Persius/hicric huggingface dataset:
Cbf1 regulatory factor gene transcriptions
"Cbf1 is a GRF that binds the palindromic E-box motif (CACGTG) and utilizes DNA shape to discriminate between potential binding sites (Gordan et al. 2013).  Like the other GRFs, almost all (88% of 113) in vivo Cbf1-bound promoter sites were also detected in vitro . There were also a substantial number of low occupancy in vitro-only sites, typically in ORFs ."

# Human genes

# Consensus sequences
"Previous studies have shown that Cbf1 prefers to bind E-boxes with a T at the 5 end of the E-box (Zhou and O'Shea 2011) . This manifests as a specific DNA shape flanking both sides of the palindromic core motif (Gordan et al. 2013). Our PB-exo experiments confirmed these preferences for Cbf1 in DNA sequence  and DNA shape readout .  While the discriminatory DNA shape (and DNA sequence) information at one end of the motif is sufficient to support binding, at the strongly bound Cbf1 motifs it is enriched at both ends ( with a T on the 5 and A on the 3 end)."
Likely consensus sequences: (TCACGTGA).

# Rossi samplings
Copying the consensus Cbf1: 3'-TCACGTGA-5' and putting the sequence in "F" finds no locations or zero for these sequences respectively between ZSCAN22 or ZNF497 and A1BG as can be found by the computer programs.
For the Basic programs (starting with SuccessablesCbf.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 looking for, and found:
- negative strand, negative direction, is SuccessablesCbf--.bas, looking for 5'-TCACGTGA-3', 0.
- negative strand, positive direction is SuccessablesCbf-+.bas, looking for 5'-TCACGTGA-3', 0.
- positive strand, negative direction is SuccessablesCbf+-.bas, looking for 5'-TCACGTGA-3', 0.
- positive strand, positive direction is SuccessablesCbf++.bas, looking for 5'-TCACGTGA-3', 0.
- complement inverse, negative strand, negative direction is SuccessablesCbfci--.bas, looking for TCACGTGA, 0.
- complement inverse, negative strand, positive direction is SuccessablesCbfci-+.bas, looking for TCACGTGA, 0.
- complement inverse, positive strand, negative direction is SuccessablesCbfci+-.bas, looking for TCACGTGA, 0.
- complement inverse, positive strand, positive direction is SuccessablesCbfci++.bas, looking for TCACGTGA, 0.

## Rossi random dataset samplings
- Cbf1Rr0: 0.
- Cbf1Rr1: 0.
- Cbf1Rr2: 0.
- Cbf1Rr3: 0.
- Cbf1Rr4: 0.
- Cbf1Rr5: 0.
- Cbf1Rr6: 0.
- Cbf1Rr7: 0.
- Cbf1Rr8: 0.
- Cbf1Rr9: 0.
Chest tube insertion (patient information)
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# Overview
A chest tube insertion involves the surgical placement of a hollow, flexible drainage tube into the chest.

# How is the Chest tube insertion done?
Chest tubes are inserted to drain blood, fluid, or air and to allow the lungs to fully expand. The tube is placed between the ribs and into the space between the inner lining and the outer lining of the lung (pleural space).
The area where the tube will be inserted is numbed (local anesthesia). Sometimes you will be given medication to make you relaxed and sleepy (sedation) through a vein (intravenously).
The chest tube is inserted through a one-inch cut in the skin between the ribs into the chest. It is connected to a bottle or canister that contains sterile water. Suction is attached to the system for drainage. A stitch (suture) and adhesive tape keep the tube in place. After every chest tube insertion, a chest x-ray is done to make sure it is in the right place.
The chest tube usually stays in place until x-rays show that all the blood, fluid, or air has drained from the chest and the lung has fully re-expanded. When the chest tube is no longer needed, it can be easily removed. Most people don't need medications to sedate or numb them while the chest tube is removed. Antibiotics may be used to prevent or treat infection.
In certain people, the chest tube may be inserted using a minimally invasive technique guided by x-ray or ultrasound. Chest tubes are usually placed during major lung or heart surgery while the person is under general anesthesia.

