Persius/hicric huggingface dataset:
Renal artery
The renal arteries normally arise off the side of the abdominal aorta, immediately below the superior mesenteric artery, and supply the kidneys with blood. Each is directed across the crus of the diaphragm, so as to form nearly a right angle with the aorta.
The renal arteries carry a large portion of total blood flow to the kidneys. Up to a third of total cardiac output can pass through the renal arteries to be filtered by the kidneys.
The arterial supply of the kidneys is variable and there may be one or more renal arteries supplying each kidney. It is located above the renal vein.

# Asymmetries before reaching kidney
Due to the position of the aorta, the inferior vena cava and the kidneys in the body, the right renal artery is normally longer than the left renal artery.
- The right passes behind the inferior vena cava, the right renal vein, the head of the pancreas, and the descending part of the duodenum.
- The left is somewhat higher than the right; it lies behind the left renal vein, the body of the pancreas and the lienal vein, and is crossed by the inferior mesenteric vein.

# At kidney
Before reaching the hilus of the kidney, each artery divides into four or five branches; the greater number of these lie between the renal vein and ureter, the vein being in front, the ureter behind, but one or more branches are usually situated behind the ureter.
Each vessel gives off some small inferior suprarenal branches to the suprarenal gland, the ureter, and the surrounding cellular tissue and muscles.
One or two accessory renal arteries are frequently found, more especially on the left side they usually arise from the aorta, and may come off above or below the main artery, the former being the more common position. Instead of entering the kidney at the hilus, they usually pierce the upper or lower part of the gland.

# Diseases of the renal arteries
Renal artery stenosis, or narrowing of one or both renal arteries will lead to hypertension as the affected kidneys release renin to increase blood pressure to preserve perfusion to the kidneys.  RAS is diagnosed with an MRA (magnet-resonance scan) of abdomen.  It is treated with the use of balloon angioplasty and stents, if necessary.
Atherosclerosis can also affect the renal arteries and can lead to poor perfusion of the kidneys leading to reduced kidney function and, possibly, renal failure.

# Additional images
- Frontal section through the kidney
- Abdominal portion of the sympathetic trunk, with the celiac and hypogastric plexuses.
- The posterior surfaces of the kidneys, showing areas of relation to the parietes.
- Front of abdomen, showing surface markings for arteries and inguinal canal.
Renal pelvis
The renal pelvis is the funnel-like dilated proximal part of the ureter in the kidney.
It is the point of convergence of two or three major calyces.  Each renal papilla is surrounded by a branch of the renal pelvis called a calyx.
The major function of the renal pelvis is to act as a funnel for urine flowing to the ureter.
Renovo, plc.
Renovo, plc. (Template:Lse) is a biopharmaceutical company based in Manchester, UK. It is the world leader in scar prevention and reduction research, and it aims "to be first to market with a scar prevention pharmaceutical drug in the US and Europe" in 2009.
The US commercial market for prevention and reduction of scarring in the skin is valued at approximately US$4 billion per annum, and the market is larger in patient volume than Depression, Osteoporosis, Asthma and Diabetes.

# Products
Currently the company doesn't have a marketed product, though its pipeline includes one drug that has recently initiated phase III clinical development, three drugs in phase II clinical development, and 13 other pre-clinical candidates.
Troglitazone
Troglitazone (Rezulin, Resulin or Romozin) is a member of the drug class of the thiazolidinediones. It was introduced in the late 1990s but turned out to be associated with an idiosyncratic reaction leading to drug-induced hepatitis. It was withdrawn from the USA market on 21 March 2000, and from other markets soon afterwards.
Troglitazone, like the other thiazolidinediones (pioglitazone and rosiglitazone), works by activating PPARs (peroxisome proliferator-activated receptors).
Troglitazone is a ligand to both PPAR and - more strongly - PPAR. Troglitazone also contains an -tocopheroyl moiety, potentially giving it vitamin E-like activity in addition to its PPAR activation. It has been shown (Aljada et al) to reduce inflammation: troglitazone use was associated with a decrease of nuclear factor kappa-B (NFB) and a concomitant increase in its inhibitor (IB). NFB is an important cellular transcription regulator for the immune response.
Right atrium

