouilly-le-Fort. The same year, Max Perutz published a vigorous defense of Pasteur in The New York Review of Books.

Sternes vaccine
The Austrian-South African immunologist Max Sterne (1905–1997) developed an attenuated live animal vaccine in 1935 that is still employed and derivatives of his strain account for almost all veterinary anthrax vaccines used in the world today. Beginning in 1934 at the Onderstepoort Veterinary Research Institute, north of Pretoria, he prepared an attenuated anthrax vaccine, using the method developed by Pasteur. A persistent problem with Pasteurs vaccine was achieving the correct balance between virulence and immunogenicity during preparation. This notoriously difficult procedure regularly produced casualties among vaccinated animals. With little help from colleagues, Sterne performed small-scale experiments which isolated the "Sterne strain" (34F2) of anthrax which became, and remains today, the basis of most of the improved livestock anthrax vaccines throughout the world.

Russian anthrax vaccines
Anthrax vaccines were developed in the Soviet Union in the 1930s and available for use in humans by 1940. A live attenuated, unencapsulated spore vaccine became widely used for humans. It was given either by scarification or subcutaneously and its developers claimed that it was reasonably well tolerated and showed some degree of protective efficacy against cutaneous anthrax in clinical field trials. The efficacy of the live Russian vaccine was reported to have been greater than that of either of the killed British or US anthrax vaccines (AVP and AVA, respectively) during the 1970s and 80s. Today both Russia and China use live attenuated strains for their human vaccines. These vaccines may be given by aerosol, scarification, or subcutaneous injection. A Georgian/Russian live anthrax spore vaccine (called STI) was based on spores from the Sterne strain of B. anthracis. It was given in a two-dose schedule, but serious side-effects restricted its use to healthy adults. It was reportedly manufactured at the George Eliava Institute of Bacteriophage, Microbiology and Virology in Tbilisi, Georgia, until 1991.

British anthrax vaccines
British biochemist Harry Smith (1921–2011), working for the UK bio-weapons program at Porton Down, discovered the three anthrax toxins in 1948. This discovery was the basis of the next generation of antigenic anthrax vaccines and for modern antitoxins to anthrax. The widely used British anthrax vaccine—sometimes called Anthrax Vaccine Precipitated (AVP) to distinguish it from the similar AVA (see below)—became available for human use in 1954. This was a cell-free vaccine in distinction to the live-cell Pasteur-style vaccine previously used for veterinary purposes. It is now manufactured by Porton Biopharma Ltd, a Company owned by the UK Department of Health.
AVP is administered at primovaccination in three doses with a booster dose after six months. The active ingredient is a sterile filtrate of an alum-precipitated anthrax antigen from the Sterne strain in a solution for injection. The other ingredients are aluminium potassium sulphate, sodium chloride and purified water. The preservative is thiomersal (0.005%). The vaccine is given by intramuscular injection and the primary course of four single injections (3 injections 3 weeks apart, followed by a 6-month dose) is followed by a single booster dose given once a year. During the Gulf War (1990–1991), UK military personnel were given AVP concomitantly with the pertussis vaccine as an adjuvant to improve overall immune response and efficacy.

