Persius/hicric huggingface dataset:
Persistent mullerian duct syndrome
Persistent mullerian duct syndrome (PMDS) refers to the presence of a uterus and sometimes other mullerian duct derivatives in a male. Typical features include undescended testes (cryptorchidism) and the presence of a small, underdeveloped uterus in a male infant or adult. This condition is usually caused by deficiency of fetal anti-mullerian hormone (AMH) effect due to mutations of the gene for AMH or the anti-Mullerian hormone receptor.

# Presentation
Because both the wolffian ducts and mullerian ducts begin to develop, the tissues are often intertwined, resulting in obstruction or nonpatency of the vas deferens or other parts of the male excretory ducts. This can result in infertility, the most serious potential problem caused by this condition.
Cryptorchidism in AMH deficiency suggests that AMH may play a role in transabdominal testicular descent, perhaps by facilitating contraction of the gubernaculum.
Other mullerian derivatives which may be present in at least a rudimentary form are the cervix, upper part of the vagina, and fallopian tubes.
The condition can come to attention because of a bulge in the inguinal canal of a male infant due to herniation of the uterus. The presence of a uterus may be noticed if an ultrasound or MRI of the pelvis is performed to locate the testes or for other reasons. Occasionally the uterus is discovered during abdominal surgery for some other purpose in later childhood or adult life.
Although persistent mullerian duct syndrome is classified as an intersex condition, it does not involve ambiguity or malformation of the external genitalia.

# Treatment
Surgery (orchiopexy) to retrieve the testes and position them in the scrotum is the primary treatment. Occasionally they are unsalvageable if located high in the retroperitoneum. During this surgery, the uterus is usually removed and attempts made to dissect away mullerian tissue from the vas deferens and epididymis for the purpose of improving the chance of fertility. Testosterone replacement will be necessary at puberty if the testes cannot be rescued.

# Molecular genetics and inheritance
PMDS type I results from mutations of the gene (AMH) for AMH on chromosome 19p3.3. 
PMDS type II results from mutations of the gene (AMH-RII) for the AMH receptor on 12q13. 
Both types of disorders are inherited as autosomal recessive conditions with expression limited to males (as females with AMH deficiency have no identified problems).
Pineocytoma Differential diagnosis

# Overview
 must be differentiated from other diseases that cause , , and , such as , , and .
OR
 must be differentiated from , , and .

# Differentiating Pineocytoma from other Diseases
Pineocytoma must be differentiated from:
- Pineal parenchymal tumor with intermediate differentiation
- Papillary tumor of the pineal region
- Pineoblastoma
- Pineal germinoma
- Pineal embryonal carcinoma
- Pineal choriocarcinoma
- Pineal yolk sac carcinoma (endodermal sinus tumor)
- Pineal teratoma
- Pineal cyst
- Astrocytoma of the pineal gland
- Meningioma near pineal gland
- Pineal metastasis
- Cavernoma in pineal region
- Aneurysm in pineal region
For differentiating pineal gland tumors from other cranial tumors click here
For differentiating among different types of pineal gland tumors click here

# Differentiating  from other Diseases
 must be differentiated from other diseases that cause , , and , such as , , and .
OR
 must be differentiated from , , and .
OR
As  manifests in a variety of clinical forms, differentiation must be established in accordance with the particular subtype.  must be differentiated from other diseases that cause , such as  and . In contrast,  must be differentiated from other diseases that cause , such as  and .

## Differentiating  from other diseases on the basis of , , and 
On the basis , , and ,  must be differentiated from , , , , , and .
Pineocytoma 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 :
Plantaris muscle or tendon rupture
Contributors:  Cafer Zorkun M.D., PhD.
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# Overview
Plantaris muscle or tendon rupture or "tennis leg" is rare but requires acute medical attention. The plantaris muscle is a rudimentary muscle located in the superficial posterior compartment of the leg and varies in its size and development.

