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Guanfacine also is used in the treatment of migraine headaches and drug withdrawal symptoms. Talk to your doctor about the possible risks of using this drug for your condition.	What information is available about Guanfacine?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What information is available about Guanfacine? [/INST] \n Guanfacine also is used in the treatment of migraine headaches and drug withdrawal symptoms. Talk to your doctor about the possible risks of using this drug for your condition.</s>
Rudolf Virchow described hypercoagulability in the mid 1800s, however, it was not until 1965 that the first descriptions of inherited thrombophilia were published. Later, in the 1990s, the more common mutations associated with primary hypercoagulable states were identified.	Can you provide an overview of thrombophilia, please?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide an overview of thrombophilia, please? [/INST] \n Rudolf Virchow described hypercoagulability in the mid 1800s, however, it was not until 1965 that the first descriptions of inherited thrombophilia were published. Later, in the 1990s, the more common mutations associated with primary hypercoagulable states were identified.</s>
On x-ray, osteoma demonstrates a dense well circumscribed mass with varying amounts of central lucency. Caldwell and Waters view are the radiographic positions of choice for the evaluation of osteomas.	How does an osteoma appear on an X-ray?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: How does an osteoma appear on an X-ray? [/INST] \n On x-ray, osteoma demonstrates a dense well circumscribed mass with varying amounts of central lucency. Caldwell and Waters view are the radiographic positions of choice for the evaluation of osteomas.</s>
The exact incidence and prevalence of milk-alkali syndrome is not known. With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention. Milk-alkali syndrome is the third most common cause of hypercalcemia in hospitalized patients after primary hyperparathyroidism and malignancies.	Can you provide an overview of milk-alkali syndrome?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide an overview of milk-alkali syndrome? [/INST] \n The exact incidence and prevalence of milk-alkali syndrome is not known. With the introduction of histamine antagonists and decrease in antacid consumption since the 1970s, the incidence of milk-alkali syndrome has decreased significantly. However, since the 1990s, there has been an increase in milk-alkali syndrome due to increase in calcium and vitamin D consumption in postmenopausal women for osteoporosis prevention. Milk-alkali syndrome is the third most common cause of hypercalcemia in hospitalized patients after primary hyperparathyroidism and malignancies.</s>
ACE inhibitors can be divided into three groups based on their molecular structure: Captopril (trade name Capoten), the first ACE inhibitor This is the largest group, including: Enalapril (Vasotec/Renitec) Ramipril (Altace/Tritace/Ramace/Ramiwin) Quinapril (Accupril) Perindopril (Coversyl/Aceon) Lisinopril (Lisodur/Lopril/Novatec/Prinivil/Zestril) Benazepril (Lotensin) Fosinopril (Monopril), the only member Casokinins and lactokinins are breakdown products of casein and whey that occur naturally after ingestion of milk products, especially cultured milk. Their role in blood pressure control is uncertain.	What does ACE inhibitor mean?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does ACE inhibitor mean? [/INST] \n ACE inhibitors can be divided into three groups based on their molecular structure: Captopril (trade name Capoten), the first ACE inhibitor This is the largest group, including: Enalapril (Vasotec/Renitec) Ramipril (Altace/Tritace/Ramace/Ramiwin) Quinapril (Accupril) Perindopril (Coversyl/Aceon) Lisinopril (Lisodur/Lopril/Novatec/Prinivil/Zestril) Benazepril (Lotensin) Fosinopril (Monopril), the only member Casokinins and lactokinins are breakdown products of casein and whey that occur naturally after ingestion of milk products, especially cultured milk. Their role in blood pressure control is uncertain.</s>
Lung cancer is a common cancer in the world. It is a leading cause of cancer death in men and women in the United States. Cigarette smoking is the main and most important cause of most lung cancers. Other risk factors include high levels of pollution, radiation and asbestos exposure. According to the pathology, lung cancer can be divided into small cell lung carcinoma and non-small cell lung carcinoma. Usual symptoms include a cough that doesn't go away and gets worse over time, constant chest pain, coughing up blood, shortness of breath, wheezing, hoarseness, repeated problems with pneumonia or bronchitis, swelling of the neck and face, loss of appetite or weight loss and fatigue. Treatments involve surgery, radiation therapy, chemotherapy, targeted therapies, or a combination. The prognosis varies widely. It mainly depends on the stage of the cancer and whether or not the tumor can be removed by surgery.	What information regarding lung cancer is available?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What information regarding lung cancer is available? [/INST] \n Lung cancer is a common cancer in the world. It is a leading cause of cancer death in men and women in the United States. Cigarette smoking is the main and most important cause of most lung cancers. Other risk factors include high levels of pollution, radiation and asbestos exposure. According to the pathology, lung cancer can be divided into small cell lung carcinoma and non-small cell lung carcinoma. Usual symptoms include a cough that doesn't go away and gets worse over time, constant chest pain, coughing up blood, shortness of breath, wheezing, hoarseness, repeated problems with pneumonia or bronchitis, swelling of the neck and face, loss of appetite or weight loss and fatigue. Treatments involve surgery, radiation therapy, chemotherapy, targeted therapies, or a combination. The prognosis varies widely. It mainly depends on the stage of the cancer and whether or not the tumor can be removed by surgery.</s>
Continued monitoring of hormone balance and careful adjustment of glucocorticoid dose is helpful in controlling infertility. In general, women with 21-hydroxylase deficiency have a lower fertility rate. To prevent adrenal crisis, all patients taking glucocorticoids replacement should take bolus dose of glucocorticoids during severe illness, surgery and severe exhaustion.	What is the strategy to prevent a deficiency in 21-hydroxylase through secondary prevention?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the strategy to prevent a deficiency in 21-hydroxylase through secondary prevention? [/INST] \n Continued monitoring of hormone balance and careful adjustment of glucocorticoid dose is helpful in controlling infertility. In general, women with 21-hydroxylase deficiency have a lower fertility rate. To prevent adrenal crisis, all patients taking glucocorticoids replacement should take bolus dose of glucocorticoids during severe illness, surgery and severe exhaustion.</s>
