Persius/hicric huggingface dataset:
Hammett acidity function
- Acid-base extraction
- Acid-base reaction
- Acid dissociation constant
- Acidity function
- Buffer solutions
- pH
- Proton affinity
- Self-ionization of water
- Acids:
Lewis acids
Mineral acids
Organic acids
Strong acids
Superacids
Weak acids
- Lewis acids
- Mineral acids
- Organic acids
- Strong acids
- Superacids
- Weak acids
- Bases:
Lewis bases
Organic bases
Strong bases
Superbases
Non-nucleophilic bases
Weak bases
- Lewis bases
- Organic bases
- Strong bases
- Superbases
- Non-nucleophilic bases
- Weak bases
edit
The Hammett acidity function is a measure of acidity that is used for very concentrated solutions of strong acids, including superacids. In such solutions, simple approximations such as the Henderson-Hasselbalch equation are no longer valid due to the variations of the activity coefficients in highly concentrated solutions. The Hammett acidity function is used in fields such as physical organic chemistry for the study of acid-catalyzed reactions, because some of these reactions use acids in very high concentrations, or even neat (pure).
The Hammett acidity function, H0, is used as a pH surrogate. It is defined as
H_{0} = -\log h_0 = -\log \left ( a_{H_3O^+} \frac{\gamma_B}{\gamma_{BH^+}} \right )
where a is the activity, and  are the activity coefficients of a base B and its conjugate acid BH+. H0 can be calculated using an equation analogous to the Henderson-Hasselbalch equation:
H_{0} = \mbox{p}K_{BH^+}  + \log \frac{}{}
where pKBH+ is log(K) for the dissociation of BH+. By using bases with very negative pKBH+ values, the H0 scale may be extended to negative values. Hammett originally used a series of anilines with electron-withdrawing groups for the bases.
On this scale, pure H2SO4 (18.4 M) has a H0 value of 12, and pyrosulfuric acid has H0 ~ 15. Take note that the Hammett acidity function clearly avoids water in its equation. It is a generalization of the pH scalein a dilute aqueous solution (where B is H2O), pH is very nearly equal to H0. By using a solvent-independent quantitative measure of acidity, the implications of the leveling effect are eliminated, and it becomes possible to directly compare the acidities of different substances (e.g. using pKa, HF is weaker than HCl in water but stronger than HCl in glacial acetic acid; however, pure HF is "stronger" than HCl because the H0 of pure HF is higher than that of pure HCl.)
H0 for some concentrated acids:
- Fluoroantimonic acid (1990): 31.3
- Magic acid (1974): 19.2
- Carborane superacid (1969): 18.0
- Fluorosulfuric acid (1944): 15.1
- Triflic acid (1940): 14.9
- Sulfuric acid 12.0
For mixtures (e.g., partly diluted acids in water), the acidity function depends on the composition of the mixture and has to be determined empirically. Graphs of H0 vs mole fraction can be found in the literature for many acids.
Although the Hammett acidity function is the best known acidity function, other acidity functions have been developed by authors such as Arnett, Cox, Katrizky, Yates, and Stevens.
Health care in Argentina
Argentinas health care system is composed of three sectors: the public sector, financed through taxes; the private sector, financed through voluntary insurance schemes, and the social security sector, financed through obligatory insurance schemes.  The Ministry of Health and Social Action (MSAS), oversees all three subsectors of the health care system and is responsible for setting of regulation, evaluation and collecting statistics.
The public sector is funded and managed by Obras Sociales, umbrella organizations for Argentine worker's unions.  There are over 300 Obras Sociales in Argentina, each chapter being organized according to the occupation of the beneficiary.   These organizations vary greatly in quality and effectiveness.   The top 30 chapters hold 73% of the beneficiaries and 75% of resources for all Obras Sociales schemes and the monthly average a beneficiary receives varies from $5-80 dollars per month.    MSAS has established a Solidarity Redistribution Fund (FSR) to try to address these beneficiary inequities.  Only workers employed in the formal sector are covered under Obras Sociales insurance schemes and after Argentinas economic crisis of 2001, the number of those covered under these schemes fell slightly (as unemployment increased and employment in the informal sector rose).  In 1999, there were 8.9 million beneficiaries covered by Obras Sociales.
The private health care sector in Argentina is characterized by great heterogeneity and is made up of a great number of fragmented facilities and small networks; it consists of over 200 organizations and covers approximately 2 million Argentines.  Private insurance often overlaps with other forms of health care coverage, thus it is difficult to estimate the degree to which beneficiaries are dependent on the public and private sectors.  According to a 2000 report by the IRBC, foreign competition has increased in Argentinas private sector, with Swiss, American and other Latin American health care providers entering the market in recent years.  This has been accompanied by little formal regulation.
The public system serves those not covered by Obras Sociales or private insurance schemes.  It also provides emergency services.  According to above-mentioned IRBC report, Argentinas public system 
exhibits serious structural deterioration and managerial inefficiency; a high degree of administrative centralization at the provincial level; rigidity in its staffing structure and labour relationships; no adequate system of incentives; inadequate information systems on which to base decision-making and control; serious deficits in facilities and equipment maintenance; and a system of management ill-suited to its size.
The public system is highly decentralized to the provincial level; often primary care is even under the purview of local townships.  Since 2001, the number of Argentines relying on public services has seen an increase.  According to 2000 figures, 37.4% of Argentines had no health insurance, 48.8 were covered under Obras Sociales, 8.6% had private insurance, and 3.8% were covered by both Obras Sociales and private insurance schemes.
Health care in Australia
Health care in Australia is provided by both private and government institutions. The subject is often debated and continues to be a political issue as services are often inadequately facilitated. The Minister for Health and Ageing, Tony Abbott administers national health policy.

