anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: BK polyomavirus (BKV) can cause permanent loss of allograft function due to BKV-associated nephropathy (BKVN) in kidney transplant recipients. Besides immunosuppression reduction, there are no consistently effective interventions for BKV infection. Study purpose was to define natural history of BKV infection, identify risk factors for BKV reactivation and BKVN in kidney transplant recipients, and inform the design/conduct of future clinical trials of BKV-targeted therapeutics.
METHODS: We conducted a multicenter prospective observational study of incident kidney transplant recipients at six U.S. transplant centers. Participants were monitored every 4 weeks for BKV reactivation and followed for up to 24 months post-transplant. We used regression models (logistic, survival, mixed models) to study relationships between BK viremia/BKVN, clinical characteristics, and allograft function.
RESULTS: We enrolled 335 participants. Fifty-eight (17%) developed BK viremia, 6 (2%) developed biopsy-proven BKVN, and 29 (9%) developed suspected/presumed BKVN (defined as BKV viral load > 10,000 copies/mL without biopsy). Male donor sex was associated with lower odds for BK viremia, whereas recipient Black race was associated with two-fold increased odds for BK viremia. Recipient female sex was associated with more rapid clearance of BK viremia. Persistent BK viremia/BKVN was associated with poorer allograft function by 24 months post-transplant.
CONCLUSIONS: We identified multiple donor and recipient demographic factors associated with risk for BKV infection and poorer allograft function by 24 months post-transplant. This may help design future clinical trials of therapies to prevent or mitigate the deleterious impact of BKV reactivation on kidney transplant outcomes.
Aspects of the present disclosure include bispecific molecules. The bispecific molecules comprise a cell-targeting moiety and a glycan-binding moiety. According to some embodiments, the cell-targeting moiety is a cancer cell-targeting moiety or an immune cell-targeting moiety. In certain embodiments, the glycan-binding moiety comprises the sialoglycan-binding domain of a lectin, non-limiting examples of which are sialic acid-binding immunoglobulin-like lectins (Siglecs). The bispecific molecules may take a variety of forms including heterodimeric molecules, fusion proteins, conjugates, and the like. Compositions, kits and methods of using the bifunctional molecules, e.g., for therapeutic purposes, are also provided.
A multicenter, randomized, open-label study was conducted in 1052 chemotherapy naive patients with Stage IIIb/IV non-small cell lung cancer to compare Paclitaxel Protein-Bound Particles for Injectable Suspension (Albumin-Bound) in combination with carboplatin to paclitaxel injection in combination with carboplatin as first-line treatment in patients with advanced non-small cell lung cancer. Paclitaxel Protein-Bound Particles for Injectable Suspension (Albumin-Bound) was administered as an intravenous infusion over 30 minutes at a dose of 100 mg/m2 on Days 1, 8, and 15 of each 21-day cycle. Paclitaxel injection was administered as an intravenous infusion over 3 hours at a dose of 200 mg/m2, following premedication. In both treatment arms carboplatin at a dose of AUC = 6 mg•min/mL was administered intravenously on Day 1 of each 21-day cycle after completion of Paclitaxel Protein-Bound Particles for Injectable Suspension (Albumin-Bound)/paclitaxel infusion. Treatment was administered until disease progression or development of an unacceptable toxicity. The major efficacy outcome measure was overall response rate as determined by a central independent review committee using RECIST guidelines (Version 1.0).

In the intent-to-treat (all-randomized) population, the median age was 60 years, 75% were men, 81% were White, 49% had adenocarcinoma, 43% had squamous cell lung cancer, 76% were ECOG PS 1, and 73% were current or former smokers. Patients received a median of 6 cycles of treatment in both study arms.

Patients in the Paclitaxel Protein-Bound Particles for Injectable Suspension (Albumin-Bound)/carboplatin arm had a statistically significantly higher overall response rate compared to patients in the paclitaxel injection/carboplatin arm [(33% versus 25%) see Table 12]. There was no statistically significant difference in overall survival between the two study arms.
We used a randomized controlled parallel group design to compare the intervention to a usual-care control group. We attempted to evaluate the effectiveness of the intervention in the "real world," rather than its ideal efficacy.

