anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PURPOSE: A composition containing Chelidonium majus var asiaticum extract is provided to activate AMPK(5'AMP-activated protein kinase) and to ensure antiobesity. CONSTITUTION: A composition for preventing and treating obesity contains 0.1-99.9 wt% of Chelidonium majus var asiaticum extract as an active ingredient. The composition is a pharmaceutical composition or food additive composition. The food composition for preventing and treating obesity contains the extract as an active ingredient. The extract is a hot water extract or ethanol extract. The composition is manufactured in the form of beverage, gum, tea, vitamin complex, pill, powder, granule, tablet, or capsule.
The present invention provides a denatured albumin lamina, useful for repairing lesions on solid visceral organs. The lamina comprises human serum albumin, formed into a thin, pliant sheet and denatured. The denatured lamina can be sterilized and stored until used. As well, it can be impregnated with a variety of bioagents. A method for repairing a lesion on a solid visceral organ includes applying an energy-absorbing proteinaceous material to a lesion site on the solid visceral organ lesion; irradiating the proteinaceous material with energy sufficient to fuse the energy-absorbing material at least partially to the lesion site; applying a biocompatible denatured albumin lamina onto the proteinaceous material on the lesion site; and irradiating the biocompatible albumin lamina and the proteinaceous material with energy sufficient to fuse the biocompatible albumin lamina to the proteinaceous material and/or the lesion site. A laser solder can be deployed beneath the lamina to aid in welding it to the organ surface using laser light energy.
Fine particulate matter (PM2.5) as an environmental pollutant is related with respiratory and cardiovascular diseases. Pulmonary arterial hypertension (PAH) was characterized by incremental pulmonary artery pressure and pulmonary arterial remodeling, leading to right ventricular hypertrophy, and finally cardiac failure and death. The adverse effects on pulmonary artery and the molecular biological mechanism underlying PM2.5-caused PAH has not been elaborated clearly. In the current study, the ambient PM2.5 exposure mice model along with HPASMCs models were established. Based on bioinformatic methods and machine learning algorithms, the hub genes in PAH were screened and then adverse effects on pulmonary artery and potential mechanism was studied. Our results showed that chronic PM2.5 exposure contributed to increased pulmonary artery pressure, pulmonary arterial remodeling and right ventricular hypertrophy in mice. In vitro, PM2.5 induced phenotypic switching in HPASMCs, which served as the early stage of PAH. In mechanism, we investigated that PM2.5-mediated mitochondrial dysfunction could induce phenotypic switching in HPASMCs, which was possibly through reprogramming lipid metabolism. Next, we used machine learning algorithm to identify ELK3 as potential hub gene for mitochondrial fission. Besides, the effect of DNA methylation on ELK3 was further detected in HPASMCs after PM2.5 exposure. The results provided novel directions for protection of pulmonary vasculature injury, against adverse environmental stimuli. This work also provided a new idea for the prevention of PAH, as well as provided experimental evidence for the targeted therapy of PAH.
BACKGROUND: Prior literature has reported inferior surgical outcomes and reduced access to minimally invasive procedures at safety-net hospitals. However, this relationship has not yet been elucidated for elective colectomy. We sought to characterize the association between safety-net hospitals and likelihood of minimally invasive resection, perioperative outcomes, and costs.
METHODS: All adult (≥18 years) hospitalization records entailing elective colectomy were identified in the 2016-2020 National Inpatient Sample. Centers in the top quartile of safety-net burden were considered safety-net hospitals (others: non-safety-net hospitals). Multivariable regression models were developed to assess the impact of safety-net hospitals status on key outcomes.
RESULTS: Of ∼532,640 patients, 95,570 (17.9%) were treated at safety-net hospitals. The safety-net hospitals cohort was younger and more often of Black race or Hispanic ethnicity. After adjustment, care at safety-net hospitals remained independently associated with reduced odds of minimally invasive surgery (adjusted odds ratio 0.92; 95% confidence interval 0.87-0.97). The interaction between safety-net hospital status and race was significant, such that Black race remained linked with lower odds of minimally invasive surgery at safety-net hospitals (reference: White race). Additionally, safety-net hospitals was associated with greater likelihood of in-hospital mortality (adjusted odds ratio 1.34, confidence interval 1.04-1.74) and any perioperative complication (adjusted odds ratio 1.15, confidence interval 1.08-1.22), as well as increased length of stay (β+0.26 days, confidence interval 0.17-0.35) and costs (β+$2,510, confidence interval 2,020-3,000).
