Persius/hicric huggingface dataset:
Bradley method of natural childbirth

# Background
The Bradley Method of natural childbirth (also known as "husband-coached childbirth") is a method of natural childbirth created by Dr. Robert A. Bradley (1917-1998) and popularized by his book Husband-Coached Childbirth. Teachers of the Bradley Method believe that with adequate preparation and education along with help from a loving, supportive coach, most women can give birth naturally - without drugs or surgery. The Bradley Method emphasizes measures that can be taken to stay healthy and low-risk to help avoid complications that may lead to medical intervention.
The primary goal of the Bradley Method is healthy mothers and healthy babies. The method holds that in most circumstances, a natural childbirth (drug free) is the best way to achieve that goal. Over 86% of Bradley moms having vaginal births do so without drugs. The classes teach nutrition,  relaxation and natural breathing as pain management techniques, and active participation of the husband as coach. Parents-to-be are taught to be consumers of birth services and to take responsibility to make informed decisions regarding procedures, attendants and the birth place.
Dr. Bradley developed his method during the era of what he referred to as "knock-em-out, drag-em-out obstetrics," when "twilight sleep" and general anesthesia were common in hospital deliveries. Having been raised on a farm and having witnessed many animal births as a part of farm life, Dr. Bradley believed that human women, like the animals he had observed growing up, could give birth without drugs. Based on observations of perspiring mammals during labor and birth, he developed a childbirth method to teach human women to do the things that animal mothers do instinctively. Soon after starting to implement his new childbirth method with pregnant nurses as a trial, Dr. Bradley began to believe that the presence and support of the father during labor and birth was important to the mother's success in achieving a natural birth. He became a pioneer in including fathers in the birth process and eventually expanded his childbirth method to include extensive instruction of the father as labor coach.
Bradley Method instructors are certified by the American Academy of Husband-Coached Childbirth (AAHCC). The terms "Husband-Coached Childbirth" and "The Bradley Method" have been registered in order to protect the consumer, ensuring that only those currently certified by the AAHCC can teach the Bradley Method.
Breast Cancer historical perspective

# Overview

# Historical Perspective

## Discovery
- There is limited information about the historical perspective of .
OR
-  was first discovered by , a , in /during/following .
- The association between  and  was made in/during .
- In ,  was the first to discover the association between  and the development of .
- In ,  mutations were first implicated in the pathogenesis of .

## Landmark Events in the Development of Treatment Strategies

## Impact on Cultural History

## Famous Cases
The following are a few famous cases of :
Butyrophilin, subfamily 1, member A1
Butyrophilin subfamily 1 member A1 is a protein that in humans is encoded by the BTN1A1 gene.
Butyrophilin (BTN) is the major protein associated with fat droplets in the milk. It is a member of the immunoglobulin superfamily. It may have a cell surface receptor function. The human butyrophilin gene is localized in the major histocompatibility complex (MHC) class I region of 6p and may have arisen relatively recently in evolution by the shuffling of exons between 2 ancestral gene families

# Function
Btn1a1 regulates the amount of lipids and size of droplets expressed in milk.  When the gene is compromised in laboratory mice, approximately half the pups died within the first 20 days and the remainder were significantly under-weight.

# Link to multiple sclerosis
Butyrophilin has been presented as a potential antigen which may be similar enough to myelin oligodendrocyte glycoprotein (MOG) to spur the immune system to attack myelin in a process known as molecular or epitopic mimicry.  This suggests that ingestion of butyrophilin in dairy products from cows and goats may be a potential trigger for multiple sclerosis. Independent studies by a group in Germany have reached similar conclusions.
The German group have used heavy doses of butyrophilin on mice with an experimental model for multiple sclerosis called EAE. They have found that this strategy, called immune tolerance, reduces the effects of the disease.
Muscarinic acetylcholine receptor M5
The human muscarinic acetylcholine receptor M5, encoded by the CHRM5 gene, is a member of the G protein-coupled receptor superfamily of integral membrane proteins. It is coupled to Gq protein. Binding of the endogenous ligand acetylcholine to the M5 receptor triggers a number of cellular responses such as adenylate cyclase inhibition, phosphoinositide degradation, and potassium channel modulation. Muscarinic receptors mediate many of the effects of acetylcholine in the central and peripheral nervous system. The clinical implications of this receptor have not been fully explored; however, stimulation of this receptor is known to effectively decrease cyclic AMP levels and downregulate the activity of protein kinase A (PKA).

