<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 Streptococcus agalactiae and explain in detail? [/INST] Streptococcus agalactiae (also known as group B streptococcus or GBS) is a gram-positive coccus (round bacterium) with a tendency to form chains (as reflected by the genus name Streptococcus). It is a beta-hemolytic, catalase-negative, and facultative anaerobe.S. agalactiae is the most common human pathogen of streptococci belonging to group B of the Rebecca Lancefield classification of streptococci. GBS are surrounded by a bacterial capsule composed of polysaccharides (exopolysacharide). The species is subclassified into ten serotypes (Ia, Ib, II–IX) depending on the immunologic reactivity of their polysaccharide capsule.The plural term group B streptococci (referring to the serotypes) and the singular term group B streptococcus (referring to the single species) are both commonly encountered (even though S. halichoeri and S. pseudoporcinus are also group B Streptococci).
In general, GBS is a harmless commensal bacterium being part of the human microbiota colonizing the gastrointestinal and genitourinary tract of up to 30% of healthy human adults (asymptomatic carriers). Nevertheless, GBS  can cause severe invasive infections especially in newborns, the elderly, and people with compromised immune systems.
S. agalactiae is also a common veterinary pathogen, because it can cause bovine mastitis (inflammation of the udder) in dairy cows. The species name agalactiae meaning "of no milk", alludes to this.

Laboratory identification
GBS grows readily on blood agar plates as colonies surrounded by a narrow zone of β-hemolysis. GBS is characterized by the presence in the cell wall of the antigen group B of Lancefield classification (Lancefield grouping) that can be detected directly in intact bacteria using latex agglutination tests. The CAMP test is also another important test for identification of GBS. The CAMP factor produced by GBS acts synergistically with the staphylococcal β-hemolysin inducing enhanced hemolysis of sheep or bovine erythrocytes. GBS is also able to hydrolyze hippurate and this test can also be used to identify presumptively GBS.
Hemolytic GBS strains produce an orange-brick-red non-isoprenoid polyene (ornithine rhamnolipid) pigment (granadaene) when cultivated on granada medium that allows its straightforward identification.
GBS can also be identified using MALDI-TOF (Matrix Assisted Laser Desorption/Ionization-Time of Flight) instruments.
GBS colonies can additionally be identified tentatively after their appearance in chromogenic agar media, nevertheless GBS-like colonies that develop in chromogenic media should be confirmed as GBS using additional reliable tests (e.g.latex agglutination or the CAMP test) to avoid potential mis-identification.
A summary of the laboratory techniques for GBS identification is depicted in Ref 7.

GBS colonization
GBS is a normal component of the intestinal and vaginal microbiota in some women, GBS is an asymptomatic (presenting no symptoms) colonizer of the gastrointestinal tract and vagina in up to 30% of otherwise healthy adults, including pregnant women. GBS colonization may be permanent, intermittent or temporary. In different studies, GBS vaginal colonization rate ranges from 0% to 36%, most studies reporting colonization rates in sexually active women over 20%. It has been estimated that maternal GBS colonization worldwide is 18%, with regional variation from 11% to 35%.
These variations in the reported prevalence of asymptomatic GBS colonization could be related to the detection methods used, and differences in populations sampled.

Virulence
As other virulent bacteria, GBS harbors an important number of virulence factors (virulence factors are molecules produced by bacteria that boosts their capacity to infect and damage human tissues), the most important being the capsular polysaccharide (rich in sialic acid)
and a pore-forming toxin, β-hemolysin.
Today it is considered that GBS pigment and hemolysin are identical or closely related molecules.