# National health policy
Following the global trend, services have been moving from a mostly publicly-funded health care model to a mixed market with a growing health care industry responsible for health care management. Essentially this has been driven by two-tier health care policy where payment methods have been encouraged via third party insurers who charge an annual fee to cover potential heath care costs, from the fee free model based bulk billing service by a general practitioner.

## Programs
The federal government agency Medicare Australia is responsible for administering programs like the universal health care-based Medicare and medicine subsidies under the Pharmaceutical Benefits Scheme.
The federal government provides a health care card to low income earners that entitles the holder to reduced costs for some services such as dental and eye-wear.
The Australian Organ Donor Register is also maintained by the federal government.

# Issues
Cigarette smoking is the largest preventable cause of death and disease in Australia. 
State governments are responsible for managing hospitals and community health care centres.  Services across the country have been routinely criticised for lengthy waiting times in emergency rooms and for non-life threatening operations.
Many parts of remote and rural Australia suffer from a shortage of doctors and health care services, so the federal government started the Medical Rural Bonded Scheme to encourage medical practitioners to settle in rural areas.
The quality of aged care is another problem in some parts of the country.

# Peak bodies
- Australian Medical Association
- Royal Australian College of General Practitioners
Hemolysis (microbiology)

# Overview
Hemolysis is used in the empirical identification of microorganisms based on the ability of bacterial colonies grown on agar plates to break down red blood cells in the culture. When the organism has been grown on blood agar plates, it can be classified with regard to whether or not it has caused hemolysis in the red blood cells (RBCs) incorporated in the medium.  This is of particular importance in the classification of streptococcal species.  A substance that causes hemolysis is a hemolysin.
While a blood agar plate may contain varying concentrations of RBCs and may use blood from a variety of animals, clinical results are  most often reported on 5-10% sheep blood agar plates (SBAP).

# Types of hemolysis
- Alpha hemolysis (-hemolysis) is present if there is a greenish darkening of the agar under the colonies. Streptococcus pneumoniae and Streptococcus viridans display alpha hemolysis.  This is sometimes called green hemolysis because of the color change in the agar.  Other synonymous terms are incomplete hemolysis and partial hemolysis. Alpha hemolysis is generally caused by peroxides produced by the bacterium.
- Beta hemolysis (-hemolysis) is caused by a complete lysis of the red cells in the media. The area around and under the colonies are lightened and transparent. Streptococcus pyogenes, or Group A beta-hemolytic Strep, displays beta hemolysis. Hemolytic tests are also used to differentiate Staphylococcus aureus, which displays beta-hemolysis, from S. epidermidis, a non-hemolytic, commensal species. Beta hemolysis is sometimes called complete hemolysis. Beta hemolysis is caused by hemolysins.
Some weakly beta hemolytic species will cause intense beta hemolysis when grown together with a strain of Staphylococcus. This is called the CAMP test1. Streptococcus agalactiae displays this property. Clostridium perfringens can be identified presumptively with this test.
- Some weakly beta hemolytic species will cause intense beta hemolysis when grown together with a strain of Staphylococcus. This is called the CAMP test1. Streptococcus agalactiae displays this property. Clostridium perfringens can be identified presumptively with this test.
- If an organism does not cause hemolysis, it is said to display gamma hemolysis (-hemolysis): the agar under and around the colony is unchanged (this is also called non-hemolytic). Enterococcus faecalis (formerly called Group D Strep) displays gamma hemolysis.

