anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Techniques are disclosed herein for generating microbiome fingerprints, dietary fingerprints, and microbiome ancestry. Microbiome data associated with an individual is analyzed to generate a microbiome fingerprint, and a dietary fingerprint for a user. A “microbiome fingerprint” uniquely identifies the microbiome of a user at a particular point in time and is based on a combination of different profiles generated from the microbiome data. The dietary fingerprint identifies how the microbiome of a user is associated with one or more different indexes, such as a dietary index and/or a particular characteristic (e.g., a Mediterranean diet index, a vegetarian diet index, a fast food index, an internal fat index, a fat-digesting index, a carbohydrate-digesting index, a health index, a fasting index, a ketogenic index, . . . ). The microbiome data may also be utilized to determine microbiome ancestry for the user that indicates other users to which the user is related to.
<P>PROBLEM TO BE SOLVED: To provide a diagnosis marker capable of rapidly and competently judging the morbidity of live body disintegrative syndrome originated from various diseases.  <P>SOLUTION: This marker peptide set of live body disintegrative syndrome comprises at least one peptide being a decomposition product of proteins existing in a live body, and detected in the biological fluid of a live body disintegrative syndrome patient and that of a healthy person with a statistically significant difference. This antibody recognizes either one of peptides of the marker peptide set. This therapeutic agent of the syndrome replenishes the parent protein of the marker peptide or contains a substance which is the marker itself or simultaneously regulates the quantity or the activity of a physiologically active peptide capable of acting in the direction of healing or worsening the disease. A judging method of the stage of live body disintegrative syndrome, by detecting at least one peptide constituting the marker peptide set in the live body sample which is derived from the patient affected a basic disease to result in live body disintegrative syndrome, an evaluation method of treatment effect, and an estimation method of the abolition of the function of part/organ of a patient and/or the danger of life continuation are also invented.  <P>COPYRIGHT: (C)2008,JPO&INPIT
It will be consisted of 16 women complaining from mild to moderate Carpel Tunnel Syndrome after 6 weeks from delivery diagnosed by electrophysiological study. They will receive wrist exercises (strengthening exercises for thenar muscles, wrist flexors. Extensors, grip strengthening, stretching, nerve glide, neurodynamic technique and tendon glide) for 15 minutes, three times per week for 4 weeks (total of 12 sessions) and home advices only.
Amyotrophic lateral sclerosis (ALS) is neurodegenerative disease characterized by a progressive loss of motor neurons resulting in paralysis and muscle atrophy. One of the most prospective hypothesis on the ALS pathogenesis suggests that excessive inflammation and advanced glycation end-products (AGEs) accumulation play a crucial role in the development of ALS in patients and SOD1 G93A mice. Hence, we may speculate that RAGE, receptor for advanced glycation end-products and its proinflammatory ligands such as: HMGB1, S100B and CML contribute to ALS pathogenesis. The aim of our studies was to decipher the role of RAGE as well as provide insight into RAGE signaling pathways during the progression of ALS in SOD1 G93A and RAGE-deficient SOD1 G93A mice. In our study, we observed alternations in molecular pattern of proinflammatory RAGE ligands during progression of disease in RAGE KO SOD1 G93A mice compared to SOD1 G93A mice. Moreover, we observed that the amount of beta actin (ACTB) as well as Glial fibrillary acidic protein (GFAP) was elevated in SOD1 G93A mice when compared to mice with deletion of RAGE. These data contributes to our understanding of implications of RAGE and its ligands in pathogenesis of ALS and highlight potential targeted therapeutic interventions at the early stage of this devastating disease. Moreover, inhibition of the molecular cross-talk between RAGE and its proinflammatory ligands may abolish neuroinflammation, gliosis and motor neuron damage in SOD1 G93A mice. Hence, we hypothesize that attenuated interaction of RAGE with its proinflammatory ligands may improve well-being and health status during ALS in SOD1 G93A mice. Therefore, we emphasize that the inhibition of RAGE signaling pathway may be a therapeutic target for neurodegenerative diseases.