GBS infection in newborns
GBS colonization usually does not cause problems in healthy women, nevertheless during pregnancy it can sometimes cause serious illness for the mother and the newborn. GBS is the leading cause of bacterial neonatal infection in the baby during gestation and after delivery with significant mortality rates in premature infants. GBS infections in the mother can cause chorioamnionitis (a severe infection of the placental tissues) infrequently, postpartum infections (after birth) and it had been related with prematurity and fetal death. GBS urinary tract infections (UTI) may also induce labor and cause premature delivery.
In the western world, GBS (in the absence of effective prevention measures) is the major cause of several bacterial infections of the newborn neonatal infection sepsis, pneumonia, and meningitis, which can lead to death or long-term sequelae.GBS neonatal infection typically originates in the lower reproductive tract of infected mothers.
GBS infections in newborns are separated into two clinical syndromes, early-onset disease (EOD) and late-onset disease (LOD).
EOD manifests from 0 to 7 living days in the newborn, most of the cases of EOD being apparent within 24h of birth. The most common clinical syndromes of EOD are sepsis without apparent focus, pneumonia, and less frequently meningitis. EOD is acquired vertically (vertical transmission),  through exposure of the fetus or the baby to GBS from the vagina of a colonized woman, either intrautero or during birth after rupture of membranes. Infants can be infected during passage through the birth canal, nevertheless newborns that acquire GBS through this route can become only colonized, and these colonized infants habitually do not develop EOD. Roughly 50% of newborns to GBS colonized mothers are also GBS colonized and (without prevention measures) 1–2% of these newborns will develop EOD. In the past, the incidence of EOD ranged from 0.7 to 3.7 per thousand live births in the US and from 0.2 to 3.25 per thousand in Europe. In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis (IAP), the CDC reported an incidence of 0.28 cases of EOD per thousand live births in the US.Multistate surveillance 2006-2015 shows a decline in EOD from 0.37 to 0.23 per 1000 live births in the US but LOD remains steady at 0.31 per 1000 live births.It has been indicated that where there was a policy of providing IAP for GBS colonized mothers the overall risk of EOGBS is 0.3%. Since 2006 to 2015 the incidence of GBS EOD decreased from 0.37 to 0.23 per thousand live births in the US.Though maternal GBS colonization is the key determinant for EOD, other factors also increase the risk. These factors include onset of labor before 37 weeks of gestation (premature birth), prolonged rupture of membranes (≥18h before delivery), intra-partum fever (>38 °C,  >100.4 °F), amniotic infections (chorioamnionitis), young maternal age, and low levels of GBS anticapsular polysaccharide antibodies in the mother. Nevertheless, most babies who develop EOD are born to GBS colonized mothers without any additional risk factor. A previous sibling with EOD is also an important risk factor for development of the infection in subsequent deliveries, probably reflecting a lack of GBS polysaccharides protective antibodies in the mother.
Heavy GBS vaginal colonization is also associated with a higher risk for EOD.
Overall, the case–fatality rates from EOD have declined, from 50% observed in studies from the 1970s to 2 to 10% in recent years, mainly as a consequence of improvements in therapy and management. Fatal neonatal infections by GBS are more frequent among premature infants.GBS LOD affects infants from 7 days to 3 months of age and is more likely to cause bacteremia or meningitis. LOD can be acquired from the mother or from environmental sources. Hearing loss and mental impairment can be a long-term sequela of GBS meningitis. In contrast with EOD, the incidence of LOD has remained unchanged at 0.26 per 1000 live births in the US. S. agalactiae neonatal meningitis does not present with the hallmark sign of adult meningitis, a stiff neck; rather, it presents with nonspecific symptoms, such as fever, vomiting and irritability, and can consequently lead to a late diagnosis.

Prevention of neonatal infection
The only reliable way to prevent EOD currently is intrapartum antibiotic prophylaxis (IAP), that is to say administration of antibiotics during delivery.  It has been proved that intravenous penicillin or ampicillin administered for at least 4 hours before delivery to GBS colonized women is very effective at preventing vertical transmission of GBS from mother to baby and EOD. Intravenous penicillin remains the agent of choice for IAP, with intravenous ampicillin as an acceptable alternative. For penicillin allergic women, the laboratory requisitions for ordering antepartum GBS screening cultures should indicate clearly the presence of penicillin allergy.Cefazolin, clindamycin, and vancomycin are used to prevent EOD in infants born to penicillin-allergic mothers.
Intravenous vancomycin is recommended for IAP in women colonized with a clindamycin-resistant Group B Streptococcus strain and a severe penicillin allergy.There are two ways to identify female candidates to receive intrapartum antibiotic prophylaxis: a risk-based approach or a culture-based screening approach. The culture-based screening approach identifies candidates to receive IAP using lower vaginal and rectal cultures obtained between 36 and 37 weeks gestation (32–34 weeks of gestation for women with twins) and IAP is administered to all GBS colonized women. The risk-based strategy identifies candidates to receive IAP by the aforementioned risk factors known to increase the probability of EOD without considering if the mother is or is not a GBS carrier.IAP is also recommended for women with intrapartum risk factors if their GBS carrier status is not known at the time of delivery, for women with GBS bacteriuria during their pregnancy, and for women who have had an infant with EOD previously.
The risk-based approach for IAP is in general less effective than the culture-based approach because in most of the cases EOD develops among newborns, which are born to mothers without risk factors.In 2010, the Centers for Disease Control and Prevention (CDC), in collaboration with several professional groups, issued its revised GBS prevention guidelines.In 2018, the task of revising and updating the GBS prophylaxis guidelines was transferred from the CDC   to ACOG (American College of Obstetricians and Gynecologists), the American Academy of Pediatrics and to the American Society for Microbiology. The ACOG committee issued an update document on Prevention of Group B Streptococcal Early-Onset Disease in Newborns in 2019. This document does not introduce important changes from the CDC guidelines. The key measures necessary for preventing neonatal GBS early onset disease continue to be universal prenatal screening by culture of GBS from swabs collected from the lower vagina and rectum, correct collection and microbiological processing of the samples, and proper implementation of intrapartum antibiotic prophylaxis. The ACOG now recommends performing universal GBS screening between 36 and 37 weeks of gestation.
This new recommendation provides a five-week window  for valid culture results that includes births that occur up to a gestational age of at least 41 weeks.
The culture-based screening approach is followed in most developed countries such as the United States,  France, Spain, Belgium, Canada, Argentina, and Australia. The risk-based strategy is followed in the United Kingdom, and the Netherlands.

