anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
INTRODUCTION: Photobiomodulation (PBM) has been studied since the 1960s as a clinical tool. More recently, PBM has been observed to reduce compound action potential components and hypersensitivities associated with neuropathic pains. However, no definitive description of efficacious light parameters has been determined. Some reasons may be that previous meta-analyses and reviews have focused on emitter output rather than the light at the target tissue and have included data sets that are large but with notable variability (e.g., combining data from various disease etiologies, and data from PBM at various wavelengths). This fact has made it difficult to successfully define the range of effective parameters.
METHODS: In this study, photon propagation software was used to estimate irradiance at a target nerve using several published data sets chosen for their narrow criteria to minimize variability. Utilizing these estimates, effective and ineffective light irradiances at the nerve of interest for wavelengths of 633 nm or 808-830 nm were examined and estimated. These estimates are focused on the amount of light required to achieve a reduction in pain or a surrogate measure via a hypothesized nerve block mechanism.
RESULTS: Accounting for irradiance at the target nerve yielded a clear separation of PBM doses that achieved small-fiber nerve block from those that did not. For both the 633 nm group and the 808-830 group, the irradiance separation threshold followed a nonlinear path with respect to PBM application duration, where shorter durations required higher irradiances, and longer durations required lower irradiances. Using the same modeling methods, irradiance was estimated as a function of depth from a transcutaneous source (distance from skin surface) for emitter output power using small or large emitter sizes.
CONCLUSION: Taken together, the results of this study can be used to estimate effective PBM dosing schemes to achieve small-fiber inhibition for various anatomical scenarios.
Patients receive 6 cycles of NALIRIFOX. Then undergo surgery and receive 6 cycles of NALIRIFOX after surgery. NALIRIFOX consists of irinotecan liposome injection, oxaliplatin, 5 FU/LV.
<P>PROBLEM TO BE SOLVED: To provide a drink and food, a medicine, a cosmetic, or the like containing a new ellagic acid derivative and a xanthin-oxydase activity inhibitor.  <P>SOLUTION: The new ellagic acid derivative (1) is expressed by a formula of the figure. The xanthin-oxydase activity inhibitor (2) contains the new ellagic acid derivative expressed by the formula as an effective component. A preventive or therapeutic agent (3) for hyperuricemia contains the new ellagic acid derivative expressed by the formula as an effective component. The new ellagic acid derivative (4) expressed by the formula is also obtained as a component extracted from Punica granatum.  <P>COPYRIGHT: (C)2007,JPO&INPIT
1. A method for preparing a drug complex in which a polysaccharide derivative having carboxyl groups and a residue of a drug compound are bound to each other by means of a spacer comprising an amino acid or a spacer comprising peptide-bonded 2 to 8 amino acids, characterized in that an organic amine salt of the polysaccharide derivative having carboxyl groups is reacted with the spacer bound to the drug compound in a non-aqueous system. 2. A method for preparing a drug complex in which a polysaccharide derivative having carboxyl groups and a residue of a drug compound are bound to each other by means of a spacer comprising an amino acid or a spacer comprising peptide bonded 2 to 8 amino acids, wherein the method comprises the steps of: (1) converting an alkali metal salt of the polysaccharide derivative having carboxyl groups into an organic amine salt thereof, and (2) reacting the organic amine salt with the spacer bound to the drug compound in a non-aqueous system. 3. The method according to Claim 1 or Claim 2, wherein the polysaccharide derivative having carboxyl groups is a carboxy(C1-4)alkyldextran polyalcohol. 4. The method according to Claim 3, wherein the dextran polyalcohol that constitutes the carboxy(C1-4)alkyldextran polyalcohol is a dextran polyalcohol obtained by treating a dextran under conditions that enable substantially complete polyalcoholization. 5. The method according to Claim 3 or Claim 4, wherein the carboxy(C1-4)alkyldextran polyalcohol is a carboxymethyldextran polyalcohol. 6. The method according to any one of Claims 1 to 5, wherein the drug compound is an antineoplastic agent or an anti-inflammatory agent. 7. The method according to any one of Claims 1 to 5, wherein the drug compound is a drug compound which can form a lactone ring. 8. The method according to any one of Claims 1 to 7, wherein a spacer bound to a drug compound having a lactone ring formed is used for the reaction of the organic amine salt with the spacer bound to the drug compound. 9. The method according to Claim 8, wherein the drug compound which can form a lactone ring described in Claim 7 is (1S,9S)-1-amino-9-ethyl-5-fluoro-2,3-dihydro-9-hydroxy-4-methyl-1H,12H-benzo[de]pyrano[3',4':6,7]indolizino[1,2-b]quinoline-10,13(9H,15H)-dione. 10. An organic amine salt and a polysaccharide derivative having carboxyl groups for the use for preparing a drug complex in which the polysaccharide derivative having carboxyl groups and a residue of a drug compound are bound to each other by means of a spacer comprising an amino acid or peptide-bonded 2 to 8 amino acids.