# Ligands
No highly selective agonists or antagonists for the M5 receptor have been discovered as of 2018, but several non-selective muscarinic agonists and antagonists have significant affinity for M5.
The lack of selective M5 receptor ligands is one of the main reasons that the medical community has such a limited understanding of the M5 receptors effects as the possibility that any and/or all effects of non-selective ligands may be due to interactions with other receptors can not be ruled out. Some data may be obtained by observing which effects are common among semi-selective ligands (ex. a ligand of M1 and M5, a ligand of M2 and M5, and a ligand of M3 and M5), but until both a selective agonist and a selective antagonist of the M5 receptor are developed this data must be considered merely theoretical.

## Agonists
- Milameline ((E)-1,2,5,6-Tetrahydro-1-methyl-3-pyridinecarboxaldehyde-O-methyloxime, CAS# 139886-32-1)
- Sabcomeline

## Positive allosteric modulators
- ML-380
- ML-326
- VU-0238429: EC50 = 1.16 M; >30-fold selectivity versus M1 and M3, inactive at M2 and M4.

## Negative allosteric modulators
- ML375

## Antagonists
- VU-0488130 (ML381)
- Xanomeline
Cefadroxil dosage and administration

# Dosage and Administration
DURICEF is acid-stable and may be administered orally without regard to meals. Administration with food may be helpful in diminishing potential gastrointestinal complaints occasionally associated with oral cephalosporin therapy.

## Adults
Urinary Tract Infections: For uncomplicated lower urinary tract infections (i.e., cystitis) the usual dosage is 1 or 2 g per day in a single (q.d.) or divided doses (b.i.d.).
For all other urinary tract infections the usual dosage is 2 g per day in divided doses (b.i.d.).
Skin and Skin Structure Infections: For skin and skin structure infections the usual dosage is 1 g per day in single (q.d.) or divided doses (b.i.d.).
Pharyngitis and Tonsillitis: Treatment of group A beta-hemolytic streptococcal pharyngitis and tonsillitis1 g per day in single (q.d.) or divided doses (b.i.d.) for 10 days.

## Children
For urinary tract infections, the recommended daily dosage for children is 30 mg/kg/day in divided doses every 12 hours. For pharyngitis, tonsillitis, and impetigo, the recommended daily dosage for children is 30 mg/kg/day in a single dose or in equally divided doses every 12 hours. For other skin and skin structure infections, the recommended daily dosage is 30 mg/kg/day in equally divided doses every 12 hours. In the treatment of beta-hemolytic streptococcal infections, a therapeutic dosage of DURICEF should be administered for at least 10 days.
See chart for total daily dosage for children.

## Renal Impairment
In patients with renal impairment, the dosage of cefadroxil monohydrate should be adjusted according to creatinine clearance rates to prevent drug accumulation. The following schedule is suggested. In adults, the initial dose is 1000 mg of DURICEF and the maintenance dose (based on the creatinine clearance rate ) is 500 mg at the time intervals listed below.
Patients with creatinine clearance rates over 50 mL/min may be treated as if they were patients having normal renal function.
Ceftibuten dosage and administration
The recommended doses of CEDAX Oral Suspension are presented in the table below. CEDAX Oral Suspension must be administered at least 2 hours before or 1 hour after a meal.
Pediatric patients weighing more than 45 kg should receive the maximum daily dose of 400 mg.

# Renal Impairment
CEDAX Capsules and CEDAX Oral Suspension may be administered at normal doses in the presence of impaired renal function with creatinine clearance of 50 mL/min or greater. The recommendations for dosing in patients with varying degrees of renal insufficiency are presented in the following table.
Hemodialysis Patients
In patients undergoing hemodialysis two or three times weekly, a single 400-mg dose of ceftibuten capsules or a single dose of 9 mg/kg (maximum of 400 mg of ceftibuten) oral suspension may be administered at the end of each hemodialysis session.
Directions for Mixing CEDAX Oral Suspension
After mixing, the suspension may be kept for 14 days and must be stored in the refrigerator. Keep tightly closed. Shake well before each use. Discard any unused portion after 14 days.
Cephalexin dosage and administration
Cephalexin is administered orally.