# Symptoms
- Calf pain
- Calf tenderness
- Exercise induced foot pain
- Foot pain
- Heel pain
- Leg pain
- Lower extremity pains
- Midfoot pain
- Pain in plantar area

# Differential Diagnosis
- Plantar fasciitis
- Tarsal tunnel syndrome

# Diagnostic Findings
Images courtesy of RadsWiki
- MRI: Plantaris tendon rupture
- MRI: Plantaris tendon rupture
- MRI: Plantaris tendon rupture
- MRI: Plantaris tendon rupture
- MRI: Plantaris tendon rupture
- MRI: Plantaris tendon rupture
- MRI: Plantaris tendon rupture
Posaconazole indications and usage

# Indications And Usage

## Prophylaxis of Invasive Aspergillus and Candida Infections
Noxafil delayed-release tablets and oral suspension are indicated for:
- Prophylaxis of invasive Aspergillus
- Prophylaxis of Candida infections
in patients with
- 13 years of age and older
- High risk of developing these infections
- Severely immunocompromised, such as hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD) or those with hematologic malignancies with prolonged neutropenia from chemotherapy.

## Treatment of Oropharyngeal Candidiasis Including Oropharyngeal Candidiasis Refractory to Itraconazole and/or Fluconazole
Noxafil oral suspension is indicated for the treatment of oropharyngeal candidiasis, including oropharyngeal candidiasis refractory to itraconazole and/or fluconazole.
Posterior superior alveolar artery
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# Overview
The posterior superior alveolar artery (posterior dental artery) is given off from the internal maxillary, frequently in conjunction with the infraorbital just as the trunk of the vessel is passing into the pterygopalatine fossa.
Descending upon the tuberosity of the maxilla, it divides into numerous branches, some of which enter the alveolar canals, to supply the molar and premolar teeth and the lining of the maxillary sinus, while others are continued forward on the alveolar process to supply the gums.
Praziquantel clinical pharmacology

# Clinical Pharmacology
Praziquantel induces a rapid contraction of schistosomes by a specific effect on the permeability of the cell membrane. The drug further causes vacuolization and disintegration of the schistosome tegument.
After oral administration BILTRICIDE is rapidly absorbed (80%), subjected to a first pass effect, metabolized and eliminated by the kidneys. Maximal serum concentration is achieved 1-3 hours after dosing. The half-life of praziquantel in serum is 0.8-1.5 hours.

### Special Populations
The pharmacokinetics of praziquantel were studied in 40 patients with Schistosoma mansoni infections with varying degrees of hepatic dysfunction (See table1). In patients with schistosomiasis, the pharmacokinetic parameters did not differ significantly between those with normal hepatic function (Group 1) and those with mild (Child-Pugh class A) hepatic impairment. However, in patients with moderate-to-severe hepatic dysfunction (Child-Pugh class B and C), praziquantel half-life, Cmax, and AUC increased progressively with the degree of hepatic impairment. In Child-Pugh class B, the increases in mean half-life, Cmax, and AUC relative to Group 1 were 1.58-fold, 1.76-fold, and 3.55-fold, respectively. The corresponding increases in Child-Pugh class C patients were 2.82-fold, 4.29-fold, and 15-fold for half-life, Cmax, and AUC.
Precursor B lymphoblastic leukemia
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# Overview
Precursor T acute lymphoblastic leukemia/lymphoma is a form of lymphoid leukemia.
It consists of the following subtypes:
- t(9;22)-BCR/ ABL
- t(v;11q23)-MLL rearrangement
- t(1;19)-E2A/PBX1
- t(12;21)-ETV/ CBF
Preparation of the patient for PCI

# Overview
There are several steps involved in preparing patients for PCI, which include the use of premedications and the use of a Heart Team approach. Attention should be given to possible adverse reactions to contrast, possible anaphylactoid reactions, use of statins, bleeding risk in patients, and the presence of on-site surgical backup services.