Gastroenteropancreatic neuroendocrine tumors are classified based on their origin from the embryonic divisions of the alimentary tract into foregut (bronchial, stomach), midgut (small intestine, appendix, cecum) and hindgut (distal colon, rectum, genitourinary) tumours.	What exactly is carcinoid syndrome?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What exactly is carcinoid syndrome? [/INST] \n Gastroenteropancreatic neuroendocrine tumors are classified based on their origin from the embryonic divisions of the alimentary tract into foregut (bronchial, stomach), midgut (small intestine, appendix, cecum) and hindgut (distal colon, rectum, genitourinary) tumours.</s>
About half of people with DVT have no symptoms at all. The following are the most common symptoms of DVT that occur in the affected part of the body (usually the leg or arm): Swelling of your leg or arm Pain or tenderness that can not be explained Skin that is warm to the touch Redness of the skin PE can be present without any symptoms of a DVT. Symptoms of a PE can include: Difficulty breathing Faster than normal or irregular heartbeat Chest pain or discomfort, which usually worsens with a deep breath or coughing Anxiety Coughing up blood Lightheadedness, or fainting	What is the connection between deep vein thrombosis and economy class syndrome?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the connection between deep vein thrombosis and economy class syndrome? [/INST] \n About half of people with DVT have no symptoms at all. The following are the most common symptoms of DVT that occur in the affected part of the body (usually the leg or arm): Swelling of your leg or arm Pain or tenderness that can not be explained Skin that is warm to the touch Redness of the skin PE can be present without any symptoms of a DVT. Symptoms of a PE can include: Difficulty breathing Faster than normal or irregular heartbeat Chest pain or discomfort, which usually worsens with a deep breath or coughing Anxiety Coughing up blood Lightheadedness, or fainting</s>
Avoid direct contact with the skin lesions. Do not share towels with other people. Avoiding sex can also prevent molluscum virus and other STDs. You can also avoid STDs by having a monogamous sexual relationship with a partner known to be disease-free. Male and female condoms cannot fully protect you, as the virus can be on areas not covered by the condom. Nonetheless, condoms should still be used every time the disease status of a sexual partner is unknown. They reduce your chances of getting or spreading STDs. It is advisable to use condoms containing spermicide such as nonoxynol 9.	What information is available on Molluscum contagiosum?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What information is available on Molluscum contagiosum? [/INST] \n Avoid direct contact with the skin lesions. Do not share towels with other people. Avoiding sex can also prevent molluscum virus and other STDs. You can also avoid STDs by having a monogamous sexual relationship with a partner known to be disease-free. Male and female condoms cannot fully protect you, as the virus can be on areas not covered by the condom. Nonetheless, condoms should still be used every time the disease status of a sexual partner is unknown. They reduce your chances of getting or spreading STDs. It is advisable to use condoms containing spermicide such as nonoxynol 9.</s>
Normally, the atrioventricular node (AVN) can generate an escape rhythm of 40-60 beats per minute in case the sinoatrial node (SA node) or atrial pacemakers fail (sinus arrest) or slow (sinus bradycardia) or if there is complete heart block. This junctional escape rhythm generates a normal, narrow QRS complex rhythm at a rte below 60 beats per minute (junctional bradycardia) as the electrical impulses once they are generated are conducted with normal velocity down the His-Purkinje system. Retrograde P waves (i.e. upside down) due to retrograde or backward conduction may or may not be present in junctional bradycardia. In contrast to a junctional escape rhythm or junctional bradycardia at a rate of 40-60 beats per minute, junctional tachycardia is faster, at a rate > 60 beats per minute. Junctional tachycardia generates a normal, narrow QRS complex rhythm as the electrical impulses are conducted with normal velocity down the His-Purkinje system. Retrograde P waves (i.e. upside down) P waves due to retrograde or backward conduction may or may not be present. The cause of the more rapid firing of the atrioventricular node is thought to be due to enhanced automaticity as a result of abnormal Calcium metabolism in the sarcoplastic reticulum.	What is the physiological mechanism behind junctional tachycardia?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the physiological mechanism behind junctional tachycardia? [/INST] \n Normally, the atrioventricular node (AVN) can generate an escape rhythm of 40-60 beats per minute in case the sinoatrial node (SA node) or atrial pacemakers fail (sinus arrest) or slow (sinus bradycardia) or if there is complete heart block. This junctional escape rhythm generates a normal, narrow QRS complex rhythm at a rte below 60 beats per minute (junctional bradycardia) as the electrical impulses once they are generated are conducted with normal velocity down the His-Purkinje system. Retrograde P waves (i.e. upside down) due to retrograde or backward conduction may or may not be present in junctional bradycardia. In contrast to a junctional escape rhythm or junctional bradycardia at a rate of 40-60 beats per minute, junctional tachycardia is faster, at a rate > 60 beats per minute. Junctional tachycardia generates a normal, narrow QRS complex rhythm as the electrical impulses are conducted with normal velocity down the His-Purkinje system. Retrograde P waves (i.e. upside down) P waves due to retrograde or backward conduction may or may not be present. The cause of the more rapid firing of the atrioventricular node is thought to be due to enhanced automaticity as a result of abnormal Calcium metabolism in the sarcoplastic reticulum.</s>
Immediate stabilization of patients is the first step. Then the radial fracture and the DRUJ stabilization is recommended in these cases. Open forearm fractures considered as a surgical emergency. Humerus fracture occurs in younger patients who are skeletally immature; the normally they treated using a closed reduction and casting. Since closed reduction and cast application have led to unsatisfactory results. Then, Almost always the open reduction are necessary for the Humerus fracture. There are controversies regarding the indications for intramedullary nailing of forearm fractures.	What kind of injury is classified as an avulsion fracture?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What kind of injury is classified as an avulsion fracture? [/INST] \n Immediate stabilization of patients is the first step. Then the radial fracture and the DRUJ stabilization is recommended in these cases. Open forearm fractures considered as a surgical emergency. Humerus fracture occurs in younger patients who are skeletally immature; the normally they treated using a closed reduction and casting. Since closed reduction and cast application have led to unsatisfactory results. Then, Almost always the open reduction are necessary for the Humerus fracture. There are controversies regarding the indications for intramedullary nailing of forearm fractures.</s>
