Persius/hicric huggingface dataset:
Penicillin G benzathine description

# Description
Bicillin L-A (penicillin G benzathine injectable suspension) is available for deep intramuscular injection. Penicillin G benzathine is prepared by the reaction of dibenzylethylene diamine with two molecules of penicillin G. It is chemically designated as (2S, 5R, 6R )-3,3-Dimethyl-7-oxo-6-(2-phenylacetamido)-4-thia-1-azabicycloheptane-2-carboxylic acid compound with N,N' -dibenzylethylenediamine (2:1), tetrahydrate. It occurs as a white, crystalline powder and is very slightly soluble in water and sparingly soluble in alcohol. Its chemical structure is as follows:
Bicillin L-A contains penicillin G benzathine in aqueous suspension with sodium citrate buffer and, as w/v, approximately 0.5% lecithin, 0.6% carboxymethylcellulose, 0.6% povidone, 0.1% methylparaben, and 0.01% propylparaben.
Bicillin L-A suspension in the disposable-syringe formulation is viscous and opaque. It is available in a 1 mL, 2 mL, and 4 mL sizes containing the equivalent of 600,000, 1,200,000 and 2,400,000 units respectively of penicillin G as the benzathine salt. Read CONTRAINDICATIONS, WARNINGS, PRECAUTIONS, and DOSAGE AND ADMINISTRATION sections prior to use.
Penicillin G potassium how supplied

# How Supplied
Buffered Penicillin G Potassium for Injection, USP, is supplied in dry powder form in vials containing 1,000,000 units (1 million units)  10's (NDC 0781-6134-95), 5,000,000 units (5 million units)  10's (NDC 0781-6135-95), and 20,000,000 units (20 million units)  1's (NDC 0781-6136-94) of crystalline penicillin G as the potassium salt; buffered with sodium citrate and citric acid to an optimum pH.

## Storage
Store the dry powder at 20-25C (68-77F) (see USP controlled room temperature).
Sterile constituted solution may be kept in refrigerator 2-8C (36-46F) for 7 days without significant loss of potency.
Penicillin V potassium how supplied

# How Supplied
Penicillin - VK Tablets (Penicillin V Potassium Tablets USP), 250 mg (400,000 units) are round, biconvex white tablets, debossed PVK 250 and break scored on one side and GG 949 on the reverse side.
NDC 0781-1205-01 .......bottles of 100
NDC 0781-1205-10 .......bottles of 1000
Penicillin - VK Tablets (Penicillin V Potassium Tablets USP), 500 mg (800,000 units) are oblong, biconvex white tablets, debossed PVK 500 on one side and GG 950 on the reverse side and break scored on both sides.
NDC 0781-1655-01 .......bottles of 100
NDC 0781-1655-10 .......bottles of 1000
Store at 20 - 25C (68 - 77F) (see USP Controlled Room Temperature).
Keep tightly closed. Dispense in a tight container, as defined in the USP.
Peptidoglycan recognition protein 1
Peptidoglycan recognition protein 1, also known as TAG7, is a protein that in humans is encoded by the PGLYRP1 gene.

# Tissue distribution and secretion
The PGLYRP1 gene is highly expressed in bone marrow, circulating Polymorphonuclear leukocytes (PMLs), and in the corneal epithelium. The PGLYRP1 protein is primarily found in the granules of PMLs.

# Structure
As with most PGRPs, PGLYRP1 has one carboxy-terminal type 2 amidase domain (also known as a PGRP domain) and consists of three alpha helices, five beta strands and coils, and has three pairs of conserved cysteins which form three disulphide bonds.  PGLYRP1 can form homodimers for its antimicrobial activity, and can complex with HSP70 for its cytotoxic activity.

# Function
The PGLYRP1 protein plays an important role in the innate immune response.  It is bactericidal against gram-positive bacteria such as S. aureus, S. epidermidis, and L. monocytogenes and generally has proinflammatory effects, inducing TNF-a and IFN-g in many tissues.  PGLYRP-1 is also known to form a cytotoxic complex with HSP-70, suggesting it may also have a role in anti-cancer defense.  As a pathogen recognition protein with antimicrobial properties, PGLYRP-1 is suspected to play an important role in maintaining the gut microbial flora.

