Persius/hicric huggingface dataset:
Seed-specific element gene transcriptions
Seed-specific element (CATGCATG).

# Human genes

# Consensus sequences
Consensus sequence is CATGCATG.

# SEED samplings
Copying the apparent consensus sequence for the seed-specific element (CATGCATG) and putting it in "F" finds none located between ZSCAN22 and A1BG or between ZNF497 and A1BG as can be found by the computer programs.
For the Basic programs testing consensus sequence CATGCATG (starting with SuccessablesSEED.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:
- negative strand, negative direction, looking for CATGCATG, 0.
- positive strand, negative direction, looking for CATGCATG, 0.
- positive strand, positive direction, looking for CATGCATG, 0.
- negative strand, positive direction, looking for CATGCATG, 0.
- complement, negative strand, negative direction, looking for GTACGTAC, 0.
- complement, positive strand, negative direction, looking for GTACGTAC, 0.
- complement, positive strand, positive direction, looking for GTACGTAC, 0.
- complement, negative strand, positive direction, looking for GTACGTAC, 0.
- inverse complement, negative strand, negative direction, looking for CATGCATG, 0.
- inverse complement, positive strand, negative direction, looking for CATGCATG, 0.
- inverse complement, positive strand, positive direction, looking for CATGCATG, 0.
- inverse complement, negative strand, positive direction, looking for CATGCATG, 0.
- inverse negative strand, negative direction, looking for GTACGTAC, 0.
- inverse positive strand, negative direction, looking for GTACGTAC, 0.
- inverse positive strand, positive direction, looking for GTACGTAC, 0.
- inverse negative strand, positive direction, looking for GTACGTAC, 0.
Selective progesterone receptor modulator
A selective progesterone receptor modulator (SPRM) is an agent that acts on the progesterone receptor. A characteristic that distinguishes such substances from receptor full agonists (such as progesterone) and full antagonists (such as RU 486) is that their action differs in different tissues (agonist in some while antagonist in others).  This mixed agonist/agonist profile of action leads to selective stimulation or inhibition progesterone-like action in different tissues and furthermore raises the possibility of dissociation of desirable therapeutic effects from undesirable side effects in synthetic progesterone receptor drug candidates.

# Members
Members include:
- Asoprisnil (J867)
- CDB-4124 (ProellexTM, ProgentaTM)

# Uses
SPRMs are in limited use:
- Asoprisnil and CDB-4124 are both under investigation (2005) for the medical treatment of uterine leiomyoma.

# Mechanism of action
Synthetic SPRMs differ in chemical structure from the endogenous hormone progesterone, but nevertheless bind to the same progesterone receptor.  In humans, there is only one gene (PGR) that codes for the receptor, but two splice variants (PR-A and -B) arising from this single gene each with a somewhat different tissue distribution and intrinsic functional activity in response to ligand binding (agonist vs. antagonist).  In addition, synthetic SPRMs may have some binding selectivity between the two isoforms, although this is unlikely as the ligand binding domains of the two isoforms are identical.
A more likely origin of the tissue selectivity of SPRMs is what conformational preference these ligands induce in the receptor.  The ligand binding domain of the receptor is in equilibrium between two different conformations.  The first is an agonist conformation which favors the binding of coactivator proteins which in turn favors upregulation of gene transcription.  The second is an antagonistic conformation which in contrast favors the binding of corepressors and as a consequence down regulation of gene expression.  Full agonists such as progesterone which display agonist properties in all tissues, strongly shift the conformational equilibrium in the agonist direction.  Conversely full antagonists such as RU-486 strongly shift the equilibrium in the antagonist direction.  Finally, the overall ratio of concentrations of coactivator to corepressor may differ in different cell types.
When SPRMs bind to the progesterone receptor, the equilibrium between the two conformational states is more closely balanced and hence more easily perturbed by differences in the cellular environment.  In tissues where the concentration of coactivators is higher than corepressors, the excess coactivators drive the equilibrium in the agonist direction.  Conversely in tissues where corepressor concentration is higher the equilibrium is driven in the antagonist direction.  Hence SPRMs display agonist activity in tissues where coactivators predominate and antagonist activity where corepressors are in excess.
Signaling lymphocytic activation molecule
Signaling lymphocytic activation molecule is a family of genes.  Homophilic binding between SLAMs is involved in cellular adhesion 
Signaling lymphocytic activation molecule (SLAM) is a CD2-related surface receptor expressed by activated T cells and B cells. SLAM is a self ligand and enhances T cellular proliferation and IFN-gamma production.
A defective SLAM associated protein (SAP) causes X-linked lymphoproliferative syndrome (XLP), a frequently lethal mononucleosis based on the inability to control EBV
Members of the family include:
- SLAMF1 (CD150)
- SLAMF2 (CD48)
- SLAMF3 (CD229, LY9)
- SLAMF4 (CD244)
- SLAMF5 (CD84)
- SLAMF6 (CD352)
- SLAMF7 (CD319)
- SLAMF8 (CD353)
- SLAMF9
Silver sulfadiazine clinical pharmacology