Subependymoma must be differentiated from: Neoplasms of the ventricular wall and septum pellucidum Ependymoma Central neurocytoma Subependymal giant cell astrocytoma Neoplasms of the choroid plexus Choroid plexus papilloma and carcinoma Others Intraventricular meningioma Intraventricular metastasis Oligodendroglioma Pilocytic astrocytoma Glioblastoma multiforme Medulloblastoma Intraventricular teratoma	What is Subependymoma, and how can it be distinguished from other illnesses?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is Subependymoma, and how can it be distinguished from other illnesses? [/INST] \n Subependymoma must be differentiated from: Neoplasms of the ventricular wall and septum pellucidum Ependymoma Central neurocytoma Subependymal giant cell astrocytoma Neoplasms of the choroid plexus Choroid plexus papilloma and carcinoma Others Intraventricular meningioma Intraventricular metastasis Oligodendroglioma Pilocytic astrocytoma Glioblastoma multiforme Medulloblastoma Intraventricular teratoma</s>
Physical findings for effusions are determined by the volume of pleural fluid and the extent of lung compression. Pleural fluid also interferes with transmission of low-frequency vibrations and results in diminished tactile fremitus, asymmetric chest expansion, decreased or absent fremitus posteriorly and laterally, dullness on percussion, decreased or absent breath sounds, and reduced vocal resonance.	What does the physical examination entail for Pleural effusion?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does the physical examination entail for Pleural effusion? [/INST] \n Physical findings for effusions are determined by the volume of pleural fluid and the extent of lung compression. Pleural fluid also interferes with transmission of low-frequency vibrations and results in diminished tactile fremitus, asymmetric chest expansion, decreased or absent fremitus posteriorly and laterally, dullness on percussion, decreased or absent breath sounds, and reduced vocal resonance.</s>
Patients with Warthin's tumor are usually well-appearing. Mobile non-tender mass which is firm, solitary, and normal in color and appearance On oral examination, redness or bulging may be present	What does a physical examination for a Warthin's tumor involve?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does a physical examination for a Warthin's tumor involve? [/INST] \n Patients with Warthin's tumor are usually well-appearing. Mobile non-tender mass which is firm, solitary, and normal in color and appearance On oral examination, redness or bulging may be present</s>
Viral parotitis is caused by the infiltration of respiratory droplets containing the mumps virus. Mumps virus is a member of the paramyoxoviridae family with a single-strand, negative-sense RNA molecule. The mumps HN and F glycoproteins reach the surface of the infected host cell through the endoplasmic reticulum and Golgi complex. Virions emerge from the infected cells due to the M protein facilitating the localization of the viral ribonucleic proteins onto the host cell membrane. The virus binds with the neighboring host cells via sialic acid through HN glycoprotein. Both HN and F glycoproteins mediate the fusion of virus and host cell, as well as cell and cell - membrane fusion, to perpetuate the spread of the virus throughout the host. The virus replicates in the nasopharynx and regional lymph nodes. Upon replication, viremia occurs for three to five days, spreading to the salivary glands. The parotid gland particularly susceptible to parotitis due to the lower rate of secretion. Salivary flow rate is reduced due to the inflammation response. Reduced saliva flow rate in the parotid gland leads to a reduction in the salivary defense proteins IgA (sIgA) and IgG, increasing vulnerability of the parotid gland to infection. Parotitis results from the inflammatory response to the presence of mumps virus in the parotid salivary gland. Bacterial parotitis is most commonly caused by staphylococcus aureus, a gram-positive coccal bacterium often found in the respiratory tract. Staphylococcus aureus infects the host through skin to skin or skin to surface contact with an infected individual or object.	What is the mechanism of action that causes Parotitis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the mechanism of action that causes Parotitis? [/INST] \n Viral parotitis is caused by the infiltration of respiratory droplets containing the mumps virus. Mumps virus is a member of the paramyoxoviridae family with a single-strand, negative-sense RNA molecule. The mumps HN and F glycoproteins reach the surface of the infected host cell through the endoplasmic reticulum and Golgi complex. Virions emerge from the infected cells due to the M protein facilitating the localization of the viral ribonucleic proteins onto the host cell membrane. The virus binds with the neighboring host cells via sialic acid through HN glycoprotein. Both HN and F glycoproteins mediate the fusion of virus and host cell, as well as cell and cell - membrane fusion, to perpetuate the spread of the virus throughout the host. The virus replicates in the nasopharynx and regional lymph nodes. Upon replication, viremia occurs for three to five days, spreading to the salivary glands. The parotid gland particularly susceptible to parotitis due to the lower rate of secretion. Salivary flow rate is reduced due to the inflammation response. Reduced saliva flow rate in the parotid gland leads to a reduction in the salivary defense proteins IgA (sIgA) and IgG, increasing vulnerability of the parotid gland to infection. Parotitis results from the inflammatory response to the presence of mumps virus in the parotid salivary gland. Bacterial parotitis is most commonly caused by staphylococcus aureus, a gram-positive coccal bacterium often found in the respiratory tract. Staphylococcus aureus infects the host through skin to skin or skin to surface contact with an infected individual or object.</s>
Chiggers do burrow into the skin but do not suck blood. It attaches to its host, injects digestive enzymes into the bite wound, and then sucks up the digested tissue. Warm, rainy days make these parasitic and predatory mites reproduce into large populations. Once the ground temperature is regularly above 60°F, the harvest mite lays eggs, and “chigger season” is underway. This season typically begins in April and ends in the early autumn/first “frost.” Chiggers do not like sunlight or humidity. During the wet season, chiggers are usually found in tall grass and other vegetation. During dry seasons, chiggers are most found underneath brush and shady areas.	What is the explanation for Chigger and its pathophysiology?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the explanation for Chigger and its pathophysiology? [/INST] \n Chiggers do burrow into the skin but do not suck blood. It attaches to its host, injects digestive enzymes into the bite wound, and then sucks up the digested tissue. Warm, rainy days make these parasitic and predatory mites reproduce into large populations. Once the ground temperature is regularly above 60°F, the harvest mite lays eggs, and “chigger season” is underway. This season typically begins in April and ends in the early autumn/first “frost.” Chiggers do not like sunlight or humidity. During the wet season, chiggers are usually found in tall grass and other vegetation. During dry seasons, chiggers are most found underneath brush and shady areas.</s>
Exanthem subitum; Sixth disease.	What information do you have about Roseola?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What information do you have about Roseola? [/INST] \n Exanthem subitum; Sixth disease.</s>