# Mechanism of action
As an antimicrobial, the binding of PGLYRP1 to its target does not permeabilize the bacterial cell wall like defensins and other antimicrobial peptides.  Instead, PGLYRP1 binding activates a bacterial stress response that causes the bacterium to shut down transcription and translation, and induces oxidative stress. As a cytotoxic agent, the PGLYRP1-HSP70 complex

# Possible pathological role
In humans, single nuclear polymorphisms of the PGLYRP1 gene have been associated with the development of ulcerative colitis.
In mice, the lack of PGLYRP1 is associated with increased susceptibility to infectious disease, but also decreased susceptibility to autoimmune disease. The lack of PGLYRP1 was found to have increased susceptibility to corneal infections, reduced corneal wound healing, and increased scarification of the cornea when infected by P. aeruginosa. But PGLYRP1-deficient mice also had decreased severity of atopic dermatitis and contact dermatitis.  and may play a role in the development of asthma.
Pericarditis in malignancy overview

# Overview
Many malignant neoplasms such as lung cancer, breast cancer, esophageal cancer, lymphomas, melanomas, kaposi's sarcoma and leukemias may metastasize to pericardium causing pericarditis, effusion, cardiac tamponade and pericardial constriction. Malignant pericardial effusion is seen in approximately 50-60% of patients presenting with pericardial effusion who have a history of malignancy. Among patients presenting with pericarditis or pericardial effusion with no history of malignancy, undiagnosed underlying malignancy was detected in 4-7%.
Malignancy related pericardial disease can manifest as pericarditis, pericardial effusion, cardiac tamponade or pericardial constriction.

# Pathophysiology
The pericardium may be involved by direct local spread from neoplasms such as breast and lung carcinomas or by metastatic spread via blood stream and lymphatics as in melanomas, lymphomas and leukemias.
Pericardial effusion in such situations may occur either secondary to pericardial inflammation or obstruction of lymphatic drainage by enlarged mediastinal nodes.
Persistent genital arousal disorder
Persistent Genital Arousal Disorder (formerly known as Persistent Sexual Arousal Syndrome) results in a spontaneous and persistent genital arousal, with or without orgasm or genital engorgement, unrelated to any feelings of sexual desire. It was first documented by Dr. Sandra Leiblum in 2001, only recently characterized as a distinct syndrome in medical literature. In particular, it is not related to hypersexuality, sometimes known as nymphomania or satyriasis. In addition to being very rare, the condition is also frequently unreported by sufferers who may consider it shameful or embarrassing.
Physical arousal caused by this syndrome can be very intense and persist for extended periods, days or weeks at a time. Orgasm can sometimes provide temporary relief, but within hours the symptoms return. The symptoms can be debilitating, preventing concentration on mundane tasks. Some situations, such as riding in an automobile or train, vibrations from mobile phones, and even going to the toilet can aggravate the syndrome unbearably. 

# Possible causes and treatment
There is not enough known about Persistent Genital Arousal Disorder to definitively pinpoint a cause. Medical professionals think it is caused by an irregularity in sensory nerves, and note that the disease has a tendency to strike post-menopausal women in their 40s and 50s, or those who've undergone hormonal treatment. But, there have also been cases reported among women in their 30s.
Some drugs such as trazodone may cause it as a side effect, in which case discontinuing the medication may give relief. Additionally, the condition can sometimes start only after the discontinuation of SSRIs.  In some recorded cases, the syndrome was caused by a pelvic arterial-venous malformation with arterial branches to the penis or clitoris; surgical treatment was effective in this case.
In other situations where the cause is unknown or less easily treatable, the symptoms can sometimes be reduced by the use of antidepressants, antiandrogenic agents and anaesthetising gels. Psychotherapy with cognitive reframing of the arousal as a healthy response may also be used.
Phosphoinositide-dependent kinase-1
In the field of biochemistry, PDPK1 refers to the protein 3-phosphoinositide-dependent protein kinase-1, an enzyme which is encoded by the PDPK1 gene in humans. It is implicated in the development and progression of melanomas.