The CHWs used protocols that specified education content, participant skill development and participant and CHW actions. The CHWs modified their approach to meet the priorities of participants using motivational interviewing techniques. They addressed asthma patho-physiology, reliever and controller medication use, self-monitoring, use of an asthma action plan, environmental assessment, trigger avoidance, effective use of the health care system, successful communication with health care providers, and weight control (obesity is associated with increased asthma symptoms). Participants also received low-literacy educational materials, in English or Spanish. The education concepts and environmental assessment activities were based on our prior healthy homes work modified for adults.
Subjects who have a mixed (nociceptive and neuropathic) pain conditions will receive a mixed pain cream combined of Ketamine 10%/Gabapentin 6%/Diclofenac 3%/baclofen 2%/Cyclobenzaprine 2% and Lidocaine 2% or placebo. They will be told to use the pain cream 3 times per day. Each will receive cream in identical dispensers. Cream is dispensed by rotating the base of the device and each rotation also produces a clicking sound. The number of clicks will be standardized so that all doctors utilize the same prescription depending on the size of the patient's pain location.
TAK-931 50 mg (2x25 mg or 5x10 mg), capsules, orally, QD for 14 days, followed by a 7-day washout period (14 days on and 7 days off study drug), in 21-day cycles until disease progression or unacceptable treatment-related toxicity up to 8 cycles. Participants with metastatic sqEC who had progressed after at least 1 line of standard chemotherapy were included in this cohort.
When the patient is switching from a 21-day regimen of tablets, she should wait 7 days after her last tablet before she starts FALMINA. She will probably experience withdrawal bleeding during that week. She should be sure that no more than 7 days pass after her previous 21-day regimen. When the patient is switching from a 28-day regimen of tablets, she should start her first pack of FALMINA on the day after her last tablet. She should not wait any days between packs. The patient may switch any day from a progestin-only pill and should begin FALMINA the next day. If switching from an implant or injection, the patient should start FALMINA on the day of implant removal or, if using an injection, the day the next injection would be due. In switching from a progestin-only pill, injection, or implant, the patient should be advised to use a nonhormonal back-up method of birth control for the first 7 days of tablet-taking.
The control group was collected from the period immediately before the study's initiation (from Jun 2012 to September 2013). This cohort was comprised of preterm infants of less than 32 WG who met the inclusion criteria.
BACKGROUND: Necrotizing myopathies and muscle necrosis can be caused by immune-mediated mechanisms, drugs, ischemia, and infections, and differential diagnosis may be challenging.
CASE PRESENTATION: We describe a case of diabetic myonecrosis complicated by pyomyositis and abscess caused by Escherichia coli. A white woman in her late forties was admitted to the hospital with a 1.5 week history of bilateral swelling, weakness, and mild pain of the lower extremities and inability to walk. She had a history of type 1 diabetes complicated by diabetic retinopathy, neuropathy, nephropathy, and end-stage renal disease. C-reactive protein was 203 mg/l, while creatinine kinase was only mildly elevated to 700 IU/l. Magnetic resonance imaging of her lower limb muscles showed extensive edema, and muscle biopsy was suggestive of necrotizing myopathy with mild inflammation. No myositis-associated or myositis-specific antibodies were detected. Initially, she was suspected to have seronegative immune-mediated necrotizing myopathy, but later her condition was considered to be explained better by diabetic myonecrosis with multifocal involvement. Her symptoms alleviated without any immunosuppressive treatment. After a month, she developed new-onset and more severe symptoms in her right posterior thigh. She was diagnosed with emphysematous urinary tract infection and emphysematous myositis and abscess of the right hamstring muscle. Bacterial cultures of drained pus from abscess and urine were positive for Escherichia coli. In addition to abscess drainage, she received two 3-4-week courses of intravenous antibiotics. In the discussion, we compare the symptoms and findings typically found in pyomyositis, immune-mediated necrotizing myopathy, and diabetic myonecrosis (spontaneous ischemic necrosis of skeletal muscle among people with diabetes). All of these diseases may cause muscle weakness and pain, muscle edema in imaging, and muscle necrosis. However, many differences exist in their clinical presentation, imaging, histology, and extramuscular symptoms, which can be useful in determining diagnosis. As pyomyositis often occurs in muscles with pre-existing pathologies, the ischemic muscle has likely served as a favorable breeding ground for the E. coli in our case.
