Persius/hicric huggingface dataset:
Post pneumonectomy syndrome

# Overview
Postpneumonectomy syndrome is a delayed complication seen primarily in children and young adults within a year after surgery.  Most cases of postpneumonectomy syndrome have been described as occurring after right pneumonectomy, when the powerful negative pressure of the involved hemithorax and over-expansion of the remaining lung move the mediastinum rightward. The frequency with which this syndrome occurs in infants, young children, and women is believed to be related to the increased elasticity and compliance of their lungs and mediastinum, compared with those of older patients and men.

# Diagnosis
The syndrome is manifested in exertional dyspnea, inspiratory stridor, and recurrent pulmonary infections.
Imaging findings are,
- Overexpanding lung displacing the mediastium away from it.
- CT images show abnormal narrowing of the distal part of the trachea and the left main bronchus because of compression of the airway between the pulmonary artery anteriorly and the aorta and spine posteriorly.
- As the overexpanded lung further displaces the mediastinum toward the right side, the heart descends in the hemithorax and rotates counterclockwise along its main axis.
- The trachea also is displaced toward the right side, with resultant stretching of the left main bronchus, which is compressed downward by the aortic arch and the left main pulmonary artery.

# Treatment
Various surgical procedures have been used to reposition the mediastinum. Silicone breast implants have been used in the postpneumonectomy space to prevent rotational shifting after pneumonectomy in children, a method that has brought good results.
Posterior intercostal veins
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The posterior intercostal veins are veins that drain the intercostal spaces posteriorly.  They run with their corresponding posterior intercostal artery on the underside of the rib, the vein superior to the artery.
There are eleven posterior intercostal veins on each side.  Their patterns are variable, but they are commonly arranged as:
- The 1st posterior intercostal vein, supreme intercostal vein, drains into the brachiocephalic vein or the vertebral vein.
- The 2nd and 3rd (and often 4th) posterior intercostal veins drain into the superior intercostal vein.
- The remaining posterior intercostal veins drain into the azygos vein on the right, or the hemiazygos vein on the left.
Potassium chloride overdose

# Overdosage topics
Overview
Treatment

## Overview
The administration of oral potassium salts to persons with normal excretory mechanisms for potassium rarely causes serious hyperkalemia. However, if excretory mechanisms are impaired or if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can result. It is important to recognize that hyperkalemia is usually asymptomatic and may be manifested only by an increased serum potassium concentration (6.5-8.0 mEq/L) and characteristic electrocardiographic changes (peaking of T-waves, loss of P-waves, depression of S-T segment, and prolongation of the QT-interval). Late manifestations include muscle-paralysis and cardiovascular collapse from cardiac arrest. (9-12 mEq/L). Return to top

## Treatment
Treatment measures for hyperkalemia include the following:
- Elimination of foods and medications containing potassium and of any agents with potassium-sparing properties.
- Intravenous administration of 300 to 500 mL/hr of 10% dextrose solution containing 10-20 units of crystalline insulin per 1,000 mL.
- Correction of acidosis, if present, with intravenous sodium bicarbonate.
- Use of exchange resins, hemodialysis, or peritoneal dialysis.
In treating hyperkalemia, it should be recalled that in patients who have been stabilized on digitalis, too rapid a lowering of the serum potassium concentration can produce digitalis toxicity. Return to top
Adapted from the FDA Package Insert.
Principal investigator role

# Definition
Principal investigator (PI) is an individual who actually conducts a study (i.e. under whose immediate direction the drug is dispensed to a subject). If an investigation is conducted by a team of individuals, the investigator is the responsible leader of the team.

## FDA Expectations of Clinical Investigators
The FDA requires the investigator to adhere to the code of federal regulations and to have complete knowledge and understanding of the clinical investigators regulations and responsibilities.

