Persius/hicric huggingface dataset:
Chalazion (patient information)
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# Overview
A chalazion is a small bump in the eyelid caused by a blockage of a tiny oil gland.

# What are the symptoms of Chalazion?
- Eyelid tenderness
- Increased tearing
- Painful swelling on the eyelid
- Sensitivity to light

# What causes Chalazion?
A chalazion develops in the glands that produce the fluid that lubricates the eye. These are called Meibomian glands. The eyelid has approximately 100 of these glands, which are located near the eyelashes.
A chalazion is caused by a blockage of the duct that drains one of these glands.

# Diagnosis
An exam of the eyelid confirms the diagnosis.
Rarely, the Meibomian gland duct may be blocked by a skin cancer. If this is suspected, you may need a biopsy.

# When to seek urgent medical care?
Apply warm compresses and call your health care provider if the swelling gets worse or continues for longer than 1 month.
Call for an appointment with your health care provider if lumps on the eyelid continue to get bigger despite treatment, or you have an area of eyelash loss.

# Treatment options
A chalazion will often disappear without treatment in a month or so.
The primary treatment is to apply warm compresses for 10-15 minutes at least four times a day. This may soften the hardened oils blocking the duct, and promote drainage and healing.
If the chalazion continues to get bigger, it may need to be removed with surgery. This is usually done from underneath the eyelid to avoid a scar on the skin.
Antibiotic eye drops are usually used several days before and after the cyst is removed. However, they are not much use otherwise in treating a chalazion.
Steroid injection is another treatment option.

# Where to find medical care for Chalazion?
Directions to Hospitals Treating Chalazion

# What to expect (Outlook/Prognosis)?
Chalazia usually heal on their own. The outcome with treatment is usually excellent.

# Possible complications
A large chalazion can cause astigmatism due to pressure on the cornea. This will get better when the chalazion is treated.

# Prevention of Chalazion
Properly cleaning the eyelid may prevent the condition from returning in people who are prone to chalazia. Cleaning the eyelash area with baby shampoo will help reduce clogging of the ducts.

# Sources
Chris Hani Baragwanath Hospital
Chris Hani Baragwanath Hospital is the largest hospital in the world, occupying 173 acres, with 3200 beds and 6760 staff members. The hospital is in Soweto, South Africa - just outside Johannesburg. It is one of the 40 Gauteng provincial hospitals, and is financed and run by the Gauteng provincial Health Authorities.
Opened in 1941 by Prime Minister Smuts as the Royal Imperial Hospital, Baragwanath, the facility was known as Baragwanath Hospital from 1948. The name Chris Hani was added in 1997 to honour a slain African National Congress and South African Communist Party member.
More than two thousand patients check in to the hospital daily and nearly half of them are HIV positive.
Cidofovir clinical pharmacology

# Clinical Pharmacology

## PHARMACOKINETICS
VISTIDE must be administered with probenecid. The pharmacokinetics of cidofovir, administered both without and with probenecid, are described below.
The pharmacokinetics of cidofovir without probenecid were evaluated in 27 HIV-infected patients with or without asymptomatic CMV infection. Dose-independent pharmacokinetics were demonstrated after one hr infusions of 1.0 (n = 5), 3.0 (n = 10), 5.0 (n = 2) and 10.0 (n = 8) mg/kg (See Table 2 for pharmacokinetic parameters). There was no evidence of cidofovir accumulation after 4 weeks of repeated administration of 3 mg/kg/week (n = 5) without probenecid. In patients with normal renal function, approximately 80 to 100% of the VISTIDE dose was recovered unchanged in urine within 24 hr (n = 27). The renal clearance of cidofovir was greater than creatinine clearance, indicating renal tubular secretion contributes to the elimination of cidofovir.
The pharmacokinetics of cidofovir administered with probenecid were evaluated in 12 HIV-infected patients with or without asymptomatic CMV infection and 10 patients with relapsing CMV retinitis. Dose-independent pharmacokinetics were observed for cidofovir, administered with probenecid, after one hr infusions of 3.0 (n = 12), 5.0 (n = 6), and 7.5 (n = 4) mg/kg (See Table 2). Approximately 70 to 85% of the VISTIDE dose administered with concomitant probenecid was excreted as unchanged drug within 24 hr. When VISTIDE was administered with probenecid, the renal clearance of cidofovir was reduced to a level consistent with creatinine clearance, suggesting that probenecid blocks active renal tubular secretion of cidofovir.
In vitro, cidofovir was less than 6% bound to plasma or serum proteins over the cidofovir concentration range 0.25 to 25 g/mL. CSF concentrations of cidofovir following intravenous infusion of VISTIDE 5 mg/kg with concomitant probenecid and intravenous hydration were undetectable (< 0.1 g/mL, assay detection threshold) at 15 minutes after the end of a 1 hr infusion in one patient whose corresponding serum concentration was 8.7 g/mL.