# Overview
The right atrium (in older texts termed the right auricle) is one of four chambers (two atria and two ventricles) in the human heart. It receives de-oxygenated blood from the superior and inferior vena cavae and the coronary sinus, and pumps it into the right ventricle through the tricuspid valve.
The sinoatrial node (SAN) is located within this chamber next to the vena cava. This is a group of pacemaker cells which spontaneously depolarise to create an action potential. The cardiac action potential then spreads across both atria causing them to contract forcing the blood they hold into their corresponding ventricles.
In early life, when a fetus is in the womb, the right atrium has a hole within its septum through to the left atrium, this makes them continuous with each other which is essential for fetal circulation.  This junction is called the foramen ovale. Once born (usually within a year's time) the foreman ovale seals over and it is renamed as the fossa ovalis.  The fossa ovalis is seen as an embryonic remnant.  In some cases, the formane ovale fails to close and is present in 20% of the general population, however it does not cause problems in the vast majority. This is known as patent foramen ovale.
Within the fetal right atrium, blood from the inferior vena cava and the superior vena flow in separate streams to different locations in the heart, and this has been reported to occur through the Coanda effect.
The right atrium also holds the coronary sinus which is the opening of the vein that drains the myocardium itself. 
Attached to the right atrium is the right auricular appendix.

# Additional images
- Heart seen from above.
Right to die
The term "right to die"  refers to various issues around the death of an individual when that person could continue to live with the aid of life support, or in a diminished or enfeebled capacity. In some cases, it refers to the idea that a person with a terminal illness and in serious condition should be allowed to commit suicide before death would otherwise occur. The concept is often referred to as dying with dignity.
In most countries in the Western world, people do not, legally speaking, have the right to die.
Suicide is often frowned upon, and euthanasia is only legal in a handful of countries. In some East Asian countries, suicide may be acceptable in cases such as ritual suicide.
Most often, the idea of the right to die is related to a person's wish that caregivers allow deathfor example, by not providing life support or vital medication under certain conditions when recovery is highly unlikely or impossible. It may also refer to issues regarding physician-assisted suicide. It may be called passive euthanasia in cases where the patient is unable to make decisions about treatment. Living wills and Do Not Resuscitate orders are legal instruments that make a patient's treatment decisions known ahead of time; allowing a patient to die based on such decisions is not considered to be euthanasia. Usually these patients have also made explicit their wish to receive only palliative care to reduce pain and suffering.
Although specialized legal instruments differ from place to place, there are two more that are important in this context. The Five Wishes document allows a person to state in advance the priorities and values they wish to have honored at the end of life. And the Medical Durable Power of Attorney (or MDPOA) designates an agent to make decisions in case of incapacity, and can be used to give written guidance regarding end of life decision making. The MDPOA is generally considered to be the most powerful of all such instruments. All others may require interpretation on the part of health care providers or even court-appointed guardians; the MDPOA takes the job of interpretation out of the hands of strangers and gives it to a person selected and trusted by the individual.
Rigor mortis
Rigor mortis is one of the recognizable signs of death (Latin mors, mortis) that is caused by a chemical change in the muscles after death, causing the limbs of the corpse to become stiff (Latin rigor) and difficult to move or manipulate. Eerily, during rigor mortis, muscles may contract in seemingly random and bizarre ways even though the body is dead.

# Biochemistry
After a muscle contracts, ATP expenditure is required to release the myosin head of a thick filament from its binding site on the thin filament. Since all metabolic processes have come to a halt in a dead body, no ATP is being produced. Therefore, because of a lack of ATP, the myosin head cannot be released from the actin filament, and the sarcomere cannot relax. 
Because this happens in muscles all over the body, they become "stiff" and "locked" into place.
To understand the contractions associated with rigor mortis, it's important to know that ATP is required to reuptake calcium into the sarcomere's sarcoplasmic reticulum. Additionally, when a muscle is relaxed, the myosin heads are returned to their "high energy" position, ready and waiting for a binding site on the actin filament to become available. Because there is no ATP available, previously released calcium ions cannot be reuptaken into the SR. These leftover calcium ions move around inside the sarcomere and may eventually find their way to a binding site on the thin filament's regulatory protein. Since the myosin head is already ready to bind, no addition ATP expenditure is required and the sarcomere contracts. When this process occurs on a larger scale, the disturbing twitches and gruesome postures associated with rigor mortis can occur.
After about 72 hours, the body relaxes again, this time as a result of decomposition. This is known as resolution of rigor.