# Who needs Chest tube insertion?
Chest tubes are used to treat conditions that can cause the lung to collapse, such as:
- After surgery or trauma in the chest (pneumothorax or hemothorax).
- Air leaks from the lung into the chest (pneumothorax).
- Bleeding into the chest (hemothorax).
- Collection of fat in the chest (chylothorax).
- Lung abscesses or pus in the chest (empyema).

# Where to find centers that perform Chest tube insertion?
Directions to Hospitals Performing Chest tube insertion

# Possible complications
Risks from any anesthesia are:
- Problems breathing.
- Reactions to medications.
Risks from any surgery are:
- Bleeding.
- Infection.
Risks from the procedure itself:
- Accidental movement of the tube.
- Buildup of pus (empyema).
- Improper placement of the tube--into the tissues, abdomen, or too far in the chest.
- Injury to the lung or heart.
- Injury to the spleen, liver, stomach, or diaphragm.

# What to expect (Outlook/Prognosis)?
You will stay in the hospital until the chest tube is removed. While the chest tube is in place, the nursing staff will carefully check for possible air leaks, breathing difficulties, and the need for oxygen. You'll need to breathe deeply and cough often to help re-expand the lung, help with drainage, and prevent fluids from collecting in the lungs.
Chest x-rays are done often while a chest tube is in place to make sure that all of the air, blood, and other fluids are being removed.

# Sources
Chinese Classification of Mental Disorders

# Overview
The Chinese Classification of Mental Disorders (CCMD), published by the Chinese Society of Psychiatry (CSP), is a clinical guide used in China for the diagnosis of mental disorders. It is currently on a third version, the CCMD-3, written in Chinese and English. It is intentionally similar in structure and categorisation to the ICD and DSM, the two most well-known diagnostic manuals, though includes some variations on their main diagnoses and around 40 culturally-related diagnoses.

# History
The first published Chinese psychiatric classificatory scheme appeared in 1979. A revised classification system, the CCMD-1, was made available in 1981 and further modified in 1984 (CCMD-2-R). The CCMD-3 was published in 2001. 
Many Chinese psychiatrists believed the CCMD had special advantages over other manuals, such as simplicity, stability, the inclusion of culture-distinctive categories, and the exclusion of certain Western diagnostic categories. The Chinese translation of the ICD-10 was seen as linguistically complicated, containing very long sentences and awkward terms and syntax.

# Diagnostic categories
The diagnosis of depression is included in the CCMD, with many similar criteria to the ICD or DSM, with the core having been translated as 'low spirits'. However, Neurasthenia is a more central diagnosis. Although also found in the ICD, its diagnosis takes a particular form in China, called 'shenjing shuairuo', which emphasizes somatic (bodily) complaints as well as fatigue or depressed feelings. Neurasthenia is a less stigmatizing diagnosis than depression in China, being conceptually distinct from psychiatric labels, and is said to fit well with a tendency to express emotional issues in somatic terms. The concept of neurasthenia as a nervous system disorder is also said to fit well with the traditional Chinese epistemology of disease causation on the basis of disharmony of vital organs and imbalance of qi.
The diagnosis of Schizophrenia is included in the CCMD. It is applied quite readily and broadly in Chinese psychiatry.
Rather than borderline personality disorder as in the DSM, or emotionally unstable personality disorder (borderline type) as in the ICD, the CCMD has impulsive personality disorder.
Diagnoses that are more specific to Chinese or Asian culture, though they may also be outlined in the ICD (or DSM glossary section), include:
- Mental disorder due to Qigong. Qigong is a Chinese method of meditation/posture/exercise. It has been linked in Chinese psychiatry to psychosis.
- Koro - excessive fear in men of the penis shrinking or drawing back in to the body. This has been associated with cultures placing a heavy emphasis on balance, or on fertility and reproduction.
- Mental disorders due to superstition or witchcraft.
- Travelling psychosis
The CCMD-3 retains a category of 'ego-dystonic homosexuality'.
Chronic recurrent multifocal osteomyelitis
Chronic recurrent multifocal osteomyelitis (CRMO) is an inflammatory condition that mainly affects children around the age of ten. Chronic because it lasts for years, usually six to ten. Recurrent because the condition comes and goes. Multifocal because it affects different areas. Osteomyelitis because the bones have lesions. Although the bones have legions, there is no no infection. A bone biopsy will come back negative for bacteria. CRMO usually affects the long bones but can affect any bone in the body. Some believe that SAPHO is the adult version of the same condition, but that is disputed by others.
CRMO is rare in that it only affect one in a million, usually children (average mean age 10), and usually girls. The lack of a large study group makes it difficult to outline and detail the condition. The rarity also explains the shortage of experts in the field. For this reason, there are probably some children who have CRMO but are never diagnosed, or better said the children are not correctly diagnosed. Currently, more cases are diagnosed in Europe and Scandinavia when compared to all other areas of the world.
Some children have fever, but some do not. Most have painful skeletal (bone) areas. Some children have stomach aches. Antibiotics do not help. A diet that reduces inflammation along with antiinflammatory medicines such as NSAIDS, in particular naproxen (aleve), appear to help the most.
CRMO can easily be mistaken for other illnesses or diseases. CRMO can be mistaken for growing pains. Since CRMO does resolve itself over the years, a child could go undiagnosed. Another example of misdiagnosis, one neurosurgeon did a biopsy on a seven year old's cervical vertebrae. He thought it was cancer and considered removing the bone immediately. Fortunately, he decided to confer with the other doctors first. The child was in the hospital for about one month before diagnosed with CRMO. Over time, the vertebra healed. In another case, an eleven year old boy was home bound on antibiotic IVs, which do not help CRMO patients. After a year, CRMO was diagnosed.
Laboratory tests may help discover the inflammation: C-reactive protein level, erythrocyte sedimentation rate, level of peripheral leukocytes, ferritin level, antinuclear antibody level, and rheumatoid factor status. BUT usually, it is just an MRI that reveals the legions.
Chronic tic disorder (patient information)
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Synonyms and Keywords: Chronic vocal tic disorder