The incidence Eosinophilic esophagitis (EoE) is approximately 10 per 100,000 individuals worldwide. The prevalence of EoE is approximately 50-100 per 100,000 individuals worldwide. Patients of all age groups may develop EoE. It usually affects individuals of the white race. Males are more commonly affected by EoE than females. EoE is a rare disease that tends to affect people with a history of European ancestry.	Can you provide a summary of eosinophilic esophagitis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide a summary of eosinophilic esophagitis? [/INST] \n The incidence Eosinophilic esophagitis (EoE) is approximately 10 per 100,000 individuals worldwide. The prevalence of EoE is approximately 50-100 per 100,000 individuals worldwide. Patients of all age groups may develop EoE. It usually affects individuals of the white race. Males are more commonly affected by EoE than females. EoE is a rare disease that tends to affect people with a history of European ancestry.</s>
The most important risk factor in the development of peritoneal carcinomatosis include: Ovarian cancer Colon cancer Gastric cancer Pancreatic cancer	Could you provide the current phrasing of the sentence for me to rephrase it?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Could you provide the current phrasing of the sentence for me to rephrase it? [/INST] \n The most important risk factor in the development of peritoneal carcinomatosis include: Ovarian cancer Colon cancer Gastric cancer Pancreatic cancer</s>
The symptoms of the inherited condition manifest themselves at around four years old. The symptoms will often improve with age, although they may grow more severe again in old age. The acquired variant usually becomes evident during adulthood. The condition is not life-threatening; the impact on the patient, who has a mild case, is generally restricted to mild itching and the social impact of having skin with an unusual appearance. People afflicted with "mild" cases have symptoms which include " mosaic lines" or scaly patches on the shins, fine white scales on the forearms and rough palms. However, severe cases, although rare, do exist. Severe cases would entail the build up of scales everywhere, with areas of the body that have a concentration of sweat glands being least affected. Areas where the skin rubs against each other, such as the arm pits, the groin, and the "folded" areas of the elbow and knees, would also be less affected. When the build up of scales is bad, the person with a severe case would suffer from "prickly itch" when he or she needs to sweat but cannot as a result of the scales.	What is the meaning of ichthyosis vulgaris?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the meaning of ichthyosis vulgaris? [/INST] \n The symptoms of the inherited condition manifest themselves at around four years old. The symptoms will often improve with age, although they may grow more severe again in old age. The acquired variant usually becomes evident during adulthood. The condition is not life-threatening; the impact on the patient, who has a mild case, is generally restricted to mild itching and the social impact of having skin with an unusual appearance. People afflicted with "mild" cases have symptoms which include " mosaic lines" or scaly patches on the shins, fine white scales on the forearms and rough palms. However, severe cases, although rare, do exist. Severe cases would entail the build up of scales everywhere, with areas of the body that have a concentration of sweat glands being least affected. Areas where the skin rubs against each other, such as the arm pits, the groin, and the "folded" areas of the elbow and knees, would also be less affected. When the build up of scales is bad, the person with a severe case would suffer from "prickly itch" when he or she needs to sweat but cannot as a result of the scales.</s>
In patients with stable angina, beta blockers are used as a first line of therapy for both, symptomatic relief and the prevention of ischemic events. The physiologic mechanism of benefit of this therapy is a marked reduction in myocardial oxygen consumption by reducing the heart rate and myocardial contractility. Selective beta-1 blockers are preferred to non-selective beta-blockers due to fewer associated side effects. The most commonly used selective beta-1 blockers are metoprolol, atenolol, and bisoprolol.	In chronic cases, what is the prescribed treatment for stable angina using beta blockers?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: In chronic cases, what is the prescribed treatment for stable angina using beta blockers? [/INST] \n In patients with stable angina, beta blockers are used as a first line of therapy for both, symptomatic relief and the prevention of ischemic events. The physiologic mechanism of benefit of this therapy is a marked reduction in myocardial oxygen consumption by reducing the heart rate and myocardial contractility. Selective beta-1 blockers are preferred to non-selective beta-blockers due to fewer associated side effects. The most commonly used selective beta-1 blockers are metoprolol, atenolol, and bisoprolol.</s>
Nitric oxide The normal physiology of nitric oxide can be understood as follows: The endothelium (inner lining) of blood vessels use nitric oxide to signal the surrounding smooth muscle to relax, thus dilating the artery and increasing blood flow. This underlies the action of nitroglycerin, amyl nitrate, "poppers" (isobutyl nitrite or similar) and other nitrate derivatives in the treatment of heart disease: The compounds are converted to nitric oxide (by a process that is not completely understood), which in turn dilates the coronary artery (blood vessels around the heart), thereby increasing its blood supply. Nitric oxide also acts on cardiac muscle to decrease contractility and heart rate. The vasodilatory actions of nitric oxide play a key role in renal control of extracellular fluid homeostasis. Nitric oxide also plays a role in erection of the penis. Nitric oxide is also a second messenger in the nervous system and has been associated with neuronal activity and various functions like avoidance learning. Nitric oxide is synthesized by nitric oxide synthase (NOS). There are three isoforms of the NOS enzyme: endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) - each with separate functions. The neuronal enzyme (NOS-1) and the endothelial isoform (NOS-3) are calcium-dependent and produce low levels of gas as a cell-signaling molecule. The inducible isoform (NOS-2) is calcium-independent and produces large amounts of gas which can be cytotoxic. Nitric Oxide (NO) is of critical importance as a mediator of vasorelaxation in blood vessels. Platelet-derived factors, shear stress, angiotensin II, acetylcholine, and cytokines stimulate the production of NO by endothelial nitric oxide synthase (eNOS). eNOS synthesizes NO from the terminal guanidine-nitrogen of L-arginine and oxygen and yields citrulline as a byproduct. NO production by eNOS is dependent on calcium - calmodulin and other cofactors. NO, a highly reactive free radical then diffuses into the smooth muscle cells of the blood vessel and interacts with soluble guanylate cyclase. Nitric oxide stimulates the soluble guanylate cyclase to generate the second messenger cyclic GMP (3’,5’ guanosine monophosphate)from guanosine triphosphate (GTP). The soluble cGMP activates cyclic nucleotide-dependent protein kinase G (PKG or cGKI). PKG is a kinase that phosphorylates a number of proteins that regulate calcium concentrations, calcium sensitization, hyperpolarize cell through potassium channels, actin filament and myosin dynamic alterations that result in smooth muscle relaxation.