Screening for GBS colonization
Though the GBS colonization status of women can change during pregnancy, cultures to detect GBS carried out ≤5 weeks before delivery predict quite accurately the GBS carrier status at delivery.
In contrast, if the prenatal culture is performed more than five weeks before delivery it is unreliable for predicting accurately the GBS carrier status at delivery.The clinical specimens recommended for culture of GBS at 36–37 weeks’ gestation, this recommendation provides a 5-week window for valid culture results that includes births that occur up to a gestational age of at least 41 weeks  (32–34 weeks of gestation for women with twins) are swabs collected the lower vagina (near the introitus) and then from the rectum (through the anal sphincter) without use of a speculum. Vaginal-rectal samples should be collected using a flocked swab preferably, since flocked swabs releases samples and microorganisms more effectively than fiber swabs. Following the recommendations of the Centers for Disease Control and Prevention of United States  (CDC) these swabs should be placed into a non-nutritive transport medium and later inoculated into a selective enrichment broth, Todd Hewitt broth with selective antibiotics  (enrichment culture). After incubation the enrichment broth is subcultured to blood agar plates and GBS like colonies are identified by the CAMP test or using latex agglutination with GBS antisera. After incubation the enrichment broth can also be subcultured to granada medium agar  where GBS grows as pink-red colonies or to chromogenic agars, where GBS grows as colored colonies. GBS-like colonies that develop in chromogenic media should be confirmed as GBS using additional reliable tests to avoid mis-identification.Nucleic acid amplification tests (NAAT) such as polymerase chain reaction (PCR) and DNA hybridization probes have been developed for identifying GBS directly from recto-vaginal samples, but they still cannot replace antenatal culture for the most accurate detection of GBS carriers.
 Intrapartum NAAT without enrichment has a high false negative rate and the use of intrapartum NAAT without enrichment to rule out the need for IAP.

Vaccination
Though IAP for EOD prevention is associated with a large decline in the incidence of the disease, there is, however, no effective strategy for preventing late-onset neonatal GBS disease.Vaccination is considered an ideal solution to prevent not only EOD and LOD but also GBS infections in adults at risk. Nevertheless, though research and clinical trials for the development of an effective vaccine to prevent GBS infections are underway, no vaccine was available in 2020.
The capsular polysaccharide of GBS is not only an important GBS virulence factor but it is also an excellent candidate for the development of an effective vaccine. Protein-based vaccines are also in development.

GBS infection in adults
GBS is also an important infectious agent able to cause invasive infections in adults </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 Protrusio acetabuli and explain in detail? [/INST] Protrusio acetabuli is an uncommon defect of the acetabulum, the socket that receives the femoral head to make the hip joint. The hip bone of the pelvic bone/girdle is composed of three bones, the ilium, the ischium and the pubis </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 Opisthorchiasis and explain in detail? [/INST] Opisthorchiasis is a parasitic disease caused by certain species of genus Opisthorchis (specifically, Opisthorchis viverrini and Opisthorchis felineus). Chronic infection may lead to cholangiocarcinoma, a cancer of the bile ducts.
Medical care and loss of wages caused by Opisthorchis viverrini in Laos and in Thailand costs about $120 million annually. In Asia, infection by Opisthorchis viverrini and  other liver flukes affects the poorest people. Along with other foodborne trematode infections such as clonorchiasis, fascioliasis and paragonimiasis, opisthorchiasis is listed among the World Health Organizations list of neglected tropical diseases.

Signs and symptoms
Symptoms of opisthorchiasis are indistinguishable from clonorchiasis. About 80% of infected people have no symptoms, though they can have eosinophilia. Asymptomatic infection can occur when there are less than 1000 eggs in one gram of feces. Infection is considered heavy when there are 10,000-30,000 eggs in one gram of feces. Symptoms of heavier infections may include diarrhea, epigastric and right upper quadrant pain, lack of appetite, fatigue, yellowing of the eyes and skin and mild fever.These parasites are long-lived and cause heavy chronic infections that may lead to accumulation of fluid in the legs (edema) and in the peritoneal cavity (ascites), enlarged non-functional gallbladder and also ascending cholangitis, which can lead to periductal fibrosis, cholecystitis and cholelithiasis, obstructive jaundice, hepatomegaly and/or portal hypertension.