## SPECIAL POPULATIONS
Renal Insufficiency
Pharmacokinetic data collected from subjects with creatinine clearance values as low as 11 mL/min indicate that cidofovir clearance decreases proportionally with creatinine clearance.
High-flux hemodialysis has been shown to reduce the serum levels of cidofovir by approximately 75%.
Initiation of therapy with VISTIDE is contraindicated in patients with serum creatinine > 1.5 mg/dL, a calculated creatinine clearance  55 mL/min, or a urine protein  100 mg/dL (equivalent to 2+ proteinuria) (See CONTRAINDICATIONS).
Geriatric/Gender/Race
The effects of age, gender, and race on cidofovir pharmacokinetics have not been investigated.
Ciprofloxacin direction for use

# Instructions To The Pharmacist For Use/Handling Of CIPRO Oral Suspension:
CIPRO Oral Suspension is supplied in 5% (5 g ciprofloxacin in 100 mL) and 10% (10 g ciprofloxacin in 100 mL) strengths. The drug product is composed of two components (microcapsules and diluent) which must be combined prior to dispensing.
One teaspoonful (5 mL) of 5% ciprofloxacin oral suspension = 250 mg of ciprofloxacin.
One teaspoonful (5 mL) of 10% ciprofloxacin oral suspension = 500 mg of ciprofloxacin.
Appropriate Dosing Volumes of the Oral Suspensions:
Preparation of the suspension:
1. The small bottle contains the microcapsules, the large bottle contains the diluent.
2. Open both bottles. Child-proof cap: Press down according to instructions on the cap while turning to the left.
3. Pour the microcapsules completely into the larger bottle of diluent. Do not add water to the suspension.
4. Remove the top layer of the diluent bottle label (to reveal the CIPRO Oral Suspension label). Close the large bottle completely according to the directions on the cap and shake vigorously for about 15 seconds. The suspension is ready for use.
No additions should be made to the mixed final ciprofloxacin suspension. CIPRO Oral Suspension should not be administered through feeding or NG (nasogastric) tubes due to its physical characteristics.
Instruct the patient:
To shake CIPRO Oral Suspension vigorously each time before use for approximately 15 seconds
To always use the graduated measuring spoon to obtain the exact dose.
Not chew the microcapsules, but to swallow them.
That water may be taken afterwards.
Reclose the bottle properly after each use according to instructions on the cap.
After treatment has been completed, Cipro Oral Suspension should not be reused.
Cloxacillin Sodium microbiology

# Microbiology
Penicillinase-resistant penicillins exert a bactericidal action against penicillin-susceptible microorganisms during the state of active multiplication. All penicillins inhibit the biosynthesis of the bacterial cell wall.
Dicloxacillin sodium has been shown to be active against most strains of the following microorganisms, both in vitro and in clinical infections as described in the INDICATIONS AND USAGE section.
Aerobic Gram-Positive Microorganisms
Staphylococcus spp. (penicillinase producing)