CONCLUSION: Care at safety-net hospitals was linked with lower odds of minimally invasive colectomy, as well as greater complications and costs. Black patients treated at safety-net hospitals demonstrated reduced likelihood of minimally invasive surgery, relative to White patients. Further investigation is needed to elucidate the root causes of these disparities in care.
Coffin-Siris syndrome (CSS) is a rare autosomal dominant inheritance disorder characterized by distinctive facial features, hypoplasia of the distal phalanx or nail of the fifth and additional digits, developmental or cognitive delay of varying degree, hypotonia, hirsutism/hypertrichosis, sparse scalp hair and varying kind of congenital anomalies. CSS can easily be misdiagnosed as other syndromes or disorders with a similar clinical picture because of their genetic and phenotypic heterogeneity. We describde the genotype-phenotype correlation of one patient from a healthy Chinese family with a novel genotype underlying CSS, who was first diagnosed in the ophthalmology department as early-onset high myopia (eoHM). Comprehensive ophthalmic tests as well as other systemic examinations were performed on participants to confirm the phenotype. The genotype was identified using whole exome sequencing, and further verified the results among other family members by Sanger sequencing. Real-time quantitative PCR (RT-qPCR) technology was used to detect the relative mRNA expression levels of candidate genes between proband and normal family members. The pathogenicity of the identified variant was determined by The American College of Medical Genetics and Genomics (ACMG) guidelines. STRING protein-protein interactions (PPIs) network analysis was used to detect the interaction of candidate gene-related proteins with high myopia gene-related proteins. The patient had excessive eoHM, cone-rod dystrophy, coarse face, excessive hair growth on the face, sparse scalp hair, developmental delay, intellectual disability, moderate hearing loss, dental hypoplasia, patent foramen ovale, chronic non-atrophic gastritis, bilateral renal cysts, cisterna magna, and emotional outbursts with aggression. The genetic assessment revealed that the patient carries a de novo heterozygous frameshift insertion variant in the ARID1B c.3981dup (p.Glu1328ArgfsTer5), which are strongly associated with the typical clinical features of CSS patients. The test results of RT-qPCR showed that mRNA expression of the ARID1B gene in the proband was approximately 30% lower than that of the normal control in the family, suggesting that the variant had an impact on the gene function at the level of mRNA expression. The variant was pathogenic as assessed by ACMG guidelines. Analysis of protein interactions in the STRING online database revealed that the ARID1A protein interacts with the high myopia gene-related proteins FGFR3, ASXL1, ERBB3, and SOX4, whereas the ARID1A protein antagonizes the ARID1B protein. Therefore, in this paper, we are the first to report a de novo heterozygous frameshift insertion variant in the ARID1B gene causing CSS with excessive eoHM. Our study extends the genotypic and phenotypic spectrums for ARID1B-CSS and supplies evidence of significant association of eoHM with variant in ARID1B gene. As CSS has high genetic and phenotypic heterogeneity, our findings highlight the importance of molecular genetic testing and an interdisciplinary clinical diagnostic workup to avoid misdiagnosis as some disorders with similar manifestations of CSS.