# Preparation of the Patient for PCI

## Premedications
- Aspirin
- Clopidogrel

# 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization.  GENERAL PROCEDURAL ISSUES FOR PCI (Please do not edit)

## Radial and Femoral Approaches for PCI

##  Choice of Stent Type

## Use of Intravascular Imaging

## Thrombectomy

## Treatment of Calcified Lesions

## Treatment of Saphenous Vein Graft (SVG) Disease (Previous CABG)

## Treatment of CTO

## Treatment of Patients With Stent RestenosisRecommendations

## Hemodynamic Support for Complex PCI

# 2011 and 2005 ACCF/AHA/SCAI Guidelines for Percutaneous Coronary Intervention (DO NOT EDIT)

## Heart Team Approach to Revascularization Decisions (DO NOT EDIT)

## Contrast-Induced Acute Kidney Injury (DO NOT EDIT)

## Anaphylactoid Reactions (DO NOT EDIT)

## Statin Treatment (DO NOT EDIT)

## Bleeding Risk (DO NOT EDIT)

## PCI in Hospitals Without On-Site Surgical Backup (DO NOT EDIT)

## Role of Onsite Cardiac Surgical Back-Up (DO NOT EDIT)

# ACA 2021 Revascularization Guideline

## Thrombectomy
- Routine rheolytic thrombectomy did not show any benefit based on trials done on patients with ST elevation myocardial infarction undergoing primary PCI even in the presence of thrombotic occlusion.
Psychogenic non-epileptic seizures
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Psychogenic non-epileptic seizures are a manifestation or a form of conversion disorder.  They take many forms, and particularly can mimic any sort of epileptic seizure; they are distinguished from epilepsy only in that they are not associated with abnormal, rhythmic discharges of cortical neurons. The condition is not benign; people have broken bones, crashed automobiles, bitten off parts of their tongue, and even died from injuries sustained during non-epileptic seizures.
An older term for these, pseudoseizures, should not be used.  While it is correct that a non-epileptic seizure may resemble an epileptic seizure, pseudo can also connote "false, fraudulent, or pretending to be something that it is not."  Non-epileptic seizures are not false, fraudulent, or produced under any sort of pretense.

# Misdiagnosis
Confounding neurologists and other physicians, psychogenic non-epileptic seizures are frequently misdiagnosed as epilepsy; less frequently, the reverse is true.  Misdiagnosis means that appropriate treatments are not received by the patient.  In addition, the former misdiagnosis is dangerous because it can result in administration of unnecessary (and even potentially harmful) medication; the latter because a person with epilepsy is not correctly treated with medication that could help them.  Statistics on the prevalence of these misdiagnoses are not available.
Inpatient hospitalization for long term video-EEG monitoring is a costly but effective way to distinguish them from epileptic seizures.  They tend not to respond to anticonvulsant medications. Also, many persons with epilepsy experience non-epileptic seizures as well; finding evidence of one does not rule out the presence of the other.
Many physicians measure serum prolactin levels in patients who may have non-epileptic seizures, because serum levels of prolactin are often elevated just following an epileptic seizure, returning to normal within 15 minutes. Still, a negative prolactin does not rule out epileptic seizures (Ahmad & Beckett 2004).  Also, individuals with non-epileptic seizures may have elevated prolactin levels for other reasons, including intercurrent epilepsy and medication side effects.

# Treatment
The patient with psychogenic non-epileptic seizures is sometimes found to give a history of childhood physical abuse or sexual abuse or other severe emotional trauma. (Betts, 1997.)  Treatment based on insight-oriented techniques or exploring of abuse histories has not been found to be effective.
Instead, treatment with cognitive therapy or behavioral therapy is focused on concrete strategies to recognize the triggers of the seizures and use techniques to control them and eventually halt the onset.
Pulmonary Hypertension Association
The Pulmonary Hypertension Association (PHA) is a 501(c)(3) non-profit support, education, advocacy and awareness association for pulmonary hypertension (PH).  It provides information to the public about the illness and acts as a support group for those with the disease, providing medical provider location services and emotional support for those suffering from the illness.