Next 2 sites begin enrollment 6 months after Group 1. Research participants will be asked to complete weekly-check-in, 4 research surveys and engage in content available in the Connections app and with peer mentors over the course of a year.
The invention comprises an aerosol apparatus containing a non-flammable, wat er- based based composition, the viscosity of which composition is from 0.2 to 30 mPa. s at 20.degree. C , which apparatus is adapted in use to release cool water-based particles for the simultaneous topical application of thermal and mechanical kinetic energy stimuli for skin or body tissue cooling and for the generation of pulses in the body respectively, at a pressure of from 0.5 to 11 bars at 20.degree. C which pressure is creat ed by using dimethyl ether or liquefied petroleum gas or a mixture of the two to dischar ge said water-based particles at a rate of from 0.1 to 8 gm/sec at 20.degree. C at a discharge angle of from 0.0.degree. to 145.degree. at 20.degree. C, at a temperature which i s higher than 0.degree.C and lower than the ambient temperature and with a particle diameter of from 10 to 600 microns.
The present invention relates to a beneficial compound as exemplified below, which exhibits enteropeptidase-inhibiting activity, a pharmaceutically acceptable salt thereof, and a pharmaceutical composition comprising the compound or pharmaceutically acceptable salt, for use in preventing and treating metabolic diseases such as obesity, diabetes mellitus or hyperlipidemia. (see above formula) The compound of the present invention has excellent inhibitory activity against enteropeptidase, and is not absorbed into the body. Rather, it is excreted outside the body, along with fat and protein. Since not only fat but also protein are discharged together, this compound results in fewer side effects such as fatty stools. As well, because the compound acts only in the gastrointestinal tract, it has fewer side effects such as depression. It has use as a therapeutic or prophylactic drug for various metabolic diseases such as obesity, diabetes mellitus, and hyperlipidemia.
BACKGROUND: The colliding epidemic of infectious and non-communicable diseases in South Africa could potentially increase the prevalence of kidney disease in the country. This study determines the prevalence of kidney damage and known risk factors in a rural community of the Eastern Cape province, South Africa.
METHODS: This observational cross-sectional study was conducted in the outpatient department of the Mbekweni Community Health Centre in the Eastern Cape between May and July 2022. Relevant data on demography, medical history, anthropometry and blood pressure were obtained. The glomerular filtration rate was estimated using the Chronic Kidney Disease Epidemiology Collaboration Creatinine (CKD-EPICreatinine) equation and the re-expressed four-variable Modification of Diet in Renal Disease (MDRD) equation, without any adjustment for black ethnicity. Prevalence of kidney damage was defined as the proportion of individuals with low eGFR (<60mL/min per 1.73m2). The presence of proteins in the spot urine samples was determined with the use of test strips. We used the logistic regression model analysis to identify the independent risk factors for significant kidney damage.
RESULTS: The mean (±standard deviation) age of the 389 participants was 52.3 (± 17.5) years, with 69.9% female. The prevalence of significant kidney damage was 17.2% (n = 67), as estimated by the CKD-EPICreatinine, with a slight difference by the MDRD equation (n = 69; 17.7%), while the prevalence of proteinuria was 7.2%. Older age was identified as a significant risk factor for CKD, with an odds ratio (OR) = 1.08 (95% confidence interval [CI]: 1.06-1.1, p < 0.001). Hypertension was strongly associated with proteinuria (OR = 4.17, 95% CI 1.67-10.4, p<0.001).