High force lower extremity resistance training + Standard exercise care. The high force lower extremity resistance training group will participate in a 3 day per week progressive eccentric ergometry program that will be gradually increased over 3 weeks from 5-20 minutes per day and remain at that duration for the next 9 weeks. In addition, they will engage in exercises including moderate intensity aerobic training, concentric upper extremity resistance training and stretching (axial mobility exercises).
A medicine for treating insomnia is prepared from, by weight, 50 g of fresh lotus roots, 50 g of pears, 30 g of poria cocos and 20 g of the whole herb and fruit of Cynanchum thesiodes(Freyn). K.Schum. According to preparation and taking, the medicine is prepared according to the weight ratio, the fresh lotus roots are thoroughly washed, lotus root knots and peel are removed, the pears are peeled off, denucleated and cut up, and the fresh lotus roots and the cut pears are placed in clean gauze to be twisted, and juice is taken. Poria cocos and the whole herb and fruit of Cynanchum thesiodes(Freyn). K.Schum are decocted with slow fire, and the liquid of poria cocos and the whole herb and fruit of Cynanchum thesiodes(Freyn). K.Schum is taken. The juice and the liquid are combined and taken with boiled water after the dinner every day, and the problems that existing medicine for treating insomnia is large in side effect, and insomnia cannot be radically treated are solved.
The method is for treating skin. A peptide is selected that affects a receptor so that the receptor is receptive to the peptide. The selected peptide is dissolved in a solution to form a peptide solution. The skin is vibrated to generate heat without reducing the peptide in the peptide solution. The peptide solution is applied to the skin. The peptide solution increases an operational activity of the receptor in the skin.
PCT No. PCT/JP93/00436 Sec. 371 Date Feb. 9, 1994 Sec. 102(e) Date Feb. 9, 1994 PCT Filed Apr. 2, 1993 PCT Pub. No. WO93/20718 PCT Pub. Date Oct. 28, 1993.The present invention provides a food composition for inhibiting the formation of an intestinal putrefactive product, containing lactosucrose as an effective component. This food composition is low in calorific value because the lactosucrose is indigestible, and can decrease the amount of an putrefactive product to be generated in intestines. Accordingly, this food composition effectively prevents the outbreak of a variety of cancers for which the putrefactive product might serve as a promoter.
Participants receive SI-B001 as intravenous infusion for the first cycle (3 weeks). Participants with clinical benefit could receive additional treatment for more cycles. The administration will be terminated because of disease progression or intolerable toxicity occurring or other reasons.
This control group will perform general aerobic exercises. Within a 12-week period, patients will be instructed to perform a general aerobic exercise session 3 times a week.
The study group is composed of ICU care providers at the Ottawa Hospital Civic campus and the Montfort Hospital, including intensivists, fellows, nurses and allied health professionals. The study site participant breakdown is approximately 58 TOH staff respondents and 15 Montfort respondents.
NEW MATERIAL:NFA (normal fetus antigen)-1, of 20,000-30,000mol.wt. (determined by S.D.S. polyacrylamide electrophoresis). USE:Antigen for measurement of carcinoembryonic antigen (CEA) or differential diagnosis of cancers. PREPARATION:Fetus of normal persons are subjected to extraction with perchloric acid, the liquid layer is dialyzed against water to effect complete removal of perchloric acid. Then, the extract is concentrated by pressurized air drying, brought into contact with an adsorbent to which anti-CEA antibody is bonded to adsorb CEA-relating substances. Then elution is effected under acidic conditions, the eluate is neutralized, subjected to agarose gel filtration and the eluted fraction is collected. The fraction is treated with chromatography to remove strongly negative-charged brown pigment and the eluate is brought into contact with an adsorbent to which anti-NCA (nonspecific cross-reacting antigen) antibody bonds. Then, the nonreactive liquid layer is fractionated, concentrated and subjected to crosslinked dextran polymer gel filtration to collect the eluate fraction. The fraction is concentrated by pressurized air drying and subjected again to crosslinked dextran polymer gel filtration.