American anthrax vaccines
The United States undertook basic research directed at producing a new anthrax vaccine during the 1950s and 60s. The product known as Anthrax Vaccine Adsorbed (AVA)—trade name BioThrax—was licensed in 1970 by the U.S. National Institutes of Health (NIH) and in 1972 the Food and Drug Administration (FDA) took over responsibility for vaccine licensure and oversight. AVA is produced from culture filtrates of an avirulent, nonencapsulated mutant of the B. anthracis Vollum strain known as V770-NP1-R. No living organisms are present in the vaccine which results in protective immunity after 3 to 6 doses. AVA remains the only FDA-licensed human anthrax vaccine in the United States and is produced by Emergent BioSolutions, formerly known as BioPort Corporation in Lansing, Michigan. The principal purchasers of the vaccine in the United States are the Department of Defense and Department of Health and Human Services.  Ten million doses of AVA have been purchased for the U.S. Strategic National Stockpile for use in the event of a mass bioterrorist anthrax attack.
In 1997, the Clinton administration initiated the Anthrax Vaccine Immunization Program (AVIP), under which active U.S. service personnel were to be immunized with the vaccine. Controversy ensued since vaccination was mandatory and GAO published reports that questioned the safety and efficacy of AVA, causing sometimes serious side effects. A Congressional report also questioned the safety and efficacy of the vaccine and challenged the legality of mandatory inoculations. Mandatory vaccinations were halted in 2004 by a formal legal injunction which made numerous substantive challenges regarding the vaccine and its safety. After reviewing extensive scientific evidence, the FDA determined in 2005 that AVA is safe and effective as licensed for the prevention of anthrax, regardless of the route of exposure. In 2006, the Defense Department announced the reinstatement of mandatory anthrax vaccinations for more than 200,000 troops and defense contractors. The vaccinations are required for most U.S. military units and civilian contractors assigned to homeland bioterrorism defense or deployed in Iraq, Afghanistan or South Korea.

Investigational anthrax vaccines
A number of experimental anthrax vaccines are undergoing pre-clinical testing, notably the Bacillus anthracis protective antigen—known as PA (see Anthrax toxin—combined with various adjuvants such as aluminum hydroxide (Alhydrogel), saponin QS-21, and monophosphoryl lipid A (MPL) in squalene/lecithin/Tween 80 emulsion (SLT). One dose of each formulation has provided significant protection (> 90%) against inhalational anthrax in rhesus macaques.

Omer-2 trial: Beginning in 1998 and running for eight years, a secret Israeli project known as Omer-2 tested an Israeli investigational anthrax vaccine on 716 volunteers of the Israel Defense Forces.  The vaccine—given under a seven-dose schedule—was developed by the Nes Tziona Biological Institute. A group of study volunteers complained of multi-symptom illnesses allegedly associated with the vaccine and petitioned for disability benefits to the Defense Ministry, but were denied. In February 2009, a petition from the volunteers to disclose a report about Omer-2 was filed with the Israels High Court against the Defense Ministry, the Israel Institute for Biological Research at Nes Tziona, the director, Avigdor Shafferman, and the IDF Medical Corps. Release of the information was requested to support further action to provide disability compensation for the volunteers. In 2014 it was announced that the Israeli government would pay $6 million compensation to the 716 soldiers who participated in the Omer-2 trial.
In 2012, B. anthracis isolate H9401 was obtained from a Korean patient with gastrointestinal anthrax. The goal of the Republic of Korea is to use this strain as a challenge strain to develop a recombinant vaccine against anthrax.

References
Further reading
Donegan S, Bellamy R, Gamble CL (2009).  Donegan S (ed.) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Magnesium gluconate and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Telmisartan/hydrochlorothiazide and explain in detail? [/INST] Telmisartan/hydrochlorothiazide, sold under the brand name Micardis HCT among others, is a fixed-dose combination medication used to treat high blood pressure. It is a combination of telmisartan an angiotensin II receptor antagonist with hydrochlorothiazide a diuretic </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nefazodone and explain in detail? [/INST] Nefazodone, sold formerly under the brand names Serzone, Dutonin, and Nefadar among others, is an atypical antidepressant which was first marketed by Bristol-Myers Squibb (BMS) in 1994 but has since largely been discontinued. BMS withdrew it from the market by 2004 due to decreasing sales due to the rare incidence of severe liver damage and the onset of generic competition. The incidence of severe liver damage is approximately 1 in every 250,000 to 300,000 patient-years. Generic versions were introduced in 2003.Nefazodone is a phenylpiperazine compound and is related to trazodone. It has been described as a serotonin antagonist and reuptake inhibitor (SARI) due to its combined actions as a potent serotonin 5-HT2A receptor and 5-HT2C receptor antagonist and weak serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI).