## Susceptibility Testing
- Diffusion Techniques
Quantitative methods that require measurement of zone diameters provide reproducible estimates of the susceptibility of bacteria to antimicrobial compounds. One such standardized procedure1,2 that has been recommended for use with disks to test the susceptibility of microorganisms to dicloxacillin, uses the 1 mcg oxacillin disk. Interpretation involves correlation of the diameter obtained in the disk test with the minimum inhibitory concentration (MIC) for dicloxacillin.
Reports from the laboratory providing results of the standard single-disk susceptibility test with a 1 mcg oxacillin disk should be interpreted according to the criteria provided in Table 1.
- Dilution Techniques
Quantitative methods that are used to determine minimum inhibitory concentrations (MICs) provide reproducible estimates of the susceptibility of bacteria to antimicrobial compounds. One such standardized procedure1,3 uses a standardized dilution method (broth or agar) or equivalent with oxacillin powder. The MIC values obtained should be interpreted according to the criteria provided in Table 1.
A report of Susceptible (S) indicates that the pathogen is likely to be inhibited by usually achievable concentrations of the antimicrobial compound in the blood. A report of Intermediate (I) indicates that the result should be considered equivocal, and, if the microorganism is not fully susceptible to alternative, clinically feasible drugs, the test should be repeated. This category implies possible clinical applicability in body sites where the drug is physiologically concentrated or in situations where high dosage of drug can be used. This category also provides a buffer zone that prevents small uncontrolled technical factors from causing major discrepancies in interpretation. A report of Resistant (R) indicates that usually achievable concentrations of the antimicrobial compound in the blood are unlikely to be inhibitory and that other therapy should be selected.
Measurement of MIC and achieved antimicrobial compound concentrations may be appropriate to guide therapy in some infections. (See CLINICAL PHARMACOLOGY section for further information on drug concentrations achieved in infected body sites and other pharmacokinetic properties of this antimicrobial drug product.)
- Quality Control
Standardized susceptibility test procedures require the use of laboratory control microorganisms.1,2,3 The 1 mcg oxacillin disk and the standard oxacillin powder should provide respectively the following zone diameters and MIC values in these laboratory test quality control strains:
Collagenopathy, types II and XI
The type II and XI collagenopathies are a group of disorders that affect connective tissue, the tissue that supports the body's joints and organs. These disorders are caused by defects in type II or type XI collagen. Collagens are complex molecules that provide structure, strength, and elasticity  to connective tissue. Type II and type XI collagen disorders are grouped together because both types of collagen are components of the cartilage found in joints and the spinal column, the inner ear, and the jelly-like substance that fills the eyeball (the vitreous). The type II and XI collagenopathies result in similar clinical features.
Genetic changes are related to the following types of collagenopathy, types II and XI.
- achondrogenesis type 2
- hypochondrogenesis
- Kniest dysplasia
- otospondylomegaepiphyseal dysplasia
- spondyloepimetaphyseal dysplasia, Strudwick type
- spondyloepiphyseal dysplasia congenita
- spondyloperipheral dysplasia
- Stickler syndrome
- Weissenbacher-Zweymuller syndrome
The system for classifying collagenopathies is changing as researchers learn more about the genetic causes of these disorders.The clinical features of the type II and XI collagenopathies vary among the disorders, but there is considerable overlap. Common signs and symptoms include problems with bone development that can result in short stature, enlarged joints, spinal curvature, and arthritis at a young age. For some people, bone changes can be seen only on X-ray images. Problems with vision and hearing, as well as a cleft palate with a small lower jaw, are common. Some individuals with these disorders have distinctive facial features such as protruding eyes and a flat nasal bridge.
Mutations in the COL11A1, COL11A2, and COL2A1 genes cause collagenopathy, types II and XI. These genes carry instructions for the protein strands that make up type II and type XI collagen. All collagen molecules are made of three protein strands (called alpha chains). The alpha chains may be identical or different, depending on the type of collagen. Type II collagen is made by combining three copies of the alpha chain made by the COL2A1 gene. Type XI collagen, on the other hand, is composed of three different alpha chains: the products of the COL2A1, COL11A1, and COL11A2 genes.
Mutations in these genes interfere with the proper assembly of type II and XI collagens or reduce the amount of these collagens. Defective or reduced numbers of collagen molecules affect the development of bones and other connective tissues, causing the signs and symptoms of the type II and XI collagenopathies.
This article incorporates public domain text from The U.S. National Library of Medicine
Competitive exclusion principle
In community ecology, the competitive exclusion principle, sometimes referred to as Gause's Law of competitive exclusion or just Gause's Law, is a theory which states that two species competing for the same resources cannot stably coexist, if the ecological factors are constant. Either of the two competitors will always take over the other which leads to either the extinction of one of the competitors or its evolutionary or behavioural shift towards a different ecological niche.