# Adults
The adult dosage ranges from 1 to 4 g daily in divided doses. The 333 mg and 750 mg strengths should be administered such that the daily dose is within 1 to 4 grams per day. The usual adult dose is 250 mg every 6 hours. For the following infections, a dosage of 500 mg may be administered every 12 hours: streptococcal pharyngitis, skin and skin structure infections, and uncomplicated cystitis in patients over 15 years of age. Cystitis therapy should be continued for 7 to 14 days. For more severe infections or those caused by less susceptible organisms, larger doses may be needed. If daily doses of cephalexin greater than 4 g are required, parenteral cephalosporins, in appropriate doses, should be considered.

# Pediatric Patients
The usual recommended daily dosage for pediatric patients is 25 to 50 mg/kg in divided doses. For streptococcal pharyngitis in patients over 1 year of age and for skin and skin structure infections, the total daily dose may be divided and administered every 12 hours.
In severe infections, the dosage may be doubled.
In the therapy of otitis media, clinical studies have shown that a dosage of 75 to 100 mg/kg/day in 4 divided doses is required.
In the treatment of -hemolytic streptococcal infections, a therapeutic dosage of cephalexin should be administered for at least 10 days.
Directions for Mixing
125 mg per 5 mL (100 mL when mixed): Prepare suspension at time of dispensing. Add to the bottle a total of 71 mL of water. For ease in preparation, tap bottle to loosen powder, add the water in 2 portions, shaking well after each addition. The resulting suspension will contain cephalexin monohydrate equivalent to 125 mg cephalexin in each 5 mL (teaspoonful).
125 mg per 5 mL (200 mL when mixed): Prepare suspension at time of dispensing. Add to the bottle a total of 140 mL of water. For ease in preparation, tap bottle to loosen powder, add the water in 2 portions, shaking well after each addition. The resulting suspension will contain cephalexin monohydrate equivalent to 125 mg cephalexin in each 5 mL (teaspoonful).
250 mg per 5 mL (100 mL when mixed): Prepare suspension at time of dispensing. Add to the bottle a total of 71 mL of water. For ease in preparation, tap bottle to loosen powder, add the water in 2 portions, shaking well after each addition. The resulting suspension will contain cephalexin monohydrate equivalent to 250 mg cephalexin in each 5 mL (teaspoonful).
250 mg per 5 mL (200 mL when mixed): Prepare suspension at time of dispensing. Add to the bottle a total of 140 mL of water. For ease in preparation, tap bottle to loosen powder, add the water in 2 portions, shaking well after each addition. The resulting suspension will contain cephalexin monohydrate equivalent to 250 mg cephalexin in each 5 mL (teaspoonful).
- After mixing, store in refrigerator. May be kept for 14 days without significant loss of potency.
Ciliary neurotrophic factor receptor
The ciliary neurotrophic factor receptor, also known as CNTFR, binds the ciliary neurotrophic factor.  This receptor and its cognate ligand support the survival of neurons.  This receptor is most closely related to the interleukin-6 receptor.   This receptor possesses an unusual attachment to the cell membrane through a glycophosphatidylinositol linkage.

# Model organisms
Model organisms have been used in the study of CNTFR function. A conditional knockout mouse line, called Cntfrtm1a(EUCOMM)Wtsi was generated as part of the International Knockout Mouse Consortium program  a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Twenty five tests were carried out on mutant mice and one significant abnormality was observed: no homozygous mutant animals were observed at weaning. The remaining tests were therefore carried out on adult heterozygous mutant animals, but no further abnormalities were seen.
Cloxacillin Sodium drug interactions