CONCLUSIONS: This study found a high prevalence of kidney damage (17.2%) and proteinuria (7.97%) in this rural community, largely attributed to advanced age and hypertension, respectively. Early detection of proteinuria and decreased renal function at community health centres should trigger a referral to a higher level of care for further management of patients.
PURPOSE:To produce a human TNF polypeptide, by culturing a host transformed with a vector produced by integrating a DNA having a base sequence coding a polypeptide having a specific amino acid sequence into a vector. CONSTITUTION:A DNA fragment having an initiation codon ATG at the 5' terminal and a termination codon at the 3' terminal of a DNA having a base sequence coding a polypeptide variant and the DNA itself is prepared beforehand. The fragment is bonded successively to a proper promoter and an SD sequence. The product is integrated into a vector to obtain an expression vector for the production of a polypeptide variant. The expression vector is introduced e.g. into E.coli and the obtained transformant is cultured under a proper condition to produce the objective polypeptide variant.
The successful pulmonary metastasis of malignant cancer cells depends on the survival of circulating tumor cells in a distant and hostile microenvironment. The formation of a pre-metastatic niche (PMN) creates a supportive environment for subsequent metastasis. Circular RNAs (circRNAs) are increasingly acknowledged as crucial elements in the mechanisms of metastasis due to their stable structures and functions, making them promising early metastasis detection markers. However, the specific expression patterns and roles of circRNAs in the lungs before metastasis remain largely unexplored. Our research aims to chart the circRNA expression profile and assess their impact on the lung PMN. We developed a lung PMN model and employed comprehensive RNA sequencing to analyze the differences in circRNA expression between normal and pre-metastatic lungs. We identified 38 significantly different circRNAs, primarily involved in metabolism, apoptosis, and inflammation pathways. We then focused on one specific circRNA, circ:chr4:150406196 - 150406664 (circRERE-PMN), which exhibited a significant change in expression and was prevalent in myeloid-derived suppressor cells (MDSCs), alveolar epithelial cells, and macrophages within the pre-metastatic lung environment. CircRERE-PMN was found to potentially regulate apoptosis and the expression of cytokines and chemokines through its interaction with the downstream target HUR in alveolar epithelial cells. Overall, our study highlights the crucial role of circRNAs in the formation of lung PMNs, supporting their potential as diagnostic or therapeutic targets for lung metastasis.
Amotriptan malate (AXERT®) is approved for use in the treatment of acute migraine headache with or without aura in adults. Other studies have shown that almotriptan is effective and well tolerated in adults. Migraines in teenagers/adolescents are very similar to migraines in adults, except that the duration is usually less in adolescents (they last 1 to 24 hours in adolescents). This study will evaluate the usefulness of almotriptan malate (AXERT®) in treating acute migraine headaches in adolescents. This is a randomized, double-blind, parallel-group, and placebo-controlled study. During a 30-day run-in period, patients will treat their migraines as they normally would. During this time, the frequency and severity of headaches will be recorded. At the second visit, patients will be randomized (like with the toss of a coin) to a treatment group to receive one oral dose of almotriptan malate (AXERT®) 6.25, 12.5, or 25 milligrams or placebo. Approximately the same number of patients will be assigned to each of the four treatment groups. Patients will take this one-time dose when the next migraine of at least moderate severity occurs. Patients will record assessments in a diary for up to 24 hours after the study drug is given to help determine the drug's effect on headache pain intensity. Patients will return for a third visit within 2 to 14 days from taking the study medication. A physical examination, electrocardiogram (a painless test of the heart), and laboratory tests will be performed at the first and third visits. The objective of this study is to determine the effectiveness and tolerability of 3 dosage strengths of almotriptan malate (AXERT®) in adolescents with migraine headaches.