# Function
PDPK1 is a master kinase, which is crucial for the activation of AKT/PKB and many other AGC kinases including PKC, S6K, SGK. An important role for PDPK1 is in the signalling pathways activated by several growth factors and hormones including insulin signaling.
Mice lacking PDPK1 die during early embryonic development, indicating that this enzyme is critical for transmitting the growth-promoting signals necessary for normal mammalian development.
Mice that are deficient in PDPK1 have a 40% decrease in body mass, mild glucose intolerance, and are resistant to cancer brought about by hyperactivation of the PI3K pathway (PTEN+/-).

# Etymology
PDPK1 stands for 3-phosphoinositide-dependent protein kinase 1. PDPK1 functions downstream of PI3K through PDPK1's interaction with membrane phospholipids including phosphatidylinositols, phosphatidylinositol (3,4)-bisphosphate and phosphatidylinositol (3,4,5)-trisphosphate. PI3K indirectly regulates PDPK1 by phosphorylating phosphatidylinositols which in turn generates phosphatidylinositol (3,4)-bisphosphate and phosphatidylinositol (3,4,5)-trisphosphate. However, PDPK1 is believed to be constitutively active and does not always require phosphatidylinositols for its activities.
Phosphatidylinositols are only required for the activation at the membrane of some substrates including AKT. PDPK1 however does not require membrane lipid binding for the efficient phosphorylation of most of its substrates in the cytosol (not at the cell membrane).

# Structure
The structure of PDPK1 can be divided into two domains; the kinase or catalytic domain and the PH domain. The PH domain functions mainly in the interaction of PDPK1 with phosphatidylinositol (3,4)-bisphosphate and phosphatidylinositol (3,4,5)-trisphosphate which is important in localization and activation of some of membrane associated PDPK1's substrates including AKT.
The kinase domain has three ligand binding sites; the substrate binding site, the ATP binding site, and the docking site (also known as PIF pocket). Several PDPK1 substrates including S6K and Protein kinase C, require the binding at this docking site. Small molecule allosteric activators of PDPK1 were shown to selectively inhibit activation of substrates that require docking site interaction. These compounds do not bind to the active site and allow PDPK1 to activate other substrates that do not require docking site interaction. PDPK1 is constitutively active and at present, there is no known inhibitor proteins for PDPK1.
The activation of PDPK1's main effector, AKT, is believed to require a proper orientation of the kinase and PH domains of PDPK1 and AKT at the membrane.

# Interactions
Phosphoinositide-dependent kinase-1 has been shown to interact with:
- AKT1,
- PKN2,
- PRKACA,
- PRKCD,
- PRKCI,
- Protein kinase M,
- Protein kinase N1,
- SGK,
- SLC9A3R2,  and
- YWHAH
Phosphopantothenatecysteine ligase
In enzymology, a phosphopantothenate-cysteine ligase also known as phosphopantothenoylcysteine synthetase  (PPCS) is an enzyme that catalyzes the chemical reaction which constitutes the second of five steps involved in the conversion of pantothenate to Coenzyme A. The reaction is:
The nucleoside triphosphate (NTP) involved in the reaction varies from species to species. Phosphopantothenatecysteine ligase from the bacterium Escherichia coli uses cytidine triphosphate (CTP) as an energy donor, whilst the human isoform uses adenosine triphosphate (ATP).

# Nomenclature
This enzyme belongs to the family of ligases, specifically those forming carbon-nitrogen bonds as acid-D-amino-acid ligases (peptide synthases).  The systematic name of this enzyme class is (R)-4'-phosphopantothenate:L-cysteine ligase. This enzyme is also called phosphopantothenoylcysteine synthetase.

# Gene
Phosphopantothenoylcysteine synthetase in humans is encoded by the PPCS gene.

# Protein structure
As of late 2007, 5 structures have been solved for this class of enzymes, with PDB accession codes 1P9O, 1U7U, 1U7W, 1U7Z, and 1U80.
Posterior humeral circumflex artery
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# Overview
The posterior humeral circumflex artery (posterior circumflex artery, posterior circumflex humeral artery) arises from the axillary artery at the lower border of the Subscapularis, and runs backward with the axillary nerve through the quadrangular space.
It winds around the neck of the humerus and is distributed to the Deltoideus and shoulder-joint, anastomosing with the anterior humeral circumflex and profunda brachii.