# Overview
Chronic motor tic disorder involves quick, uncontrollable movements or vocal outbursts (but not both).

# What are the symptoms of Chronic tic disorder?
- Symptoms include:
- Excessive blinking
- Grimaces of the face
- Quick movements of the arms, legs, or other areas
- Sounds (grunts, throat clearing, contractions of the abdomen or diaphragm)
- People can hold off these symptoms for a short period of time, but they feel a sense of relief when they carry out these movements. Patients typically describe them as responding to an inner urge and may have abnormal sensations in the area of the tic prior to the tic occurring.
- Tics may continue during all stages of sleep. They may get worse with:
- Excitement
- Fatigue
- Heat
- Stress

# What causes Chronic tic disorder?
- About 1 to 2% of the population has chronic motor tic disorder.
- The condition is more common than Tourette syndrome. However, it is not as common as transient tic disorder.
- Chronic tics may be forms of Tourette syndrome.

# When to seek urgent medical care?
- There is usually no need to see the health care provider for a tic unless it is severe or disrupts your life.
- If you cannot tell whether your movements are a tic or something more serious (such as a seizure), call your health care provider.

# Diagnosis
- The doctor can usually diagnose a tic during a physical examination. Tests are generally not needed.
- To be diagnosed with the disorder:
- You must have had the tics nearly every day for more than a year
- You have not had a tic-free period longer than 3 months

# Treatment options
- Treatment depends on how bad the tics are and how the condition affects you.
- Medicines and psychotherapy are used only when the tics have a major impact on daily activities, such as school and job performance.
- Drugs used to treat tics include dopamine blockers, such as fluphenazine, haloperidol, pimozide and risperidone. These medicines can help control or reduce tics, but they have side effects such as movement disorders and cognitive dulling.
- Botulinium toxin injections is used to treat certain form of dystonic tics.
- In recent years, brain stimulation using permanently implanted electrodes in the brain has shown promising results.

# Where to find medical care for Chronic tic disorder?
Directions to Hospitals Treating Chronic tic disorder

# What to expect (Outlook/Prognosis)?
- Children who develop this disorder between ages 6 and 8 usually do very well. Symptoms may last 4 to 6 years, and then stop without treatment in early adolescence.
- When the disorder begins in older children and continues into the 20s, it may become a life-long condition

# Possible complications
There are usually no complications.

# Source
Coiled-Coil Domain Containing Protein  25
The Coiled-Coil Domain Containing Protein  25 (CCDC25) is a human protein whose function is not presently understood.

# Gene
The gene encoding the CCDC25 protein is located at 8p21.1, on the short arm of human chromosome 8, and is transcribed into an mRNA product approximately 3,583 nucleotides in length.