Growth failure and GH/IgF-1 deficiency has been described in patients diagnosed with Ataxia telangiectasia (AT) \[Boder et al.,1958\]. This condition is a fatal inherited disease caused by a mutation of the ATM gene on chromosome 11 leading to chromosomal instability, immunodeficiency, cancer susceptibility and and endocrinological abnormalities. In this regard, several groups demonstrated a cross-linking of ATM with growth factor pathways. Participation of the ATM protein in insulin signaling through phosphorylation of eIF-4E-binding protein 1 has been postulated \[Yang et al.,2000\]. Peretz et al.\[2001\] described that expression of the insulin-like growth factor-I receptor is (IGF-I R) ATM dependent in a pathway regulating radiation response. In addition, Shahrabani-Gargir et al.\[2004\] found that the ATM gene controls IGF-I R gene expression in a DNA damage response pathway. Suzuki et al.\[2004\] described that IGF-I phosphorylates AMPK-alpha, a key regulator of cholesterol and fatty acid synthesis, acts in an ATM-dependent manner . We have recently demonstrated reduced levels of circulating Insulin-like growth factor-I (IGF-I) and its main binding protein 3 (IGFBP-3) in AT patients accompanied with decreased body mass index \[Schubert et al.,2005\]. Furthermore, apart from regulating somatic growth and metabolism, evidence suggests that the GH/IGF-I axis is involved in the regulation of brain growth, development and myelination. Moreover, GH and particularly IGF-1 have potential neuroprotective effects in different in vitro and in vivo experimental models. In addition we have recently shown that extracerebellar MRI-lesions in AT go along with deficiency of the GH/IGF-1 Axis, markedly reduced body weight, high ataxia scores and advanced age \[Kieslich et al.,2009\]. Supplementation with these growth hormones might overcome the progressive dystrophy and may have clinical benefits against the progression of neurodegeneration and immunodeficiency.

We found that supplementation with GH significantly increased longevity of Atm-deficient mice and improve T-cell immunity and locomotor behaviour \[Schubert et al.,2009\]. Surprisingly IGF-1 was not generated in the ATM deficient mice, indicating that the GH/IGF-1 signalling is impaired. Taken this into account a accurate diagnostic approach of the GH/IGF-1 axis is mandatory including a IGF-1 generation test before long term treatment either with GH or IGF-1 is justified in humans.
PURPOSE: To obtain a sucralfate preparation having a small dispersion particle size, high affinity for plasma protein and excellent medication, by melting and granulating pulverized sucralfate by using a water-soluble low-melting wax. CONSTITUTION: Dried powder of sucralfate is further ground to give pulverized sucralfate comprising >=90% powder having <=50μm particle diameter, which is mixed with >=5wt% of a water-soluble low-melting wax (e.g. polyethylene glycol). The mixture is heated, the wax is melted and sucralfate particles are stuck to the wax and granulated. The pulverized sucralfate can be properly mixed with an excipient, a spice, a sweetener, etc., besides the water-soluble low-melting wax. The prepared sucralfate preparation is applicable to a medicine for internal use such as fine granule, tablet and capsule and/or a medicine for external use.
Sarcopenia is associated with mortality in patients with nonalcoholic steatohepatitis (NASH). Angiotensin II receptor blocker (ARB) has been suggested to prevent sarcopenia, but reports on its effect on NASH-derived skeletal muscle atrophy in conjunction with insulin-like growth factor 1 (IGF-1)-mediated muscle homeostasis are few. Our aim was to examine the combined effect of the ARB losartan and IGF-1 replacement on skeletal muscle atrophy in a methionine-choline deficient (MCD) diet-fed murine steatohepatitis model. The MCD-fed mice developed steatohepatitis and skeletal muscle atrophy, as indicated by the reduction of psoas muscle mass and attenuation of forelimb and hindlimb grip strength. Significantly suppressed steatohepatitis and skeletal muscle atrophy was observed after single treatment with ARB or IGF-1, and these effects were augmented after combination treatment. Treatment with ARB and IGF-1 effectively inhibited ubiquitin proteasome-mediated protein degradation by reducing forkhead box protein O1 (FOXO1) and FOXO3a transcriptional activity in the skeletal muscle. Combined ARB and IGF-1 decreased the intramuscular expression of proinflammatory cytokines (i.e., TNFα, IL6, and IL1β) and increased the Trolox equivalent antioxidant capacity and antioxidant enzymes (CAT, GPX1, SOD2, and CYTB). This antioxidant effect was based on downregulation of NADPH oxidase (NOX) 2, normalization of mitochondrial biogenesis and dynamics. Moreover, ARB increased the hepatic and plasma IGF-1 levels and improved steatohepatitis, leading to enhanced skeletal muscle protein synthesis mediated by IGF-1/ AKT/ mechanistic target of rapamycin signaling. Collectively, combined ARB and IGF-1 replacement could be a promising new therapeutic target for NASH-derived skeletal muscle wasting.