(see smooth muscle article). . Angiogenesis The underlying mechanisms behind angiogenesis are beginning to be discovered. The process may begin with vasodilatation mediated by nitric oxide followed by an increase in permeability mediated by VEGF. This increased permeability allows for plasma protein extravasation and scaffold formation. Endothelial cell migration is supported by adhesion molecules such as PECAM-1 and cadherins. The vascular smooth muscle cells detaching and loosening signaled by Ang2 enables the migration and sprouting of endothelial cells. The process of angiogenesis is initiated by VEGF by Ang1 and is required to stabilize the endothelial networks and to increase periendothelial cell interactions. Platelet-derived growth factor (PDGF) stimulates inflammatory cells and promotes cell-cell interactions by molecules such as integrin. VEGF has morphogenic effects which allow endothelial cells cords to acquire and enlarge their lumen. Unfortunately, muscularization of the network is poorly understood. The process appears to be tissue-specific. In the coronary arteries, the epicardial layer appears to be the source of smooth muscle cells which migrate under PDGF-BB and VEGF stimulation. TGF-beta and downstream transcription factors Smads promote extracellular matrix production and solidify cell-cell interactions. FGF can help further this process resulting in arteriogenesis. In pathologic conditions such as ischemic myocardium, arteriogenesis can allow for as much as a 20-fold enlargement of collateral network vessels. Chemokines and cytokines are upregulated by increased collateral flow which results in monocyte recruitment. Monocytes produce proteinases which cause medial destruction and further remodeling. Hypoxia-inducible transcription factors (HIF), and their stabilization by peptide regulator 39 help induce and potentiate the neovascularization process. Newer imaging techniques utilize knowledge of molecular mechanisms to help enhance image resolution and improve sensitivity and specificity. Pulmonary microvascular dilation and angiogenesis are two central pathogenic features that drive abnormal pulmonary gas exchange in experimental hepatopulmonary syndrome, and thus might underlie hepatopulmonary syndrome in humans. Vasodilators The exact pathogenesis of the hepatopulmonary syndrome is not completely understood. It is thought that hepatopulmonary syndrome is the result of microscopic intrapulmonary arteriovenous dilatations due to either increased liver production or decreased liver clearance of vasodilators, possibly involving nitric oxide. The progression to hepatopulmonary syndrome is believed that involves the nitric oxide metabolism. The dilation of these blood vessels causes overperfusion relative to ventilation, leading to ventilation-perfusion mismatch and hypoxemi a. 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 hepatopulmonary syndrome 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 positio n 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. Angiogenesis As discussed below a variety of angiogenesis-related genes polymorphism has been linked to hepatopulmonary syndrome. An increased levels of endothelin-1 in cirrhotic patients have been correlated with intrapulmonary molecular and gas exchange abnormalities, hypothesizing a probable contribution to the pathogenesis of hepatopulmonary syndrome.	What is the underlying abnormal physiological condition that causes hepatopulmonary syndrome?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the underlying abnormal physiological condition that causes hepatopulmonary syndrome? [/INST] \n Nitric oxide The normal physiology of nitric oxide can be understood as follows: The endothelium (inner lining) of blood vessels use nitric oxide to signal the surrounding smooth muscle to relax, thus dilating the artery and increasing blood flow. This underlies the action of nitroglycerin, amyl nitrate, "poppers" (isobutyl nitrite or similar) and other nitrate derivatives in the treatment of heart disease: The compounds are converted to nitric oxide (by a process that is not completely understood), which in turn dilates the coronary artery (blood vessels around the heart), thereby increasing its blood supply. Nitric oxide also acts on cardiac muscle to decrease contractility and heart rate. The vasodilatory actions of nitric oxide play a key role in renal control of extracellular fluid homeostasis. Nitric oxide also plays a role in erection of the penis. Nitric oxide is also a second messenger in the nervous system and has been associated with neuronal activity and various functions like avoidance learning. Nitric oxide is synthesized by nitric oxide synthase (NOS). There are three isoforms of the NOS enzyme: endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) - each with separate functions. The neuronal enzyme (NOS-1) and the endothelial isoform (NOS-3) are calcium-dependent and produce low levels of gas as a cell-signaling molecule. The inducible isoform (NOS-2) is calcium-independent and produces large amounts of gas which can be cytotoxic. Nitric Oxide (NO) is of critical importance as a mediator of vasorelaxation in blood vessels. Platelet-derived factors, shear stress, angiotensin II, acetylcholine, and cytokines stimulate the production of NO by endothelial nitric oxide synthase (eNOS). eNOS synthesizes NO from the terminal guanidine-nitrogen of L-arginine and oxygen and yields citrulline as a byproduct. NO production by eNOS is dependent on calcium - calmodulin and other cofactors. NO, a highly reactive free radical then diffuses into the smooth muscle cells of the blood vessel and interacts with soluble guanylate cyclase. Nitric oxide stimulates the soluble guanylate cyclase to generate the second messenger cyclic GMP (3’,5’ guanosine monophosphate)from guanosine triphosphate (GTP). The soluble cGMP activates cyclic nucleotide-dependent protein kinase G (PKG or cGKI). PKG is a kinase that phosphorylates a number of proteins that regulate calcium concentrations, calcium sensitization, hyperpolarize cell through potassium channels, actin filament and myosin dynamic alterations that result in smooth muscle relaxation.(see smooth muscle article). . Angiogenesis The underlying mechanisms behind angiogenesis are beginning to be discovered. The process may begin with vasodilatation mediated by nitric oxide followed by an increase in permeability mediated by VEGF. This increased permeability allows for plasma protein extravasation and scaffold formation. Endothelial cell migration is supported by adhesion molecules such as PECAM-1 and cadherins. The vascular smooth muscle cells detaching and loosening signaled by Ang2 enables the migration and sprouting of endothelial cells. The process of angiogenesis is initiated by VEGF by Ang1 and is required to stabilize the endothelial networks and to increase periendothelial cell interactions. Platelet-derived growth factor (PDGF) stimulates inflammatory cells and promotes cell-cell interactions by molecules such as integrin. VEGF has morphogenic effects which allow endothelial cells cords to acquire and enlarge their lumen. Unfortunately, muscularization of the network is poorly understood. The process appears to be tissue-specific. In the coronary arteries, the epicardial layer appears to be the source of smooth muscle cells which migrate under PDGF-BB and VEGF stimulation. TGF-beta and downstream transcription factors Smads promote extracellular matrix