Persius/hicric huggingface dataset:
Time of Useful Consciousness
Time of useful consciousness (TUC) is defined as the amount of time an individual is able to perform flying duties efficiently in an environment of inadequate oxygen supply. It is the period of time from the interruption of the oxygen supply or exposure to an oxygen-poor environment to the time when useful function is lost, and the individual is no longer capable of taking proper corrective and protective action. It is not the time to total unconsciousness. The TUC has also been called Effective Performance Time (EPT). At the higher altitudes, the TUC becomes very short; considering this danger, the emphasis is on prevention rather than cure.

# Medical analysis and variations
There are many individual variations of hypoxia, even within the same person.  Generally, old age tends to reduce the efficiency of the pulmonary system, and can cause the onset of hypoxia symptoms sooner.  Smoking drastically reduces oxygen intake efficiency, and can have the effect of reducing tolerance by 1,000-2,000 meters.  Hypoxia can be simulated in an altitude chamber.  This can be useful for identifying individual symptoms of hypoxia, along with rough estimates of the altitude that causes problems for each person.    Identifying symptoms is often helpful for self-diagnosis in order to realize when altitude should be reduced.  Although the times in the table below are often called average TUCs, an average failure is meaningless to a person who has a shorter TUC.
The table below reflects various altitudes with the corresponding average TUC. These times have been established from observations over a period of years and are for an individual at rest. Any exercise will reduce the time considerably. For example, usually upon exposure to hypoxia at FL 250, an average individual has a TUC of 3 to 5 minutes. The same individual, after performing 10 deep knee bends, will have a TUC in the range of 1 to 1.5 minutes.
A rapid decompression can reduce the TUC by up to 50 percent caused by the forced exhalation of the lungs during decompression and the extremely rapid rate of ascent.
Tinidazole adverse reactions

# Adverse Reactions

## Clinical Studies Experience
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
Among 3669 patients treated with a single 2 g dose of tinidazole, in both controlled and uncontrolled trichomoniasis and giardiasis clinical studies, adverse reactions were reported by 11.0% of patients. For multi-day dosing in controlled and uncontrolled amebiasis studies, adverse reactions were reported by 13.8% of 1765 patients. Common ( 1% incidence) adverse reactions reported by body system are as follows. (Note: Data described in Table 1 below are pooled from studies with variable designs and safety evaluations.)
Other adverse reactions reported with tinidazole include:
- Central Nervous System: Two serious adverse reactions reported include convulsions and transient peripheral neuropathy including numbness and paresthesia . Other CNS reports include vertigo, ataxia, giddiness, insomnia, drowsiness.
- Gastrointestinal: tongue discoloration, stomatitis, diarrhea
- 'Hypersensitivity: urticaria, pruritis, rash, flushing, sweating, dryness of mouth, fever, burning sensation, thirst, salivation, angioedema
- Renal: darkened urine
- Cardiovascular: palpitations
- Hematopoietic: transient neutropenia, transient leukopenia
- Other: Candida overgrowth, increased vaginal discharge, oral candidiasis, hepatic abnormalities including raised transaminase level, arthralgias, myalgias, and arthritis.
Rare reported adverse reactions include bronchospasm, dyspnea, coma, confusion, depression, furry tongue, pharyngitis and reversible thrombocytopenia.
Adverse Reactions in Pediatric Patients: In pooled pediatric studies, adverse reactions reported in pediatric patients taking tinidazole were similar in nature and frequency to adult findings including nausea, vomiting, diarrhea, taste change, anorexia, and abdominal pain.
Bacterial vaginosis: The most common adverse reactions in treated patients (incidence >2%), which were not identified in the trichomoniasis, giardiasis and amebiasis studies, are gastrointestinal: decreased appetite, and flatulence; renal: urinary tract infection, painful urination, and urine abnormality; and other reactions including pelvic pain, vulvo-vaginal discomfort, vaginal odor, menorrhagia, and upper respiratory tract infection .