Chronic opisthorchiasis and cholangiocarcinoma
Both experimental and epidemiological evidence strongly implicates Opisthorchis viverrini infections in the etiology of a malignant cancer of the bile ducts (cholangiocarcinoma) in humans which has a very poor prognosis.  Clonorchis sinensis and Opisthorchis viverrini are both categorized by the International Agency for Research on Cancer (IARC) as Group 1 carcinogens.In humans, the onset of cholangiocarcinoma occurs with chronic opisthorchiasis, associated with hepatobiliary damage, inflammation, periductal fibrosis and/or cellular responses to antigens from the infecting fluke. These conditions predispose to cholangiocarcinoma, possibly through an enhanced susceptibility of DNA to damage by carcinogens. Chronic hepatobiliary damage is reported to be multi-factorial and considered to arise from a continued mechanical irritation of the epithelium by the flukes present, particularly via their suckers, metabolites and excreted/secreted antigens as well as immunopathological processes. In silico analyses using techniques of genomics and bioinformatics is unraveling information on molecular mechanisms that may be relevant to the development of cholangiocarcinoma.In regions where Opisthorchis viverrini is highly endemic, the incidence of cholangiocarcinoma is unprecedented. For instance, cholangiocarcinoma represents 15% of primary liver cancer worldwide, but in Thailands Khon Kaen province, this figure escalates to 90%, the highest recorded incidence of this cancer in the world. Of all cancers recorded worldwide in 2002, 0.02% were cholangiocarcinoma caused by Opisthorchis viverrini. Cancer of the bile ducts caused by opisthorchiasis occurs in the ages 25–44 years in Thailand. A few cases have appeared in later life among U.S. veterans of the Vietnam War, who consumed poorly cooked fish from streams in endemic areas near the border of Laos and Vietnam.

Diagnosis
The medical diagnosis is usually established by finding eggs of Opisthorchis viverrini in feces using the Kato technique.
Alternatively, an antigen of Opisthorchis viverrini can be detected by ELISA test. A polymerase chain reaction test that can be performed on faeces has been developed and evaluated in a rural community in central Thailand.

Prevention
Cholangiocarcinoma is typically incurable at diagnosis. Because of this, intervention strategies are focused on the prevention or treatment of liver fluke infection. Prevention can be accomplished through education (by persuading people not to consume raw or undercooked fish), but the ancient cultural custom to consume raw, undercooked or freshly pickled fish persists in endemic areas. One community health program, known as the Integrated Opisthorchiasis Control Program, has achieved success in the Lawa Lakes region south of Khon Kaen.Cooking or deep-freezing (-20 °C for 7 days) of food made of fish is an effective method of prevention. Methods for prevention of Opisthorchis viverrini in aquaculture fish ponds have also been proposed.

Treatment
Treatment of opisthorchiasis is usually accomplished with praziquantel. A single dose of praziquantel of 40 mg/kg is effective against opisthorchiasis (and also against schistosomiasis). Despite the efficacy of this compound, the lack of acquired immunity to infection predisposes humans to reinfection in endemic regions. In addition, under experimental conditions, the treatment of Opisthorchis viverrini-infected hamsters with praziquantel induced a dispersion of parasite antigens, resulting in adverse immunopathological changes following re-infection with Opisthorchis viverrini, a process which has been proposed to initiate and/or promote the development of cholangiocarcinoma in humans. Albendazole can be used as an alternative.A randomized controlled trial published in 2011 showed that tribendimidine, a broad-spectrum anthelmintic, appears to be at least as efficacious as praziquantel </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 Low milk supply and explain in detail? [/INST] In breastfeeding women, low milk supply, also known as lactation insufficiency, insufficient milk syndrome,  agalactia, agalactorrhea, hypogalactia or hypogalactorrhea, is the production of breast milk in daily volumes that do not fully meet the nutritional needs of her infant.
Breast milk supply augments in response to the babys demand for milk, and decreases when milk is allowed to remain in the breasts. Low milk supply is usually caused by allowing milk to remain in the breasts for long periods of time, or insufficiently draining the breasts during feeds. It is usually preventable, unless caused by medical conditions that have been estimated to affect five to fifteen percent of women.Several common misconceptions often lead mothers to believe they have insufficient milk when they are in fact producing enough. Actual low milk supply is likely if the baby is latching and swallowing well at the breast, is nevertheless not growing well or is showing signs of dehydration or malnutrition, and does not have a medical condition that would explain the lack of growth. The main method for increasing milk supply is improved breastfeeding practices and/or expressing milk through pumping or hand expression. The medication domperidone increases milk supply for some women. For mothers who cannot breastfeed exclusively, breastfeeding as much as possible, with supplementary formula feeding as necessary, offers many benefits over formula alone.