Medical uses
Nefazodone is used to treat major depressive disorder, aggressive behavior, anxiety, and panic disorder.

Available forms
Nefazodone is available as 50 mg, 100 mg, 150 mg, 200 mg, and 250 mg tablets for oral ingestion.

Contraindications
Side effects
Nefazodone can cause severe liver damage, leading to a need for liver transplant, and death. The incidence of severe liver damage is approximately 1 in every 250,000 to 300,000 patient-years. By the time that it started to be withdrawn in 2003, nefazodone had been associated with at least 53 cases of liver injury, with 11 deaths, in the United States, and 51 cases of liver toxicity, with 2 cases of liver transplantation, in Canada. In a Canadian study which found 32 cases in 2002, it was noted that databases like that used in the study tended to include only a small proportion of suspected drug reactions.Protocols are that nefazodone should not be used in patients who have a pre-existing liver condition. Prior to treatment liver enzymes should be tested to make sure there is not an underlying liver condition.  If serum AST or serum ALT levels are more than 3 times the upper limit of normal (ULN) should be permanently withdrawn from the drug.  Regular enzyme labs should be done every 6 months.  Due to liver issues Nefazodone should not be a first line treatment. Common and mild side effects of nefazodone reported in clinical trials more often than placebo include dry mouth (25%), sleepiness (25%), nausea (22%), dizziness (17%), blurred vision (16%), weakness (11%), lightheadedness (10%), confusion (7%), and orthostatic hypotension (5%). Rare and serious adverse reactions may include allergic reactions, fainting, painful/prolonged erection, and jaundice.Nefazodone is not especially associated with increased appetite and weight gain.

Interactions
Nefazodone is a potent inhibitor of CYP3A4, and may interact adversely with many commonly used medications that are metabolized by CYP3A4.

Pharmacology
Pharmacodynamics
Nefazodone acts primarily as a potent antagonist of the serotonin 5-HT2A receptor and to a lesser extent of the serotonin 5-HT2C receptor. It also has high affinity for the α1-adrenergic receptor and serotonin 5-HT1A receptor, and relatively lower affinity for the α2-adrenergic receptor and dopamine D2 receptor. Nefazodone has low but significant affinity for the serotonin, norepinephrine, and dopamine transporters as well, and therefore acts as a weak serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI). It has low but potentially significant affinity for the histamine H1 receptor, where it is an antagonist, and hence may have some antihistamine activity. Nefazodone has negligible activity at muscarinic acetylcholine receptors, and accordingly, has no anticholinergic effects.

Pharmacokinetics
The bioavailability of nefazodone is low and variable, about 20%. Its plasma protein binding is approximately 99%, but it is bound loosely.Nefazodone is metabolized in the liver, with the main enzyme involved thought to be CYP3A4. The drug has at least four active metabolites, which include hydroxynefazodone, para-hydroxynefazodone, triazoledione, and meta-chlorophenylpiperazine. Nefazodone has a short elimination half-life of about 2 to 4 hours. Its metabolite hydroxynefazodone similarly has an elimination half-life of about 1.5 to 4 hours, whereas the elimination half-lives of triazoledione and mCPP are longer at around 18 hours and 4 to 8 hours, respectively. Due to its long elimination half-life, triazole is the major metabolite and predominates in the circulation during nefazodone treatment, with plasma levels that are 4 to 10 times higher than those of nefazodone itself. Conversely, hydroxynefazodone levels are about 40% of those of nefazodone at steady state </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Rimexolone and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bepotastine and explain in detail? [/INST] Bepotastine (Talion, Bepreve) is a 2nd generation antihistamine. It was approved in Japan for use in the treatment of allergic rhinitis and urticaria/pruritus in July 2000 and January 2002, respectively. It is currently marketed in the United States as an eye drop under the brand-name Bepreve, by ISTA Pharmaceuticals, a subsidiary of Bausch + Lomb.

