anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
To breach the current controversies, there is an urgent need for well-designed controlled human intervention trials evaluating the true impact of boiled potato consumption as part of a healthy dietary pattern on cardiometabolic health. There are two important issues that need to be addressed when designing such an intervention study: First, the longer-term effects of boiled potato consumption on established fasting and postprandial cardiovascular risk markers should be addressed. Second, the effect of boiled potatoes should be studied using an iso-energetic exchange for other traditionally main carbohydrate sources. These carbohydrate-sources will be part of a recommended healthy dietary pattern to mimic as closely as possible current dietary guidelines, facilitating the implementation of the outcomes. Effects will be studied in both fasting and postprandial conditions. In fact, the evidence is accumulating that optimizing postprandial glucose and lipid responses are important targets for maintaining health. Since potatoes, white rice and white pasta are all products with a high glycemic index and concomitant relatively steep glucose excursions after intake, the question is how long-term intake of these products affects the metabolic capacity of our body to respond to postprandial challenges. Interestingly, potatoes are not only rich in complex carbohydrates but are also more nutrient-dense (a wide variety of minerals, vitamins, and micronutrients) as compared to white rice and white pasta. In addition, potatoes provide large amounts of fiber and are more satiating than other carbohydrate sources. This nutrient profile might beneficially impact the resilience of the metabolic machinery and as such improve postprandial cardiometabolic plasma profiles (glucose, insulin, and triacylglycerol). In other words, there might be a beneficial effect of longer-term potato consumption in comparison with longer-term white pasta and white rice consumption will not only be present in fasting conditions but particularly in the postprandial state when the cardiometabolic system is challenged.
Inflammatory Bowel Disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract characterized by disrupted immune function. Indeed, gut microbiota dysbiosis and metabolomic profile alterations, are hallmarks of IBD. In this scenario, metabolite-sensing G-protein coupled receptors (GPCRs), involved in several biological processes, have emerged as pivotal players in the pathophysiology of IBD. The aim of this study was to characterize the axis microbiota-metabolite-GPCR in intestinal surgical resections from IBD patients. Results showed that UC patients had a lower microbiota richness and bacterial load, with a higher proportion of the genus Cellulosimicrobium and a reduced proportion of Escherichia, whereas CD patients showed a decreased abundance of Enterococcus. Furthermore, metabolomic analysis revealed alterations in carboxylic acids, fatty acids, and amino acids in UC and CD samples. These patients also exhibited upregulated expression of most metabolite-sensing GPCRs analysed, which positively correlated with pro-inflammatory and pro-fibrotic markers. The role of GPR109A was studied in depth and increased expression of this receptor was detected in epithelial cells and cells from lamina propria, including CD68+ macrophages, in IBD patients. The treatment with β-hydroxybutyrate increased gene expression of GPR109A, CD86, IL1B and NOS2 in U937-derived macrophages. Besides, when GPR109A was transiently silenced, the mRNA expression and secretion of IL-1β, IL-6 and TNF-α were impaired in M1 macrophages. Finally, the secretome from siGPR109A M1 macrophages reduced the gene and protein expression of COL1A1 and COL3A1 in intestinal fibroblasts. A better understanding of metabolite-sensing GPCRs, such as GPR109A, could establish their potential as therapeutic targets for managing IBD.
Patients with Polycystic ovary syndrome (PCOS) have chronic low-grade ovarian inflammation. Inflammation can cause telomere dysfunction, and telomere and telomerase complex are also involved in regulating inflammation. However, the specific mechanisms of inflammatory signaling feedback and telomere-telomerase mutual regulation remain to be discovered. This study elucidates the role of Nuclear factor kappa-B (NF-κB)-Telomerase reverse transcriptase (TERT) feedback in PCOS granulosa cell apoptosis. Using letrozole and a high-fat diet, a PCOS rat model was established, along with a Lipopolysaccharide (LPS) -treated KGN cell inflammation model was established. NF-κB and TERT inhibitors (BAY 11-7082 and BIBR1532) were then administered to LPS-induced KGN cells. PCOS rats displayed disrupted estrous cycles, increased weight, elevated serum testosterone, cystic follicles, granulosa cell layer thinning, and reduced corpora lutea count (P are all less than 0.05). In PCOS rat ovaries, NF-κB, Interleukin-6 (IL-6), Tumor Necrosis Factor α (TNF-α), TERT, Bax, and Caspase-3 exhibited notable upregulation, while Bcl-2 decreased, with telomere elongation (P are all less than 0.05). There were significant correlations among NF-κB-related inflammatory factors, TERT and apoptotic factors, and they were positively correlated with Bax and Caspase-3, and negatively correlated with Bcl-2 (P are all less than 0.05). LPS-treated KGN cells demonstrated increased expression of inflammatory and pro-apoptotic factors, later restored post-treatment with NF-κB and TERT inhibitors (P are all less than 0.05). In conclusion, TERT may induce granulosa cell apoptosis by participating in the regulation of the NF-κB signaling pathway, thereby mediating the chronic inflammatory response of PCOS through downstream inflammatory factors IL-6 and TNF-α.