## Responsibilities of Principal Investigator
- Principal investigators are in charge and can be held accountable if required.
- They are required to control the investigational drug.
- They are responsible for record keeping and retention.
- They have to maintain adequate records of the disposition of the drug.
- They are responsible for accurate case histories that record all observations and other data pertinent to the investigation on each individual administered the investigational drug or employed as a control in the investigation.
- They are not permitted to delegate their general responsibilities to Contract Research Organizations (CRO) or site management organizations, subinvestigators, or study staff.
- An investigator is required to maintain investigation records for:
2 years following the date a marketing application is approved for the drug for the indication for which it is being investigated.
2 years after the investigation is discontinued and FDA is notified if no application is to be filed or if the application has not been approved for such indication.
- 2 years following the date a marketing application is approved for the drug for the indication for which it is being investigated.
- 2 years after the investigation is discontinued and FDA is notified if no application is to be filed or if the application has not been approved for such indication.
Prokaryotic release factors
There are three known prokaryotic release factors involved in the termination of  translation.
- RF1 recognizes the stop codon UAG
- RF2 recognizes the stop codon UGA (both RF1 and RF2 recognize the stop codon UAA)
- RF3 promotes termination by either factor by accelerating dissociation.
The release factors provide the means of termination by having a conformation that mimics that of tRNA molecules.  The decoding release factor binds to the A site of the ribosome and directly recognise the stop codon .  Once RF1 (or RF2) and RF3 are bound to the ribosome, the polypeptide is released, and the ribosome and release factors dissasemble, thus completing the process of translation .
Propionic acidemia overview
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# Overview
Propionic acidemia, also known as propionic aciduria, propionyl-CoA carboxylase deficiency and ketotic glycinemia, is an autosomal recessive metabolic disorder, classified as a branched-chain organic acidemia.
The disorder presents in the early neonatal period with progressive encephalopathy. Death can occur quickly, due to secondary hyperammonemia, infection, cardiomyopathy, or basal ganglial stroke.
Propionic acidemia is a rare disorder that is inherited from both parents. Being autosomal recessive, neither parent shows symptoms, but both carry a defective gene responsible for this disease. It takes two faulty genes to cause PA, so there is a 1 in 4 chance for these parents to have a child with PA.

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Propionic acidemia from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Protein K (gene expression)
Protein K is a human protein found in the cell nucleus that binds to pre-messenger RNA (mRNA) as a component of heterogeneous ribonucleoprotein particles. The simian homolog is known as protein H16. Both proteins bind to single-stranded DNA as well as to RNA and can stimulate the activity of RNA polymerase II, the protein responsible for most gene transcription. The relative affinities of the proteins for DNA and RNA vary with solution conditions and are inversely correlated, so that conditions promoting strong DNA binding result in weak RNA binding.
RNA binding protein domains in other proteins that are similar to the RNA binding domain of protein K are called K-homology or KH domains.
Protein K has been the subject of study related to colorectal cancer, in which an RNA editing event inducing the expression of an isoform containing a point mutation was found to be specific to cancerous cells.
Protein disulfide isomerase
Protein disulfide isomerase or PDI (EC 5.3.4.1) is an enzyme in the endoplasmic reticulum in eukaryotes or periplasmic space of prokaryotes that catalyzes the formation and breakage of disulfide bonds between cysteine residues within proteins as they fold.  This allows proteins to quickly find the correct arrangement of disulfide bonds in their fully-folded state, and therefore the enzyme acts to catalyze protein folding.
In contrast, reduced (dithiol) form of PDI is able to catalyse a reduction of mispaired thiol residues of a particular substrate, acting as an isomerase.  Therefore, PDI is capable of catalyzing the post-translational disulfide exchange.  Such exchange reactions can occur intramolecularly, leading to the rearrangement of disulphide bonds in a single protein.
Another major function of PDI relates to its activity as a chaperone, i.e., it aids wrongly-folded proteins to reach a correctly-folded state without the aid of enzymatic disulfide shuffling.
PDI has been found to be involved in the breaking of bonds on the HIV gp120 protein during HIV infection of CD4 positive cells, and is required for HIV infection of lymphocytes and monoctyes. Some studies have shown it to be available for HIV infection on the surface of the cell clustered around the CD4 protein.  Yet conflicting studies have shown that it is not available on the cell surface, but instead is found in significant amounts in the blood plasma.
Oxidized PDI can catalyze the formation of a disulfide bridge. This reduces PDI and a protein called Ero1 oxidizes it again.

# Other functions
PDI helps load antigenic peptides into MHC class I molecules.  These molecules (MHC I) are related to the peptide presentation by APC in the immunity response.