# History
The PHA was formed in 1987 or 1988 by three pulmonary hypertension patients.  By 1990, it had 100 members and started its newsletter, the Pathlight.  In 1992 it established the Doctor's List (a list of doctors treating PH).  By 2004, it had grown to over 3,400 members and had an annual budget of over $5 million.  Presently it has more than 8,000 members.

# Activities

## Help line
The Association maintains a help line at +1-800-748-7274 staffed by persons living with PH to support and provide information to those with PH.

## Support groups
PHA supports a network of more than 145 local support groups.  They meet personally and via E-mail and LISTSERV.  The Association maintains a "Find A Doctor" list.

## Conferences
Bi-Annually, PHA hosts an international conference dedicated to scientific and medical teaching on the topic of PH.  The 2006 International PH Conference was attnded by more than 300 medical professionals and researchers and featured more than 60 research abstracts.

## Awareness publications
PHA funds and distributes a host of literature regarding PH, including the Patient's Guide to Pulmonary Hypertension, Pathlight, and Persistent Voices.  Advances in Pulmonary Hypertension is distributed quarterly to more than 35,000 medical professionals.

## Research
PHA raises research funds through golf tournaments, charity auctions, and other events.  PHA funds a number of research projects with the proceeds.  PHA jointly funds research with the National Heart, Lung, and Blood Institute, the American Thoracic Society, and completely funds two grants per year in PH research.

## Advocacy
The Association has been instrumental in the Pulmonary Hypertension Research Act (H.R. 3005, S. 1774, now co-sponsored by 247 members of the House and 13 members of the Senate), dealing with governmental officials over airline oxygen portability, and the placement of PH on the National Institutes of Health priority list.

# Notes and References
- Pulmonary Hypertension Association

## International affiliations
PHA has a memorandum of understanding with these organizations:
- British Columbia Pulmonary Hypertension Society
- The Manitoba Pulmonary Hypertension Support Group
- New Brunswick Pulmonary Hypertension Society
- PHA China
- PH Europe
- PH Israel
- Associazione Ipertensione Polmonare Italiana
- Associazione Malati Ipertensione Polmonare
- Pulmonary Hypertension Association of Japan
- Asociacion Mexicana de Hipertension Arterial Pulmonar
- PHA-Nederland
- PHA-UK
Pyrazinamide clinical pharmacology

# Clinical Pharmacology
Pyrazinamide is well absorbed from the GI tract and attains peak plasma concentrations within 2 hours. Plasma concentrations generally range from 30 to 50 mcg/mL with doses of 20 to 25 mg/kg. It is widely distributed in body tissues and fluids including the liver, lungs and cerebrospinal fluid (CSF). The CSF concentration is approximately equal to concurrent steady-state plasma concentrations in patients with inflamed meninges.1 Pyrazinamide is approximately 10% bound to plasma proteins.2 The half-life (t 1/2) of pyrazinamide is 9 to 10 hours in patients with normal renal and hepatic function. The plasma half-life may be prolonged in patients with impaired renal or hepatic function. Pyrazinamide is hydrolyzed in the liver to its major active metabolite, pyrazinoic acid. Pyrazinoic acid is hydroxylated to the main excretory product, 5-hydroxypyrazinoic acid.3
Approximately 70% of an oral dose is excreted in the urine, mainly by glomerular filtration within 24 hours.3
Pyrazinamide may be bacteriostatic or bactericidal against Mycobacterium tuberculosis depending on the concentration of the drug attained at the site of infection. The mechanism of action is unknown. In vitro and in vivo the drug is active only at a slightly acidic pH.
Pyrazinamide indications and usage