## Postmarketing Experience
The following adverse reactions have been identified and reported during post-approval use of Tindamax. Because the reports of these reactions are voluntary and the population is of uncertain size, it is not always possible to reliably estimate the frequency of the reaction or establish a causal relationship to drug exposure.
Severe acute hypersensitivity reactions have been reported on initial or subsequent exposure to tinidazole. Hypersensitivity reactions may include urticaria, pruritis, angioedema, Stevens-Johnson syndrome and erythema multiforme.
Tipranavir adverse reactions

# Adverse Reactions
The following adverse reactions are described, in greater detail, in other sections:
- Hepatic Impairment and Toxicity
- Intracranial Hemorrhage
- Rash
Due to the need for co-administration of APTIVUS with ritonavir, please refer to ritonavir prescribing information for ritonavir-associated adverse reactions.
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice.
Tipranavir contraindications

# Contraindications

## Hepatic Impairment
APTIVUS is contraindicated in patients with moderate or severe (Child-Pugh Class B or C, respectively) hepatic impairment.

## Drug Interactions
Co-administration of APTIVUS/ritonavir with drugs that are highly dependent on CYP 3A for clearance or are potent CYP 3A inducers are contraindicated (see Table 1). These recommendations are based on either drug interaction studies or they are predicted interactions due to the expected magnitude of interaction and potential for serious events or loss of efficacy. For information regarding clinical recommendations .
Due to the need for co-administration of APTIVUS with ritonavir, please refer to the ritonavir prescribing information for a description of ritonavir contraindications.
Tobramycin adverse reactions

# Adverse Reactions
TOBI was generally well tolerated during two clinical studies in 258 cystic fibrosis patients ranging in age from 6 to 48 years. Patients received TOBI in alternating periods of 28 days on and 28 days off drug in addition to their standard cystic fibrosis therapy for a total of 24 weeks.
Voice alteration and tinnitus were the only adverse experiences reported by significantly more TOBI -treated patients. Thirty-three patients (13%) treated with TOBI complained of voice alteration compared to 17 (7%) placebo patients. Voice alteration was more common in the on-drug periods.
Eight patients from the TOBI group (3%) reported tinnitus compared to no placebo patients. All episodes were transient, resolved without discontinuation of the TOBI treatment regimen, and were not associated with loss of hearing in audiograms. Tinnitus is one of the sentinel symptoms of cochlear toxicity, and patients with this symptom should be carefully monitored for high frequency hearing loss. The numbers of patients reporting vestibular adverse experiences such as dizziness were similar in the TOBI and placebo groups.
Nine (3%) patients in the TOBI group and nine (3%) patients in the placebo group had increases in serum creatinine of at least 50% over baseline. In all nine patients in the TOBI group, creatinine decreased at the next visit.
Table 1 lists the percent of patients with treatment-emergent adverse experiences (spontaneously reported and solicited) that occurred in >5% of TOBI patients during the two Phase III studies.
Adverse drug reactions (<5%) occurring more frequently with TOBI in the placebo-controlled studies and assessed as drug-related in 1% of patients:

### Ear and labyrinth disorders
Tinnitus (3.1%, vs 0% for placebo)

### Musculoskeletal and connective tissue disorders
Myalgia (4.7%, vs 2.7% for placebo)

### Infections and infestations
Laryngitis (4.3%, vs 3.1% for placebo)

## Adverse drug reactions derived from spontaneous reports
The following adverse reactions have been identified during postapproval use of TOBI. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.