# Assays used for PDI activity
Insulin Turbidity Assay: PDI breaks the two disulfide bonds between two insulin (a and b) chains that results in precipitation of b chain. This precipitation can be monitored at 620 nm, which is indirectly used monitor PDI activity. Sensitivity of this assay is in micromolar range.
ScRNase assay: PDI converts scrambled (inactive) RNase into native (active) RNase that further acts on its substrate. The sensitivty is in micromolar range.
Di-E-GSSG assay: This is the fluorometric assay that can detect picomolar quantities of PDI and therefore is the most sensitive assay to date for detecting PDI activity. Di-E-GSSG has two eosin molecules attached to oxidized glutathione (GSSG).  The proximity of eosin molecules leads to the quenching of its fluorescence. However, upon breakage of disulfide bond by PDI, fluorescence increases 70-fold.
Psilocybe ovoideocystidiata
Psilocybe ovoideocystidiata is a psilocybin-containing mushroom first documented in Pennsylvania and also known from Michigan, Ohio and West Virginia.  This mushroom bruises blue where handled and has been put into the Stuntzii section of Psilocybe because it has subrhomboid thick walled spores and an annulus.  It is closely related to to P. subaeruginascens from Java, P. septentrionalis from Japan, and P. wayanadensis from India.
This mushroom was first documented by Richard V. Gaines in Montgomery County in June of 2003 and has become common in the Ohio river valley.
Its range and appearance are similar to Psilocybe caerulipes, and it can be distinguished by its rhomboid spores and membranous annulus.
Some specimens of Psilocybe ovoideocystidiata turn blue immediately when bruised, while others have a delayed or almost absent bluing reaction.  The mushroom often turns blue in the absence of bruising as it dries out.

# Description
The cap is smooth, convex to subumbonate and up to 4 cm across.  It is chestnut brown, olive green, or white and slippery when moist with striations at the edge, fading to buff as it dries and often turning blue.  The gills have adnate attachment and range from whitish to rusty brown, lavender, or dark purple brown.  The stem is 2 to 7.5 cm long, hollow, smooth at the top and often having small scales near the bottom, colored whitish with irregular yellowish, brownish, or bluish patches.   The mushroom quickly (after a few minutes) bruises blue when damaged and has a farinaceous odor.
Psychodynamic psychotherapy

# Overview
Psychodynamic psychotherapy is a form of depth psychology, the primary focus of which is to reveal the unconscious content of a client's psyche in an effort to alleviate psychic tension.    In this way, it is similar to psychoanalysis, however, psychodymanic therapy tends to be more brief and less intensive than psychoanalysis, and also relies more on the interpersonal relationship between client and therapist than do other forms of depth psychology.  In terms of approach, this form of therapy also tends to be more eclectic than others, taking techniques from a variety of sources, rather than relying on a single system of intervention. It is a focus that has been used in individual psychotherapy, group psychotherapy, family therapy, and to understand and work with institutional and organizational contexts.

# History
The principles of psychodynamics were first introduced in the 1874 publication Lectures on Physiology by German scientist Ernst von Brucke. Brucke, taking a cue from thermodynamics, suggested that all living organisms are energy systems, governed by the principle of energy conservation.  During the same year, Brucke was supervisor to first-year medical student Sigmund Freud at the University of Vienna. Freud later adopted this new construct of dynamic physiology to aid in his own conceptualization of the human psyche.  Later, both the concept and application of psychodynamics was further developed by the likes of Carl Jung, Alfred Adler, and Melanie Klein.

# Approaches
Most psychodynamic approaches centered around the idea that some maladaptive functioning is in play, and that this maladaption is, at least in part, unconscious.  The presumed maladaption develops early in life, and it is posited that in later years the client will begin to feel some dissonance in their day to day lives as a function of this paradigm.  The psychodynamic therapist first intervenes to treat the discomfort associated with the poorly formed function, then helps the client acknowledge the existence of the maladaption, while working with the client to develop strategies for change.

# Limitations
Psychodynamic psychotherapy demands considerable introspection and reflection on the part of the client.  It also relies on the client's desire to be helped to support its effectiveness, as well as the client's willingness to reveal themselves, and their level of insight.  Consequently, the client must possess enough resilience and ego-strength to manage the strong emotions this form of therapy may provoke.
Pulmonary-to-systemic shunt
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A pulmonary-to-systemic shunt is a cardiac shunt which allows, or is designed to cause, blood to flow from the pulmonary circulation to the systemic circulation. This occurs when:
- there is a passage between two or more of the great vessels; and,
- pulmonic pressure is higher than systemic pressure and/or the shunt has a one-way valvular opening.
A pulmonary-to-systemic shunt functions as follows:
- right-to-left in the absence of arterioventricular discordance.
- left-to-right if the great vessels are transposed.
Pulmonary stretch receptors
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# Overview
Pulmonary stretch receptors are mechanoreceptors found in the lungs.
When the lung expands, the receptors imitate the Hering-Breuer reflex, which reduces the respiratory rate.  Increased firing from the stretch receptors also increases production of pulmonary surfactant.
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Quinine sulfate description