production and solidify cell-cell interactions. FGF can help further this process resulting in arteriogenesis. In pathologic conditions such as ischemic myocardium, arteriogenesis can allow for as much as a 20-fold enlargement of collateral network vessels. Chemokines and cytokines are upregulated by increased collateral flow which results in monocyte recruitment. Monocytes produce proteinases which cause medial destruction and further remodeling. Hypoxia-inducible transcription factors (HIF), and their stabilization by peptide regulator 39 help induce and potentiate the neovascularization process. Newer imaging techniques utilize knowledge of molecular mechanisms to help enhance image resolution and improve sensitivity and specificity. Pulmonary microvascular dilation and angiogenesis are two central pathogenic features that drive abnormal pulmonary gas exchange in experimental hepatopulmonary syndrome, and thus might underlie hepatopulmonary syndrome in humans. Vasodilators The exact pathogenesis of the hepatopulmonary syndrome is not completely understood. It is thought that hepatopulmonary syndrome is the result of microscopic intrapulmonary arteriovenous dilatations due to either increased liver production or decreased liver clearance of vasodilators, possibly involving nitric oxide. The progression to hepatopulmonary syndrome is believed that involves the nitric oxide metabolism. The dilation of these blood vessels causes overperfusion relative to ventilation, leading to ventilation-perfusion mismatch and hypoxemi a. 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 hepatopulmonary syndrome 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 positio n 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. Angiogenesis As discussed below a variety of angiogenesis-related genes polymorphism has been linked to hepatopulmonary syndrome. An increased levels of endothelin-1 in cirrhotic patients have been correlated with intrapulmonary molecular and gas exchange abnormalities, hypothesizing a probable contribution to the pathogenesis of hepatopulmonary syndrome.</s>
Marburg hemorrhagic fever must be differentiated from other viral hemorrhagic fevers that may cause fever, abdominal pain,and bleeding such as Ebola, Crimean-Congo hemorrhagic fever (CCHF), Hantavirus Infection, Rift Valley fever, Lujo hemorrhagic fever and Lassa fever. SInce many of the signs and symptoms of marburg hemorrhagic fever are similar to those of other infectious diseases such as malaria or typhoid fever, leptospirosis, marburg hemorrhagic fever must also be differentiated from those infections.	Could you provide me with the given sentence so I can rephrase it for you?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Could you provide me with the given sentence so I can rephrase it for you? [/INST] \n Marburg hemorrhagic fever must be differentiated from other viral hemorrhagic fevers that may cause fever, abdominal pain,and bleeding such as Ebola, Crimean-Congo hemorrhagic fever (CCHF), Hantavirus Infection, Rift Valley fever, Lujo hemorrhagic fever and Lassa fever. SInce many of the signs and symptoms of marburg hemorrhagic fever are similar to those of other infectious diseases such as malaria or typhoid fever, leptospirosis, marburg hemorrhagic fever must also be differentiated from those infections.</s>
GERD can be classified based on the endoscopic appearance of the esophageal mucosa and the clinical presentation of the disease.	Could you provide me with the text that needs to be rephrased?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Could you provide me with the text that needs to be rephrased? [/INST] \n GERD can be classified based on the endoscopic appearance of the esophageal mucosa and the clinical presentation of the disease.</s>
Effective measures for the secondary prevention of ascites include: Water and sodium intake restriction Diuretic use Antibiotic prophylaxis for spontaneous bacterial peritonitis (SBP).	What does secondary prevention for Ascites entail?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does secondary prevention for Ascites entail? [/INST] \n Effective measures for the secondary prevention of ascites include: Water and sodium intake restriction Diuretic use Antibiotic prophylaxis for spontaneous bacterial peritonitis (SBP).</s>
In the circulatory system, a vein is a blood vessel that carries blood toward the heart. The majority of veins in the body carry low-oxygen blood from the tissues back to the heart; the exceptions being the pulmonary and umbilical veins which both carry oxygenated blood.	Could you please explain what Vein and Overview mean?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Could you please explain what Vein and Overview mean? [/INST] \n In the circulatory system, a vein is a blood vessel that carries blood toward the heart. The majority of veins in the body carry low-oxygen blood from the tissues back to the heart; the exceptions being the pulmonary and umbilical veins which both carry oxygenated blood.</s>
Cryptococci were first identified in 1894 by German pathologist Otto Busse in a patient with chronic periostitis of the tibia. He described the isolated organism as a " Saccharomyces -like" pathogen. The infection was referred to as "Busse-Buschke" disease named after Busse and his colleague, dermatologist Abraham Buschke. Busse later named the organism Saccharomyces hominis. During the same time period, Francesco Sanfelice reported isolating a similar organism from fermenting peach juice. Because of its unique colony form, he referred to the species as Saccharomyces neoformans. In 1901, Jean Paul Vuillemin, a French mycologist, transferred the yeast-like fungus to the genus Cryptococcus due to the absence of ascospores in its life cycle, a defining feature of Saccharomyces. In the 1950s, four capsule serotypes (A through D) were identified using rabbit antisera. This classification was later improved by DNA sequencing, epidemiology, and pathobiology. Until 1999, Cryptococcus gattii was known as Cryptococcus neoformans var gattii, until it was recognized as separate species with distinct epidemiological patterns and clinical manifestations.	What is the historical background or context of cryptococcosis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the historical background or context of cryptococcosis? [/INST] \n Cryptococci were first identified in 1894 by German pathologist Otto Busse in a patient with chronic periostitis of the tibia. He described the isolated organism as a " Saccharomyces -like" pathogen. The infection was referred to as "Busse-Buschke" disease named after Busse and his colleague, dermatologist Abraham Buschke. Busse later named the organism Saccharomyces hominis. During the same time period, Francesco Sanfelice reported isolating a similar organism from fermenting peach juice. Because of its unique colony form, he referred to the species as Saccharomyces neoformans. In 1901, Jean Paul Vuillemin, a French mycologist, transferred the yeast-like fungus to the genus Cryptococcus due to the absence of ascospores in its life cycle, a defining feature of Saccharomyces. In the 1950s, four capsule serotypes (A through D) were identified using rabbit antisera. This classification was later improved by DNA sequencing, epidemiology, and pathobiology. Until 1999, Cryptococcus gattii was known as Cryptococcus neoformans var gattii, until it was recognized as separate species with distinct epidemiological patterns and clinical manifestations.</s>