# Rigor mortis and the meat industry
Rigor mortis is very important in meat technology. The onset of rigor mortis and its resolution partially determines the tenderness of meat. If the post-slaughter meat is immediately chilled to 15 C, a phenomenon known as cold shortening occurs, where the muscle shrinks to a third of its original size. This will lead to the loss of water from the meat along with many of the vitamins, minerals, and water soluble proteins. The loss of water makes the meat hard and interferes with the manufacturing of several meat products like cutlet and sausage.
Cold shortening is caused by the release of stored calcium ions from the sarcoplasmic reticulum of muscle fibers in response to the cold stimulus. The calcium ions trigger powerful muscle contraction aided by ATP molecules.  To prevent cold shortening, a process known as electrical stimulation is carried out, especially in beef carcass, immediately after slaughter and skinning. In this process, the carcass is stimulated with alternating current, causing it to contract and relax, which depletes the ATP reserve from the carcass and prevents cold shortening.
Rumenic acid
Rumenic acid is a conjugated linoleic acid (CLA) found in the fat of ruminants and in dairy products.  It is a omega-7 trans fat. Its lipid shorthand name is cis-9, trans-11 18:2 acid.
The name was proposed by Kramer et al in 1998.  It is  formed along with vaccenic acid by biohydrogenation of dietary polyunsaturated fatty acids in the rumen.
It can be considered as the principal dietary form, accounting for as much as 85-90% of the total CLA content in dairy products.

# Biological properties
Laboratory studies indicate that rumenic acid shows anticarcinogenic properties.
SATURN Trial

# Objective
To compare the effects of two intensive lipid lowering treatment regimens (statins) on the progression of coronary atherosclerosis and to assess their safety and side-effect profiles.

# Methods
Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) trial was a randomized trial which enrolled 1049 patients with known coronary artery disease, to study the effects of rosuvastatin and atorvastatin on the progression of coronary atherosclerosis. Percent atheroma volume and total atheroma volume were assessed by intravascular ultrasound (IVUS) at baseline and after 104 weeks of treatment with either rosuvastatin 40 daily and atorvastatin 80 mg daily.

# Results
At the end of 104 weeks:
- Serum LDL-C levels were lower in the rosuvastatin group than atorvastatin group.
- Similarly serum HDL-C levels were higher in the rosuvastatin group than in atorvastatin group.
- Percent atheroma volume (PAV), decreased by 0.99% with atorvastatin and by 1.22% with rosuvastatin.