Almotriptan oral tablets, 6.25, 12.5, or 25 milligrams, or placebo
Synthetic hypocalcemic peptides which are similar in biological properties to native calcitonins as clinically useful agents. The peptides comprise analogues of native calcitonins having amino acid substitutions and deletions which act to improve potency, prolong duration of the hormonal effect, enhance receptor binding, and increase oral or nasal bioavailability. The calcitonin peptide analogues are less expensive and more easily synthesized than native calcitonins, and have improved resistance to inactivation or degradation. Methods are provided for the synthesis of these peptides. Also, disclosed are novel cyclic peptides, including calcitonin, having increased stability with respect to proteolysis. Methods for the synthesis of these peptides are provided, comprising converting disulfide cyclic peptides and proteins to enzymatically and chemically stable cyclic peptide structures by the replacement of cysteine residues with dicarboxylic acids and diamino acids. The method is applicable to various naturally occurring peptides, their synthetic analogues or derivatives, and proteins.
Glioblastoma (GBM) is a highly aggressive and treatment-resistant brain tumor, necessitating novel therapeutic strategies. In this study, we present a mechanistic breakthrough by designing and evaluating a series of abiraterone-installed hydroxamic acids as potential dual inhibitors of CYP17A1 and HDAC6 for GBM treatment. We established the correlation of CYP17A1/HDAC6 overexpression with tumor recurrence and temozolomide resistance in GBM patients. Compound 12, a dual inhibitor, demonstrated significant anti-GBM activity in vitro, particularly against TMZ-resistant cell lines. Mechanistically, compound 12 induced apoptosis, suppressed recurrence-associated genes, induced oxidative stress and initiated DNA damage response. Furthermore, molecular modeling studies confirmed its potent inhibitory activity against CYP17A1 and HDAC6. In vivo studies revealed that compound 12 effectively suppressed tumor growth in xenograft and orthotopic mouse models without inducing significant adverse effects. These findings highlight the potential of dual CYP17A1 and HDAC6 inhibition as a promising strategy for overcoming treatment resistance in GBM and offer new hope for improved therapeutic outcomes.
The invention relates to a medicament for treating epilepsy and a preparation method thereof. The medicament comprises the following raw materials by weight proportion: 0.7 to 1.2 parts of rhinoceros horn, 0.5 to 1.1 parts of bezoar, 12 to 18 parts of Chinese eaglewood, 1 to 3 parts of natural bezoar, 3 to 7 parts of henon bamboo leaves, 10 to 18 parts of juncus, 4 to 7 parts of mus covite, 0.5 to 1.1 parts of pig zinnober (concretion from pig viscera), 1 to 3 parts of succinite, 0.8 to 1.1 parts of musk, 0.8 to 1.2 parts of cinnabar and 3 to 6 parts of bamboo shavings. The medicament is good for treating epilepsy. The curative ratio is high, and the effect for treating epilepsy is obvious; one-time seizure epileptics, or long-term epileptics who are not cured for years or more than ten years can be cured without relapse, and medicament resistance or side effect does not exist. The medicament has better curative effect to hysteria majors caused by intimidation, startle, inheritance epilepsy, high fever, fidget, invasion of pericardium by evil, shutting-off of brain information, cardio-cerebral disharmony, having ants in the pants and the like. The preparing procedures of the medicament is easy to be operated; and the medicament has no toxic and side effect, is convenient to be used, and has obvious treating effect and low cost.
INTRODUCTION: Older adults with advanced chronic diseases and palliative care needs are more exposed to polypharmacy and use of potentially inappropriate medication, which generates a high risk of adverse events and impaired quality of life. The objective of this study was to describe the frequency of potentially inappropriate medication use among older adults with palliative care needs receiving home care services after hospital discharge.
METHODS: Observational cross-sectional study of pharmacy dispensing and electronic health records, of older adults in a home care system and with palliative care needs according to the screening with the NECPAL tool or the PROFUND and/or PALIAR indexes. Dispensed medications during 180 days after admission to home care were analyzed. Medications were classified as potentially inappropriate according to the LESS-CHRON criteria.
RESULTS: We included 176 patients, mean age 87.4 years, 67% were women; 73% were pluripathologic patients and 22% had one chronic progressive disease. Mortality at 6 months was 73%. Median frequency of dispensed medications per patient was 9.1 (IQR = 4-9.7). The frequency of potentially inappropriate medication dispensation among patients was 87%, mainly antihypertensives, benzodiazepines and antipsychotics.
CONCLUSION: This study observed that dispensation of potentially inappropriate medication among older adults with palliative care needs and home care services is very high. This emphasizes the need for effective patient-centered interventions to prevent inadequate prescription and stimulate de-prescription.