Current literature suggests that in patients with refractory chronic rhinosinusitis endoscopic sinus surgery(ESS) is superior to continued medical therapy in terms of symptom relief, quality of life and cost effectiveness with reported incremental cost effectiveness ratio (ICER) of five to thirteen thousand dollars per quality adjusted life year (QALY). Medical therapy mostly helps maintain the quality of life and health-state utility of the patients. Biologic therapies such as mepolizumab, omalizumab and dupilumab are recently introduced as alternative therapies for sever cases of chronic rhinosinusitis. To date, there has been insufficient evidence in the literature regarding their health care, social and economic cost effectiveness. It is suggested that use of biologic agents could prevent recurrence of the disease, and subsequently decrease the direct and indirect costs of the surgery. On the other hand the their high cost and need for multiple visits to the health care provider, should be considered. Thus, it is not easy to determine the cost-effectiveness of biologic agents in treatment of chronic rhinosinusitis and further prospective research with longer follow-up period is required.	How cost-effective is therapy for treating rhinosinusitis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: How cost-effective is therapy for treating rhinosinusitis? [/INST] \n Current literature suggests that in patients with refractory chronic rhinosinusitis endoscopic sinus surgery(ESS) is superior to continued medical therapy in terms of symptom relief, quality of life and cost effectiveness with reported incremental cost effectiveness ratio (ICER) of five to thirteen thousand dollars per quality adjusted life year (QALY). Medical therapy mostly helps maintain the quality of life and health-state utility of the patients. Biologic therapies such as mepolizumab, omalizumab and dupilumab are recently introduced as alternative therapies for sever cases of chronic rhinosinusitis. To date, there has been insufficient evidence in the literature regarding their health care, social and economic cost effectiveness. It is suggested that use of biologic agents could prevent recurrence of the disease, and subsequently decrease the direct and indirect costs of the surgery. On the other hand the their high cost and need for multiple visits to the health care provider, should be considered. Thus, it is not easy to determine the cost-effectiveness of biologic agents in treatment of chronic rhinosinusitis and further prospective research with longer follow-up period is required.</s>
Patient #1	What does the term unicornuate uterus mean?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does the term unicornuate uterus mean? [/INST] \n Patient #1</s>
There are no known secondary preventive measures of fungal meningitis.	What is the secondary prevention strategy for fungal meningitis?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the secondary prevention strategy for fungal meningitis? [/INST] \n There are no known secondary preventive measures of fungal meningitis.</s>
The prevalence of heart failure has been increasing due to the increase in the aging population, the early detection, preventive measures and improvement in the therapy. The prevalence of heart failure in the United States was estimated in 2006 to be 5.8 million people of all ages with an estimated incidence of 10/1000 for individuals older than 65 years of age.	Can you provide a description or summary of heart failure?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Can you provide a description or summary of heart failure? [/INST] \n The prevalence of heart failure has been increasing due to the increase in the aging population, the early detection, preventive measures and improvement in the therapy. The prevalence of heart failure in the United States was estimated in 2006 to be 5.8 million people of all ages with an estimated incidence of 10/1000 for individuals older than 65 years of age.</s>
† Criteria fulfilled for the past 3 months and symptom onset at least 6 months before diagnosis. American Gastroenterological Association, however have stopped using the term functional constipation because a subset these patients have slow colonic transit that has been associated with a marked reduction in colonic intrinsic nerves and interstitial cells of Cajal which is against the true definition of functional disorder.	What is the purpose of constipation?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the purpose of constipation? [/INST] \n † Criteria fulfilled for the past 3 months and symptom onset at least 6 months before diagnosis. American Gastroenterological Association, however have stopped using the term functional constipation because a subset these patients have slow colonic transit that has been associated with a marked reduction in colonic intrinsic nerves and interstitial cells of Cajal which is against the true definition of functional disorder.</s>
Iron deficiency anemia was discovered in 1852 by Karl Vierordt and his student H. Welcher. Over the next century, the details of iron regulation were elucidated.	What does iron deficiency anemia mean?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What does iron deficiency anemia mean? [/INST] \n Iron deficiency anemia was discovered in 1852 by Karl Vierordt and his student H. Welcher. Over the next century, the details of iron regulation were elucidated.</s>
Glycogen storage disease type 1 is diagnosed by identification of proband by either of the following: Molecular genetic testing Enzyme activity assay Molecular genetic testing shows: Biallelic pathogenic variants in G6PC for patients with GSD type 1a Biallelic pathogenic variants in SLC37A4 for patients with GSD type 1b Molecular genetic testing Genetic testing Analysis performed Serial single-gene testing First sequence analysis of G6PC is done Sequence analysis of SLC37A4 if no G6PC pathogenic variants identified Targeted analysis For G6PC pathogenic variant Ashkenazi Jewish ancestry p.Arg83Cys analysis For G6PD pathogenic variant Old Order Amish ancestry p.Gln347Ter analysis Multigene panel Multiple genes are sequenced at the same time including G6PC, SLC37A4 and other related genes when differential diagnosis is considered Comprehensive genomic testing Exome sequencing Considered if the diagnosis is not confirmed by serial single-gene testing and/or use of a multigene panel in an individual with features of GSD type I Genome sequencing Molecular genetic testing is preferred over enzyme activity assay due to: Relatively high sensitivity Need for liver biopsy for enzyme activity assay Enzyme activity assay is performed on frozen liver (ample of 15-20 mg) obtained by percutaneous or open liver biopsy. Transport should be done on dry ice via overnight delivery to the clinical diagnostic laboratory. Enzyme activity assay performed are: Glucose-6-phosphatase (G6Pase) catalytic activity Glucose-6-phosphate exchanger SLC37A4 (transporter) activity	What is the preferred diagnostic test for detecting Glycogen storage disease type I?