CONCLUSIONS: Identifying the etiology of necrotizing myopathy is a diagnostic challenge and often requires a multidisciplinary assessment of internists, pathologists, and radiologists. Moreover, the presence of two rare conditions concomitantly is possible in cases with atypical features.
BACKGROUND: Healthcare-associated infections (HAIs) represent the most frequent adverse event in healthcare systems around the world. From a forensic point of view, HAIs show various legal implications. Therefore, it is essential in cases of death or injury from a suspected nosocomial infection that the infection itself, the source and the method of contamination are correctly diagnosed in order to evaluate any profiles of professional liability.
METHODS: This study combined a minireview of the scientific literature using the Pubmed search engine, the website of the Higher Institute of Health and the member states information sessions on infection prevention and control (IPC).
DISCUSSION: Despite the significant impact that HAIs have on healthcare systems, their severity is often not fully understood by healthcare professionals, leading to insufficient responses. In the autopsy setting, the diagnosis of these infections is not always simple due to the risk of post-mortem contamination determined by the endogenous bacterial flora. In the forensic field, the medical examiner during the autopsy can use various diagnostic techniques and investigative tools to identify the infection. Some usefulpp approaches include: 1) Macroscopic examination of the organs; 2) Histopathological investiga-tions; 3) Microbiological analyzes with the performance of swabs; 4) Immunofluorescence tests for the detection of antigens or antibodies on biological liquids; 5) Molecular tests. The choice of methods will depend on the nature of the suspected infection and the availability of diagnostic resources.
Employing race-specific resistance genes remains an effective strategy to protect wheat from leaf rust caused by Puccinia triticina (Pt) worldwide, while the newly emerged Pt races, owing to rapid genetic evolution, frequently overcome the immune response delivered by race-specific resistance genes. The molecular mechanisms underlying the newly evolved virulence Pt pathogen remain unknown. Here, we identified an avirulence protein AvrLr15 from Pt that induced Lr15-dependent immune responses. Heterologously produced AvrLr15 triggered pronounced cell death in Lr15-isogenic wheat leaves. AvrLr15 contains a functional signal peptide, localized to the plant nucleus and cytosol and can suppress BAX-induced cell death. Evasion of Lr15-mediated resistance in wheat was associated with a deletion and point mutations of amino acids in AvrLr15 rather than AvrLr15 gene loss in the Lr15-breaking Pt races, implying that AvrLr15 is required for the virulence function of Pt. Our findings identified the first molecular determinant of wheat race-specific immunity and facilitated the identification of the first AVR/R gene pair in the Pt-wheat pathosystem, which will provide a molecular marker to monitor natural Pt populations and guide the deployment of Lr15-resistant wheat cultivars in the field.
The object is to isolate and identify human and mouse adiponectin receptors, to provide a novel protein having adiponectin binding ability, and to provide a screening method and screening kit for a ligand, agonist and antagonist to an adiponectin receptor using such protein. To achieve this object, a protein is used, as novel protein having adiponectin binding ability, that is (a) a protein comprising an amino acid sequence according to Seq. No. 2, 4, 6 or 8, or (b) a protein comprising an amino acid sequence according to Seq. No. 2, 4, 6 or 8 with one or more amino acids deleted, replaced or added, and having adiponectin binding ability.
PURPOSE:To obtain a lipid endoplasmic reticulum which maintains physical and chemical stability, has high decomposing property in a living body, and is suitable for making liposome medicine by incorporating a specified polymerizable phospholipid and non-polymerizable lipid and specifying the ratio of the non-polymerizable phospholipid to the polymerizable phospholipid. CONSTITUTION:The material to form lipid endoplasmic reticulum consists of (A) polymerizable phospholipid expressed by formula (wherein R<1>, R<2> are acyl residues produced from polymerizable fatty acid and X is a phospholipid polar group) and (B) non-polymerizable lipid. The ratio of the component (B) non- polymerizable phospholipid to 1mol of the component (A) polymerizable phospholipid is specified to 0.3-3mol. The forming material is used as a member to constitute the membrane of the lipid endoplasmic reticulum. Further, the lipid endoplasmic reticulum is subjected to polymn. treatment. Thereby, the obtd. lipid endoplasmic reticulum maintains physical and chemical stability, has high decomposing property in a living body, is fast metabolized and decomposed, and suitable as such a liposome medicine that the period of accumulation in a living body is decreased.