# Clinical Pharmacology
Silver sulfadiazine has broad antimicrobial activity.  It is bactericidal for many gram-negative and gram-positive bacteria as well as being effective against yeast.  Results from in vitro testing are listed below.
Sufficient data have been obtained to demonstrate that silver sulfadiazine will inhibit bacteria that are resistant to other antimicrobial agents and that the compound is superior to sulfadiazine.
Studies utilizing radioactive micronized silver sulfadiazine, electron microscopy, and biochemical techniques have revealed that the mechanism of action of silver sulfadiazine on bacteria differs from silver nitrate and sodium sulfadiazine.  Silver sulfadiazine acts only on the cell wall to produce its bactericidal effect.
Results of In Vitro Testing With Silver Sulfadiazine Cream, 1% Concentration of Silver Sulfadiazine
Number of Sensitive Strains / Total Number of Strains Tested
Silver sulfadiazine is not a carbonic anhydrase inhibitor and may be useful in situations where such agents are contraindicated.
Solitary pulmonary nodule pathophysiology

# Overview

# Pathophysiology
Several features help to distinguish benign conditions from possible lung cancer. The first parameter is the size of the lesion: the smaller, the less risk for malignant cancer. Benign causes tend to have a well defined border, whereas lobulated lesions or those with an irregular margin extending into the neighbouring tissue tend to be malignant.
If there is a central cavity, then a thin wall points to a benign cause whereas a thick wall is associated with malignancy (especially 4mm or less versus 16mm or more). In lung cancer, cavitation can represent central tumor necrosis (tissue death) or secondary abces formation. If the walls of an airway are visible (air bronchogram), bronchioloalveolar carcinoma is a possibility.
An SPN often contains calcifications. Certain patterns of calcification are reassuring, such as the popcorn-like appearance of hamartoma. An SPN with a density below 15 Hounsfield units on computed tomography tends to be benign, whereas malignant tumors often measure more than 20 Hounsfield units. Fatty tissue inside hamartomas will have a strongly negative value on the Hounsfield scale.
The growth velocity of a lesion is also informative: very fast or very slow growing tumors are rarely malignant, in contrary to inflammatory or congenital conditions. It is therefore important to retrieve previous imaging studies to see if a lesion was presented and how fast its volume is increasing. This is more difficult for nodules smaller than 1 centimeter. Moreover, the predictive value of stable lesion over a period of 2 years has been found to be rather low and unreliable.
Splinter hemorrhage (patient information)
For the WikiDoc page for this topic, click here

# Overview
Splinter hemorrhages are small areas of bleeding (hemorrhage) under the fingernails or toenails.
Splinter hemorrhages look like thin, red to reddish-brown lines of blood under the nails. They run in the direction of nail growth.
They are named splinter hemorrhages because they look like a splinter under the fingernail.

# What causes splinter hemorrhages?
Splinter hemorrhages can occur with infection of the heart valves (endocarditis). They may be caused by vessel damage from swelling of the blood vessels (vasculitis) or tiny clots that damage the small capillaries (microemboli). Injury to the nail can also cause splinter hemorrhages.

