Persius/hicric huggingface dataset:
Ceftaroline description
Teflaro is a sterile, semi-synthetic, broad-spectrum, prodrug antibacterial of cephalosporin class of beta-lactams (-lactams). Chemically, the prodrug, ceftaroline fosamil monoacetate monohydrate is (6R,7R)-7-{(2Z)-2-(ethoxyimino)-2-acetamido}-3-{sulfanyl}-8-oxo-5-thia-1-azabicyclooct-2-ene-2-carboxylate monoacetate monohydrate. Its molecular weight is 762.75. The empirical formula is C22H21N8O8PS4.C2H4O2.H2O.
Teflaro vials contain either 600 mg or 400 mg of anhydrous ceftaroline fosamil. The powder for injection is formulated from ceftaroline fosamil monoacetate monohydrate, a pale yellowish-white to light yellow sterile powder. All references to ceftaroline activity are expressed in terms of the prodrug, ceftaroline fosamil. The powder is constituted for IV injection.
Each vial of Teflaro contains ceftaroline fosamil and L-arginine, which results in a constituted solution at pH 4.8 to 6.5.
Ceftibuten how supplied
CEDAX Capsules, containing 400 mg of ceftibuten (as ceftibuten dihydrate) are white, opaque capsules imprinted with the product name and strength, are available as follows:
20 Capsules/Bottle (NDC 59630-820-20)
Store the capsules between 2 and 25C (36 and 77F). Replace cap securely after each opening.
CEDAX Oral Suspension is an off-white to cream-colored powder that, when reconstituted as directed, contains ceftibuten equivalent to 90 mg/5 mL, supplied as follows:
Ceftizoxime description