# Protein

## General
The protein is highly conserved among mammals as well as eukaryotes as diverse as Arabidopsis thaliana.  CCDC25 is made up of a single polypeptide chain 208 amino acids in length and is expressed at a high level, nearly 4.2 times that of a normal human protein.  Its expression is nearly ubiquitous in human tissues with little indication that its expression level changes drastically in diseased tissues.  Despite currently lacking a well understood function, CCDC25 is predicted to localize to the nucleus and was shown by a microarray experiment to be upregulated in Metaphase II oocytes.

## Interactions
CCDC25 was shown by a yeast-two-hybrid assay to interact with Smad2, a latent transcription factor that is part of the TGF- signaling pathway. The protein is a predicted substrate of Casein Kinase 1, Casein Kinase 2, cGMP-dependent protein kinase, and the Insulin Receptor; all of which have well defined roles in cell signaling.
Congenital cystic adenomatoid malformation

# Overview
Congenital cystic adenomatoid malformation (CCAM) is a congenital disorder similar to bronchopulmonary sequestration. In CCAM, usually an entire lobe of lung is replaced by a non-working cystic piece of abnormal lung tissue. This abnormal tissue will never function as normal lung tissue.
In most cases the outcome of a fetus with CCAM is very good. However in a rare few cases the cystic mass grows so large as to limit the growth of the surrounding lung and cause pressure against the heart. In these situations, the CCAM can be life-threatening for the fetus.

# Diagnosis
CCAMs are often identified during routine prenatal ultrasonography. Indentifying characteristics on the sonogram include: an echogenic (bright) mass appearing in the chest of the fetus, displacement of the heart from its normal position, a flat or everted (pushed downward) diaphragm, or the absence of visible lung tissue.
CCAMS are classified into three different types based largely on their gross appearance.  Type I has large (>2 cm) multiloculated cysts.  Type II has smaller uniform cysts.  Type III is not grossly cystic, referred to as the "adenomatoid" type.  Microscopically, the lesions are not true cysts, but communicate with the surrounding parenchyma.

# Treatment
In most cases, a fetus with CCAM is closely monitored during pregnancy and the CCAM is removed via surgery after birth. A few fetuses may develop fluid collections within the chest cavity and in those situations a Harrision catheter shunt can be used to drain the fluid into the amniotic fluid.
Very large cystic masses might pose dangerous during birth because of the airway compression. In this situation, a special surgical type of delivery called the EXIT procedure may be used.
In rare extreme cases, where fetus's heart is in danger, fetal surgery can be performed to remove the CCAM. If non-immune hydrops fetalis develop, there is a near universal mortality of the fetus. Fetal surgery can improve the survival percentage up to 50-60%.
Percutaneous umbilical cord blood sampling

# Overview
Percutaneous umbilical cord blood sampling (PUBS), also called cordocentesis, is a diagnostic genetic test that examines blood from the fetal umbilical cord to detect fetal abnormalities. PUBS provides a means of rapid chromosome analysis and is useful when information cannot be obtained through amniocentesis, CVS, or ultrasound (or if the results of these tests were inconclusive). This test carries a significant risk of complication and is typically reserved for pregnancies determined to be at high risk for genetic defect.

# Procedure
PUBS is similar to amniocentesis, but instead of sampling the amniotic fluid which surrounds the fetus, PUBS examines fetal blood. An advanced imaging ultrasound determined the location for needle insertion into the placenta, and the needle is guided through the mother's abdomen and uterine wall into the fetal vein of the umbilical cord, where a fetal blood sample is removed. The sample can then be sent for chromosomal analysis. The entire process lasts 45 minutes to an hour. Because the fetal vein is fragile early in pregnancy, PUBS is performed no earlier than 17 weeks into pregnancy.
PUBS testing has a turnaround time of about 72 hours and can detect chromosomal abnormalities, blood disorder, some metabolic disorders, infections, and some causes of structural problems. PUBS has largely replaced fetoscopy, which has a much higher rate of miscarriage.