The invention provides an anti-CLL1 antibody and application thereof, wherein the variable region of the anti-CLL1 antibody comprises CDRs of SEQ ID NO. 1-6, SEQ ID NO. 5 and SEQ ID NO. 7-11 or SEQ ID NO. 12-17. The anti-CLL1 antibody has obvious binding capacity to both free CLL1 and cell surface CLL1, further improves the affinity of the antibody and CLL1 after humanized modification, and has important application prospect in the clinical diagnosis and/or treatment of tumors.
PROBLEM TO BE SOLVED: To improve the operability of the chart/receipt generation process by providing a temporary disease name memory means storing a presented disease name candidate list in relation with the action portion to be treated, erasing the stored presented disease name candidate list for the action portion specified with the disease name, and registering the specified disease name as the established disease name. SOLUTION: When the therapeutic input process is selected for a treatment and receipt generation via a dental information processing device, the display of a display section 41 is shifted to the input screen of the therapeutic portion of a therapeutic input screen. The tooth number of the therapeutic portion is inputted from an operation section 43, and the therapeutic portion including a missing tooth is established. After the input is finished, the disease name input process is started. When the disease name is not established yet, unestablished disease name data are registered for the patient temporary establishment region data. When the function key of the operation section 43 is depressed after the function key allocation display is confirmed, the display screen is shifted to a disease name input screen, and the established disease name is inputted.
Cystic fibrosis is an autosomal recessive disorder caused by mutations of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most recent therapeutic approach to cystic fibrosis aims to correct structural and functional abnormalities of CFTR protein. CFTR modulators including ivacaftor-tezacaftor-elexacaftor are used in patients with F508del mutation, with clinical improvement. To date, there are no experiences of CFTR modulator therapy in cystic fibrosis patients with organ transplantation and severe renal impairment. We report the case of a patient diagnosed with cystic fibrosis with F508del mutation, who underwent liver transplantation at the age of 19 and started hemodialysis at the age of 24 due to end-stage renal disease secondary to membranous glomerulonephritis. She was treated with Kaftrio (ivacaftor-tezacaftor-elexacaftor) with clinical benefits on appetite, improvement of body mass index, and reduction of pulmonary exacerbations. A reduction of dosage to 75% of the standard dose was required due to alterations of the liver function. Conclusions. Use of CFTR modulators in patient with cystic fibrosis, liver transplant and end-stage renal disease could be considered safe but a clinical and laboratoristic monitoring of hepatic function is needed.
A high-throughput screening assay for identifying small molecule agonists for the TrkA receptor is described. One such agonist, gambogic amide, selectively binds to TrkA but not TrkB or C, robustly induces its tyrosine phosphorylation and downstream signaling activation including Akt and MAP kinases. Further, it strongly prevents glutamate-induced neuronal cell death and provokes prominent neurite outgrowth in PC 12 cells. Gambogic amide specifically interacts with the cytoplasmic juxtamembrane domain of TrkA receptor and triggers its dimerization. Administration of this molecule in mice substantially diminishes Kainic acid-triggered neuronal cell death and decreases infarct volume in transient middle cerebral artery occlusion (MCAO) model of stroke. Thus, gambogic amide and other selective TrkA agonists can provide effective treatments for debilitating neurodegenerative diseases and provide neuroprotection from patients suffering from stroke or other ischemic events.
BACKGROUND: Atrial fibrillation (AF) is known to be a strong risk factor for stroke. However, the risk of stroke recurrence in patients with cryptogenic stroke with AF detected after stroke by an insertable cardiac monitor (ICM) is not well known. We sought to evaluate the risk of ischemic stroke recurrence in patients with cryptogenic stroke with and without ICM-detected AF.
METHODS AND RESULTS: We retrospectively reviewed patients with cryptogenic stroke who underwent ICM implantation at 8 stroke centers in Japan. Cox regression models were developed using landmark analysis and time-dependent analysis. We set the target sample size at 300 patients based on our estimate of the annualized incidence of ischemic stroke recurrence to be 3% in patients without AF detection and 9% in patients with AF detection. Of the 370 patients, 121 were found to have AF, and 110 received anticoagulation therapy after AF detection. The incidence of ischemic stroke recurrence was 4.0% in 249 patients without AF detection and 5.8% in 121 patients with AF detection (P=0.45). In a landmark analysis, the risk of ischemic stroke recurrence was not higher in patients with AF detected ≤90 days than in those without (hazard ratio, 1.47 [95% CI, 0.41-5.28]). In a time-dependent analysis, the risk of ischemic stroke recurrence did not increase after AF detection (hazard ratio, 1.77 [95% CI, 0.70-4.47]).