Causes
Low milk supply can be either primary (caused by medical conditions or anatomical issues in the mother), secondary (caused by not thoroughly and regularly removing milk from the breasts) or both. Secondary causes are far more common than primary ones. One study found that 15% of healthy first-time mothers had low milk supply 2–3 weeks after birth, with secondary causes accounting for at least two-thirds of those cases.Breastfeeding management issues that can interfere with regular milk drainage from the breast include poor latch, unnecessary use of supplemental formula, timed or scheduled feedings (as opposed to on-demand feedings), and overuse of pacifiers. Medical conditions in the infant that result in weak or unco-ordinated sucking can cause low milk supply by inhibiting the transfer of milk to the baby. These conditions include tongue-tie, congenital heart defects,  prematurity, and Down syndrome.Primary causes of low milk supply include:

insufficient glandular tissue, also known as primary lactation failure. Breasts with insufficient glandular tissue often have a tubular shape, with a large space between the breasts, and often do not grow during pregnancy.
retained placenta
Sheehans syndrome
prior breast surgery (especially breast reduction)
prior nipple piercing
polycystic ovary syndrome (PCOS)
hypothyroidism
hypoprolactinemia
theca lutein cysts
hypertension
pregnancySmoking more than 15 cigarettes per day is associated with reduced milk production. Many medications are known to significantly suppress milk production, including pseudoephedrine, diuretics, and contraceptives that contain estrogen. It is suspected that some herbs, particularly sage and peppermint, suppress milk production.

Mechanism
The physiological mechanisms that regulate breast milk supply are poorly understood. High levels of prolactin are necessary for lactation, however there is no direct correlation between baseline levels of prolactin and quantity of milk production. One aspect of supply regulation that has been identified is that breast milk contains a peptide called feedback inhibitor of lactation (FIL).  When milk is present in the breast, FIL inhibits the secretion of milk.
After a mothers milk comes in, a reduction in supply is inevitable unless milk is removed regularly and thoroughly from the breasts.Surgery or injury to the breast can decrease supply by disrupting milk ducts that carry milk from the alveoli, where milk is produced, to the nipple. Retained placenta results in high levels of progesterone, a hormone that inhibits lactation.

Diagnosis
A womans belief that her milk supply is insufficient is one of the most common reasons for discontinuing breastfeeding. In many of those cases, the womans milk supply is actually normal. After a few weeks or months of breastfeeding, changes that are commonly mistaken for signs of low milk supply include breasts feeling softer (this is normal after 1–3 months), more frequent demands by the infant to feed, feeds becoming shorter over time, baby colic, the perception that the baby is more satisfied after being fed infant formula, and a slowdown in growth after three months.To evaluate whether milk supply is actually insufficient, qualitative parameters should be used such as the following:

By 3–5 days, of age, the infant should be stooling 3–4 times per day and urinating 3—5 times per day. By 5–7 days of age, there should be 3—6 stools per day and 4—6 urines.
The infant should be alert, have good muscle tone, and show no signs of dehydration.
The infant should be consistently gaining weight and growing. In newborns, a loss of more than 5 to 7 percent of birth weight warrants investigation. The use of IV fluids in labour tends to artificially increase the birth weight of the baby, and subsequently inflate the babys weight loss. Newborns should regain their birth weight by two weeks of age, and gain at least 150 g per week.If an infant is not showing these signs of growing well, other possible causes include:

Poor milk transfer due to tongue-tie, or cleft palate.
Medical conditions in the infant, such as malabsorption of nutrients.

Definition
A mother is considered to have low milk supply if she produces less breast milk than her infant requires. The term is used only after a mothers milk "comes in", which usually occurs around 30–40 hours after delivery of a full-term infant. Low milk supply is distinct from the scenario in which the mothers milk comes in later than normal but is thereafter produced in sufficient quantities; this is known as delayed onset of lactation (delayed lactogenesis II).

Prevention
The first week after birth is a critical window for establishing milk supply. The Ten Steps of the Baby Friendly Hospital Initiative describe some maternity hospital practices that promote the development of a good milk supply, such as rooming in (allowing mothers and infants to remain together 24 hours a day) and having trained staff available to help mothers with breastfeeding. Supplemental formula or donor milk should be given only when medically necessary.
There is increasing evidence that suggests that early skin-to-skin contact between mother and baby stimulates breastfeeding behavior in the baby. Newborns who are immediately placed on their mothers skin have a natural instinct to latch on to the breast and start nursing, typically within one hour of birth. Immediate skin-to-skin contact may provide a form of imprinting that makes subsequent feeding significantly easier.  Interrupting the process, such as removing the baby to weigh him/her, may complicate subsequent feeding.Frequent suckling in the first days of life is correlated with higher milk production. Infants should be fed when they show signs of hunger. It is common for breastfed babies to feed during the night for the first six months. Usually feedings last 10–15 minutes in the early days.If the infant is unable to breastfeed, it is recommended that pumping or hand expression of milk begin within two hours of delivery, and be done at least eight times every 24 hours.