# Experimental basis
Russian ecologist Georgii Frantsevich Gause, formulated the law of competitive exclusion based on laboratory competition experiments using two species of Paramecium, the Paramecium aurelia and Paramecium caudatum. Following a lag phase, the Paramecium aurelia was  consistently able to drive the other to extinction. The conditions were to add fresh water everyday and input a constant flow of food.
On the other hand, Gause was able to let the Paramecium caudatum survive by driving differently the environmental parameters (food, water): that explains why the Gause law is valid only if the ecological factors are constant.

# Prediction
Competitive exclusion is predicted by a number of mathematical and theoretical models, such as the Lotka-Volterra models of competition. However, for reasons that are poorly understood, competitive exclusion is rarely observed in natural ecosystems, and many biological communities appear to violate Gause's Law. The best known example is the paradox of the plankton (or short diversity paradox): All plankton species live on a very limited number of resources, primarily solar energy and minerals that are dissolved in the water. According to the competitive exclusion principle, only a small number of plankton species should be able to coexist on these resources. Nevertheless, large numbers of plankton species coexist within small regions of open sea.

# Paradoxical traits
A partial solution to the paradox lies in raising the dimensionality of the system. Spatial heterogeneity, multiple resource competition, competition-colonization trade-offs, and lag prevent exclusion (ignoring stochastic extinction over longer time-frames). However, such systems tend to be analytically intractable. In addition, many can theoretically support an unlimited number of species. A new paradox is created: Most well-known models that allow for stable coexistence allow for unlimited number of species to coexist, yet in nature, any community contains just a handful of species.

# Re-definition
Recent studies that address some of the assumptions made for the models predicting competitive exclusion have shown that these assumptions need to be reconsidered. For example, a slight modification of the assumption of how growth and body size are related leads to a different conclusion, namely that for a given ecosystem a certain range of species may coexist while others become outcompeted.
Familial amyloid polyneuropathy
Synonyms and keywords: Transthyretin-related hereditary amyloidosis; Transthyretin amyloidosis abbreviated also as ATTR ( hereditary form);  Corino de Andrade's disease

# Overview
Familial amyloid polyneuropathy (FAP) or Corino de Andrade's disease, a form of Paramyloidosis, is a neurodegenerative autosomal dominant genetically transmitted disease, first identified and described by Portuguese neurologist Mario Corino da Costa Andrade, in the 50s. It is a fatal and incurable disease.

# Cause
Being an autosomal dominant genetically transmitted disease, FAP is transmitted from parents to sons, one mutated gene being enough (in only one of the alleles), in any of the progenitors, for the disease to be passed on.

# Pathology
FAP is characterized by the systemic deposition of amyloidogenic variants of the transthyretin protein, especially in the peripheral nervous system, causing a progressive sensory and motorial polyneuropathy.

# Symptoms
Usually manifesting itself between 20 and 40 years of age, it is characterized by pain, paresthesia, muscular weakness and autonomic dysfunction. In its terminal state, the kidneys and the heart are affected.
In the absence of a liver transplant, FAP is invariably fatal.

# Epidemiology
This disease is endemic in Portuguese locations Povoa de Varzim and Vila do Conde (Caxinas), with more than 1000 affected people, coming from about 500 families, where 70% of the people develop the illness. It was brought by Vikings from Scandinavia during the Middle Age. In northern Sweden, more specifically Pitea, Skelleftea and Umea, 1.5% of the population has the mutated gene. There are many other populations in the world who exhibit the illness after having developed it independently.