Pharmacology
Bepotastine is available as an ophthalmic solution and oral tablet. It is a direct H1-receptor antagonist that inhibits the release of histamine from mast cells. The ophthalmic formulation has shown minimal systemic absorption, between 1 and 1.5% in healthy adults. Common side effects are eye irritation, headache, unpleasant taste, and nasopharyngitis. The main route of elimination is urinary excretion, 75-90% excreted unchanged.

Marketing history
It is marketed in Japan by Tanabe Seiyaku under the brand name Talion. Talion was co-developed by Tanabe Seiyaku and Ube Industries, the latter of which discovered bepotastine. In 2001, Tanabe Seiyaku granted Senju, now owned by Allergan, exclusive worldwide rights, with the exception of certain Asian countries, to develop, manufacture and market bepotastine for ophthalmic use. Senju, in turn, has granted the United States rights for the ophthalmic preparation to ISTA Pharmaceuticals.

Sales and patents
In 2011, ISTA pharmaceuticals experienced a 2.4% increase in net revenues from 2010, which was driven by the sales of Bepreve. Their net revenue for 2011 was $160.3 million. ISTA Pharmaceuticals was acquired by Bausch & Lomb in March 2012 for $500 million </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Vecuronium bromide and explain in detail? [/INST] Vecuronium bromide, sold under the brand name Norcuron among others, is a medication used as part of general anesthesia to provide skeletal muscle relaxation during surgery or mechanical ventilation. It is also used to help with endotracheal intubation; however, suxamethonium (succinylcholine) is generally preferred if this needs to be done quickly. It is given by injection into a vein. Effects are greatest at about 4 minutes and last for up to an hour.Side effects may include low blood pressure and prolonged paralysis. Allergic reactions are rare. It is unclear if use in pregnancy is safe for the baby. Vecuronium is in the aminosteroid neuromuscular-blocker family of medications and is of the non-depolarizing type. It works by blocking the action of acetylcholine on skeletal muscles.Vecuronium was approved for medical use in the United States in 1984. It is on the World Health Organizations List of Essential Medicines. Vecuronium is available as a generic medication. The effects may be reversed with a combination of neostigmine and atropine.

Mechanism of action
Vecuronium operates by competing for the cholinoceptors at the motor end plate, thereby exerting its muscle-relaxing properties, which are used adjunctively to general anesthesia. Under balanced anesthesia, the time to recovery to 25% of control (clinical duration) is approximately 25 to 40 minutes after injection and recovery is usually 95% complete approximately 45 to 65 minutes after injection of an intubating dose. The neuromuscular blocking action of vecuronium is slightly enhanced in the presence of potent inhalation anesthetics. If vecuronium is first administered more than 5 minutes after the start of the inhalation of enflurane, isoflurane, or halothane, or when a steady state has been achieved, the intubating dose of vecuronium may be decreased by approximately 15%.
Vecuronium has an active metabolite, 3-desacetyl-vecuronium, that has 80% of the effect of vecuronium. Accumulation of this metabolite, which is cleared by the kidneys, can prolong the duration of action of the drug, particularly when an infusion is used in a person with kidney failure.Reversal of vecuronium can be accomplished by administration of sugammadex which is a γ-cyclodextrin which encapsulates vecuronium preventing it from binding to receptors. Reversal can also be accomplished with neostigmine or other cholinesterase inhibitors, but their efficacy is lower than that of sugammadex.

History
As long ago as 1862, adventurer Don Ramon Paez described a Venezuelan poison, guachamaca, which the indigenous peoples used to lace sardines as bait for herons and cranes. If the head and neck of a bird so killed was cut off, the remainder of the flesh could be eaten safely. Paez also described the attempt of a Llanero woman to murder a rival to her lovers affections with guachamaca and unintentionally killed 10 other people when her husband shared his food with their guests. It is probable that the plant was Malouetia nitida or Malouetia schomburgki.The genus Malouetia (family Apocynaceae) is found in both South America and Africa. The botanist Robert E </s>