Management
Attempts to increase milk supply should begin promptly as the longer low supply continues, the more difficult it is to reverse. The primary method for increasing milk supply is to increase the frequency and the thoroughness of milk drainage from the breasts, and to increase breast stimulation.For mothers of healthy term infants who are able to nurse, very strong evidence supports improving breastfeeding practices as a primary treatment. Increasing skin-to-skin contact between mother and baby, and allowing unrestricted breastfeeding, aid in stimulating the milk ejection reflex and promote frequent feeds. If the babys latch is not optimal, improving the latch will help the baby drink more milk. Making the mother comfortable, particularly by resolving nipple pain, is essential. Breast self-massage is recommended to stimulate the milk ejection reflex and to physically promote the flow of milk. Some experts recommend using a breast pump after each breastfeeding session.If the baby cannot nurse effectively, frequent drainage of milk from the breasts through hand expression and/or an electric double breast pump is recommended.The mothers use of medications and herbs should be evaluated, as some substance suppress lactation. The Academy of Breastfeeding Medicine protocol for low milk supply recommends that the mother be evaluated for medical causes of the problem, however health professionals and breastfeeding counsellors often do not do this.

Medications and herbs
After the above treatment methods have been attempted, many breastfeeding specialists and lactation consultants recommend medications or herbs that are believed to increase milk supply (galactagogues).  In 2010, a randomized, double-blinded, placebo-controlled study demonstrated that domperidone increased milk production in mothers of preterm infants. Another very small study of domperidone found that some women respond to it and others do not. As the effects of domperidone stop when use of the drug is stopped, it is sometimes used for months </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 Endometrial hyperplasia and explain in detail? [/INST] Endometrial hyperplasia is a condition of excessive proliferation of the cells of the endometrium, or inner lining of the uterus.
Most cases of endometrial hyperplasia result from high levels of estrogens, combined with insufficient levels of the progesterone-like hormones which ordinarily counteract estrogens proliferative effects on this tissue. This may occur in a number of settings, including obesity, polycystic ovary syndrome, estrogen producing tumours (e.g. granulosa cell tumour) and certain formulations of estrogen replacement therapy.
Endometrial hyperplasia with atypia is a significant risk factor for the development or even co-existence of endometrial cancer, so careful monitoring and treatment of women with this disorder is essential.

Classification
Like other hyperplastic disorders, endometrial hyperplasia initially represents a physiological response of endometrial tissue to the growth-promoting actions of estrogen. However, the gland-forming cells of a hyperplastic endometrium may also undergo changes over time which predispose them to cancerous transformation </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 Vesicointestinal fistula 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 Healing and explain in detail? [/INST] With physical trauma or disease suffered by an organism, healing involves the repairing of damaged tissue(s), organs and the biological system as a whole and resumption of (normal) functioning. Medicine includes the process by which the cells in the body regenerate and repair to reduce the size of a damaged or necrotic area and replace it with new living tissue. The replacement can happen in two ways: by regeneration in which the necrotic cells are replaced by new cells that form "like" tissue as was originally there; or by repair in which injured tissue is replaced with scar tissue. Most organs will heal using a mixture of both mechanisms.Within surgery, healing is more often referred to as recovery, and postoperative recovery has historically been viewed simply as restitution of function and readiness for discharge. More recently, it has been described as an energy‐requiring process to decrease physical symptoms, reach a level of emotional well‐being, regain functions, and re‐establish activitiesHealing is also referred to in the context of the grieving process.In psychiatry and psychology, healing is the process by which neuroses and psychoses are resolved to the degree that the client is able to lead a normal or fulfilling existence without being overwhelmed by psychopathological phenomena. This process may involve psychotherapy, pharmaceutical treatment or alternative approaches such as traditional spiritual healing.

Regeneration
In order for an injury to be healed by regeneration, the cell type that was destroyed must be able to replicate. Cells also need a collagen framework along which to grow. Alongside most cells there is either a basement membrane or a collagenous network made by fibroblasts that will guide the cells growth.  Since ischaemia and most toxins do not destroy collagen, it will continue to exist even when the cells around it are dead.

Example
Acute tubular necrosis (ATN) in the kidney is a case in which cells heal completely by regeneration. ATN occurs when the epithelial cells that line the kidney are destroyed by either a lack of oxygen (such as in hypovolemic shock, when blood supply to the kidneys is dramatically reduced), or by toxins (such as some antibiotics, heavy metals or carbon tetrachloride).Although many of these epithelial cells are dead, there is typically patchy necrosis, meaning that there are patches of epithelial cells still alive. In addition, the collagen framework of the tubules remains completely intact.The existing epithelial cells can replicate, and, using the basement membrane as a guide, eventually bring the kidney back to normal. After regeneration is complete, the damage is undetectable, even microscopically.Healing must happen by repair in the case of injury to cells that are unable to regenerate (e.g. neurons). Also, damage to the collagen network (e.g. by enzymes or physical destruction), or its total collapse (as can happen in an infarct) cause healing to take place by repair.

Genetics
Many genes play a role in healing. For instance, in wound healing, P21 has been found to allow mammals to heal spontaneously. It even allows some mammals (like mice) to heal wounds without scars. The LIN28 gene also plays a role in wound healing. It is dormant in most mammals. Also, the proteins MG53 and TGF beta 1 play important roles in wound healing.