# Indications and Usage
Pyrazinamide is indicated for the initial treatment of active tuberculosis in adults and children when combined with other antituberculous agents. (The current recommendation of the CDC for drugsusceptible disease is to use a six-month regimen for initial treatment of active tuberculosis, consisting of isoniazid, rifampin and pyrazinamide given for 2 months, followed by isoniazid and rifampin for 4 months.*4)
(Patients with drug-resistant disease should be treated with regimens individualized to their situation. Pyrazinamide frequently will be an important component of such therapy.)
(In patients with concomitant HIV infection, the physician should be aware of current recommendation of CDC. It is possible these patients may require a longer course of treatment)
It is also indicated after treatment failure with other primary drugs in any form of active tuberculosis.
Pyrazinamide should only be used in conjunction with other effective antituberculous agents.
- See recommendations of Center for Disease Control (CDC) and American Thoracic Society for complete regimen and dosage recommendations.4
Pyruvate dehydrogenase phosphatase
pyruvate dehyrogenase phosphatase catalytic subunit 1 (PDPC 1), also known as protein phosphatase 2C, is an enzyme that in humans is encoded by the PDP1 gene. PDPC 1 is an enzyme which serves to reverse the effects of pyruvate dehydrogenase kinase upon pyruvate dehydrogenase.

# Function
Pyruvate dehydrogenase (E1) is one of the three components (E1, E2, and E3) of the large pyruvate dehydrogenase complex. Pyruvate dehydrogenase kinases catalyze phosphorylation of serine residues of E1 to inactivate the E1 component and inhibit the complex. Pyruvate dehydrogenase phosphatases catalyze the dephosphorylation and activation of the E1 component to reverse the effects of pyruvate dehydrogenase kinases. Pyruvate dehydrogenase phosphatase is a heterodimer consisting of catalytic and regulatory subunits. Two catalytic subunits have been reported; one is predominantly expressed in skeletal muscle and another one is much more abundant in the liver. The catalytic subunit, encoded by this gene, is the former, and belongs to the protein phosphatase 2C (PP2C) superfamily. Along with the pyruvate dehydrogenase complex and pyruvate dehydrogenase kinases, this enzyme is located in the mitochondrial matrix.

# Regulation
Pyruvate dehydrogenase phosphatase is stimulated by insulin, PEP, and AMP, but competitively inhibited by ATP, NADH, and Acetyl-CoA.

# Clinical significance
Mutation in this gene causes pyruvate dehydrogenase phosphatase deficiency.
Queen Elizabeth Hospital, Adelaide
The Queen Elizabeth Hospital (TQEH) is a 340 bed acute tertiary referral hospital in the western suburbs of Adelaide, South Australia.

# History
The hospital opened in 1954 in order to service the western area but is now the second most utilised hospital in South Australia by patients from the central northern region of Adelaide.
The Queen Elizabeth Hospital was the first unit in Australia to perform kidney transplantation successfully. The hospital houses the Australian and New Zealand Dialysis and Transplant Registry (ANZDATA) which collects national statistics on the treatment of those patients with end stage renal failure.

# Teaching
The Queen Elizabeth Hospital is a teaching hospital for the University of Adelaide's medical school and provides clinical attachments in a variety of specialties for undergraduate medical students, including Medicine, Surgery, Emergency Medicine, and Psychiatry.
The Discipline of Medicine has broad ranging functions in undergraduate and postgraduate teaching, research and clinical service and management. The Discipline of Surgery has a large academic surgical department and is a major centre for surgical research and postgraduate teaching in a wide range of fields.

# Services
The hospital provides mental health services through community response teams, TQEH's Emergency Department and via a 40 bed purpose built inpatient unit. The inpatient unit, Cramond Clinic, was named after Professor William Cramond the foundation Chair in Psychiatry at the University of Adelaide. Cramond pioneered the delivery of mental health care to renal patients at TQEH in the 1960s. In 2002-3, the TQEH community mental health teams provided services to 48,621 individuals which was the second largest number for services in the central northern health region.