# Description
Cefizox (ceftizoxime injection) in the Galaxy plastic container (PL 2040) contains ceftizoxime as ceftizoxime sodium. It is a sterile, semisynthetic, broad spectrum, cephalosporin antibiotic for intravenous administration.
Chemically, it is the sodium (6R, 7R)78oxo5thia1azabicyclooct2ene2carboxylate 72-(Z)-(O-methyloxime). The molecular formula is C13H12N5NaO5S2  and the molecular weight is 405.38. The structural formula of ceftizoxime sodium is as follows:
efizox (ceftizoxime injection) in the Galaxy plastic container is a frozen iso-osmotic, sterile, nonpyrogenic premixed 50 mL solution containing 1 g or 2 g of ceftizoxime as ceftizoxime sodium. Dextrose, USP has been added to these dosages to adjust osmolality (approximately 1.9 g and 950 mg to the 1 g and 2 g dosages as dextrose hydrous, respectively). Thawed solutions range from very pale yellow to yellow. The pH of thawed solutions range from 5.5 to 8.0. After thawing to room temperature, the solution is intended for intravenous use only.
The Galaxy container is fabricated from a specially designed multilayer plastic (PL 2040). Solutions are in contact with the polyethylene layer of this container and can leach out certain chemical components of the plastic in very small amounts within the expiration dating period. The suitability of the plastic has been confirmed in tests in animals according to the USP biological tests for plastic containers, as well as by tissue culture toxicity studies.
Ceftriaxone description
Ceftriaxone for Injection, USP is a sterile, semisynthetic, broad-spectrum cephalosporin antibiotic for intravenous or intramuscular administration. Ceftriaxone sodium is (6R, 7R)-7--8-oxo-3-methyl]-5-thia-1-azabicyclooct-2-ene-2-carboxylic acid, 72-(Z)-(O-methyloxime), disodium salt, sesquaterhydrate.
The chemical formula of ceftriaxone sodium is C18H16N8Na2O7S33.5H2O. It has a calculated molecular weight of 661.59 and the following structural formula:
Ceftriaxone for Injection, USP is a white to yellowish-orange crystalline powder which is readily soluble in water, sparingly soluble in methanol and very slightly soluble in ethanol. The pH of a 1% aqueous solution is approximately 6.7. The color of Ceftriaxone for Injection, USP solutions ranges from light yellow to amber, depending on the length of storage, concentration and diluent used.
Each Pharmacy Bulk Package is supplied as a dry powder in vials containing sterile ceftriaxone sodium, USP equivalent to 10 grams of ceftriaxone and is intended for intravenous infusion only. Ceftriaxone for Injection, USP contains approximately 83 mg (3.6 mEq) of sodium per gram of ceftriaxone activity.
A Pharmacy Bulk Package is a container of a sterile preparation for parenteral use that contains many single doses. The contents are intended for use in a pharmacy admixture program and are restricted to the preparation of admixtures for intravenous infusion. FURTHER DILUTION IS REQUIRED BEFORE USE. (See DOSAGE AND ADMINISTRATION, and DIRECTIONS FOR PROPER USE OF PHARMACY BULK PACKAGE.)
Cefuroxime how supplied
ZINACEF in the dry state should be stored between 15 and 30C (59 and 86F) and protected from light. ZINACEF is a dry, white to off-white powder supplied in vials as follows:
NDC 0173-0352-10 750-mg- Vial (Tray of 10)
NDC 0173-0354-10 1.5-g- Vial (Tray of 10)
NDC 0173-0400-00 7.5-g- Pharmacy Bulk Package (Tray of 6)
NDC 0173-0436-00 750-mg ADD-Vantage Vial (Tray of 25)
NDC 0173-0437-00 1.5-g ADD-Vantage Vial (Tray of 10)
(The above ADD-Vantage vials are to be used only with Abbott ADD-Vantage diluent containers.)
ZINACEF frozen as a premixed solution of cefuroxime injection should not be stored above -20C. ZINACEF is supplied frozen in 50-mL, single-dose, plastic containers as follows:
NDC 0173-0424-00 750-mg- Plastic Container (Carton of 24)
NDC 0173-0425-00 1.5-g- Plastic Container (Carton of 24)
- Equivalent to cefuroxime.
Cell fate determination
Cell fate determination is the programming of a cell to follow a specified path of cell differentiation. Often, cells are discussed in terms of their terminal differentiation state. During development, fates of some few cells may be specified at certain times. When referring to developmental fate or cell fate, one is talking about everything that happens to that cell and its progeny after that point in development.
The process of a cell to be committed to a certain state can be divided into two stages: specification and determination. Specification is not a permanent stage and cells can be reversed based upon different cues. In contrast, determination refers to when cells are irreversibly committed to a particular fate. This is a process influenced by the action of the extracellular environment and the contents of the cell's genome. Determination is not something that is visible under the microscope- cells do not change their appearance when they become determined. Determination is followed by differentiation, the actual changes in biochemistry, structure, and function that result in cells of different types. Differentiation often involves a change in appearance as well as function.
The state of commitment of a cell is also known as its developmental potential. When the developmental potential is less than or equal to the developmental fate, the cell is exhibiting mosaic behavior. When the developmental potential is greater than the developmental fate, the cell is exhibiting regulative behavior.
Embryos can use a combination of methods and exhibit a combination of behaviors throughout its development.

# Types of specification
There are three major ways that developmental fates become specified: autonomous specification, conditional specification and syncytial specification.

## Autonomous specification
This type of specification results from cell-intrinsic properties; it gives rise to mosaic development. The cell-intrinsic properties arise from a cleavage of a cell with asymmetric cytoplasmic determinants or morphogenetic determinants. Thus, the fate of the cell depends on factors segregated into the cytoplasm during cleavage. Early examples of autonomous specification came from the work of Whittaker in tunicate embryos.

## Conditional specification
In contrast to the autonomous specification, this type of specification is a cell-extrinsic process that relies on cues and interactions between cells or from concentration-gradients of morphogens. These interactions can be either stimulatory or inhibitory. This type of specification was discovered from the result of transplantation experiments and isolation experiments.

## Syncytial specification
This type of a specification is a hybrid of the autonomous and conditional that occurs in insects. This method involves the action of morphogen gradients within the syncytium. As there are no cell boundaries in the syncytium, these morphogens can influence nuclei in a concentration-dependent manner.
Link to: Cellular determination
Central DuPage Hospital
Central DuPage Hospital, or CDH, is an independent hospital system located throughout DuPage County, Illinois in the United States. Its primary facility is a 361-bed hospital located in Winfield, Illinois. There are an additional twenty primary care facilities located throughout the county, and four retirement communities. Central DuPage Hospital was the first hospital in the county to perform open heart surgery, and is currently the second busiest surgical center in the state.