# Risks
Miscarriage is the primary risk associated with PUBS and occurs in 1-2% of procedures. Additional possible complications are similar to those for amniocentesis and include blood loss at the puncture site, infection, and premature rupture of membranes. During the procedure, the mother may feel discomfort similar to a menstrual cramp.
Corticotropin-releasing hormone receptor 2
Corticotropin-releasing hormone receptor 2 (CRHR2) is a protein, also known by the IUPHAR-recommended name CRF2, that is encoded by the CRHR2 gene and occurs on the surfaces of some mammalian cells. CRF2 receptors are type 2 G protein-coupled receptors for corticotropin-releasing hormone (CRH) that are resident in the plasma membranes of hormone-sensitive cells. CRH, a peptide of 41 amino acids synthesized in the hypothalamus, is the principal neuroregulator of the hypothalamic-pituitary-adrenal axis, signaling via guanine nucleotide-binding proteins (G proteins) and downstream effectors such as adenylate cyclase. The CRF2 receptor is a multi-pass membrane protein with a transmembrane domain composed of seven helices arranged in a V-shape. CRF2 receptors are activated by two structurally similar peptides, urocortin II, and urocortin III, as well as CRH.

# Properties
The human CRHR2 gene contains 12 exons. Three major functional isoforms, alpha (411 amino acids), beta (438 amino acids), and gamma (397 amino acids), encoded by transcripts with alternative first exons, differ only in the N-terminal sequence comprising the signal peptide and part of the extracellular domain (amino acids 18-108 of CRHR2 alpha); the unique N-terminal sequence of each isoform (34 amino acids in CRHR2 alpha; 61 amino acids in Hs CRHR2 beta; 20 amino acids in CRHR2 gamma) is followed by a sequence common to all isoforms (377 amino acids) comprising most of the multi-pass transmembrane domain followed by a cytoplasmic domain of 47 amino acids.
CRHR2 beta is expressed in human brain; CRHR2 alpha predominates in peripheral tissues. The N-terminal signal peptides of corticotropin-releasing hormone receptor 1 and CRHR2 beta are cleaved off in the endoplasmic reticulum to yield the mature receptors. In contrast, CRHR2 alpha contains a unique pseudo signal peptide that is not removed from the mature receptor. In adenylate cyclase activation assays, CRH-related peptides are 10 times more potent at stimulating CRHR2 beta than CRHR2 alpha and CRHR2 gamma, suggesting that the N-terminal sequence is involved in the ligand-receptor interaction.
Corticotropin releasing hormone antagonist

# Overview
A Corticotropin releasing hormone antagonist is a specific type of receptor antagonist which blocks the receptor sites for Corticotropin releasing hormone (also known as Corticotropin releasing factor (CRF)).
There are four subtypes of this receptor known at present, defined as CRF-1, CRF-2a, CRF-2b and CRF-2g. Three of these receptors are expressed only in the brain, CRF-1 in the cortex and cerebrum, CRF-2a in the lateral septum and hypothalamus and CRF-2g in the amygdala. CRF-2b is expressed in the choroid plexus and cerebral arterioles in the brain, but is mainly expressed peripherally, on the heart and skeletal muscle tissue.
The main research into CRF antagonists to date has focused on antagonists selective for the CRF-1 subtype. Several antagonists for this receptor have been developed and are widely used in research, with the best-known agents being the selective CRF-1 antagonist antalarmin and a newer drug pexacerfont, although several other ligands for this receptor are used in research, such as LWH-234, CP-154,526, NBI-27914 and R-121,919. Antagonists acting at CRF-2 have also been developed, such as the peptide Astressin-B, but so far no highly selective agents for the different CRF-2 subtypes are available.
Dihydropyrimidine dehydrogenase deficiency
Dihydropyrimidine dehydrogenase deficiency (DPD deficiency) is a condition in which there is absent or significantly decreased activity of dihydropyrimidine dehydrogenase. Individuals with this condition may develop life-threatening toxicity following exposure to 5-fluorouracil (5-FU), a chemotherapy drug that is used in the treatment of cancer.
Current research suggests that nearly 8% of the population has at least partial DPD deficiency. A diagnostics determination test for DPD deficiency is available and it is expected that with a potential 500,000 people in North America using 5-FU this form of testing will increase.
For a thorough scientific overview of Dihydropyrimidine dehydrogenase deficiency, one can consult chapter 91 of OMMBID.  For more online resources and references, see inborn errors of metabolism.