The 35,000 women randomised to the no intervention arm will continue in the Swedish National Breast Cancer Screening Program. This means that they are invited for the next mammography screening after 24 months.
Glatiramer acetate, the active ingredient of Glatopa, consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000 – 9,000 daltons. Glatiramer acetate is identified by specific antibodies.

Chemically, glatiramer acetate is designated L-glutamic acid polymer with L-alanine, L-lysine and L-tyrosine, acetate (salt). Its structural formula is:

Glatopa is a clear, colorless to slightly yellow, sterile, nonpyrogenic solution for subcutaneous injection. Each 1 mL of glatiramer acetate injection solution contains 20 mg or 40 mg of glatiramer acetate and the following inactive ingredient: 40 mg of mannitol. The pH of the solutions is approximately 5.5 to 7. The biological activity of glatiramer acetate is determined by its ability to block the induction of experimental autoimmune encephalomyelitis (EAE) in mice.
This is a double-blind, randomized, placebo-controlled study. Approximately 450 subjects will be randomized in a 1:1:1 ratio to receive daily oral doses of serlopitant 1 mg, 5 mg, or placebo for 6 weeks. During the screening period, subjects will be provided with an electronic device for recording electronic diary (eDiary) assessments throughout the study. This eDiary will be used to capture efficacy endpoint data and treatment information. At the Baseline visit, eligible subjects will be randomized, and study drug dispensed beginning with a loading dose of 3 tablets to be taken at bedtime that same day. Starting on Study Day 2, subjects will take one tablet per day at bedtime. Treatment will continue for 6 weeks. The primary efficacy endpoint will be assessed during Week 6. After completion of the 6-week treatment period, all subjects will enter a 4-week follow-up period.
NEW MATERIAL:A compound shown by the formula I (R is 6-30C alkyl; A is 0 or NH). EXAMPLE:3-O-Laurylallose. USE:A drug having anticancer action, plant growth regulating action and antimicrobial action. PREPARATION:For example, 1,2:5,6-di-O-isopropylidene-alpha-D-allofuranose shown by the formula II is reacted with a compound (e.g., lauryl bromide, etc.) shown by the formula RX (X is active group) to give a 3-O-alkyl-1,2:5,6-di-O- isopropylidene-alpha-D-allofuranose, which is then hydrolyzed to give a compound shown by the formula I (A is O). Or, 1,2:5,6-di-O-isopropylidene-alpha-D-ribo- hexofuranose-3-ulose is reacted with a compound (e.g., stearylamine, etc.) shown by the formula RNH2 to give a Schiff base, which is reduced and hydrolyzed to give a compound shown by the formula I (R is NH).
The presence of feathers is a vital characteristic among birds, yet most modern birds had no feather on their feet. The discoveries of feathers on the hind limbs of basal birds and dinosaurs have sparked an interest in the evolutionary origin and genetic mechanism of feathered feet. However, the majority of studies investigating the genes associated with this trait focused on domestic populations. Understanding the genetic mechanism underpinned feathered-foot development in wild birds is still in its infancy. Here, we assembled a chromosome-level genome of the Asian house martin (Delichon dasypus) using the long-read High Fidelity sequencing approach to initiate the search for genes associated with its feathered feet. We employed the whole-genome alignment of D. dasypus with other swallow species to identify high-SNP regions and chromosomal inversions in the D. dasypus genome. After filtering out variations unrelated to D. dasypus evolution, we found six genes related to feather development near the high-SNP regions. We also detected three feather development genes in chromosomal inversions between the Asian house martin and the barn swallow genomes. We discussed their association with the wingless/integrated (WNT), bone morphogenetic protein, and fibroblast growth factor pathways and their potential roles in feathered-foot development. Future studies are encouraged to utilize the D. dasypus genome to explore the evolutionary process of the feathered-foot trait in avian species. This endeavor will shed light on the evolutionary path of feathers in birds.