# Additional images
- Suprascapular and axillary nerves of right side, seen from behind.
Postoperative cognitive dysfunction
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Postoperative Cognitive Dysfunction (POCD) refers to cognitive problems (with memory, learning and the ability to concentrate) following surgery.
Recent studies suggest that the incidence of POCD increases with age.
There has been very limited research into POCD, but existing reports suggest that it can last for long periods of time, with 2-3 months considered long-term.
Prostatic intraepithelial neoplasia
Steven C. Campbell, M.D., Ph.D.
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# Overview
Prostatic intraepithelial neoplasia (PIN) is a non-invasive lesion in the prostate gland which is though to be a precursor to prostate cancer. Microscopically, PIN is a collection of irregular cells which are fully contained within the gland structure and have not spread to the surrounding tissue. This may be proven by the identification of basal cells forming the supporting layer of the gland. PIN does not require specific therapy, but close follow-up with additional biopsies is warranted. PIN may disappear, remain unchanged, or progress to prostate cancer, often over as many as ten years.

# Histopathological Findings: Intraepithelial Neoplasia (PIN)
Pyrimethamine indications and usage

# Indications And Usage

## Treatment of Toxoplasmosis
DARAPRIM is indicated for the treatment of toxoplasmosis when used conjointly with a sulfonamide, since synergism exists with this combination.

## Treatment of Acute Malaria
DARAPRIM is also indicated for the treatment of acute malaria. It should not be used alone to treat acute malaria. Fast-acting schizonticides such as chloroquine or quinine are indicated and preferable for the treatment of acute malaria. However, conjoint use of DARAPRIM with a sulfonamide (e.g., sulfadoxine) will initiate transmission control and suppression of susceptible strains of plasmodia.

## Chemoprophylaxis of Malaria
DARAPRIM is indicated for the chemoprophylaxis of malaria due to susceptible strains of plasmodia. However, resistance to pyrimethamine is prevalent worldwide. It is not suitable as a prophylactic agent for travelers to most areas.
Quantum well infrared photodetector
A quantum well infrared photodetector (QWIP), is an infrared photodetector made from semiconductor materials which contain one or more quantum wells. These can be integrated together with electronics and optics to make infrared cameras for thermography. A very common well material is gallium arsenide, used with barrier material aluminium gallium arsenide. There are several companies world-wide manufacturing infrared systems which use QWIPs. It is also considered a game changing technology in the field of air to air missiles (within visual range).

# Detection description
QWIPs operate by photoexcitation of electrons between ground and first excited state subbands of multi-quantum wells which are artificially fabricated by placing thin layers of two different, high-bandgap semiconductor materials alternately. The bandgap discontinuity of two materials creates quantized subbands in the potential wells associated with conduction bands or valence bands. The structure parameters are designed so that the photo-excited carriers can escape from the potential wells and be collected as photocurrent.
The lattice matched GaAs/AlGaAs material system is commonly used to create a QWIP structure. Highly uniform and pure crystal layers of such semiconductors can be grown on large substrate wafers, with control of each layer thickness down to a fraction of a molecular layer, using modern crystal-growth methods like molecular beam epitaxy (MBE). Thus, by controlling the quantum well width and the barrier height (which depends on the Al molar ratio of the alloy), this intersubband transition energy can be varied over a wide enough range to enable light detection at any wavelength range between 6-20 m (infrared).
Spectral responsivity peak wavelength of a QWIP is determined by the energy difference between 
ground and excited states of the quantum well. Unlike the responsivity spectra of intrinsic infrared detectors, QWIPs spectra are much narrower and sharper due to their resonance intersubband absorption. Typically, responsivity spectra of the bound and quasibound excited state QWIPs are much narrower than the continuum QWIPs. This is because when the excited state is placed in the continuum band above the barrier the energy width associated with the state becomes wide. Spectral band width of these QWIPs can be further increased by replacing single quantum wells with small superlattice structures (several quantum wells separated by thin barriers) in the multi-quantum well structure. Such a scheme creates an excited state miniband due to overlap of the excited state wavefunctions of quantum wells.
The dominant noise in QWIP devices is due to the shot noise resulting from the total current in the device. Unlike conventional detectors, there is no significant thermal noise in QWIPs. In addition QWIP have good noise stability (low 1/f noise), enabling long integration times and scanning strategies commonly required in focal plane array imaging applications.