CONCLUSIONS: The risk of ischemic stroke recurrence in patients with cryptogenic stroke with ICM-detected AF, 90% of whom were subsequently anticoagulated, was not higher than in those without ICM-detected AF.
BIA 2-093 200mg with 200 ml potable water. Identical placebo administered as oral tablets.
The invention provides a pig 4-1BB receptor molecule, which is the flowing protein (1) or (2): the protein (1) is composed of amino acid sequences shown in SEQ ID NO. 3 or 4, and the protein (2) is derived from the protein (1) by substitution, deletion or insertion of one or more amino acids in the amino acid sequences shown in SEQ ID NO. 3 or 4, and has the same activity. . The invention also provides a gene for encoding the pig 4-1BB receptor, which has nucleotide sequences shown in SEQ ID NO. 1 or 2. The costimulatory receptor 4-1BB provided by the invention is specifically and highly expressed in peripheral blood T cells of pig, can enhance activation, proliferation and secretion activity of cell factor when transgenic T cells are suffered from antigenic stimulation, thus enhance acquired immunity response of host and immunity effect of vaccine.
Exposure to winter cold causes an increase in energy demands to meet the challenge of thermoregulation. In small rodents, this increase in cardiac output leads to a profound cardiac hypertrophy, 2-3 times that typically seen with exercise training. The nature of this hypertrophy and its relevance to winter mortality remains unclear. Our goal was to characterize cold-induced cardiac hypertrophy and to assess its similarity to either exercise-induced (physiological) hypertrophy or the pathological hypertrophy of hypertension. We hypothesized that cold-induced hypertrophy will most closely resemble exercise-induced hypertrophy, but be another unique pathway for physiological cardiac growth. We found that cold-induced hypertrophy was largely reversed after a return to warm temperatures. Further, metabolic rates were elevated while gene expression and mitochondrial enzyme activities indicative of pathology were absent. A gene expression panel comparing hearts of exercised and cold-exposed mice further suggests that these activities are similar, although not identical. In conclusion, we found that chronic cold led to a phenotype that most closely resembled physiological hypertrophy, with enhanced metabolic rate, without induction of fetal genes, but with decreased expression of genes associated with fatty acid oxidation, suggesting that heart failure is not a cause of winter mortality in small rodents and identifying a novel approach for the study of cardiac growth.
Within two weeks of enrollment, patients receive allogeneic adenovirus-specific CTLs IV over 30 minutes. Patients may receive additional allogeneic adenovirus-specific CTL infusions at the discretion of the investigator in the absence of disease progression or unacceptable toxicity.
This invention relates to an improved integrated process in the recovery of pectin and polyphenolic compositions from mango peels. In this improved process, the pectin containing material is subjected to acid hydrolysis to extract the pectin, separation of the filtrate containing the pectin material by a simple decantation and/or filtration step, and recovery of the pectin material by alcoholic precipitation. The pectin precipitate may be further dried and milled to obtain the pectin powder. Further, the improved process is characterized by its pectin yield of 30% or greater. The pectin obtained herein is further characterized by its galacturonic acid content of 70% or higher and high methoxyl content with a degree of esterification of 65% or greater, as it employs the  defatted mango peel powder  obtained in the integrated process of a related invention. In addition, the improved process results in the efficient use of alcohol as precipitating agent for pectin as it employs the combined purification and alcohol recovery methods in the subsequent preparation of the polyphenolic composition.
Cohort A3 will include patients with ER positive breast tumor. Patients will be treated with one injection of Pembrolizumab (Keytruda®) administered intravenously at 200 mg 10 +/- 4 days before surgery.
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.

In a 12-week randomized, placebo-controlled, double-blind, fixed-dose study of SOMAVERT in subjects with acromegaly, 32 subjects received placebo and 80 subjects received SOMAVERT once daily [see Clinical Studies (14)]. A total of 108 subjects (30 placebo, 78 SOMAVERT) completed 12 weeks of study treatment.