# When to seek urgent medical care?
Contact your health care provider if:
- You notice splinter hemorrhages and you haven't had any recent injury to the nail
Note: Splinter hemorrhages usually appear late in endocarditis. Likely other symptoms will cause you to visit your health care provider before splinter hemorrhages appear.

# Diagnosis
Your health care provider will examine you to determine the cause of splinter hemorrhages. The health care provider may ask you the following medical history questions:
- When did you first notice this?
- Have you had an injury to the nails recently?
- Do you have endocarditis, or has your health care provider suspected that you have endocarditis?
- What other symptoms do you have, such as shortness of breath, fever, general ill feeling, or muscle aches?
Physical examination may include special attention to the heart and blood circulation systems.
Laboratory studies may include:
- Blood cultures
- Complete blood count (CBC)
- Erythrocyte sedimentation rate (ESR)
In addition, your health care provider may order:
- Chest x-ray
- ECG
- Echocardiogram
After seeing your health care provider, you may want to add a diagnosis of splinter hemorrhages to your personal medical record.

# Treatment options
There is no specific care for splinter hemorrhages. Follow your health care provider's instructions for treating endocarditis.

# Where to find medical care for splinter hemorrhages?
Directions to Hospitals Treating Splinter Hemorrhages

# Sources
Sulconazole topical (patient information)

# Why is this medication prescribed
Sulconazole is used to treat skin infections such as athlete's foot (cream only), jock itch, and ringworm.
This medication is sometimes prescribed for other uses; ask your doctor or pharmacist for more information.

# How should this medicine be used
Sulconazole comes as a cream and solution to apply to the skin. It is usually used once or twice a day, in the morning and evening, for 2 to 4 weeks. Some infections require up to 6 weeks of treatment. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Use sulconazole exactly as directed. Do not use more or less of it or use it more often than prescribed by your doctor.
Thoroughly clean the infected area, allow it to dry, and then gently rub the medication in until most of it disappears. Use just enough medication to cover the affected area. You should wash your hands after applying the medication.
Continue to use sulconazole even if you feel well. Do not stop using sulconazole without talking to your doctor.

# What special precautions should I follow
Before using sulconazole:
- tell your doctor and pharmacist if you are allergic to sulconazole or any other drugs.
- tell your doctor and pharmacist what prescription and nonprescription drugs you are taking, including vitamins.
- tell your doctor if you are pregnant, plan to become pregnant, or are breast-feeding. If you become pregnant while using sulconazole, call your doctor.

# What should I do if I forget a dose
Apply the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule. Do not apply a double dose to make up for a missed one.

# Side effects
Sulconazole may cause side effects. If you experience any of the following symptoms, call your doctor immediately:
- itching
- rash
- burning
- irritation or stinging
- redness
If you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) MedWatch Adverse Event Reporting program online  or by phone .

# What storage conditions are needed for this medicine
Keep this medication in the container it came in, tightly closed, and out of reach of children. Store it at room temperature and away from excess heat and moisture (not in the bathroom). Throw away any medication that is outdated or no longer needed. Talk to your pharmacist about the proper disposal of your medication.

# What other information should I know
Keep all appointments with your doctor. Sulconazole is for external use only. Do not let sulconazole get into your eyes or mouth, and do not swallow it. Do not apply cosmetics, lotions, or other skin medications to the area being treated unless your doctor tells you.
Do not let anyone else use your medication. Ask your pharmacist any questions you have about refilling your prescription. If you still have symptoms of infection after you finish the sulconazole, call your doctor.

# Brand names
- Exelderm
Surgeon General of the United States Army
The Surgeon General of the United States Army is the senior-most officer of the Army Medical Department of the U.S. Army.  By law, the Surgeon General may be appointed from any of the six branches of the Army Medical Department.  Also by law, the Surgeon General is appointed in the grade of Lieutenant General.  By policy, the Surgeon General also serves as Commanding General, U.S. Army Medical Command (MEDCOM) and head of the U.S. Army Medical Department (AMEDD). His (or her) office and staff are known as the Office of the Surgeon General (OTSG) and are located in Falls Church, Virginia.