# Notes
1The CAMP test is so called from the initials of those who initially described it, R. Christie, N. E. Atkins, and E. Munch-Peterson.
Retroperitoneal hematoma

# Overview
Retroperitoneal hemorrhage and retroperitoneal hematoma are potentially life-threatening conditions. Common causes of retroperitoneal hemorrhage are cardiac catheterization and trauma.

# Symptoms
The patient may complain of intense flank pain or back pain.

# Signs
The patient may develop tachycardia and hypotension if the rate of hemorrhage is rapid.
Rarely, later in the course, the patient may develop a Grey-Turner's sign with bulging flanks, and a bluish discoloration in the region of the flank.  Again, it should be emphasized that this sign appears 24 to 48 hours after a severe retroperitoneal bleed and should not be used to gauge whether a retroperitoneal bleed is present acutely.

# Differentiating retroperitoneal heamatoma from other diseases
High endothelial venules
High endothelial venules, or HEVs, are a subtype of blood endothelium present within lymph nodes; used by various leukocytes to gain entry into the lymph node via the blood.
The HEVs are made up of cuboidal endothelial cells, with various receptors to allow entry/rolling interactions between leukocytes and the endothelium.
High endothelial venules are found in lymph nodes and tonsils and Peyer's patches, but not in the thymus or spleen.
High triglyceride causes

# Overview
Hypertriglyceridemia can occur due to various causes, including genetics, familial, metabolic and drugs.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
Hypertriglyceridemia does not have life threatening causes.

## Common Causes
- Diabetes mellitus
- Obesity

## Causes by Organ System

## Causes in Alphabetical Order
Diagnosis

# 2018 AHA ACC Guideline on the Management of Blood Cholesterol. Hypertriglyceridemia Recommendations
Supreme intercostal vein
The supreme intercostal vein (highest intercostal vein) is a paired vein that drains the first intercostal space on its corresponding side.
It can drain into either the brachiocephalic vein, the superior intercostal vein, or the vertebral vein of its corresponding side.
This vein does not have valves, this is an important point when it comes to spread of cancerous secondaries.

# Additional images
- Diagram showing completion of development of the parietal veins.
Superior thoracic artery
The superior thoracic artery (highest thoracic artery) is a small vessel, which may arise from the thoracoacromial.
Running forward and medialward along the upper border of the Pectoralis minor, it passes between it and the Pectoralis major to the side of the chest.
It supplies branches to these muscles, and to the parietes of the thorax, and anastomoses with the internal mammary and intercostal arteries.
Superior thoracic artery is the first division of the axillary artery. Axillary artery can be divided into three sections based on its location relative to the pectoralis minor muscle.
Hydatiform mole overview
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# Overview
Hydatidiform mole (or mola hydatidiforma) is a common complication of pregnancy, occurring once in every 1000 pregnancies in the US, with much higher rates in Asia (e.g. up to one in 100 pregnancies in Indonesia). It consists of a nonviable embryo which implants and proliferates within the uterus.  The term is derived from hydatidiform ("like a bunch of grapes") and mole (from Latin mola = millstone).
Most moles present with painless vaginal bleeding during the second trimester of pregnancy. They are diagnosed by ultrasound imaging. Extremely high levels of human chorionic gonadotropin (HCG) are suggestive, but not diagnostic, of molar pregnancy. Today moles are surgically removed by curettage, in order to avoid the risks of choriocarcinoma.
Hypertensive retinopathy
Hypertensive retinopathy is damage to the retina due to high blood pressure (i.e. hypertension).