Doctors may be matched with patients desiring or needing medical care. A doctor computing device may be used to manage workload, to set an on call status, to receive patient requests for medical services and associated information, to communicate with a potential patient, to navigate to a patient location, to create or process medical records, to process billing, and other purposes. A doctor may be matched to a patient request for medical services by a coordination component. Doctor/patient matches may be made based upon location information, the medical needs of the patient, the medical practice of the doctor, gender, language skills, or any other criteria. A doctor may accept or decline a request for medical services from a patient. A bi-directional and at least partially anonymized communication may be initiated by a doctor to permit the doctor to evaluate the medical needs of a patient.
A method may include: a message is received from one or more data systems. A machine learning model may be applied to the message to determine whether the message is an actionable or non-actionable message. In response to the message being an actionable message, the machine learning model is applicable to extract clinical meaning data from the message. One or more tasks may be performed based on the clinically significant data. The one or more tasks may include performing resource allocation of a clinical workflow associated with a data system based on the clinically significant data. The one or more tasks may also include detecting system inefficiencies and bottlenecks associated with the clinical workflow. Related methods and articles, including computer program products, are also provided.
D-dimer is a fibrin degradation product and its measurement is affected by hemolysis. This study was designed to reveal the value of hemolysis affecting D-dimer in our laboratory. In this study, hemolysate samples obtained by both mechanical and freezing methods were used. D-dimer levels of all plasmas were measured with Improgen Diagnostic kit by immune-turbidimetric method. Numerical change in hemolyzed samples was evaluated by calculating the percentage difference, and clinically significant differences were evaluated by calculating the maximum acceptable bias (MAB). In the hemolysate study prepared by both freeze-thaw and mechanical methods, it was observed that low D-dimer levels did not exceed the total allowable error (TAE) (30%) up to +2 hemolysis (corresponds to hemoglobin = 1.01-2 g/l) and did not exceed the MAB (65%) even at +4 hemolysis (corresponds to hemoglobin = 1.01-2 g/l). High D-dimer levels did not exceed the limit values of both TAE (30%) and MAB (68%) even in +4 hemolysis. The D-dimer test was affected by lower levels of hemolysis compared to both other studies and the values in the kit insert (hemoglobin >5 g/l corresponds to +4 hemolysis index). We verified the hemolysis interference in the D-dimer test, which we thought was not compatible with the kit insert, under our own laboratory conditions. This is the first hemolysis interference study performed with the Improgen brand d-dimer kit. In samples with a hemolysis rate of +2 and above, it would be more accurate to reject the D-dimer result as a 'hemolyzed sample'.
When prescribing, do not convert a patient to OTFC from any other fentanyl product on a mcg per mcg basis as OTFC and other fentanyl products are not equivalent on a microgram per microgram basis.

OTFC is not a generic version of other transmucosal immediate release fentanyl (TIRF) formulations. When dispensing, do not substitute an OTFC prescription for any other TIRF formulation under any circumstances. Other TIRF formulations and OTFC are not equivalent. Substantial differences exist in the pharmacokinetic profile of OTFC compared to other fentanyl products including other TIRF formulations that result in clinically important differences in the rate and extent of absorption of fentanyl. As a result of these differences, the substitution of OTFC for any other fentanyl product may result in a fatal overdose.