# History
Congress established the Medical Service of the Continental Army on July 27, 1775 and emplaced a "Chief physician & director general" of the Continental Army as its head at that time. The first five surgeons general of the U.S. Army served under this title. An Act of May 28, 1789 established a "Physician general" of the U.S. Army (only Doctors Richard Allison and  James Craik served according to this nomenclature). An Act of March 13, 1813 cited the "Physician & surgeon general" of the U.S. Army. This nomenclature remained in place until the U.S. Army Medical Corps (or Medical Department) was established  by the Reorganization Act of April 14, 1818. (Physicians assigned to the U.S. Army were not accorded military rank until 1847.)

# List of Surgeons General of the United States Army
- Note: The AMEDD Museum at Fort Sam Houston, San Antonio, Texas has a display on the Army Surgeons General including images of all of them except Dr. Richard Allison.

# References and notes
-  MG Pollock, a U.S. Army Nurse Corps officer, served as Acting Surgeon General for nine months after LTG Kiley resigned in the wake of the 2007 Walter Reed Army Medical Center neglect scandal. (Army News Release)
Ticarcillin clavulanate adverse reactions

# Adverse Reactions
The following are discussed in more detail in other sections of the labeling:
-Anaphylactic Reactions 
-Clostridium difficile Associated Diarrhea 
- Clinical Trials 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.
Adverse reactions occurring in 1% of 867 patients receiving TIMENTIN 3.1 grams in clinical studies included rash, nausea, diarrhea, and phlebitis at the injection site. The most common laboratory abnormalities (3%) were elevations in eosinophils, serum aspartate aminotransferase (AST), and serum alanine aminotransferase (ALT).
Available safety data for pediatric patients treated with TIMENTIN demonstrate a similar adverse event profile to that observed in adult patients.
- Postmarketing Experience
In addition to adverse reactions reported from clinical trials, the following adverse reactions have been identified during postmarketing use of TIMENTIN. Because they are reported voluntarily from a population of unknown size, estimates of frequency cannot be made. These adverse reactions have been chosen for inclusion due to a combination of their seriousness, frequency of reporting, or potential causal connection to TIMENTIN.
Hypersensitivity Reactions: Skin rash, pruritus, urticaria, arthralgia, myalgia, drug fever, chills, chest discomfort, anaphylactic reactions, and bullous reactions (including erythema multiforme, toxic epidermal necrolysis, and StevensJohnson syndrome).
Central Nervous System: Headache, giddiness, neuromuscular hyperirritability, or convulsive seizures.
Gastrointestinal Disturbances: Disturbances of taste and smell, stomatitis, flatulence, nausea, vomiting and diarrhea, epigastric pain, and pseudomembranous colitis have been reported. Onset of pseudomembranous colitis symptoms may occur during or after antibacterial treatment .
Hemic and Lymphatic Systems: Thrombocytopenia, leukopenia, neutropenia, eosinophilia, reduction of hemoglobin or hematocrit, and prolongation of prothrombin time and bleeding time.
Abnormalities of Hepatic Function Tests: Elevation of AST, ALT, serum alkaline phosphatase, serum LDH, and serum bilirubin. There have been reports of transient hepatitis and cholestatic jaundice, as with some other penicillins and some cephalosporins.
Renal and Urinary Effects: Hemorrhagic cystitis, elevation of serum creatinine and/or BUN, hypernatremia, reduction in serum potassium, and uric acid.
Local Reactions: Pain, burning, swelling, and induration at the injection site and thrombophlebitis with intravenous administration.
Ticarcillin clavulanate drug interactions

