Persius/hicric huggingface dataset:
Scanning acoustic microscope
A Scanning Acoustic Microscope (SAM) is a device which uses focused sound to investigate, measure, or image an object. It is commonly used in failure analysis and non-destructive evaluation. It also has applications in biological and medical research.  The semiconductor industry has found the Scanning Acoustic Microscope useful in detecting voids, cracks, and delaminations within microelectronic packages.

# History
The first scanning acoustic microscope was developed in 1974 by C. F. Lemons and R. A. Quate at the Microwave Laboratory of Stanford University.

# Principles of operation
Scanning Acoustic Microscopy works by directing focused sound from a transducer at a small point on a target object. Sound hitting the object is either scattered, absorbed, reflected (scattered at 180) or transmitted (scattered at 0). Typically, either the reflected or transmitted sound is gathered and measured. Based on the measurement, a value is assigned to the location investigated. The transducer (or object) is moved slightly and then insonified again. This process is repeated in a systematic pattern until the entire region of interest has been investigated. Often the values for each point are assembled into an image of the object. The contrast seen in the image is based either on the object's geometry or material composition. The resolution of the image is limited either by the physical scanning resolution or the width of the sound beam (which in turn is determined by the frequency of the sound).

# Applications

## Medicine and Biology
SAM can provide data on the elasticity of cells and tissues, which can give useful information on the physical forces holding structures in a particular shape and the mechanics of structures such as the cytoskeleton. These studies are particularly valuable in investigating processes such as cell motility.
- Flaw Detection
- Internal stress investigation
- Elastic property characterization

# Ultrasonic Direct Microscopy
Ultrasonic Direct Microscope (UDM) base on measuring the ultrasonic signal directly. The conventional sensor include a level sensor that means that the measurement instrument attitude of the signal. ADM  technique deal with ultrasonic signal as is . That make possible to produce modulate ultrasonic signal and to check not only the main frequency, and enable wide range in order to examine little chances in to material in test.
Simeprevir contraindications

# Contraindications
Contraindications to peginterferon alfa and ribavirin also apply to OLYSIO combination treatment with peginterferon alfa and ribavirin.
OLYSIO in combination with peginterferon alfa and ribavirin is contraindicated in pregnant women and in men whose female partners are pregnant because of the risks for birth defects and fetal death associated with ribavirin .
Refer to the respective prescribing information for a list of the contraindications for peginterferon alfa andribavirin.
Simeprevir drug interactions