# Bibliography
Andrade C., A peculiar form of peripheral neuropathy. Familial atypical generalized amyloidosis with special involvement of the peripheral nerves,  Brain 1952; 75:408-27.
Critical point (thermodynamics)
In physical chemistry, thermodynamics, chemistry and condensed matter physics, a critical point, also called a critical state, specifies the conditions (temperature, pressure) at which the liquid state of the matter ceases to exist.  As a liquid is heated within a confined, airtight space, its density decreases while the pressure and density of the vapor being formed increases.  The liquid and vapor densities become closer and closer to each other until the critical temperature is reached where the two densities are equal and the liquid-gas line or phase boundary disappears. Additionally, as the equilibrium between liquid and gas approaches the critical point, heat of vaporization approaches zero, becoming zero at and beyond the critical point. More generally, the critical point is the point of termination of a phase equilibrium curve, which separates two distinct phases. At this point, the phases are no longer distinguishable.
In the phase diagram shown, the phase boundary between liquid and gas does not continue indefinitely. Instead, it terminates at a point on the phase diagram called the critical point. This reflects the fact that, at extremely high temperatures and pressures, the liquid and gaseous phases become indistinguishable. In water, the critical point occurs at around 647 K (374 C or 705 F) and 22.064 MPa (3200 PSIA or 218atm).
Critical variables are useful for rewriting a varied equation of state into one that applies to all materials.  The effect is similar to a normalizing constant.
According to renormalization group theory, the defining property of criticality is that the natural length scale characteristic of the structure of the physical system, the so-called correlation length , becomes infinite.  There are also lines in phase space along which this happens: these are critical lines.
In equilibrium systems the critical point is reached only by tuning a control parameter precisely.  However, in some non-equilibrium systems the critical point is an attractor of the dynamics in a manner that is robust with respect to system parameters, a phenomenon referred to as self-organized criticality.
The critical point is described by a conformal field theory.
Cruveilhier-Baumgarten syndrome
Synonyms and keywords: Cruveilhier-Baumgarten disease, Cruveilhier-Baumgarten bruit

# Overview
A rare medical condition in which the umbilical or paraumbilical veins are distended.

# Historical perspective
It was first described by Pegot in 1833, and then by Jean Cruveilhier (1835) and Paul Clemens von Baumgarten (1907).
Armstrong et al. (1942) and Steinburg and Galambos (1967) described two different types of the condition: Cruveilhier-Baumgarten syndrome and Cruveilhier-Baumgarten disease.

# Pathophysiology
- Cruveilhier-Baumgarten syndrome: liver cirrhosis or portal hypertension is the cause of the distension of the paraumbilical veins (i.e. an acquired condition in which the veins reopen due to high portal pressure).
- Cruveilhier-Baumgarten disease: the distension of the paraumbilical veins is due to failure of umbilical vein closure, with little or no evidence of liver disease found on liver biopsy (i.e. a congenital patency of the umbilical vein leading to portal hypertension).

# Diagnosis

## Physical examination
- Abdominal wall bruit (the Cruveilhier-Baumgarten bruit)
- Palpable thrill
- Portal hypertension oesophageal varices
Hypersplenism
-esophageal varices
- Hypersplenism
- oesophageal varices
- Normal liver
Cycloserine labels and packages

# Labels and Packages

## Package Label Principal Display Panel
SEROMYCIN  cycloSERINE Capsules, USP  250mg  THE CHAO CENTER  NDC 13845-1200-3  40 capsules Rx only
Usual Initial Adult Dose: One capsule (250 mg) twice a day at 12 hour intervals. See accompanying literature. Dispense in a tight container.
WARNING: Potent drug. May cause serious reactions in some individuals. Use in patients under close medical supervision. Read accompanying literature before using.
LM000250.00
Keep tightly closed. Store at controlled room temperature, 20 degrees  to 25 degrees C (68 degrees to 77 degrees F). 
Maunfacture  The Chao center for Industrial Pharmacy and Contract Manufacturing, West Lafayette, IN 47906, USA
Expiration Date  Batch No.