Overall, eight patients with acromegaly (5.3%) withdrew from pre-marketing clinical studies because of adverse events, including two patients with marked transaminase elevations, one patient with lipohypertrophy at the injection sites, and one patient with substantial weight gain. Most adverse events did not appear to be dose-dependent. Table 3 shows the incidence of adverse events that were reported in at least two patients treated with SOMAVERT and at frequencies greater than placebo during the 12-week, placebo-controlled study.
Sinus arrest and inappropriate sinus bradycardia are sinus node dysfunction (SND), which cause loss of consciousness. Cardiac pacing is recommended in patients with symptoms, such as syncope or dizziness. Several conditions can induce these arrhythmias; however, whether or not intracranial infectious diseases, such as herpes simplex encephalitis (HSE), can cause secondary SND is unclear. We encountered a patient with sinus arrest and transient sinus bradycardia associated with HSE. Since cardiac pause was never monitored and the bradycardia improved after HSE treatment, HSE was suspected to be the cause of SND. Although the underlying mechanisms have not yet been completely elucidated, HSE may cause secondary SND.
Ultrasound is a non-invasive and non-radiated diagnostic tool in the emergency and critical care settings. In clinical practice, timely interpretation of sonographic images to facilitate decision-making is essential. However, it depends on operators' experience. As usual, it takes time for junior emergency physicians to have good diagnostic accuracy through traditional sonographic education. How to shorten the learning This proposal is for an one-year project. In this project, we aim to investigate the feasibility of using AI for sonographic image interpretation. The main project is responsible for coordination between the two sub-projects and the main project, providing image resources, and using U-Net (Convolutional Networks for Biomedical Image Segmentation) and Transfer Learning to build up the models for image recognition and validating the efficacy of the models. The purpose of Subproject 1 is to develop an image recognition system for dynamic images: pericardial effusion. After building up the model, validating the efficacy and future revision will be done. Subproject 2 comes out an image recognition system for static images: hydronephrosis. After building up the model, validating the efficacy and future revision will be done.

This pioneer study can provide two AI-assisted ultrasound image recognition systems in the real clinical conditions. They can experience of clinical applications and contribute to current medical education. Moreover, it can improve decision-making process and quality of care in the emergency and critical care units. Furthermore, the set-up models can be used in other target ultrasound image recognition in the future.
PURPOSE:To obtain an antiulcer agent exhibiting gastric acid secretion suppressing action and gastric mucosa protecting action and having excellent stability and safety, by using a specific thiomorpholin-3-one derivative as an active component. CONSTITUTION:The objective agent contains a compound of formula I (R is substituted or unsubstituted phenyl, pyridyl or cycloalkyl), e.g. 2-(m-fluorophenyl) thiomorpholin-3-one as an active component. The dose of the compound is 10-1,000mg, preferably 50-500mg daily for adult and is administered in 2-4 divided doses a day. The compound of formula I can be produced by reacting alpha-bromoethyl esters of formula II with 2-aminoethanethiol or its salt in a solvent inert to the reaction (e.g. hydrated ethanol) in the presence of potassium carbonate.
The purpose of this study is to investigate whether buprenorphine continuation at analgesic dosing is superior to full dose buprenorphine continuation in individuals presenting for elective surgery. Adults scheduled for elective surgery who are taking ≥12mg buprenorphine for OUD treatment will be eligible for this study. Enrolled participants will be randomized to receive either a reduced analgesic dose of buprenorphine (8mg) or to continue buprenorphine on the day of surgery without dose reduction. The primary outcome of interest is postoperative pain scores. The secondary outcomes of interest are opioid consumption, opioid dispensing up to 30 days following the surgical procedure and OUD related symptoms, including opioid withdrawal, cravings and relapse. The investigators hypothesis is that there will be a clinically significant increase in pain scores when buprenorphine is continued in full compared to when it is continued at a lower analgesic dose. Clinical significance will be defined as a difference in composite pain scores of greater than 20% between groups. The investigators also hypothesize that opioid consumption and opioid dispensing will be greater with full dose buprenorphine continuation compared to low-dose continuation.