# Drug Interactions
Co-administration of OLYSIO with substances that are moderate or strong inducers or inhibitors of cytochrome P450 3A (CYP3A) is not recommended as this may lead to significantly lower or higher exposure of simeprevir, respectively .
In vitro studies indicated that simeprevir is a substrate and mild inhibitor of CYP3A and a substrate and inhibitor of P-gp and OATP1B1/3. Simeprevir does not affect CYP2C9, CYP2C19 or CYP2D6 in vivo. Simeprevir does not induce CYP1A2 or CYP3A4 in vitro. In vivo, simeprevir mildly inhibits the CYP1A2 activity and intestinal CYP3A4 activity, while it does not affect hepatic CYP3A4 activity.
Simeprevir is transported into the liver by OATP1B1/3 where it undergoes metabolism by CYP3A. Based on results from in vivo studies, co-administration of OLYSIO with moderate or strong inhibitors of CYP3A may significantly increase the plasma exposure of simeprevir and co-administration with moderate or strong inducers of CYP3A may significantly reduce the plasma exposure of simeprevir, which may lead to loss of efficacy.
Drug interaction studies were performed in healthy adults with simeprevir (at the recommended dose of 150 mg once daily unless otherwise noted) and drugs likely to be co-administered or drugs commonly used as probes for pharmacokinetic interactions. The effects of co-administration of other drugs on the Cmax, AUC, and Cmin values of simeprevir are summarized in Table 6 (effect of other drugs on OLYSIO). The effect of co-administration of OLYSIO on the Cmax, AUC, and Cmin values of other drugs are summarized in Table 7 (effect of OLYSIO on other drugs). For information regarding clinical recommendations, see Drug Interactions (7).
Small nucleolar RNA SNORD102
snoRNA U102 (also known as SNORD102)  is a non-coding RNA (ncRNA) molecule which functions in the modification of other small nuclear RNAs (snRNAs). This type of modifiying RNA is usually located in the nucleolus of the eukaryotic cell which is a major site of snRNA biogenesis. It is known as a small nucleolar RNA (snoRNA) and also often referred to as a guide RNA.
snoRNA U102 belongs to the C/D box class of snoRNAs which contain the conserved sequence motifs known as the C box (UGAUGA) and the D box (CUGA). Most of the members of the box C/D family function in directing site-specific 2'-O-methylation of substrate RNAs.
U101 was identified by computational screening of the introns of ribosomal protein genes for conserved C/D box sequence motifs and expression experimentally verfied by northern blotting . It is found within intron 3 of the L21 ribosomal protein gene.  The H/ACA box snoRNA ACA27 is found in the same host gene within a different intron .
U102 is predicted to guide the 2'O-ribose methylation of 28S ribosomal RNA (rRNA) residue G4020
Small nucleolar RNA SNORD115
SNORD115 (also known as HBII-52)  is a non-coding RNA (ncRNA) molecule which functions in the modification of other small nuclear RNAs (snRNAs). This type of modifiying RNA is usually located in the nucleolus of the eukaryotic cell which is a major site of snRNA biogenesis. It is known as a small nucleolar RNA (snoRNA) and also often referred to as a guide RNA.
HBII-52 belongs to the C/D box class of snoRNAs which contain the conserved sequence motifs known as the C box (UGAUGA) and the D box (CUGA). Most of the members of the box C/D family function in directing site-specific 2'-O-methylation of substrate RNAs.
In the human genome, HBII-52 is encoded in a tandemly repeated array with another C/D box snoRNA, HBII-85, in the Prader-Willi syndrome (PWS) region of chromosome 15 .  HBII-52 is exclusively expressed in the brain but is absent in PWS patients.  HBII-52 lacks any significant complementarity with ribosomal RNAs, but does have an 18 nucleotide region of conserved complementarity to serotonin 2C receptor mRNA.

# Transcriptions
For "box C/D snoRNAs, boxes C and D and an adjoining stem form a vital structure, known as the box C/D motif."
"The  box elements are essential for snoRNA production  and for snoRNA-directed modification of rRNA nucleotides."
The "motif is necessary and sufficient for nucleolar targeting, both in yeast and mammals. Moreover, in mammalian cells, RNA is targeted to coiled bodies as well. Thus, the box C/D motif is the first intranuclear RNA trafficking signal identified for an RNA family. Remarkably, it also couples snoRNA localization with synthesis and, most likely, function. The distribution of snoRNA precursors in mammalian cells suggests that this coupling is provided by a specific protein(s) which binds the box C/D motif during or rapidly after snoRNA transcription."
"Members of the box C/D snoRNA family, which are the subject of the present report, possess characteristic sequence elements known as box C (UGAUGA) and box D (GUCUGA)."
Substituting T for U yields C box = 3'-AGTAGT-5' and D box = 3'-AGTCTG-5' in the transcription direction on the template strand.
"The antisense elements located immediately upstream of the D box and/or the D box match the sequence of the target RNA, while the areas immediately upstream of the C box and immediately downstream of the D box form a 53 terminal stem".
Small nucleolar RNA Z102/R77
Small nucleolar RNA RZ102/R77 refers to a group of related non-coding RNA (ncRNA) molecules which function in the biogenesis of other small nuclear RNAs (snRNAs). These small nucleolar RNAs (snoRNAs) are modifiying RNAs and usually located in the nucleolus of the eukaryotic cell which is a major site of snRNA biogenesis.
These two snoRNAs R77 and Z102 were identified in the plant Arabidopsis thaliana  and rice Oryza sativa  respectively. These related snoRNAs are predicted to belong to the C/D box class of snoRNAs which contain the conserved sequence motifs known as the C box (UGAUGA) and the D box (CUGA). Most of the members of the box C/D family function in directing site-specific 2'-O-methylation of substrate RNAs.
Z102 and R77 and are members of the C/D class of snoRNA which contain the C (UGAUGA) and  D (CUGA) box motifs. Most of the members of the box C/D family function in directing site-specific 2'-O-methylation of substrate RNAs .
Sodiumhydrogen antiporter 1
The sodium-hydrogen antiporter 1  (NHE-1)  also known as sodium/hydrogen exchanger 1 or SLC9A1 (SoLute Carrier family 9A1) is an isoform of sodiumhydrogen antiporter that in humans is encoded by the SLC9A1 gene.