# Pathophysiology
The retina is one of the "target organs" that are damaged by sustained hypertension.
Subjected to excessively high blood pressure over prolonged time, the small blood vessels that involve the eye are damaged, thickening, bulging and leaking.
Early signs of retinopathy correlate less well with mortality and morbidity than used to be thought, but signs of accelerated or "malignant" hypertension indicate severe illness.

# Symptoms
Most patients with hypertensive retinopathy present without visual symptoms, however, some may report decreased vision or headaches.

# Signs
Signs of damage to the retina caused by hypertension include:
- Arteriosclerotic changes
Arteriolar narrowing that is almost always bilateral
Grade I - 3/4 normal caliber
Grade II - 1/2 normal caliber
Grade III - 1/3 normal caliber
Grade IV - thread-like or invisible
Arterio-venous crossing changes (aka "AV nicking") with venous constriction and banking
Arteriolar color changes
Copper wire arterioles are those arterioles in which the central light reflex occupies most of the width.
Silver wire arterioles are those in which the central light reflex occupies all of the width of the arteriole.
Vessel sclerosis
- Arteriolar narrowing that is almost always bilateral
Grade I - 3/4 normal caliber
Grade II - 1/2 normal caliber
Grade III - 1/3 normal caliber
Grade IV - thread-like or invisible
- Grade I - 3/4 normal caliber
- Grade II - 1/2 normal caliber
- Grade III - 1/3 normal caliber
- Grade IV - thread-like or invisible
- Arterio-venous crossing changes (aka "AV nicking") with venous constriction and banking
- Arteriolar color changes
Copper wire arterioles are those arterioles in which the central light reflex occupies most of the width.
Silver wire arterioles are those in which the central light reflex occupies all of the width of the arteriole.
- Copper wire arterioles are those arterioles in which the central light reflex occupies most of the width.
- Silver wire arterioles are those in which the central light reflex occupies all of the width of the arteriole.
- Vessel sclerosis
- Ischemic changes (e.g. "cotton wool spots")
- Hemorrhages, often flame shaped.
- Edema
Ring of exudates around the retina called a "macular star"
- Ring of exudates around the retina called a "macular star"
- Papilledema, or optic disc edema, in patients with malignant hypertension
- Visual acuity loss, typically due to macular involvement

# Diagnosis
- Fluorescein angiography
- Ophthalmoscopy
- Sphygmomanometry

# Treatment and management
A major aim of treatment is to prevent, limit, or reverse such target organ damage by lowering the patient's high blood pressure. The eye is an organ where damage is easily visible at an early stage, so regular eye examinations are important.
Hyperthyroidism overview

# Overview
Hyperthyroidism is the clinical syndrome caused by an excess of circulating free thyroxine (T4) or free triiodothyronine (T3), or both.

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Hyperthyroidism from other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications and Prognosis

# Diagnosis

## History and Symptoms

## Physical Examination
Minor ocular signs, which may be present in any type of hyperthyroidism, are eyelid retraction ("stare") and lid-lag. These "fear-like" eye-signs result from thyroid hormone's exacerbation of the action of norepinephrine. In hyperthyroid stare (Dalrymple sign) the eyelids are retracted upward more than normal (the normal position is at the superior corneoscleral limbus, where the "white" of the eye begins at the upper border of the iris). In lid-lag (von Graefe's sign), when the patient tracks an object downward with their eyes, the eyelid fails to follow the downward moving iris, and the same type of upper globe exposure which is seen with lid retraction occurs, temporarily. These signs disappear with treatment of the hyperthyroidism, or treatment by certain anti-adrenergic drugs.

## Laboratory Findings
A diagnosis is suspected through blood tests, by measuring the level of thyroid-stimulating hormone (TSH) in the blood. A low TSH (the job of TSH taken over by thyroid-stimulating immunoglobulin  that act like TSH) indicates increased levels of T4 and/or T3 in the blood. Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, may contribute to the diagnosis.

## Electrocardiogram

## Chest X Ray

## CT

## MRI

## Echocardiography or Ultrasound

## Other Imaging Findings
In all patients with hyperthyroxinemia, scintigraphy is required in order to distinguish true hyperthyroidism from thyroiditis.