Wound healing
In response to an incision or wound, a wound healing cascade is unleashed.  This cascade takes place in four phases: clot formation, inflammation, proliferation, and maturation.

Clotting phase
Healing of a wound begins with clot formation to stop bleeding and to reduce infection by bacteria, viruses and fungi. Clotting is followed by neutrophil invasion three to 24 hours after the wound has been incurred, with mitoses beginning in epithelial cells after 24 to 48 hours.

Inflammation phase
In the inflammatory phase, macrophages and other phagocytic cells kill bacteria, debride damaged tissue and release chemical factors such as growth hormones that encourage fibroblasts, epithelial cells and endothelial cells which make new capillaries to migrate to the area and divide.

Proliferative phase
In the proliferative phase, immature granulation tissue containing plump, active fibroblasts forms. Fibroblasts quickly produce abundant type III collagen, which fills the defect left by an open wound. Granulation tissue moves, as a wave, from the border of the injury towards the center.As granulation tissue matures, the fibroblasts produce less collagen and become more spindly in appearance. They begin to produce the much stronger type I collagen. Some of the fibroblasts mature into myofibroblasts which contain the same type of actin found in smooth muscle, which enables them to contract and reduce the size of the wound.

Maturation phase
During the maturation phase of wound healing, unnecessary vessels formed in granulation tissue are removed by apoptosis, and type III collagen is largely replaced by type I. Collagen which was originally disorganized is cross-linked and aligned along tension lines. This phase can last a year or longer. Ultimately a scar made of collagen, containing a small number of fibroblasts is left.

Tissue damaged by inflammation
After inflammation has damaged tissue (when combatting bacterial infection for example) and pro-inflammatory eicosanoids have completed their function, healing proceeds in 4 phases.

Recall phase
In the recall phase the adrenal glands increase production of cortisol which shuts down eicosanoid production and inflammation.

Resolution phase
In the Resolution phase, pathogens and damaged tissue are removed by macrophages (white blood cells). Red blood cells are also removed from the damaged tissue by macrophages. Failure to remove all of the damaged cells and pathogens may retrigger inflammation. The two subsets of macrophage M1 & M2 plays a crucial role in this phase, M1 macrophage being a pro inflammatory while as M2 is a regenerative and the plasticity between the two subsets determine the tissue inflammation or repair.

Regeneration phase
In the Regeneration phase, blood vessels are repaired and new cells form in the damaged site similar to the cells that were damaged and removed.  Some cells such as neurons and muscle cells (especially in the heart) are slow to recover.

Repair phase
In the Repair phase, new tissue is generated which requires a balance of anti-inflammatory and pro-inflammatory eicosanoids.  Anti-inflammatory eicosanoids include lipoxins, epi-lipoxins, and resolvins, which cause release of growth hormones.

See also
Scar free healing
Health

References
External links
How wounds heal and tumors form With this simple Flash demonstration, Harvard professor Donald Ingber explains how wounds heal, why scars form, and how tumors develop. Presented by Childrens Hospital Boston.
Wound Healing and Repair
Lorenz H.P. and Longaker M.T </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 Carcinoid syndrome and explain in detail? [/INST] Carcinoid syndrome is a paraneoplastic syndrome comprising the signs and symptoms that occur secondary to carcinoid tumors. The syndrome includes flushing and diarrhea, and less frequently, heart failure, vomiting and bronchoconstriction.  It is caused by endogenous secretion of mainly serotonin and kallikrein.

Signs and symptoms
The carcinoid syndrome occurs in approximately 5% of carcinoid tumors and becomes manifest when vasoactive substances from the tumors enter the systemic circulation escaping hepatic degradation. If the primary tumor is from the gastrointestinal tract (hence releasing serotonin into the hepatic portal circulation), carcinoid syndrome generally does not occur until the disease is so advanced that it overwhelms the livers ability to metabolize the released serotonin.
Flushing: The most important clinical finding is flushing of the skin, usually of the head and the upper part of thorax.
Diarrhea: It may be associated with abdominal cramping. This symptom is due to the action of serotonin, histamine, and gastrin
Abdominal pain: It is due to hepatomegaly, small bowel obstruction or lack of oxygen to small bowel.
Bronchoconstriction, which may be histamine or serotonin-induced, affects about 15% of those having carcinoid syndrome and often accompanies flushing, sneezing, and shortness of breath.
Carcinoid heart disease: About 19% to 60% of the those affected by carcinoid syndrome develop carcinoid heart disease. Serotonin induces fibrosis in valves of the right heart especially tricuspid valve.