# Conclusion
Maximal doses of rosuvastatin and atorvastatin resulted in significant regression of coronary atherosclerosis. Even though rosuvastatin achieved a lower LDL-C and higher HDL-C levels compared to atorvastatin, a similar degree of regression of PAV was observed in both the treatment groups.
SCN1A (gene)
The SCN1A gene is located on chromosome 2 of humans, and is made up of 26 exons spanning a total length of 6030 nucleotide base pairs (bp). Alternative splicing of exon 5 gives rise to two alternate exons. The promoter has been identified 2.5 kilobase pairs (kb) upstream of the transcription start site, and the 5- untranslated exons may enhance expression of the SCN1A gene in SH-SY5Y cells, a human cell line derived from a neuroblastoma.
The SCN1A gene codes for the alpha subunit of the voltage-gated sodium ion channel making it a member of ten paralogous gene families which code for the voltage-gated sodium transmembrane proteins NaV1.1. Within the family of genes which code for other portions of voltage-gated sodium channels, the SCN1A mutations were the first identified, since mutations to this gene caused epilepsy and febrile seizures. Indeed, the SCN1A gene is one of the most commonly mutated genes in the human genome associated with epilepsy, which has given it the title of a super culprit gene. There are 900 distinct mutations reported for the SCN1A gene, approximately half of the reported mutations are truncations which result in no protein. The remaining half of mutations are missense mutations, which are predicted to either cause loss-of-function or gain-of-function, though very few have been tested for functionality in the lab.
Subtle differences in voltage-gated sodium ion channels can have devastating physiological effects and underlie abnormal neurological functioning. Mutations to the SCN1A gene most often results in different forms of seizure disorders, the most common forms of seizure disorders are Dravet Syndrome (DS), Intractable childhood epilepsy with generalized tonic-clonic seizures (ICEGTC), and severe myoclonic epilepsy borderline (SMEB). Clinically, 70-80% of patients with DS have identified mutations specific to the SCN1A gene, which are caused by de novo heterozygous mutations of the SCN1A gene There are currently two databases on SCN1A mutations, Infobase and the SCN1A variant database.
Mice with knock-in SCN1A mutations, who are model organisms for DS quickly develop seizures, indicative of a significant reduction in the function of NaV1.1. It has been hypothesized that reduced sodium currents due to NaV1.1 mutations may cause hyper-excitability in GABAergic inhibitory interneurons leading to epilepsy. Mice in both the homozygous and heterozygous states develop the seizure phenotype and ataxia. Though homozygous mice die on average during the second to third week of life and approximately 50% of heterozygous null mice survive into adulthood.
- From a gene symbol: This is a redirect from a Human Genome Organisation (HUGO) symbol for a gene to an article about the gene.
SEARCH Study

# Objective
To study the efficacy and safety of prolonged use of more intensive cholesterol-lowering therapy in patients at high cardiovascular risk.

# Methods
Study of the effectiveness of additional reductions in cholesterol and homocysteine (SEARCH) was a randomized, double blinded study which enrolled 12,064 men and women aged 18-80 years with a history of myocardial infarction. In addition these patients were randomly assigned to homocysteine lowering with folic acid 2 mg plus vitamin B12 1 mg daily versus matching placebo. The primary endpoint was major vascular events, defined as coronary death, myocardial infarction, stroke, or arterial revascularization.

# Results
- Major vascular events occurred in 24.5% of patients receiving 80 mg simvastatin versus 25.7% of those receiving 20 mg.
- An average of 0.35 mmol/L greater reduction in LDL-C was observed in the group receiving 80 mg simvastatin compared to those receiving 20 mg.
- Overall 6% reduction in major vascular events was observed in the 80 mg group compared with the 20 mg group.
- Myopathy occurred in 0.9% patients taking 80 mg simvastatin compared with 0.03% patients in the 20 mg simvastatin group.

# Conclusion
The SEARCH study failed to find a benefit with more intensive therapy as a significant number of patients in the 20 mg simvastatin group took an additional statin off protocol as more intensive LDL-C goals were promulgated.
SPARCL Study

# Objective
To study the effects of statins on incidence of recurrent stroke after a recent episode of stroke or transient ischemic attack

# Methods
Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) was a double blinded study with subjects who had at least one episode of stroke in the last one to six months and LDL levels of 100 to 190 mg/dl with no history of coronary artery disease. These patients were randomly assorted to receive either 80 mg of atorvastatin daily or placebo. The primary end point for the study was first fatal or non-fatal stroke.

# Results
- During the mean follow up period of 4.9 years, 11.2% of patients from the atorvastatin group and 13.1% of patients from the placebo experienced fatal/non-fatal stroke, with a 5 year absolute risk reduction of 2.2%.
- The 5 year absolute risk reduction in major cardiovascular events was 3.5%.
- The overall mortality rates were similar in both the groups.

# Conclusion
Atorvastatin (80 mg daily) reduced the incidence of recurrent stroke and cardiovascular events in patients with a recent episode of stroke or transient ischemic attacks. However, the incidence of hemorrhagic stroke increased in the atorvastatin group.
STAT protein

# Overview
The Signal Transducers and Activator of Transcription (STAT) proteins regulate many aspects of cell growth, survival and differentiation.  The transcription factors of this family are activated by the Janus Kinase JAK and dysregulation of this pathway is frequently observed in primary tumors and leads to increased angiogenesis, enhanced survival of tumors and immunosuppression. Knockout studies have provided evidence that STAT proteins are involved in the development and function of the immune system and play a role in maintaining immune tolerance and tumor surveillance.