# History
The Central DuPage Hospital Association was established in 1958 when citizens from Glen Ellyn, Lombard, Wheaton, Warrenville, Winfield and West Chicago banded together to restore a sanitarium located on the hospital's current primary site. After an extensive million-dollar renovation project, Central DuPage Hospital opened on September 16, 1964 with 113 beds and 66 physicians. The hospital saw much change throughout the 1970s, with the opening of a 120-bed pavilion on December 13, 1970, small additions in 1971 and 1972, and a five-story 112-bed patient tower in 1976.

# Hospital News
In July 2007, Central DuPage Hospital (CDH) in Winfield, Ill. announced its intent to enter a joint venture with ProCure Treatment Centers Inc. and Radiation Oncology Consultants, Ltd. to bring the future of cancer treatment to Illinois. Patient treatment is expected to begin at CDH by 2010. View Press Release
Central venous pressure

# Overview
Central venous pressure (CVP) describes the pressure of blood in the thoracic vena cava, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system.
It is a good approximation of right atrial pressure, which is a major determinant of right ventricular end diastolic volume. (However, there can be exceptions in some cases.)

# Measurement
Normal CVP can be measured from two points of reference:
- Sternum: 0-5 cm H2O
- Midaxillary line: 5-10 cm H2O
CVP can be measured by connecting the patient's central venous catheter to a special infusion set which is connected to a small diameter water column. If the water column is calibrated properly the height of the column indicates the CVP.
In most progressive intensive care units in the U.S., specialized monitors are available to continuously measure CVP as well as other hemodynamic values.

# Factors affecting CVP

## Factors which increase CVP include:
- Hypervolemia
- forced exhalation
- Tension pneumothorax
- Heart failure
- Pleural effusion
- Decreased cardiac output
- Cardiac tamponade

## Factors which decrease CVP include:
- Hypovolemia
- Deep inhalation
Cephalexin how supplied
Cephalexin capsules USP
250 mg: Swedish orange body and gray cap imprinted TEVA on the cap and 3145 on the body, in bottles of 100, 500, and unit-dose boxes of 100 (10 x 10).
500 mg: Swedish orange body and Swedish orange cap imprinted TEVA on the cap and 3147 on the body, in bottles of 100, 500, and unit-dose boxes of 100 (10 x 10).
Store at 20 to 25C (68 to 77F) .
Cephalexin for oral suspension- USP
(a cherry mixed fruit flavored formula)
125 mg/5 mL: bottles of 100 mL and 200 mL.
250 mg/5 mL: bottles of 100 mL and 200 mL.
Directions for mixing are included on the label.
Store at 20 to 25C (68 to 77F) .
Shake well before using. Keep tightly closed.
- After mixing, store in refrigerator. May be kept for 14 days without significant loss of potency.
Cephalexin tablets USP
250 mg: bottles of 100. Tablet identification number and color: white, capsule-shaped tablet, debossed 2238 on one side with a score between the 2 and the 3 and TEVA on the reverse side.
500 mg: bottles of 100. Tablet identification number and color: white, capsule-shaped tablet, debossed 2240 on one side with a score between the 2 and the 4 and TEVA on the reverse side.
Store dry powder at 20 to 25C (68 to 77F) .
Charles Bonnet syndrome

# Overview
Charles Bonnet syndrome (CBS) is named after the Swiss naturalist Charles Bonnet. In 1760 he described a condition in which vivid, complex visual hallucinations (fictive visual percepts) occur in mentally healthy people. One characteristic of these hallucinations is that they usually are "lilliput hallucinations" (hallucinations in which the characters or objects are smaller than in reality).  He first documented it in his 87-year-old grandfather, who was nearly blind from cataracts in both eyes but perceived men, women, birds, carriages, buildings, tapestries, and scaffolding patterns.
Most who are affected by this are people with visual impairments due to old age, damage to the eyes or optic pathways. In particular, central vision loss due to a condition such as macular degeneration combined with peripheral vision loss from glaucoma may predispose to CBS, although most people with such deficits do not develop the syndrome.
This syndrome is well portrayed in Vilayanur S. Ramachandran's book Phantoms in the brain.
Cincinnati stroke scale

# Overview
The Cincinnati Stroke Scale is a scale used to diagnose the presence of a stroke in a patient. It tests three signs including facial droop, arm drift, and speech to find if patient is having a stroke and need more investigation. If any of the three tests shows abnormal findings, the patient may be having a stroke and should be transported to a hospital as soon as possible.