Pathophysiology
Carcinoid tumors produce several vasoactive substances, most prominently serotonin. It is commonly thought that serotonin is the cause of the flushing, but this is only partially correct. The flushing also results from secretion of kallikrein, the enzyme that catalyzes the conversion of kininogen to lysyl-bradykinin. The latter is further converted to bradykinin, one of the most powerful vasodilators known.
Other components of the carcinoid syndrome are diarrhea (probably caused by the increased serotonin, which greatly increases peristalsis, leaving less time for fluid absorption), a pellagra-like syndrome (probably caused by diversion of large amounts of tryptophan from synthesis of the vitamin B3 niacin, which is needed for NAD production, to the synthesis of serotonin and other 5-hydroxyindoles), fibrotic lesions of the endocardium, particularly on the right side of the heart resulting in insufficiency of the tricuspid valve and, less frequently, the pulmonary valve and, uncommonly, bronchoconstriction.The pathogenesis of the cardiac lesions and the bronchoconstriction is unknown, but the former probably involves activation of serotonin 5-HT2B receptors by serotonin. When the primary tumor is in the gastrointestinal tract, as it is in the great majority of cases, the serotonin and kallikrein are inactivated in the liver; manifestations of carcinoid syndrome do not occur until there are metastases to the liver or when the cancer is accompanied by liver failure (cirrhosis). Carcinoid tumors arising in the bronchi may be associated with manifestations of carcinoid syndrome without liver metastases because their biologically active products reach the systemic circulation before passing through the liver and being metabolized.In most patients, there is an increased urinary excretion of 5-HIAA (5-hydroxyindoleacetic acid), a degradation product of serotonin.The biology of these tumors differs from many other tumor types. Ongoing research on the biology of these tumors may reveal new mechanisms for tumor development.

Diagnosis
With a certain degree of clinical suspicion, the most useful initial test is the 24-hour urine levels of 5-HIAA (5-hydroxyindoleacetic acid), the end product of serotonin metabolism. Patients with carcinoid syndrome usually excrete more than 25 mg of 5-HIAA per day.

Imaging
For localization of both primary lesions and metastasis, the initial imaging method is Octreoscan, where indium-111 labelled somatostatin analogues (octreotide) are used in scintigraphy for detecting tumors expressing somatostatin receptors. Median detection rates with octreoscan are about 89%, in contrast to other imaging techniques such as CT scan and MRI with detection rates of about 80%. Gallium-68 labelled somatostatin analogues such as 68Ga-DOTA-Octreotate (DOTATATE), performed on a PET/CT scanner is superior to conventional Octreoscan.
Usually, on a CT scan, a spider-like/crab-like change is visible in the mesentery due to the fibrosis from the release of serotonin. 18F-FDG PET/CT, which evaluate for increased metabolism of glucose, may also aid in localizing the carcinoid lesion or evaluating for metastases. Chromogranin A and platelets serotonin are increased.Transthoracic echocardiogram shows valve thickening and reduction in mobility of the valves. Cardiac MRI is useful in showing ventricular anatomy and function.

Localization of tumour
Tumour localization may be extremely difficult </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 Hepatopulmonary syndrome and explain in detail? [/INST] In medicine, hepatopulmonary syndrome is a syndrome of shortness of breath and hypoxemia (low oxygen levels in the blood of the arteries) caused by vasodilation (broadening of the blood vessels) in the lungs of patients with liver disease. Dyspnea and hypoxemia are worse in the upright position (which is called platypnea and orthodeoxia, respectively).

Pathophysiology
The hepatopulmonary syndrome results from the formation of microscopic intrapulmonary arteriovenous dilatations in patients with both chronic and far less common, acute liver failure. The mechanism is unknown but is thought to be due to increased liver production or decreased liver clearance of vasodilators, possibly involving nitric oxide.The dilation of these blood vessels causes overperfusion relative to ventilation, leading to ventilation-perfusion mismatch and hypoxemia. There is an increased gradient between the partial pressure of oxygen in the alveoli of the lung and adjacent arteries (alveolar-arterial [A-a] gradient) while breathing room air. Patients with HPS have platypnea-orthodeoxia syndrome (POS); that is, because intrapulmonary vascular dilations (IPVDs) predominate in the bases of the lungs, standing worsens hypoxemia (orthodeoxia)/dyspnea (platypnea) and the supine position improves oxygenation as blood is redistributed from the bases to the apices. Additionally, late in cirrhosis, it is common to develop high output failure, which would lead to less time in capillaries per red blood cell, exacerbating the hypoxemia.

Diagnosis
The hepatopulmonary syndrome is suspected in any patient with known liver disease who reports dyspnea (particularly platypnea). Patients with clinically significant symptoms should undergo pulse oximetry. If the syndrome is advanced, arterial blood gasses should be measured on air. Hepatopulmonary syndrome (HPS) consists of the triad of liver dysfunction, otherwise unexplained hypoxemia, and intrapulmonary vascular dilation (IPVD).A useful diagnostic test is contrast echocardiography. Intravenous microbubbles (> 10 micrometers in diameter) from agitated normal saline that are normally obstructed by pulmonary capillaries (normally <8 to 15 micrometers) rapidly transit the lung and appear in the left atrium of the heart within 7 heart beats </s>