# Drug Interactions
Tetracycline, a bacteriostatic antibiotic, may antagonize the bactericidal effect of penicillin and concurrent use of these drugs should be avoided.
Probenecid administered concomitantly with penicillins increases and prolongs serum penicillin levels (see DOSAGE AND ADMINISTRATION).
Penicillinase-resistant penicillins, like other penicillins, are physically and/or chemically incompatible with aminoglycosides and can inactivate the drugs in vitro. In vitro mixing of penicillins and aminoglycosides should be avoided during concomitant therapy and the drugs should be administered separately. Penicillins can inactivate aminoglycosides in vitro in serum samples from patients receiving both drugs, which could produce falsely decreased results in serum aminoglycoside assays of the serum samples.
Dicloxacillin may reduce the anticoagulant response to dicumarol and warfarin. Careful monitoring of prothrombin times is suggested during concomitant therapy, and dosage of the anticoagulant should be adjusted as required. The mechanism of this possible interaction is unclear, but may be due to hepatic enzyme induction.
Colony stimulating factor 1 receptor
Colony stimulating factor 1 receptor (CSF1R), also known as macrophage colony-stimulating factor receptor (M-CSFR), and CD115 (Cluster of Differentiation 115), is a cell-surface protein encoded, in humans, by the CSF1R gene (known also as c-FMS). It is a receptor for a cytokine called colony stimulating factor 1.

# Genomics
The gene is located on long arm of chromosome 5 (5q32) on the Crick (minus) strand. It is 60.002 kilobases in length. The encoded protein has 972 amino acids and a predicted molecular weight of 107.984 kiloDaltons. The first intron of the CSF1R gene contains a transcriptionally inactive ribosomal protein L7 processed pseudogene, oriented in the opposite direction to the CSF1R gene.

# Function
The encoded protein is a single pass type I membrane protein and acts as the receptor for colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of macrophages. This receptor mediates most, if not all, of the biological effects of this cytokine. Ligand binding activates CSF1R through a process of oligomerization and trans-phosphorylation. The encoded protein is a tyrosine kinase transmembrane receptor and member of the CSF1/PDGF receptor family of tyrosine-protein kinases.

# Clinical significance
Increased levels of CSF1R1 are found in microglia in Alzheimer's disease and after brain injuries. The increased receptor expression causes microglia to become more active. Both CSF1R, and its ligand colony stimulating factor 1 play an important role in the development of the mammary gland and may be involved in the process of mammary gland carcinogenesis.
Mutations in CSF1R are associated with chronic myelomonocytic leukemia and type M4 acute myeloblastic leukemia.
Mutations in the tyrosine kinase domain have been associated with hereditary diffuse leukoencephalopathy with spheroids.

## As a drug target
Because CSF1R is overexpressed in many cancers and on tumor-associated macrophages (TAM), CSF1R inhibitors (and CSF1 inhibitors) have been studied for many years as a possible treatment for cancer or inflammatory diseases.  As of  2017 CSF1R inhibitors in clinical trials include : Pexidartinib, PLX7486, ARRY-382, JNJ-40346527, BLZ945, Emactuzumab, AMG820, IMC-CS4. (PD-0360324 and MCS110 are CSF1 inhibitors)
Another CSF1R inhibitor that targets/depletes TAMs is Cabiralizumab (cabira; FPA-008) which is a monoclonal antibody and is in early clinical trials for metastatic pancreatic cancer.

# Interactions
Colony stimulating factor 1 receptor has been shown to interact with:
- Cbl gene,
- FYN,
- Grb2,
- Suppressor of cytokine signaling 1, This receptor is also linked with the cells of MPS.
Congenital lacrimal duct obstruction
Congenital nasolacrimal duct obstruction (CLDO) is literally a tear duct that has failed to open at the time of birth. Around 6% of infants have CLDO, usually experiencing a persistent watery eye even when not crying.  If a secondary infection occurs, purulent (yellow / green) discharge may be present.
Most cases resolve spontaneously, with antibiotics reserved only if conjunctivitis occurs. Lacrimal sac massage has been proposed as helping to open the duct, though this is not always successful.  The aim of massage is to generate enough hydrostatic pressure (downward, toward the nose) to "pop" open any obstruction.  Additional massage may then be performed up toward the lacrimal punctum, in order to express any infectious material out of the nasolacrimal sac.  When discharge or crusting is present, the lids should be gently cleaned using cooled pre-boiled water or saline.
Referral to an ophthalmologist is indicated if symptoms are still present at 12 months, or sooner if significant symptoms or recurrent infections occur.  Nasolacrimal duct probing may be performed in the office setting (usually from 4 to 8 months of age) or under general anesthesia in an operating room for older patients.  The success rate of probing is higher for younger children.  A silastic tube or stent may be employed along with probing to maintain tear duct patency .
Greig cephalopolysyndactyly syndrome

# Overview
Greig cephalopolysyndactyly syndrome is a disorder that affects development of the limbs, head, and face. The features of this syndrome are highly variable, ranging from very mild to severe. People with this condition typically have one or more extra fingers or toes (polydactyly) or an abnormally wide thumb or big toe (hallux).