# References and external links
- NASA qwip research
- Acreo
Receptor activity-modifying protein
Receptor activity-modifying proteins (RAMPs) are a class of protein that interact with and modulate the activities of several Class B G protein-coupled receptors including the receptors for secretin, calcitonin (CT), glucagon, and vasoactive intestinal peptide (VIP). There are three distinct types of RAMPs in mammals (though more in fish), designated RAMP1, RAMP2, and RAMP3, each encoded by a separate gene.

# Function
Currently, the function of RAMPs is divided into classes of activities.  When associated with the Calcitonin receptor (CTR) or Calcitonin receptor-like (CALCRL) (below), RAMPs can change the selectivity of the receptor for a specific hormone.  In the cases of the other receptors mentioned, however, there is no evidence that they can do this, but instead function to regulate trafficking of receptors from the ER / golgi to the membrane.  These functions appear to be ones where there is redundancy, as neither RAMP1 nor RAMP3 knockout mice (KO) have grossly abnormal phenotypes.  The likelihood is that the phenotype of RAMP2 KO mice is more connected with the abolition of most adrenomedullin (AM) signalling than effects on trafficking of other receptors, as those mice are almost identical to AM KO mice and mice lacking the Calcitonin-like receptor which are unable to form either AM1 or AM-2 adrenomedullin receptors (CLR/RAMP2 and CLR/RAMP3 respectively).

# Types
Association of RAMPs with either the CT or CALCRL proteins forms 6 different receptors from the calcitonin receptor family:
Related to receptor tyrosine kinase
The related to receptor tyrosine kinase (RYK) gene encodes the protein Ryk.
The protein encoded by this gene is an atypical member of the family of growth factor receptor protein tyrosine kinases, differing from other members at a number of conserved residues in the activation and nucleotide binding domains. This gene product belongs to a subfamily whose members do not appear to be regulated by phosphorylation in the activation segment. It has been suggested that mediation of biological activity by recruitment of a signaling-competent auxiliary protein may occur through an as yet uncharacterized mechanism. Two alternative splice variants have been identified, encoding distinct isoforms.

# History
The gene encoding mouse RYK was first identified in 1992.
Subsequently, cDNA encoding the RYK protein have been isolated from the following species.
- rat
- chicken
- Human
- Zebrafish
- Drosophila and
- C. elegans

# Structure
In common with other receptor tyrosine kinase family members, RYK is composed of three domains, an N-terminal, extracellular ligand-binding domain, a transmembrane spanning domain and a C-terminal intracellular domain. However, in contrast to other receptor tyrosine kinases the C-terminal domain of RYK is devoid of detectable kinase activity.

# Function
RYK is involved in regulation of axon growth during development of the nervous system.
Respiratory system diagnostic tests

# Overview
In medicine, the respiratory examination is performed as part of a physical examination, or when a patient presents with a respiratory problem (dyspnea (shortness of breath), cough, chest pain) or a history that suggests a pathology of the lungs.

# Respiratory system diagnostic tests

## Sputum examination
- Appearance, color, presence of blood, and smell
Colorless (Bronchitis)
Green (pulmonary infection)
Red (carcinoma)
Frothy pink (pulmonary edema)
Black (pollutants)
- Colorless (Bronchitis)
- Green (pulmonary infection)
- Red (carcinoma)
- Frothy pink (pulmonary edema)
- Black (pollutants)
- Order tests - Routine microscopy (gram and ZN stain), cytology, culture

## Peak expiratory flow
- Maximal forced expiration through peak flow meter.
- Used to estimate airway caliber in COPD, and asthma

## Pulse oximetry
- Quick, non-invasive way of measurement of peripheral oxygen saturation
- Its alarm is usually set on 90%
- A decrease of oxygen saturation below 80% needs attention.
- In some cases for instance, COPD, an oxygen saturation below 80% is normal and patient is compensated
- False results may be due to:
Skin pigmentation
Nail paints
Carbon monooxide poisoning
Dyshemoglobulinemia
Poor perfusion
- Skin pigmentation
- Nail paints
- Carbon monooxide poisoning
- Dyshemoglobulinemia
- Poor perfusion

## Arterial blood gas
- Heparinized blood from peripheral arteries like radial, brachial, and femoral
- Measure pH, PaO2, PaCO2, and FiO2 (percent of inspired oxygen)
- For interpretation of ABG click here