The utility model is a medicine magnetism acupuncture point paste which can be adhered to the points of the human body. The utility model consists of a permanent magnetism paste piece, a medicine groove, adhesive plasters and a film combination. The permanent magnetism paste piece is in form of a dish, a pot bottom concave medicine groove is arranged on the front side of the permanent magnetism paste piece. The medicine groove and the permanent magnetism paste piece are integral part of each other. A round adhesive plaster is fixed on the back side of the permanent magnetism paste piece and the film is covered on the front side. When in use, take off the film, and infuse required ointment into the medicine groove to form a medicine magnetism acupuncture point paste, the adhesive plaster fixes the medicine magnetism acupuncture point paste on the points, the therapy purpose is reached by using medicine magnetic filed effect.
The invention relates to the treatment of ascites, and especially refractory ascites, with an orally bioavailable prodrug of dopamine. A preferred prodrug of dopamine is docarpamine. In one embodiment treated patients are, prior to treatment, on doses of furosemide >80 mg/day and/or spironolactone >100 mg/day or equivalent doses of an alternative loop-acting and/or distal-acting diuretic. The ascites treated by the invention are typically caused by liver cirrhosis due to alcohol or non-alcoholic fatty liver disease and generally not due to viral hepatitis or primary biliary cholangitis. Typical patients have an activated renin-angiotensin-aldosterone levels as may be indicated by elevated levels of renin and/or aldosterone. Refractory ascites treatable according to the invention are such that patients beginning treatment require large volume paracentesis at a minimum of: (a) 3 times in 60 days, (b) 4 times in 90 days or (c) at least once every 30 days over a 90-day period. The invention also contemplates treating diuretic intractable ascites. Target plasma dopamine levels are disclosed by with dosing with the contemplated dopamine prodrugs may be guided. Preferred dosing is greater that 2250 mg per day, with more preferred doses exceeding 3500 mg per day.
NEW MATERIAL:A dihydropyrimidine derivative which is tautomers expressed by formulas I and II (R<1> is lower alkyl; R<2> is phenyl, substituted phenyl, furyl or thienyl) and an acid addition salt thereof. EXAMPLE:5-Alkoxycarbonyl-2,6-dimethyl-4-phenyl-dihydropyrimidine. USE:A safe agent, having vasodilator action, and effective for treating a wide variety of cardiovascular diseases, e.g. hypertension, angina pectoris, arrhythmia, etc. and having selectivity for blood vessels. PREPARATION:A tetrahydropyrimidinol derivative expressed by formula III is treated with a dehydrating agent selected from the group consisting of phosphorus oxychloride, alumina, silica gel and acids and if desired an acid suitable to a medicine to afford the compounds expressed by formulas I and II. For example, a method of heat treatment is carried out in case and acid, e.g. p-toluenesulfonic acid, is used as the dehydrating agent.
Oxaliplatin, a platinum-based chemotherapeutic agent, frequently causes acute and chronic peripheral sensory neuropathy, for which no effective treatment has been established. In particular, chronic neuropathy can persist for years even after treatment completion, thus worsening patients' quality of life. To avoid the development of intractable adverse effects, a predictive biomarker early in treatment is awaited. In this study, we explored extracellular long non-coding RNAs (lncRNAs) released from primary sensory neurons as biomarker candidates for oxaliplatin-induced peripheral neuropathy. Because many human-specific lncRNA genes exist, we induced peripheral sensory neurons from human induced pluripotent stem cells. Oxaliplatin treatment changed the levels of many lncRNAs in extracellular vesicles (EVs) released from cultured primary sensory neurons. Among them, the levels of release of lncRNAs that were considered to be selectively expressed in dorsal root ganglia were correlated with those of lncRNAs in plasma EV obtained from healthy individuals. Several lncRNAs in plasma EVs early after the initiation of treatment showed greater changes in patients who did not develop chronic neuropathy that persisted for more than 1 year than in those who did. Therefore, these extracellular lncRNAs in plasma EVs may represent predictive biomarkers for the development of chronic peripheral neuropathy induced by oxaliplatin.