### Ear and labyrinth disorders
Hearing loss (see WARNINGS  Ototoxicity)

### Skin and subcutaneous tissue disorders
Hypersensitivity, pruritus, urticaria, rash

### Nervous system disorders
Aphonia, dysgeusia

### Respiratory, thoracic, and mediastinal disorders
Bronchospasm (see WARNINGS  Bronchospasm), oropharyngeal pain
Tracheobronchial lymph nodes
The tracheobronchial lymph nodes form four main groups:
- (a) tracheal, on either side of the trachea;
- (b) bronchial, in the angles between the lower part of the trachea and bronchi and in the angle between the two bronchi;
- (c) bronchopulmonary, in the hilus of each lung; and
- (d) pulmonary, in the lung substance, on the larger branches of the bronchi.
The afferents of the tracheobronchial glands drain the lungs and bronchi, the thoracic part of the trachea and the heart; some of the efferents of the posterior mediastinal glands also end in this group.
Their efferent vessels ascend upon the trachea and unite with efferents of the internal mammary and anterior mediastinal glands to form the right and left bronchomediastinal trunks.
Transforming Faces Worldwide
Transforming Faces Worldwide (TFW) is an international humanitarian organization which provides free surgery and rehabilitation for cleft lip and palate in developing countries.
Founded in 1999, TFW is the first organization of its kind in the world to provide both surgery and long-term rehabilitation for cleft patients in developing countries, using a multidisciplinary approach to cleft treatment.
TFW was founded on the principle of enabling medical teams to treat cleft lip and palate in their home communities.  TFW trains surgeons and specialists within partner countries to treat and rehabilitate people with cleft lip and palate.  
TFW now holds partnerships with medical teams from Ghana, Ethiopia, India, Nepal, Thailand, Peru, and Argentina.
Over the years, TFW has supported over 2,500 surgeries and over 32,000 rehabilitation treatments for children with cleft lip and palate.  Transforming Faces Worldwide is a registered Canadian charity with the Canada Revenue Agency.
Trenton Psychiatric Hospital
The Trenton Psychiatric Hospital is a state run mental hospital located in Trenton, New Jersey.
It previously operated under the name New Jersey State Hospital at Trenton and originally as the New Jersey State Lunatic Asylum.
Founded by Dorothea Lynde Dix on May 15, 1848, it was the first public mental hospital in the state of New Jersey.
Under the Hospital's first superintendent Dr. Horace A. Buttolph, the hospital admitted and treated 86 patients.
In 1907 Dr. Henry Cotton became the medical director.
Cotton's legacy of hundreds of fatalities and thousands of maimed and mutilated patients didn't end with his leaving Trenton in 1930 or his death in 1933, in fact removal of patients' teeth at the Trenton asylum was still the norm until 1960.
Triangle of Death (medicine)

# Overview
Triangle of Death is a medical term describing the fatal combination of hypothermia, acidosis and coagulopathy.
The three conditions share a complex relationship; each factor can compound the others, resulting in high mortality if the cycle continues uninterrupted.
Severe haemorrhage in trauma diminishes oxygen delivery, causing the patient's body temperature to drop (hypothermia). This in turn can halt the coagulation cascade, preventing blood from clotting (coagulopathy).
In the absence of blood-bound oxygen and nutrients (hypoperfusion), the body's cells burn glucose for energy (lactic acidosis), which in turn increases the blood's acidity (metabolic acidosis). Such an increase in acidity can reduce the efficiency of the heart muscles (myocardial performance), further reducing the oxygen delivery and hence triggering a deadly cycle.

# Related Chapters
- Hypothermia
- Coagulation
- Acidosis
Trousseau sign of malignancy

# Overview
The Trousseau sign of malignancy is a medical sign commonly found in certain cancers. It is also referred to as Trousseau syndrome and is distinct from the Trousseau sign of latent tetany.
Some malignancies, especially adenocarcinomas of the pancreas and lung, are associated with hypercoagulability (the tendency to form blood clots) for reasons that are incompletely understood, but may be related to factors secreted by the tumors. In patients with malignancy-associated hypercoagulable states, the blood may spontaneously form clots in the portal vessels, the deep veins of the extremities (such as the leg), or the superficial veins anywhere on the body. These clots present as visibly swollen blood vessels (vasculitis), especially the veins, or as intermittent pain in the affected areas.  The pathological phenomenon of clots forming, resolving and then appearing again elsewhere in the body has been named thrombophlebitis migrans or migratory thrombophlebitis.
Armand Trousseau first described this finding in himself; he was subsequently diagnosed with pancreatic cancer.

## Complete Differential Diagnosis of the Causes of Trousseau Sign of Malignancy
(In alphabetical order)
Migratory thrombophlebitis:
- Colon cancer
- Gastric carcinoma
- Lung cancer
- Ovarian cancer
- Pancreatic cancer