There are no safe conversion directions available for patients on any other fentanyl products. (Note: This includes oral, transdermal, or parenteral formulations of fentanyl.) Therefore, for opioid tolerant patients, the initial dose of OTFC should always be 200 mcg. Each patient should be individually titrated to provide adequate analgesia while minimizing side effects [see Dosage and Administration (2.4)].
In carcinogenicity tests of mebendazole in mice and rats, no carcinogenic effects were seen at doses as high as 40 mg/kg (one to two times the human dose, based on mg/m2) given daily over two years. No mutagenic activity was observed with mebendazole in a bacterial reverse gene mutation test. Mebendazole was mutagenic in the absence of S-9 when tested using a continuous (24 hour) treatment incubation period in the mouse lymphoma thymidine kinase assay. Mebendazole was aneugenic in vitro in mammalian somatic cells. In the in vivo mouse micronucleus assay, orally administered mebendazole induced an increased frequency of micronucleated polychromatic erythrocytes with evidence suggestive of aneugenicity. Doses up to 40 mg/kg in rats (2 times the total daily human dose, based on mg/m2), given to males for 60 days and to females for 14 days prior to gestation, had no effect upon fetuses and offspring.
1. A process for the preparation of eprosartan, a compound of formula (I):   or a pharmaceutically acceptable salt thereof, which process comprises reacting a compound of formula (II):   or an acid or a base addition salt thereof, with a compound of formula (III):   wherein R' is C1-4 alkyl, at reduced pressure in the presence of a catalyst, and thereafter hydrolyzing the R' ester and optionally forming a pharmaceutically acceptable salt. 2. The process according to claim 1 wherein the formula (II) compound is    3. The process according to claim 1 wherein the pharmaceutically acceptable salt of the formula (I) compound is the methanesulfonic acid salt. 4. The process according to claim 1 wherein the catalyst is piperidinium propionate and excess propionic acid. 5. The process according to claim 1 wherein the pressure is reduced to about 9-13 inches of Hg (30.5-44.0 kPa). 6. The process according to claim 1 wherein the pressure is reduced to 11 inches of Hg (37.2 kPa). 7. The process according to claim 1 wherein the catalyst is piperidine. 8. A process for the preparation of eprosartan, a compound of formula (I):   or a pharmaceutically acceptable salt thereof, which process comprises reacting a compound of formula (IV):   or an acid or a base addition salt thereof, with a compound of formula (III):   wherein R' is C1-4 alkyl, at reduced pressure in the presence of a catalyst, and thereafter hydrolyzing the R' ester and optionally forming a pharmaceutically acceptable salt. 9. The process according to claim 8 wherein the pharmaceutically acceptable salt of the formula (I) compound is the methanesulfonic acid salt. 10. The process according to claim 8 wherein the catalyst is piperidinium propionate and excess propionic acid. 11. The process according to claim 8 wherein the pressure is reduced to about 9-13 inches of Hg (30.5-44.0 kPa). 12. The process according to claim 8 wherein the pressure is reduced to 11 inches of Hg (37.2 kPa). 13. The process according to claim 8 wherein the catalyst is piperidine.
Diabetes mellitus results in numerous complications. Diabetic pulmonary fibrosis (DPF), a late pulmonary complication of diabetes, has not attracted as much attention as diabetic nephropathy and cardiomyopathy. Mangiferin (MF) is a natural small molecular compound that exhibits a variety of pharmacological effects including anti-inflammatory, anti-cancer, anti-diabetes, and anti-fibrosis effects. In this study, we investigated whether long-term diabetes shock induces DPF, and explored whether MF had a protective effect against DPF. We first examined the lung tissues and sections of 20 diabetic patients obtained from discarded lung surgical resection specimens and found that pulmonary fibrosis mainly accumulated around the pulmonary vessels, accompanied by significantly enhanced endothelial-mesenchymal transition (EndMT). We established a mouse model of DPF by STZ injections. Ten days after the final STZ injection, the mice were administered MF (20, 60 mg/kg, i.g.) every 3 days for 4 weeks, and kept feeding until 16 weeks and euthanized. We showed that pulmonary fibrotic lesions were developed in the diabetic mice, which began around the pulmonary vessels, while MF administration did not affect long-term blood glucose levels, but dose-dependently alleviated diabetes-induced pulmonary fibrosis. In human umbilical vein endothelial cells (HUVECs), exposure to high glucose (33.3 mM) induced EndMT, which was dose-dependently inhibited by treatment with MF (10, 50 μM). Furthermore, MF treatment promoted SIRT3 expression in high glucose-exposed HUVECs by directly binding to AMPK to enhance the activity of FoxO3, which finally reversed diabetes-induced EndMT. We conclude that MF attenuates DPF by inhibiting EndMT through the AMPK/FoxO3/SIRT3 axis. MF could be a potential candidate for the early prevention and treatment of DPF.