# Function
The Na+/H+ antiporter (SLC9A1) is a ubiquitous membrane-bound enzyme involved in volume- and pH-regulation of vertebrate cells. It is inhibited by the non-specific diuretic drug amiloride and activated by a variety of signals including growth factors, mitogens, neurotransmitters, tumor promoters, and others.

# Interactions
Sodiumhydrogen antiporter 1 has been shown to interact with carbonic anhydrase II and CHP. It is also the target of the experimental drug rimeporide, which is being developed for the treatment of Duchenne muscular dystrophy.
Sodiumhydrogen antiporter 3
Sodiumhydrogen antiporter 3 also known as sodiumhydrogen exchanger 3 (NHE3) or solute carrier family 9 member 3 (SLC9A3) is a protein that in humans is encoded by the SLC9A3 gene.
SLC9A3 is a sodiumhydrogen antiporter.  It is found on the apical side of the epithelial cells of the proximal tubule of the nephron of the kidney, in the apical membrane of enterocytes of the intestine, as well as the basolateral side of both duodenal and pancreatic cells responsible for the release of HCO3 into the duodenal lumen. It is primarily responsible for maintaining the balance of sodium.  It is also indirectly linked to buffering of blood pH.  The  NHE3 antiporter imports one sodium ion into the cytosol of a tubule cell as it ejects one hydrogen ion from the cell into the lumen of the proximal tubule.  The sodium within the tubule cell may then be retained by the body rather than excreted in the urine.  The NHE3 antiporter indirectly contributes to blood buffering capacity because hydrogen ions that are ejected are the products of the carbonic anhydrase enzyme, which also makes bicarbonate.

# Regulation
Protein kinase C stimulates NHE3, while protein kinase A inhibits it.
There is a specific protein functioning as an NHE3 regulator, Sodium-hydrogen antiporter 3 regulator 1.

## Inhibitors
- Tenapanor

## Stimulators
- Insulin stimulates NHE3 and thereby proximal tubule sodium absorption.

# Interactions
Sodiumhydrogen antiporter 3 has been shown to interact with CHP.
Soft tissue sarcoma overview

# Overview
A soft tissue sarcoma is a malignant (cancerous) tumor that develops in mesenchymal tissue.  Mesenchymal tissues encompass all the muscle, connective tissues, and bones of the body.
Soft tissue sarcomas can invade surrounding tissue and can metastasize (spread) to other organs of the body, forming secondary tumors. The cells of secondary tumors are similar to those of the primary (original) cancer. Secondary tumors are referred to as "metastatic soft tissue sarcoma" because they are part of the same cancer and are not a new disease.  The most common site of spread is to the lungs.
Some tumors of the soft tissue are benign (noncancerous) and are not sarcomas. These tumors do not spread and are rarely life-threatening. However, benign tumors can crowd nearby organs and cause symptoms or interfere with normal body functions.
Spaceflight gene expressions
Gene expressions is a suite of genes, and their isoforms, that appear to be biochemically involved in the appearance of a trait.
Space travel changes the way genes are expressed.
"NASAs Twins Study preliminary results have revealed that space travel causes an increase in methylation, the process of turning genes on and off, and additional knowledge in how that process works."
"Some of the most exciting things that weve seen from looking at gene expression in space is that we really see an explosion, like fireworks taking off, as soon as the human body gets into space. With this study, weve seen thousands and thousands of genes change how they are turned on and turned off. This happens as soon as an astronaut gets into space, and some of the activity persists temporarily upon return to Earth."
"This study represents one of the most comprehensive views of human biology. It really sets the bedrock for understanding molecular risks for space travel as well as ways to potentially protect and fix those genetic changes."
The image on the right shows the loss of bone mass apparently due to long-term microgravity on the International Space Station. "stronauts, on average, lost roughly 11 percent of their total hip bone mass over the course of their mission."