## Complete Differential Diagnosis of the Causes of Trousseau Sign of Malignancy:
(By organ system)
Ubiquitin-conjugating enzyme
Ubiquitin-conjugating enzymes, also known as E2 enzymes and more rarely as ubiquitin-carrier enzymes, perform the second step in the ubiquitination reaction that targets a protein for degradation via the proteasome.The ubiquitination process covalently attaches ubiquitin, a short protein of 76 amino acids, to a lysine residue on the target protein. Once a protein has been tagged with one ubiquitin molecule, additional rounds of ubiquitination form a polyubiquitin chain that is recognized by the proteasome's 19S regulatory particle, triggering the ATP-dependent unfolding of the target protein that allows passage into the proteasome's 20S core particle, where proteases degrade the target into short peptide fragments for recycling by the cell.
A ubiquitin-activating enzyme or E1 first activates the ubiquitin by covalently attaching the molecule to its active site cysteine residue. The activated ubiquitin is then transferred to an E2 cysteine. Once conjugated to ubiquitin, the E2 molecule binds one of several ubiquitin ligases or E3s via a structurally conserved binding region. The E3 molecule is responsible for binding the target protein substrate and transferring the ubiquitin from the E2 cysteine to a lysine residue on the target protein.
A particular cell usually contains only a few types of E1 molecule, a greater diversity of E2s, and a very large variety of E3s. The E3 molecules responsible for substrate identification and binding are thus the mechanisms of substrate specificity in proteasomal degradation. Each type of E2 can associate with many E3s.
Ultraviolet light and cancer

# Overview
The article examines the connection between natural ultraviolet light (UV) radiation and the incidence of cancer in human beings.
The connection between UV radiation and cancer is well known to scientists, and what is debated by public policy advocates is the role of ozone. Some researchers have claimed that Ultraviolet radiation levels are (or were) increasing at an alarming level. They concluded that cancer rater would go up accordingly, unless emissions suspected of reducing the protective effect of atmospheric ozone were banned.
In 1993, J B Kerr and C T McElroy published Evidence for large upward trends of ultraviolet-B radiation linked to ozone depletion(Science 262:1032). This was disputed by P J Michaels et al. (Science 264:1342) but Kerr and McElroy re-affirmed their original findings (Science 264:1342).
See:
- UVA
- UVB
See also:
- ozone layer
- ozone depletion
- Antarctic ozone hole
- Montreal Protocol
United Homeless Organization
The United Homeless Organization is a charity based in New York City, formed in 1987, that advocates for the homeless and solicits money at tables located in various locations in Manhattan.  More than three quarters of the workers are homeless, and all are currently or have been homeless at one time.  According to a 2001 article, at the donation tables, $15 per shift is set aside for the organization while the rest goes to the solicitor.

# Sources
-  F.Y.I. (The City Weekly Desk)
Daniel B. Schneider. New York Times (Late Edition (East Coast)). New York, N.Y.: July 1, 2001; p. 14.2 (accessed through ProQuest).
-  F.Y.I. (The City Weekly Desk) Daniel B. Schneider. New York Times (Late Edition (East Coast)). New York, N.Y.: July 1, 2001; p. 14.2 (accessed through ProQuest).
Unknown substance withdrawal

# Overview

# Differential Diagnosis
- Dose reduction after extended dosing, but not meeting the criteria for other (or unknown)substance withdrawal
- Different types of other (or unknown) substance-related disorders
- Other toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that impair brain function and cognition
- Substance withdrawal or other substance/medication-induced disorders