# Description
QUALAQUIN (quinine sulfate) is a cinchona alkaloid chemically described as cinchonan-9-ol, 6'-methoxy-, (8, 9R)-, sulfate (2:1) (salt), dihydrate with a molecular formula of (C20H24N2O2)2H2SO42H2O and a molecular weight of 782.96.
The structural formula of quinine sulfate is:
Quinine sulfate occurs as a white, crystalline powder that darkens on exposure to light. It is odorless and has a persistent very bitter taste. It is only slightly soluble in water, alcohol, chloroform, and ether.
QUALAQUIN is supplied for oral administration as capsules containing 324 mg of the active ingredient quinine sulfate USP, equivalent to 269 mg free base. Inactive ingredients: corn starch, magnesium stearate, and talc.
RAR-related orphan receptor
The RAR-related orphan receptors (RORs) are members of the nuclear receptor family of intracellular transcription factors.  There are three forms of ROR, ROR-, -, and - and each is encoded by a separate gene RORA, RORB, and RORC respectively.  The RORs are somewhat unusual in that they appear to bind as monomers to hormone response elements as opposed to the majority of other nuclear receptors which bind as dimers.

# Ligands
While the identity of natural ligands for the RORs remains controversial, similar to the liver X receptors (LXRs), it appears that the RORs are activated by oxysterols. Furthermore, the RORs appear to be constitutively active (absence of ligand) and that activity may be due to continuously bound natural ligands. Side chain oxygenated sterols (e.g., 20-hydroxycholesterol, 22R-hydroxycholesterol, and 25-hydroxycholesterol) are high affinity ROR agonists while sterols oxygenated at the 7-position, (e.g., (7-hydroxycholesterol and 7-ketocholesterol) function as inverse agonists for both RORa and ROR.   A number of other natural substances have also been reported to bind to the RORs.  These include all-trans retinoic acid binds with high affinity to ROR- and - but not ROR-. Finally the RORs may function as lipid sensors and hence may play a role in the regulation of lipid metabolism.
Melatonin has been claimed to be an endogenous ligand  for ROR- while CGP 52608 has been identified as a ROR- selective synthetic ligand.

# Tissue distribution
ROR, ROR, and ROR are primarily expressed the following tissues:
- ROR-  widely expressed in liver, skeletal muscle, skin, lung, adipose tissue, kidney, thymus, and brain.
- ROR-  expression restricted to the brain and retina.
- ROR-  highly expressed in thymus (the thymus-specific isoform is referred to as RORt), muscle, testis, pancreas, prostate, heart, and liver.

# Function
The three forms of RORs fulfill a number of critical roles including:
- ROR-   Involved in the maintenance of the circadian rhythm by positively regulating the expression of BMAL1. Development of the cerebellum and lymph nodes, lipid metabolism, immune response, maintenance of bone.
- ROR-  Circadian rhythm, bone metabolism, and retinal neurogenesis.
- ROR-  Lymph node development and immune response, survival of T helper 17 cells.

# As drug targets
A number of synthetic RORt inverse agonists are in various stages of drug development for the treatment of inflammatory diseases.  RORt agonists have also been proposed for use as immunooncology agents to activate the immune system to treat cancer.
RAS p21 protein activator 1
RAS p21 protein activator 1 or RasGAP (Ras GTPase activating protein), also known as RASA1, is a 120-kDa cytosolic human protein that provides two principal activities:
- Inactivation of Ras from its active GTP-bound form to its inactive GDP-bound form by enhancing the endogenous GTPase activity of Ras, via its C-terminal GAP domain
- Mitogenic signal transmission towards downstream interacting partners through its N-terminal SH2-SH3-SH2 domains
The protein encoded by this gene is located in the cytoplasm and is part of the GAP1 family of GTPase-activating proteins. The gene product stimulates the GTPase activity of normal RAS p21 but not its oncogenic counterpart. Acting as a suppressor of RAS function, the protein enhances the weak intrinsic GTPase activity of RAS proteins resulting in the inactive GDP-bound form of RAS, thereby allowing control of cellular proliferation and differentiation. Mutations leading to changes in the binding sites of either protein are associated with basal cell carcinomas. Alternative splicing results in two isoforms where the shorter isoform, lacking the N-terminal hydrophobic region but retaining the same activity, appears to be abundantly expressed in placental but not adult tissues.

# Domains
RasGAP contains one SH3 domain and two SH2 domains, a PH domain, and a GAP domain.

# Interactions
RAS p21 protein activator 1 has been shown to interact with:
- ANXA6,
- CAV2,
- DNAJA3,
- DOK1,
- EPHB2,
- EPHB3,
- GNB2L1 
- HCK,
- HRAS,
- HTT,
- IGF1R,
- KHDRBS1,
- NCK1,
- PDGFRB,
- PTK2B,
- SOCS3,  and
- Src.
The mRNA can interact with Mir-132 microRNA; this process is linked to angiogenesis.

# Disease database
RASA1 gene variant database