# Human genes
Gene ID: 249 ALPL alkaline phosphatase, liver/bone/kidney, alias bone alkaline phosphatase (BAP).
Gene ID: 348 APOE apolipoprotein E, one isoform (the gene itself), 19q13.32. "The protein encoded by this gene is a major apoprotein of the chylomicron. It binds to a specific liver and peripheral cell receptor, and is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. This gene maps to chromosome 19 in a cluster with the related apolipoprotein C1 and C2 genes. Mutations in this gene result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron and VLDL remnants."
Gene ID: 1277 COL1A1 collagen type I alpha 1, i.e., type 1 procollagen propeptide, procollagen C-telopeptide.
Gene ID: 5741 PTH parathyroid hormone.
Gene ID: 7415 VCP valosin-containing protein.
Gene ID: 9370 ADIPOQ adiponectin, C1Q and collagen domain containing, i.e., free and bound deoxypyridinoline.

# Hypotheses
- The transcription of each gene, or its isoforms, is the opportunity to influence under or over expression.
Specific language impairment
Specific language impairment (SLI) is a developmental language disorder that can affect both expressive and receptive language.  SLI is defined as a "pure" language impairment, meaning that is not related to or caused by other developmental disorders, hearing loss or acquired brain injury.
However, the term specific language impairment is typically used in research literature, while other equivalent terms include: language impairment, language disability, language disorder, language delay, and language deviance. All of these terms belie assumptions about the nature of normal development, and some have been dropped as new perspectives on language development arise.
An SLI therefore is a general marker meaning language disorder, and not a specific disorder or disease.
Spondyloperipheral dysplasia
Spondyloperipheral dysplasia is an inherited disorder of bone growth. The condition is characterized by flattened bones of the spine (platyspondyly) and unusually short fingers and toes (brachydactyly). Some affected individuals also have other skeletal abnormalities, short stature, nearsightedness (myopia), hearing loss, and mental retardation. Spondyloperipheral dysplasia is a subtype of collagenopathy, types II and XI.
This condition is one of a spectrum of skeletal disorders caused by mutations in the COL2A1 gene. The protein made by this gene forms type II collagen, a molecule found mostly in cartilage and in the clear gel that fills the eyeball (the vitreous). Type II collagen is essential for the normal development of bones and other connective tissues (the tissues that form the body's supportive framework).
Mutations in the COL2A1 gene interfere with the assembly of type II collagen molecules. The protein made by the altered COL2A1 gene cannot be used to make type II collagen, resulting in a reduced amount of this type of collagen in the body. Instead of forming collagen molecules, the abnormal protein builds up in cartilage cells (chondrocytes). These changes disrupt the normal development of bones, leading to the signs and symptoms of spondyloperipheral dysplasia. This condition is probably inherited in an autosomal dominant pattern, which means one copy of the altered gene is sufficient to cause the disorder.
This article incorporates public domain text from Spondyloperipheral dysplasia at NLM Genetics Home Reference
St Michael's Hospital, Hayle
St Michael's Hospital, Hayle is a small hospital located in Hayle, Cornwall, United Kingdom. The hospital carries out approximately 5,000 operations each year .
The range of operations carried out at the hospital has expanded over recent years and now includes procedures in general surgery, urology, oral surgery, and orthopaedics including hip and knee replacements. St Michael's is also a Breast Surgery unit.
St Michael's Hospital is also an outpatient centre for the county seeing approximately 17,000 patients each year and is home to the specialist rehabilitation unit, Marie Therese House, which provides in and outpatient care for patients with neurological conditions and brain injuries. Services such as physiotherapy, occupational therapy and x-ray provide essential support in the diagnosis and treatment of in and outpatients at the hospital.
Staphylococcus saprophyticus