# Historical Perspective
The condition is named for David Middleton Greig.

# Pathophysiology
Greig cephalopolysyndactyly syndrome is a chromosomal condition related to chromosome 7. Mutations in the GLI3 gene cause Greig cephalopolysyndactyly syndrome. The GLI3 gene provides instructions for making a protein that controls gene expression, which is a process that regulates whether genes are turned on or off in particular cells. By interacting with certain genes at specific times during development, the GLI3 protein plays a role in the normal shaping (patterning) of many organs and tissues before birth.
Different genetic changes involving the Gli3 gene can cause Greig cephalopolysyndactyly syndrome. In some cases, the condition results from a chromosomal abnormality, such as a large deletion or translocation of genetic material, in the region of chromosome 7 that contains the GLI3 gene. In other cases, a mutation in the GLI3 gene itself is responsible for the disorder. Each of these genetic changes prevents one copy of the gene in each cell from producing any functional protein. It remains unclear how a reduced amount of this protein disrupts early development and causes the characteristic features of Greig cephalopolysyndactyly syndrome.
This condition is inherited in an autosomal dominant pattern, which means the defective gene is located on an autosome, and only one copy of the defective GLI3 gene is sufficient to cause the disorder. In cases of dominant inheritance, an affected person inherits the genetic mutation or chromosomal abnormality from one affected parent.
Rare instances of this disorder are sporadic, and occur in people with no history of the condition in their family.

# Diagnosis

## Symptoms
Rarely, affected individuals may have more serious medical problems including seizures, mental retardation, and developmental delay.

## Physical Examination
The skin between the fingers and toes may be fused (cutaneous syndactyly). This disorder is also characterized by widely spaced eyes (ocular hypertelorism), an abnormally large head size (macrocephaly), and a high prominent forehead.
Cyclin-dependent kinase inhibitor 1C
Cyclin-dependent kinase inhibitor 1C (p57, Kip2), also known as CDKN1C, is a protein which in humans is encoded by the CDKN1C  imprinted gene.

# Function
Cyclin-dependent kinase inhibitor 1C is a tight-binding inhibitor of several G1 cyclin/Cdk complexes and a negative regulator of cell proliferation.  Mutations of CDKN1C are implicated in sporadic cancers and Beckwith-Wiedemann syndrome suggesting that it is a tumor suppressor candidate.
CDKN1C is a tumor suppressor human gene on chromosome 11 (11p15) and belongs to the cip/kip gene family. It encodes a cell cycle inhibitor that binds to G1 cyclin-CDK complexes. Thus p57KIP2 causes arrest of the cell cycle in G1 phase.

# Clinical significance
A mutation of this gene may lead to loss of control over the cell cycle leading to uncontrolled cellular proliferation. p57KIP2 has been associated with Beckwith-Wiedemann syndrome (BWS) which is characterized by increased risk of tumor formation in childhood. Loss-of-function mutations in this gene have also been shown associated to the IMAGe syndrome (Intrauterine growth restriction, Metaphyseal dysplasia, Adrenal hypoplasia congenita, and Genital anomalies).  Complete hydatidiform moles consist only of paternal DNA, and thus the cells lack p57 expression as the gene is paternally imprinted (silenced). Immuohistochemical stains for p57 can aid with the diagnosis of hydatidiform moles 

# Interactions
Cyclin-dependent kinase inhibitor 1C has been shown to interact with:
- LIMK1,
- MYBL2,
- MyoD,  and
- PCNA.
Cycloserine warnings and precautions

# Warnings
Administration of Seromycin should be discontinued or the dosage reduced if the patient develops allergic dermatitis or symptoms of CNS toxicity, such as convulsions, psychosis, somnolence, depression, confusion, hyperreflexia, headache, tremor, vertigo, paresis, or dysarthria.
The toxicity of Seromycin is closely related to excessive blood levels (above 30 g/mL), as determined by high dosage or inadequate renal clearance. The ratio of toxic dose to effective dose in tuberculosis is small.
The risk of convulsions is increased in chronic alcoholics.
Patients should be monitored by hematologic, renal excretion, blood level, and liver function studies.