# Drug Interactions
- Aminoglycosides
The mixing of TIMENTIN with an aminoglycoside in solutions for parenteral administration can result in substantial inactivation of the aminoglycoside.
- Probenecid
Probenecid interferes with the renal tubular secretion of ticarcillin, thereby increasing serum concentrations and prolonging serum halflife of ticarcillin. Probenecid does not affect the serum levels of clavulanic acid.
- Oral Contraceptives
Ticarcillin disodium/clavulanate potassium may affect the gut flora, leading to lower estrogen reabsorption and reduced efficacy of combined oral estrogen/progesterone contraceptives.
- Effects on Laboratory Tests
High urine concentrations of ticarcillin may produce falsepositive protein reactions (pseudoproteinuria) with certain methods. The bromphenol blue reagent strip test has been reported to be a reliable method for testing protein reactions .
Clavulanic acid in TIMENTIN may cause a nonspecific binding of IgG and albumin by red cell membranes, leading to a falsepositive Coombs test. A positive Coombs test should be interpreted with caution during treatment with TIMENTIN .
Transient erythroblastopenia of childhood

# Overview
Transient erythroblastopenia of childhood (TEC) is a slowly developing anemia of early childhood characterized by gradual onset of pallor.

# Historical Perspective

# Classification

# Pathophysiology

# Causes
The cause of TEC is unknown, but it has been suggested that an infection with Parvovirus B19 plays a role.

# Differentiating Transient erythroblastopenia of childhood from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis
Most patients recover completely within 1-2 months.

# Diagnosis

## Diagnostic Criteria

## History and Symptoms
Individuals with TEC have a median age of presentation of 18-26 months; however, the disorder may occur in infants younger than 6 months and in children as old as age 10 years.
Because of the gradual onset of the anemia, children are often healthier than expected from their low hemoglobin levels.

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Urinary retention resident survival guide
Synonyms and keywords:

# Overview
Urinary retention is defined as an inability to pass urine, or incomplete emptying of the bladder. It is one of the most common presenting complaints encountered in the emergency department, and can be acute or chronic. It is commonly seen in males as compared to females due to benign prostate hyperplasia. If undiagnosed or left untreated, this condition can be life-threatening as it may lead to kidney damage and severe urosepsis. Acute urinary retention can be extremely uncomfortable, and is initially managed by urethral or suprapubic  catheterization. Chronic urinary retention is often asymptomatic,  not easily identified, and is linked to increased post void residual volume. A complete detailed history about current prescription, over the counter and herbal medications is necessary along with focused physical examination that must include neurological evaluation.

# Causes

## Urinary Retention in Women
Urinary retention is overall very rare in women and can be acute or chronic. Common causes include:
- Nerve injury during surgery-For example Episiotomy-postoperative
- Medications-Atropine, Glycopyrrolate, Bupivacaine
- Fowler's syndrome
- Obstructive causes-Vaginal hematoma, Vaginal packing, Sling, Foreign body, Pelvic organ prolapse, Urethral injury

## Urinary Retention in Men
Urinary retention is more common in males, with a male to female ratio of 13:1.
Causes of Acute urinary retention in men
 Obstructive causes
 Infectious Causes
 Neurological Causes
 Detrusor Muscle Dysfunction
 Medications
Causes of Chronic urinary retention in Men
 Neurological Causes
 Detrusor Muscle Dysfunction

# Diagnosis
A detailed history and a thorough physical examination may help in diagnosing the cause behind urinary retention.

# Treatment
Acute urinary retention is treated with immediate bladder decompression with intermittent urethral catheterization or suprapubic catheterization regardless of the cause and gender. Further management depend upon the cause of retention.
Abbreviations: TwoC: trial without catheter; BPH: Benign prostate hyperplasia; TURP: Transurethral resection of prostate;POUR: postoperative urinary retention;I/V: Intravenous

# Do's
- Keep a close eye on the patient for dehydration and metabolic abnormalities which may result from post obstructive diuresis.
- Perform suprapubic catheterization in patients who had recent surgery and it should be ultrasound-guided.
- Admit the patient with urosepsis, renal failure, electrolyte imbalance, malignancy, or acute myelopathy.
- It is must to educate the patient about catheter care and urine output monitoring.

# Don'ts
- Do not perform urethral catheterization if the patient had a recent urologic surgery such as radical prostatectomy or urethral reconstruction.
- Do not start antibiotics until an infection is confirmed.