# Overview
Staphylococcus saprophyticus is a coagulase-negative species of Staphylococcus bacteria (which are catalase-positive). S. saprophyticus is often implicated in urinary tract infections. S. saprophyticus is resistant to the antibiotic Novobiocin, a characteristic that is used in laboratory identification to distinguish it from S. epidermitis, which is also coagulase- negative.
The organism is rarely found in healthy humans but is commonly isolated from animals and their carcasses.
It is implicated in 10-20% of urinary tract infections (UTI). In females between the ages of ca. 17-27 it is the second most common cause of UTIs. It may also reside in the urinary tract and bladder of sexually active females. S. saprophyticus is phosphatase-negative, urease and lipase positive.
Some of the symptoms of this bacteria are burning sensation when passing urine, the urge to go to the toilet more often than usual, the 'dripping effect' after urination, weak bladder, bloated feeling with sharp razor pains in the lower abdomen around the bladder and ovary areas and razor-like pains during sexual intercourse.
Quinolones are commonly used in treatment of S. saprophyticus urinary tract infections.

# Treatment

## Antimicrobial Regimen
- Urinary tract infections
- Preferred regimen (1): Cephalexin 500 mg PO qid
- Preferred regimen (2): Amoxicillin-Clavulanate 875/125 mg PO bid
- Preferred regimen (3): TMP-SMX 160800 mg PO bid
- Alternative regimen: Levofloxacin 500 mg PO qd
Stenotrophomonas maltophilia

# Overview
Stenotrophomonas maltophilia is an aerobic, nonfermentative,  Gram-negative bacterium which cause uncommon but difficult to treat infections in humans. Initially classified as Pseudomonas maltophilia, S. maltophilia was also grouped in the genus Xanthomonas before eventually becoming the type species of the genus Stenotrophomonas in 1993.

# Organism
S. maltophilia are slighlty smaller (0.7-1.8 x 0.4-0.7 m) than other members of the genus. They are motile due to polar flagella and grow well on MacConkey agar producing pigmented colonies. S. maltophilia are catalase positive, oxidase negative (which distinguishes them from most other members of the genus) and have a positive reaction for extracellular DNase.
S. maltophilia is ubiquitous in aqueous environments, soil and plants, including water, urine, or respiratory secretions; it has also been used in biotechnology applications. In immunocompromised patients, S. maltophilia can lead to nosocomial infections.

# Pathogenesis
S. maltophila frequently colonizes breathing tubes such as endotracheal or tracheostomy tubes, the respiratory tract and indwelling urinary catheters. Infection is usually facilitated by the presence of prosthetic material (plastic or metal), and the most effective treatment is removal of the prosthetic material (usually a central venous catheter or similar device). The growth of S. maltophilia in microbiological cultures of respiratory or urinary specimens is therefore sometimes difficult to interpret and not a proof of infection. If, however, it is grown from sites which would be normally sterile (e.g., blood), then it usually represents true infection.
In immunocompetent individuals, S. maltophila is a relatively unusual cause of pneumonia, urinary tract infection, or blood stream infection; in immunocompromised patients, however, S. maltophilia is a growing source of latent pulmonary infections. S. maltophilia colonization rates in individuals with cystic fibrosis have been increasing.
S. maltophilia is naturally resistant to many broad-spectrum antibiotics (including all carbapenems) and is thus often difficult to eradicate. Many strains of S. maltophilia are sensitive to co-trimoxazole and ticarcillin, though resistance has been increasing. It is not usually sensitive to piperacillin, and sensitivity to ceftazidime is variable.

## Antimicrobial regimen
- Stenotrophomonas maltophilia
- Preferred treatment: TMP-SMX 15-20 mg/kg/day (TMP component) IV/PO q8h
- Alternative treatment (1): Ceftazidime 2 g IV q8h
- Alternative treatment (2): Ticarcillin-clavulanate 3.1 g IV q4h
- Alternative treatment (3): Tigecycline 100 mg IV single dose THEN 50 mg IV q12h
- Alternative treatment (4): Ciprofloxacin 500-750 mg PO /400 mg IV q12h
- Alternative treatment (5): Moxifloxacin 400 mg PO/IV
- Alternative treatment (6): Levofloxacin 750 mg PO/IV .
- Alternative treatment (7) (Multiply-resistantance): Colistin 2.5 mg/kg q12h IV
- Note: Treatment duration uncertain, but usually  14 days.