<P>PROBLEM TO BE SOLVED: To provide a safe hairdye capable of dyeing the hair without adsorption of a coloring matter (an acid dye) on the skin (e.g. scalp), hardly causing discoloration of the coloring matter, and free from bad effects such as the damage of the hair, and further to provide a method for dyeing the hair by using the hairdye.  <P>SOLUTION: The hair is dyed by using (A) an acid dye having ≤1,000 molecular weight, and (B) a water-soluble polymer, especially a nonionic water-soluble polymer (e.g. a hydroxyethylcellulose) as a thickener present in (C) water and/or a water-soluble organic solvent within a neutral pH region of 6.5-7.5 without formulating an acid such as citric acid, or within an alkaline pH region of 7.0-11.0 regulated by formulating (D) a proper pH regulator when dyeing the hair by the hairdye. As a result, the dye penetrates into the inside of the hair and the inside of the hair fiber is dyed without causing adsorption of the coloring matter on the surface of the hair and the skin. The objective hairdye is provided by using the phenomena. The method for dyeing the hair by using the hairdye is also provided.  <P>COPYRIGHT: (C)2003,JPO
NEW MATERIAL:A phospholipid derivative of formula I (R<1> is 8-30C aliphatic hydrocarbon residue; R<2>-R<4> are H, lower alkyl, etc.; n is 0 or 1) and a salt thereof. EXAMPLE:Tetradecyl-2-pyridinioethyl phosphate. USE:An antitumor agent, capable of exhibiting the direct cytotoxicity to tumorous cells and further host-induced antitumor effect, and having a life prolonging effect on patients with leukemia or solid cancers, e.g. cancer of the digestive organs or lung, and useful as an antifungal, agricultural germicide and antiprotozoal agent. PROCESS:A compound of the formula R<1>OH is reacted with a compound of formula II (X and Y are halogen) in an inert solvent, e.g. benzene or toluene, to give a compound of formula III, which is then hydrolyzed with water to afford a compound of formula IV. The resultant compound of formula IV is then reacted with a compound of formula V in an inert solvent to give the aimed compound of formula I (n is 1).
Post-Traumatic Stress Disorder (PTSD) is a psychiatric disorder that can occur following exposure to a traumatic incident in which grave physical harm occurred or was threatened. PTSD is marked by clear biological changes as well as psychological symptoms. Many people with PTSD repeatedly relive the trauma in the form of flashback episodes, memories, nightmares, or frightening thoughts. Chronic PTSD can also affect the neuroendocrine system by altering functionality of some chemicals in the brain, including cortisol and catecholamines (e.g., norepinephrine). This study will determine the effectiveness of immediate treatment with prolonged exposure therapy (PE) versus delaying treatment with PE in altering neuroendocrine-related symptoms of post-traumatic stress disorder in women.

This single-blind study will randomly assign two thirds of participants to PE therapy immediately following a traumatic event and one third to a waitlist condition (WL), in which they will receive no treatment until a later date. Participants assigned to receive PE will do so once weekly for 10 weeks. Participants assigned to the WL condition will receive no treatment for 10 weeks, and then will begin PE therapy once weekly for an additional 10 weeks. Study visits will occur at baseline, Week 10, and 6 months post-treatment for those in both conditions, with additional visits 10 weeks and 6 months post-PE therapy for those in the WL condition. Psychological measurements to be assessed at these visits will include PTSD symptoms, anxiety, depression, and PTSD-related cognitions. Physical assessments will include urine and saliva tests, as well as a dexamethasone-suppression test. Participants in the PE condition will also provide saliva samples at points throughout the study to monitor changes in cortisol and catecholamines.