NEW MATERIAL:A compound obtained by the esterification of a polymeric polyol of the formula (n1, n2, n3=2-25; m1, m2, m3=0-7; the average molecular weight of the polymeric ethylene oxide is 0-30wt% of the total molecular weight) with a saturated aliphatic dicarboxylic acid and/or an oxydicarboxylic acid. EXAMPLE:A hydrophilic esterified product obtained by the esterification of ''Adeka'' polyether G-1500( product of Asahi Denka Kogyo KK) with succinic acid. USE:A raw material of cosmetics and pharmaceuticals. Esp. it is suitable as a composition base of hair dressings. Non-corrosive to cellulose nitrate. Hydrophilic oil soluble to dilute water-containing ethanol. Excellent hair fixfng performance. PROCESS:The addition polymerization of glycerine with e.g. ethylene oxide gives a compound of the formula. The compound is allowed to react with a saturated aliphatic dicarboxylic acid or oxydicarboxylic acid to give an esterified product.
Aromatherapy with inhalers will be carried out in an open clinical setting. Three drops of sweet orange oil will be dispensed into a cotton wick of the inhaler, The children will be asked to inhale the aroma from the inhalers for 2 minutes followed by an induction period of 15 minutes.
Adenylate cyclase 3 (ADCY3) is a transmembrane protein predominantly expressed in the primary cilia of neurons. It plays a vital role in converting ATP to cAMP, a secondary messenger that regulates various downstream signaling pathways such as carbohydrates and lipids metabolism. Homozygous loss-of-function variants in the ADCY3 gene lead to severe early-onset obesity and insulin resistance whereas gain-of-function variants protect against obesity. To describe a novel pathogenic ADCY3 variant implicated in early-onset obesity and functionally characterize this variant via in vitro and in silico validation, we identified a novel homozygous nonsense variant c.2520C>G, p.Thr840X in the ADCY3 gene using gene panel sequencing in a four-year-old girl. She was born to first-cousin consanguineous parents. The patient presented with severe obesity, and exhibited hepatomegaly and insulin resistance, with other biochemical and hormonal tests being normal. In vitro and in silico functional analyses showed downregulation and impaired activation of the ADCY3 protein. Our findings contribute to existing research that supports the role of ADCY3 in the genetic pathogenesis of early-onset obesity. In vitro and in silico functional characterization of the novel p.Thr840X variant showed impaired enzymatic activity leading to receptor loss of function, consistent with the patient's phenotype. Genetic testing is essential in severe early-onset obesity and early diagnosis could benefit patients with personalized treatment strategies.
PURPOSE: An antibiotic composition containing plant or extract thereof against pathogenic microorganism is provided to ensure strong antibacterial activity against Burkholderia sp. CONSTITUTION: An antibiotic composition against Burkholderia sp. contains Sesbania grandiflora L. or plant thereof as an active ingredient. The extract is isolated using an organic solvent. The organic solvent is ethanol, methanol, propanol, butanol, methyl acetate, ethyl acetate, methyl ethyl ether, methylene chloride, chloroform, benzene, or acetone. The composition is used for preventing or treating respiratory diseases.
Patients receive paclitaxel IV on days 1, 8, and 15 of each cycle, and carboplatin IV on day 1 of each cycle. Treatment repeats every 28 days for up to 6 cycles in the absence of disease progression or unacceptable toxicity.
Single ascending dose (SAD) cohort 1 will participate in three dosing periods separated by 2 weeks. Eight subjects will be enrolled, 6 will receive RX-10001 and 2 will receive vehicle control. The starting dose will be 300 mg. Subsequent doses will be determined by the pk and safety data from previous cohorts.