# Cincinnati Prehospital Stroke Scale

## Calculation of the Cincinnati Prehospital Stroke Scale
The Cincinnati Stroke Scale is a scale used to diagnose the presence of a stroke in a patient. It tests three signs including facial droop, arm drift, and speech to find if patient is having a stroke and need more investigation.
Check all boxes that apply to your patient:
function calcScore(){
var score = 0;
if(document.forms.checked == 1){score += 0;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 0;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 0;}
if(document.forms.checked == 1){score += 1;}
document.forms.value = score;
if(score == 0){document.forms.value = "Stroke is unlikely";} 
if(score >=1){document.forms.value = "Patient may have a stroke and should be transported to a hospital as soon as possible";}

## Interpretation of the Cincinnati Prehospital Stroke Scale
If any of the three tests shows abnormal findings, the patient may be having a stroke and should be transported to a hospital as soon as possible.
Cofactor (biochemistry)
A cofactor is a non-protein chemical compound that is bound (either tightly or loosely) to an enzyme and is required for catalysis. They can be considered "helper molecules/ions" that assist in biochemical transformations. Certain substances such as water and various abundant ions may be bound tightly by enzymes, but are not considered to be cofactors since they are ubiquitous and rarely limiting. Some sources limit the use of the term "cofactor" to inorganic substances.
Cofactors can be divided into two broad groups: coenzymes and prosthetic groups. Coenzymes are small organic non-protein molecules that carry chemical groups between enzymes. These molecules are not bound tightly by enzymes and are released as a normal part of the catalytic cycle. In contrast, prosthetic groups form a permanent part of the protein structure.

# Apoenzymes and holoenzymes
An enzyme without a cofactor is referred to as an apoenzyme, and the completely active enzyme (in addition to the cofactor) is called a holoenzyme.
Apoenzyme + cofactor  Holoenzyme

# Metal ion cofactors
Metal ions are common cofactors. In nutrition, the list of essential trace elements reflects their role as cofactors. This list includes manganese, iron, cobalt, nickel, copper, zinc, and molybdenum. Other organisms require additional metals, such as vanadium and tungsten. The study of these cofactors falls under the area of bioinorganic chemistry.
In many cases, the cofactor includes both an inorganic and organic component. One diverse set of examples are the haem proteins, which consists of a porphyrin ring coordinated to iron.

# Cofactors and coenzymes
Cofactors vary in their location and the tightness of their binding to the host enzyme. When bound tightly to the enzyme, cofactors are called prosthetic groups. Loosely-bound cofactors typically associate in a similar fashion to enzyme substrates. These are better described as coenzymes, which are organic substances that directly participate as substrates in an enzyme reaction. Vitamins can serve as precursors to coenzymes (e.g. vitamins B1, B2, B6, B12, niacin, folic acid) or as coenzymes themselves (e.g. vitamin C).
Cold agglutinin disease
Synonyms and keywords:

# Overview
Cold agglutinin disease is an autoimmune disease characterized by the presence of high concentrations of circulating antibodies directed against red blood cells. It is a form of autoimmune hemolytic anemia, specifically one in which antibodies only bind red blood cells at low temperatures, typically 28-31C.