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the preferred diagnostic test for detecting Glycogen storage disease type I? [/INST] \n Glycogen storage disease type 1 is diagnosed by identification of proband by either of the following: Molecular genetic testing Enzyme activity assay Molecular genetic testing shows: Biallelic pathogenic variants in G6PC for patients with GSD type 1a Biallelic pathogenic variants in SLC37A4 for patients with GSD type 1b Molecular genetic testing Genetic testing Analysis performed Serial single-gene testing First sequence analysis of G6PC is done Sequence analysis of SLC37A4 if no G6PC pathogenic variants identified Targeted analysis For G6PC pathogenic variant Ashkenazi Jewish ancestry p.Arg83Cys analysis For G6PD pathogenic variant Old Order Amish ancestry p.Gln347Ter analysis Multigene panel Multiple genes are sequenced at the same time including G6PC, SLC37A4 and other related genes when differential diagnosis is considered Comprehensive genomic testing Exome sequencing Considered if the diagnosis is not confirmed by serial single-gene testing and/or use of a multigene panel in an individual with features of GSD type I Genome sequencing Molecular genetic testing is preferred over enzyme activity assay due to: Relatively high sensitivity Need for liver biopsy for enzyme activity assay Enzyme activity assay is performed on frozen liver (ample of 15-20 mg) obtained by percutaneous or open liver biopsy. Transport should be done on dry ice via overnight delivery to the clinical diagnostic laboratory. Enzyme activity assay performed are: Glucose-6-phosphatase (G6Pase) catalytic activity Glucose-6-phosphate exchanger SLC37A4 (transporter) activity</s>
It has been reported (Heard & Ashworth 1968 apud Basrani et al. 2007) that, when placed in an aqueous solution, Chlorhexidine Gluconate (antiseptic) slowly hydrolyzes and forms para-chloroaniline (4-Chloroaniline, p-Chloroaniline or PCA). Para-chloroaniline (PCA) has been shown to be toxic. As an aromatic amine, the primary toxic effect is methemogloblin formation. Toxicological studies in rats and mice have shown that the hemopoietic system is the major target for PCA.	What is the historical context or background of Methemoglobinemia?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the historical context or background of Methemoglobinemia? [/INST] \n It has been reported (Heard & Ashworth 1968 apud Basrani et al. 2007) that, when placed in an aqueous solution, Chlorhexidine Gluconate (antiseptic) slowly hydrolyzes and forms para-chloroaniline (4-Chloroaniline, p-Chloroaniline or PCA). Para-chloroaniline (PCA) has been shown to be toxic. As an aromatic amine, the primary toxic effect is methemogloblin formation. Toxicological studies in rats and mice have shown that the hemopoietic system is the major target for PCA.</s>
Estriol (also oestriol) is one of the three main estrogens produced by the human body. It is only produced in significant amounts during pregnancy as it is made by the placenta. In pregnant women with multiple sclerosis (MS), estriol reduces the disease's symptoms noticeably, according to researchers at UCLA's Geffen Medical School. Levels of estriol in non-pregnant women do not change much after menopause, and levels are not significantly different from levels in men.	Could you provide an explanation and overview of Estriol, please?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: Could you provide an explanation and overview of Estriol, please? [/INST] \n Estriol (also oestriol) is one of the three main estrogens produced by the human body. It is only produced in significant amounts during pregnancy as it is made by the placenta. In pregnant women with multiple sclerosis (MS), estriol reduces the disease's symptoms noticeably, according to researchers at UCLA's Geffen Medical School. Levels of estriol in non-pregnant women do not change much after menopause, and levels are not significantly different from levels in men.</s>
Many cases of atrial fibrillation (AF) have no definite cause, it may be the result of various other problems. Nevertheless, thyroid function tests are required, especially for a first episode of atrial fibrillation (AF), when the ventricular rate is difficult to control, or when atrial fibrillation (AF) recurs unexpectedly after cardioversion. Renal function and electrolytes are routinely performed in patients suffering from atrial fibrillation. In addition, in acute-onset atrial fibrillation associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered.	What are the laboratory results that can be linked to atrial fibrillation?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What are the laboratory results that can be linked to atrial fibrillation? [/INST] \n Many cases of atrial fibrillation (AF) have no definite cause, it may be the result of various other problems. Nevertheless, thyroid function tests are required, especially for a first episode of atrial fibrillation (AF), when the ventricular rate is difficult to control, or when atrial fibrillation (AF) recurs unexpectedly after cardioversion. Renal function and electrolytes are routinely performed in patients suffering from atrial fibrillation. In addition, in acute-onset atrial fibrillation associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered.</s>
In juvenile myoclonic epilepsy, seizures usually involve the neck, shoulders, and upper arms. These seizures typically occur shortly after waking up. They normally begin between puberty and early adulthood. They can usually be controlled with medication, but it must be taken for life. In rare cases, myoclonic seizures can be symptomatic of Lennox-Gastaut syndrome, beginning in early childhood and usually involving the face, neck, shoulders, and upper arms. In these cases, the seizures tend to be strong and difficult to control.Progressive myoclonic epilepsy includes both myoclonic and tonic-clonic seizures. Treatment is not normally successful for any extended period of time.	What is the definition of myoclonus and how is it categorized?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is the definition of myoclonus and how is it categorized? [/INST] \n In juvenile myoclonic epilepsy, seizures usually involve the neck, shoulders, and upper arms. These seizures typically occur shortly after waking up. They normally begin between puberty and early adulthood. They can usually be controlled with medication, but it must be taken for life. In rare cases, myoclonic seizures can be symptomatic of Lennox-Gastaut syndrome, beginning in early childhood and usually involving the face, neck, shoulders, and upper arms. In these cases, the seizures tend to be strong and difficult to control.Progressive myoclonic epilepsy includes both myoclonic and tonic-clonic seizures. Treatment is not normally successful for any extended period of time.</s>
To determine whether your pains are osteochondritis dissecans, an MRI or X-Ray can be performed to show whether the loose piece of bone is still in place. In specific cases if caught early enough, a harmless dye will be injected into your blood stream to show where the calcium will most likely continue to build up. Doing this makes the removal process much easier..	What is osteochondritis, and how can it be diagnosed?	Answer the question truthfully, you are a medical professional.	<s>[INST] Answer the question truthfully, you are a medical professional. This is the question: What is osteochondritis, and how can it be diagnosed? [/INST] \n To determine whether your pains are osteochondritis dissecans, an MRI or X-Ray can be performed to show whether the loose piece of bone is still in place. In specific cases if caught early enough, a harmless dye will be injected into your blood stream to show where the calcium will most likely continue to build up. Doing this makes the removal process much easier..</s>