Tumor-associated macrophages (TAMs) are known to promote tumor growth, invasion, metastasis, and protumor angiogenesis, but the role of TAMs in evading radiotherapy in esophagus cancer remains unclear. In this study, we first induced TAMs from human monocytes (THP-1) and identified using immunofluorescence and Western blotting assays. We then co-cultured them with human esophageal cancer cell lines. CCK-8, colony formation, Transwell, scratch test, and TUNEL assays showed that TAMs could promote proliferation, survival rate, invasion, migration, and radioresistance and could inhibit apoptosis of the esophageal squamous carcinoma cell lines KYSE-150 and TE-1 before and after radiotherapy both in vivo and in vitro. Using LV-VEGFA-RNAi lentiviral vectors, we also found that TAMs could increase the expression of VEGFA and that inhibition of VEGFA could inhibit the biological function caused by TAMs. Finally, a Western blotting assay was used to evaluate the expression of various factors underlying the mechanism of TAMs. VEGFA, MAPK, P-MAPK, BCL-2, and Snail proteins were found to be overexpressed in co-cultured groups, whereas after VEGFA inhibition, MAPK, P-MAPK, BCL-2, and Snail proteins were found to be significantly downregulated in the radiotherapy group. These study results offer important information regarding the mechanism of radioresistance in esophageal cancer.
BACKGROUND/AIMS: In Saudi Arabia, students with intellectual disabilities (ID) receive some of their education through textbooks. However, using textbooks with students with ID contradicts the principles of providing services based on individuals with ID needs personalized plans to develop their individual abilities. This study aimed to investigate family and teacher perceptions of middle and high school curricula for students with ID in Saudi Arabia. This study focused specifically on the extent to which these curricula contribute to the development of academic and life skills among these students.
METHOD AND PROCEDURE: A 21-item scale was used to measure the perceptions of family members and teachers of individuals with intellectual disability. The scale validity and reliability were examined and supported. The sample comprised of 113 family members and 111 teachers of students with ID.
OUTCOMES AND RESULTS: Family members and teachers both expressed low satisfaction regarding the improvement in academic and life skills of students as a result of the current curricular in the surveyed programs. Additionally, they conveyed dissatisfaction with the overall outcomes of services provided for individuals with intellectual disabilities.
CONCLUSIONS AND IMPLICATIONS: This study highlights the inadequacies of a one-size-fits-all approach to designing curricula for students with ID. There is a need to improve and enhance curriculum content to meet the diverse learning needs of these individuals.
Disclosed are pharmaceutical compositions containing oligopeptides comprising a sequence derived by a computer program, with the general formula B-X-X-X-B-X-X-X-J-Tyr, wherein: B is Lys or Arg; X is any amino acid other than a charged or polar aliphatic amino acid or the D-isomer thereof; and J is Gly, B or an aliphatic hydrophobic amino acid from 5 to 6 carbons, preferably Lys or Arg. Such compositions are useful in inhibiting cytotoxic activity of lymphocytic cells, inhibiting the production of inflammatory cytokines and inflammatory responses associated with those cytokines, inhibiting the activity of heme-containing enzymes and delaying the onset of an autoimmune disease in a mammal at risk of developing the disease. By combining the subject compositions with mixtures of cells comprising lymphocytic cells and cells that would otherwise activate the lymphocytic cells, lysis of the target cells can be substantially inhibited. The oligopeptides may be joined to a wide variety of other groups or compounds for varying the activity of the subject compositions. The subject compositions may be administered by any convenient means to a host to inhibit lymphocytic attack on tissue, particularly involved with xenogeneic or allogeneic transplants or to inhibit the production of inflammatory cytokines and inflammatory responses associated therewith. The subject compositions may also be used in the inhibition of the activity of heme-containing enzymes.
Regarding the demand for a duly documented efficacy of the therapy applied, a standardized procedure is imperative to show the medical and economic advantages of a given therapy. To obtain valid results, it is necessary to use a standardized process, monitored with a validated questionnaire.

In this multi-center study the Activity Index Questionnaire will be tested regarding its outcome quality regarding usability and patient acceptance. Each center collects data of 10 patients with injection pain therapy. Each patient is interviewed twice and after the 2nd interview each patient will fill out a feasibility questionnaire. During the whole study, the use and consumption of oral analgetic drugs are monitored in a diary. The statistical Analysis is done descriptive. Before entering the study, each patient has to give informed consent to participate. National Registration Guidelines for post market surveillance will be obtained.