# Historical Perspective

# Classification

# Pathophysiology
All individuals have circulating antibodies directed against red blood cells, but their concentrations are often too low to trigger disease (titers under 1:64 at 4C). In individuals with cold agglutinin disease, these antibodies are in much higher concentrations (titers over 1:1000 at 4C).
At temperatures of 28-31C, such as those encountered during winter months, and occasionally at 37C, antibodies bind to the polysaccharide region of glycoproteins on the surface of red blood cells (typically the I antigen, i antigen, and Pr antigens). IgM-type antibodies are typically responsible for this action. Binding of antibodies to red blood cells activates the classical pathway of the complement system. If the complement response is sufficient, red blood cells are damaged by the membrane attack complex, an effector of the complement cascade. In the formation of the membrane attack complex, several complement proteins are inserted into the red blood cell membrane, forming pores that lead to membrane instability and intravascular hemolysis (destruction of the red blood cell within the blood vessels).
If the complement response is insufficient to form membrane attack complexes, then extravascular lysis will be favored over intravascular red blood cell lysis. In lieu of the membrane attack complex, complement proteins (particularly C3b and C4b) are deposited on red blood cells. This opsonization enhances the clearance of red blood cell by phagocytes in the liver, spleen, and lungs, a process termed extravascular hemolysis.
Individuals with cold agglutinin disease present with signs and symptoms of hemolytic anemia. Those with secondary agglutinin disease may also present with an underlying disease.

# Causes
There are two forms of cold agglutinin disease: primary and secondary. The primary form is by definition idiopathic, a disease for which no cause is known.
Secondary cold agglutinin disease is a result of an underlying condition. In adults, this is typically due to a lymphoproliferative disease such as lymphoma and chronic lymphoid leukemia. In children, cold agglutinin disease is often secondary to an infection, such as Mycoplasma pneumonia, mononucleosis, and HIV.

# Differentiating Cold Agglutinin Disease from Other Diseases

# Epidemiology and Demographics

## Age

## Gender

## Race

# Risk Factors

# Natural History, Complications and Prognosis

# Diagnosis

## Diagnostic Criteria

## Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Colombian Sign Language
Colombian  Sign Language is a language used by a rough estimated of 250 000 colombian  deaf people. (50,000 deaf in Bogota in 1992).

# Description
The development of the signs have influences of  Spanish sign language and USA sign language.   Also similarities with El Salvador signs have been noticed. 

# Teaching
There are two sign language schools in Bogota (the first started in 1929), two in Medellin and one in Cali.  Countrywide, three different institutions of support for deaf promotes the learning of the language.   The national Committee for the sign language promotes the research in the area, distributes the manual alphabet for spelling and the Grammar Dictionary and supports the organization for sign language teachers.   The national central of telecommunications TELECOM distributes a CD-ROM software for self-learning.

# Relevancy
There is a growing interest for learning the sign language between the hearing people.  Some schools use sign language in the classroom. Interpreters are provided at important public events, and for college students.

# References and External links
- Colombian sign language software available in :  Lengua de Sen~as Colombianas (software). Divisio'n de Investigacio'n
ITEC - TELECOM Colombia. /
Combined hyperlipidemia
In medicine, combined hyperlipidemia (or -aemia) is a commonly occurring form of hypercholesterolemia (elevated cholesterol levels) characterised by increased LDL and triglyceride concentrations, often accompanied by decreased HDL. On lipoprotein electrophoresis (a test now rarely performed) it shows as a  hyperlipoproteinemia type IIB.
The elevated triglyceride levels (>5 mmol/l) are generally due to an increase in VLDL (very low density lipoprotein), a class of lipoprotein that is prone to cause atherosclerosis.

# Types
There are roughly two forms of this lipid disorder:
- Familial combined hyperlipidemia (FCH) is the familiar occurrence of this disorder, probably caused by polymorphisms in molecules and enzymes that participate in lipoprotein metabolism, such as ApoCII and ApoCIII and CETP (cholesterylester transferring protein).
- Acquired combined hyperlipidemia is extremely common in patients who suffer from other diseases from the metabolic syndrome ("syndrome X", incorporating diabetes mellitus type II, hypertension, central obesity and CH). Excessive free fatty acid production by various tissues leads to increased VLDL synthesis by the liver. Initially, most VLDL is converted into LDL until this mechanism is saturated, after which VLDL levels elevate.

# Treatment
Both conditions are treated with fibrate drugs, which act on the peroxisome proliferator-activated receptors (PPARs), specifically PPAR, to decrease free fatty acid production.
Statin drugs, especially the synthetic statins (atorvastatin and rosuvastatin) can decrease LDL levels by increasing hepatic reuptake of LDL due to increased LDL-receptor expression.