# STAT family
The first two STAT proteins were identified in the interferon system
The seven mammalian STAT family members identified are: STAT1, STAT2, STAT3, STAT4, STAT5 a and b, and STAT6.
STAT1 homodimers are involved in type II interferon signalling, and binds to the GAS (Interferon-Gamma Activated Sequence) promoter to induce expression of ISG (Interferon Stimulated Genes).  In type I interferon signaling, STAT1-STAT2 heterodimer combines with IRF9 (Interferon Response Factor) to form ISGF3 (Interferon Stimulated Gene Factor), which binds to the ISRE (Interferon Stimulated Response Element) promoter to induce ISG expression.

# Function
STAT proteins were originally described as latent cytoplasmic transcription factors that require phosphorylation for nuclear retention. The unphosphorylated STAT proteins shuttles between cytosol and the nucleus waiting for its activation signal. Once the activated transcription factors reaches the nucleus it binds to consensus DNA-recognition motif called gamma activated sites (GAS) in the promoter region of cytokine inducible genes and activates transcription of these genes.

# Activation
Extracellular binding of cytokines induces activation of the intracellular Janus kinase that phosphorylates a specific tyrosine residue in the STAT protein which promotes the dimerization of STAT monomers via their SH2 domain. The phosphorylated dimer is then actively transported in the nucleus via importin a/b and RanGDP  complex. Once inside the nucleus the active STAT dimer binds to cytokine inducible promoter regions of genes containing gamma activated site (GAS) motif and activate transcription of these genes. The STAT protein can be dephosphorylated by nuclear phosphatases which leads to inactivation of STAT and the transcription factor becomes transported out of the nucleus by exportin crm1/RanGTP.
Sal ammoniac
Sal ammoniac is a rare mineral composed of ammonium chloride, NH4Cl. It forms colorless to white to yellow-brown crystals in the isometric-hexoctahedral class. It has very poor cleavage and a brittle to conchoidal fracture. It is quite soft, with a Mohs hardness of 1.5 to 2, and has a low specific gravity of 1.5. It is water-soluble.
It typically forms as encrustations formed by sublimation around volcanic vents. It is found around volcanic fumaroles, guano deposits and burning coal seams. Associated minerals include sodium alum, native sulfur and other fumarole minerals. Notable occurrences include Tadzhikistan; Mt. Vesuvius, Italy; and Paricutin, Michoacan, Mexico.
Sal ammoniac is also the archaic name for the chemical compound ammonium chloride; from Greek,   hals ammoniakos, salt of Ammon, because of its early manufacture in Egypt.
It is commonly used as a flux in the soldering of stained-glass windows. In both jewelery-making and the refining of precious metals, potassium carbonate (cream of tartar) is added to gold and silver in a borax-coated crucible to purify iron or steel filings that may have contaminated the scrap. It is then air-cooled and remelted with a one-to-one mixture of powdered charcoal and sal ammoniac to yield a sturdy ingot of the respective metal or alloy in the case of sterling silver (0.75% copper) or karated gold. Anything other than 24-karat gold has silver and copper added. Usually the addition of silica, zinc, and deoxidants in very small amounts relative to the pennyweight (dwt.) of gold are processed into gold from as low as 8-karat to as high as 23.5-karat gold. This is added to prevent porosity or cracking while milling the ingot further into wire, sheet, or tubing. Without those additives an otherwise poor-quality ingot will result in open crucible melting with a hand torch or blowpipe and flame, as was done before electric melting furnaces were invented for use in the precious metals industry. These practices are still used by metalsmiths and jewelers today.
Sal ammoniac has also been used in the past in bakery products to give cookies a very crisp texture, although that application is rapidly dying due to the general disuse of it as an ingredient. However, in some areas of Europe, particularly Scandinavia, it is still widely used in the production of salty licorice candy known as Salmiak. The term sal ammoniac has largely fallen out of general use in the 20th century.