Subjects randomized to LAMS plus double pigtail stent will undergo EUS-guided transmural placement of a single Axios stent with a 15 mm luminal diameter. Following this, wire access across the stent lumen will be achieved using a 0.035 inch hydrophilic guidewire, and a double pigtail plastic biliary stent (6 French, 7 French, or 10 French at the discretion of the endoscopist) will be deployed over the wire.
BACKGROUND: Enzalutamide (Enz) resistance is a poor prognostic factor for patients with castration-resistant prostate cancer (CRPC), which often involves aberrant expression of the androgen receptor (AR). Myosin VI (MYO6), one member of the myosin family, plays an important role in regulating cell survival and is highly expressed in prostate cancer (PCa). However, whether MYO6 is involved in Enz resistance in CRPC and its mechanism remain unclear.
METHODS: Multiple open-access databases were utilized to examine the relationship between MYO6 expression and PCa progression, and to screen differentially expressed genes (DEGs) and potential signaling pathways associated with the MYO6-regulated Enz resistance. Both in vitro and in vivo tumorigenesis assays were employed to examine the impact of MYO6 on the growth and Enz resistance of PCa cells. Human PCa tissues and related clinical biochemical data were utilized to identify the role of MYO6 in promoting PCa progression and Enz resistance. The molecular mechanisms underlying the regulation of gene expression, PCa progression, and Enz resistance in CRPC by MYO6 were investigated.
RESULTS: MYO6 expression increases in patients with PCa and is positively correlated with AR expression in PCa cell lines and tissues. Overexpression of AR increases MYO6 expression to promote PCa cell proliferation, migration and invasion, and to inhibit PCa cell apoptosis; whereas knockdown of MYO6 expression reverses these outcomes and enhances Enz function in suppressing the proliferation of the Enz- sensitive and resistant PCa cells both in vitro and in vivo. Mechanistically, AR binds directly to the promoter region (residues - 503 to - 283 base pairs) of MYO6 gene and promotes its transcription. Furthermore, MYO6 activates focal adhesion kinase (FAK) phosphorylation at tyrosine-397 through integrin beta 8 (ITGB8) modulation to promote PCa progression and Enz resistance. Notably, inhibition of FAK activity by Y15, an inhibitor of FAK, can resensitize CRPC cells to Enz treatment in cell lines and mouse xenograft models.
CONCLUSIONS: MYO6 has pro-tumor and Enz-resistant effects in CRPC, suggesting that targeting MYO6 may be beneficial for ENZ-resistant CRPC therapy through the AR/MYO6/FAK signaling pathway.
With new daily discoveries about the long-term impacts of COVID-19, there is a clear need to develop in vitro models that can be used to better understand the pathogenicity and impact of COVID-19. Here, we demonstrate the utility of developing a model of endothelial dysfunction that utilizes human induced pluripotent stem cell-derived endothelial progenitors encapsulated in collagen hydrogels to study the effects of COVID-19 on the endothelium. These cells form capillary-like vasculature within 1 week after encapsulation and treating these cell-laden hydrogels with SARS-CoV-2 spike protein resulted in a significant decrease in the number of vessel-forming cells as well as vessel network connectivity quantified by our computational pipeline. This vascular dysfunction is a unique phenomenon observed upon treatment with SARS-CoV-2 SP and is not seen upon treatment with other coronaviruses, indicating that these effects were specific to SARS-CoV-2. We show that this vascular dysfunction is caused by an increase in inflammatory cytokines, associated with the COVID-19 cytokine storm, released from SARS-CoV-2 spike protein treated endothelial cells. Following treatment with the corticosteroid dexamethasone, we were able to prevent SARS-CoV-2 spike protein-induced endothelial dysfunction. Our results highlight the importance of understanding the interactions between SARS-CoV-2 spike protein and the endothelium and show that even in the absence of immune cells, the proposed 3D in vitro model for angiogenesis can reproduce COVID-19-induced endothelial dysfunction seen in clinical settings. This model represents a significant step in creating physiologically relevant disease models to further study the impact of long COVID and potentially identify mitigating therapeutics.