## Other Diagnostic Studies

# Treatment

## Medical Therapy
The major and generally accepted modalities for treatment of hyperthyroidism in humans involve initial temporary use of suppressive thyrostatics medication, and possibly later use of permanent surgical or radioisotope therapy. All approaches may cause under active thyroid function (hypothyroidism) which is easily managed with levothyroxine supplementation.

## Surgery
Surgery as an option predates the use of the less invasive radioisotope therapy, but is still required in cases where the thyroid gland is enlarged and causing compression to the neck structures, or the underlying cause of the hyperthyroidism may be cancerous in origin.

## Primary Prevention

## Secondary Prevention

## Cost-Effectiveness of Therapy

## Future or Investigational Therapies

# Case Studies

## Case #1
IMITREX spray overdosage

# Overdosage
In clinical trials, the highest single doses of IMITREX Nasal Spray administered without significant reactions were 40 mg to 12 volunteers and 40 mg to 85 subjects with migraine, which is twice the highest single recommended dose. In addition, 12 volunteers were administered a total daily dose of 60 mg (20 mg 3 times daily) for 3.5 days without significant adverse reactions.
Overdose in animals has been fatal and has been heralded by convulsions, tremor, paralysis, inactivity, ptosis, erythema of the extremities, abnormal respiration, cyanosis, ataxia, mydriasis, salivation, and lacrimation.
The elimination halflife of sumatriptan is approximately 2 hours , and therefore monitoring of patients after overdose with IMITREX Nasal Spray should continue for at least 10 hours or while symptoms or signs persist.
It is unknown what effect hemodialysis or peritoneal dialysis has on the serum concentrations of sumatriptan.
IMPROVEDD VTE risk score
Synonyms and keywords:

# Overview
The IMPROVEDD VTE Risk Score, which incorporates D-dimer measurement into the IMPROVE (International Medical Prevention Registry on Venous Thromboembolism) score, refines the prediction of symptomatic venous thromboembolism (including symptomatic deep-vein thrombosis, nonfatal pulmonary embolism, and death related to venous thromboembolism) events in acutely ill hospitalized patients up to 77 days of hospitalization.

# IMPROVEDD VTE Risk Score
The IMPROVEDD VTE Risk Score, which incorporates D-dimer measurement into the IMPROVE (International Medical Prevention Registry on Venous Thromboembolism) score, refines the prediction of symptomatic venous thromboembolism (including symptomatic deep-vein thrombosis, nonfatal pulmonary embolism, and death related to venous thromboembolism) events in acutely ill hospitalized patients up to 77 days of hospitalization.

# IMPROVEDD VTE Risk Score Calculator
Shown below is the calculator for IMPROVEDD Score for VTE (check all the boxes that apply):
function calcScore(){
var score = 0;
if(document.forms.checked == 1){score += 3;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 2;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 2;
document.forms.value = score;
if(score == 0){document.forms.value = "0.4% at 3542 days; 0.5% at 77 days";}
if(score == 1){document.forms.value = "0.6% at 3542 days; 0.7% at 77 days";}
if(score == 2){document.forms.value = "0.8% at 3542 days; 1.0% at 77 days";}
if(score == 3){document.forms.value = "1.2% at 3542 days; 1.4% at 77 days";}
if(score == 4){document.forms.value = "1.6% at 3542 days; 1.9% at 77 days";}
if(score >= 5 && score <= 10){document.forms.value = "2.2% at 3542 days; 2.7% at 77 days";}

# Interpretation
- Score = 0: Predicted Risk of Symptomatic VTE is 0.4% at 35-42 days and 0.5% at 77 days
- Score = 1: Predicted Risk of Symptomatic VTE is 0.6% at 35-42 days and 0.7% at 77 days
- Score = 2: Predicted Risk of Symptomatic VTE is 0.8% at 35-42 days and 1.0% at 77 days
- Score = 3: Predicted Risk of Symptomatic VTE is 1.2% at 35-42 days and 1.4% at 77 days
- Score = 4: Predicted Risk of Symptomatic VTE is 1.6% at 35-42 days and 1.9% at 77 days
- Score  5: Predicted Risk of Symptomatic VTE is 2.2% at 35-42 days and 2.7% at 77 days