# Epidemiology and Demographics

## Prevalence
The prevalence of  Other (or Unknown) Substance Withdrawal is unknown.

# Diagnostic Criteria

## DSM-V Diagnostic Criteria for Other (or Unknown) Substance Withdrawal
Valproate sodium description

# Description
Depacon (valproate sodium) is the sodium salt of valproic acid designated as sodium 2-propylpentanoate. Valproate sodium has the following structure:
Valproate sodium has a molecular weight of 166.2. It occurs as an essentially white and odorless, crystalline, deliquescent powder.
Depacon solution is available in 5 mL single-dose vials for intravenous injection. Each mL contains valproate sodium equivalent to 100 mg valproic acid, edetate disodium 0.40 mg, and water for injection to volume. The pH is adjusted to 7.6 with sodium hydroxide and/or hydrochloric acid. The solution is clear and colorless.
Vancomycin adverse reactions
Infusion-Related Events
During or soon after rapid infusion of vancomycin, patients may develop anaphylactoid reactions, including hypotension (see ANIMAL PHARMACOLOGY), wheezing, dyspnea, urticaria, or pruritus. Rapid infusion may also cause flushing of the upper body (red neck) or pain and muscle spasm of the chest and back. These reactions usually resolve within 20 minutes but may persist for several hours. Such events are infrequent if vancomycin is given by a slow infusion over 60 minutes. In studies of normal volunteers, infusion-related events did not occur when vancomycin was administered at a rate of 10 mg/min or less.
Nephrotoxicity
Renal failure, principally manifested by increased serum creatinine or BUN concentrations, especially in patients administered large doses of vancomycin, has been reported rarely. Cases of interstitial nephritis have also been reported rarely. Most of these have occurred in patients who were given aminoglycosides concomitantly or who had preexisting kidney dysfunction. When vancomycin was discontinued, azotemia resolved in most patients.
Gastrointestinal
Onset of pseudomembranous colitis symptoms may occur during or after antibiotic treatment (see WARNINGS).
Ototoxicity
A few dozen cases of hearing loss associated with vancomycin have been reported. Most of these patients had kidney dysfunction or a preexisting hearing loss or were receiving concomitant treatment with an ototoxic drug. Vertigo, dizziness, and tinnitus have been reported rarely.
Hematopoietic
Reversible neutropenia, usually starting 1 week or more after onset of therapy with vancomycin or after a total dosage of more than 25 g, has been reported for several dozen patients. Neutropenia appears to be promptly reversible when vancomycin is discontinued. Thrombocytopenia has rarely been reported. Although a causal relationship has not been established, reversible agranulocytosis (granulocytes <500/mm3) has been reported rarely.
Phlebitis
Inflammation at the injection site has been reported.
Miscellaneous
Infrequently, patients have been reported to have had anaphylaxis, drug fever, nausea, chills, eosinophilia, rashes including exfoliative dermatitis, Stevens-Johnson syndrome, and vasculitis in association with administration of vancomycin.
Chemical peritonitis has been reported following intraperitoneal administration of vancomycin (see PRECAUTIONS).
Post Marketing Reports
The following adverse reactions have been identified during post-approval use of vancomycin. Because these reactions are reported voluntarily from a population of uncertain size, it is not possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Skin and Subcutaneous Tissue Disorders
Drug Rash with Eosinophilia and Systemic Symptoms (DRESS)
Ventricular action potential

# Overview
The ventricular action potential is composed of four phases: phase 0 is depolarization, phase 1 is early repolarization, phase 2 is a plateau, phase 3 is rapid repolarization and phase 4 is the resting potential.  The different phases depend on the opening and/or closure of specific ion channels.

# Ventricular Action Potential
At rest, the ventricular myocyte membrane potential is about -90 mV, which is close to the potassium reversal potential.  When an action potential is generated, the membrane potential rises above this level in four distinct phases.
The beginning of the action potential, phase 1, specialized membrane proteins (voltage-gated sodium channels) in the cell membrane selectively allow sodium ions to enter the cell.  This causes the membrane potential to rise at a rate of about 300 V/s.  As the membrane voltage rises (to about 40 mV) sodium channels close due to a process called inactivation.
The sodium channel opening is followed by inactivation.  Sodium inactivation comes with slowly inactivating Ca2+ channels at the same time as a few fast K+ channels open. There is a balance between the centrifugal flow of K+ and the centripetal flow of Ca2+ causing a plateau of length in variables.  The delayed opening of more Ca2+-activated K+ channels, which are activated by build-up of Ca2+ in the sarcoplasm, while the Ca2+ channels close, ends the plateau. This leads to repolarisation.
The depolarization of the membrane allows calcium channels to open as well.  As sodium channels close calcium provides current to maintain the potential around 10 mV.  The plateau lasts on the order of 100 ms.  At the time that calcium channels are getting activated, channels that mediate the transient outward potassium current open as well.  This outward potassium current causes a small dip in membrane potential shortly after depolarization.  This current is observed in human and dog action potentials, but not in guinea pig action potentials.
Repolarization is accomplished by channels that open slowly and are mostly activated at the end of the action potential (slow delayed-rectifier channels), and channels that open quickly but are inactivated until the end of the action potential (rapid delayed rectifier channels).  Fast delayed rectifier channels open quickly but are shut by inactivation at high membrane potentials.  As the membrane voltage begins to drop the channels recover from inactivation and carry current.
Shown below is an image summarizing the phases of the ventricular action potential.