Succinate, traditionally viewed as a mere intermediate of the tricarboxylic acid (TCA) cycle, has emerged as a critical mediator in inflammation. Disruptions within the TCA cycle lead to an accumulation of succinate in the mitochondrial matrix. This excess succinate subsequently diffuses into the cytosol and is released into the extracellular space. Elevated cytosolic succinate levels stabilize hypoxia-inducible factor-1α by inhibiting prolyl hydroxylases, which enhances inflammatory responses. Notably, succinate also acts extracellularly as a signaling molecule by engaging succinate receptor 1 on immune cells, thus modulating their pro-inflammatory or anti-inflammatory activities. Alterations in succinate levels have been associated with various inflammatory disorders, including rheumatoid arthritis, inflammatory bowel disease, obesity, and atherosclerosis. These associations are primarily due to exaggerated immune cell responses. Given its central role in inflammation, targeting succinate pathways offers promising therapeutic avenues for these diseases. This paper provides an extensive review of succinate's involvement in inflammatory processes and highlights potential targets for future research and therapeutic possibilities development.
Considerable research has been conducted on the effects of environmental exposure on human diseases. This is also known as "exposome" research. However, there is limited research on the impact of beneficial exposomes found in the natural environment. The researchers would like to identify and measure the benefits of these naturally occurring compounds on holistic human health.

Through blood specimens, the researchers will observe biomarkers such as cortisol levels and inflammatory markers. Data will be collected from wearable sensors to observe the effects of beneficial exposomes on areas such as cardiovascular health and sleep quality. There will be surveys to understand well-being, stress, and mood. Through such observations, this study aims to understand the positive impacts of intentional exposure to selected compounds found in nature.
Adults often experience a loss of social relations and sense of belonging in later life, leading to the risk of social isolation. Municipal senior centres offer a potential site for intervention, as they provide social communities targeting older people. However, not all older people find it easy to access these social communities due to experiencing physical and/or psychosocial frailties and could therefore continue to experience a decline in social relations and sense of belonging, which potentiates poor physical and psychosocial health and well-being. To date, there are limited evidence-based interventions in Denmark. The present article describes the development of an intervention to increase belongingness and decrease social isolation among older people with frailties who attend Danish municipal senior centres. The development process was conducted with reference to the INDEX (IdentifyiNg and assessing different approaches to DEveloping compleX intervention) guidance. The development process resulted in a 6-month supportive intervention, consisting of four elements: skills development workshops for all staff members; a start conversation including frailty screening; allocation of a 'buddy' among existing service users; and monthly follow-up conversations with staff members. This theory-informed approach can progress to feasibility testing and outcome evaluation in order to generate an evidence base. Concurrently, the article reflects on current guidance for intervention development and how it may be used and optimized to strengthen developmental processes in the future.
This is a proposal to conduct a small clinical trial for proof in principle that vilazodone reduces the frequency and severity of menopausal hot flashes. An additional exploratory aim is to identify improvement in menopause-related quality of life. Healthy, perimenopausal women ages 45-60 with an average of 4 or more moderate or severe hot flashes/night sweats per day for 3 screening weeks will be randomized to 8 weeks of treatment in a 2:1 ratio of vilazodone or matching placebo pills. Flexible dosing of vilazodone will start at 10 mg once/day for 7 days, increase to 20 mg/day for 1 more week and increase to 40 mg once/day at week 3 if unimproved. The primary outcome assessments are the frequency and severity of hot flashes at week 4 and week 8 as assessed by prospective daily diaries (using 7-day mean scores from the daily diaries). The secondary outcome is clinical improvement, defined as hot flash frequency \>=50% decrease from baseline. Treatment-emergent adverse events will be monitored and patient ratings of tolerability will be obtained.
The present disclosure relates to methods of initiating brexpiprazole treatment in patients with schizophrenia or major depressive disorder. In embodiments, an increased dose (relative to the usual dose) is administered to said patients during treatment initiation. The present disclosure further relates to modified dosing regimens for patients that are obese and/or CYP2D6 poor metabolizers. The inventors have discovered that the pharmacokinetics of brexpiprazole are substantively different in obese patients. Consequently, dosing changes are required when initiating treatment with brexpiprazole to achieve the same clinical response: effective treatment of schizophrenia and major depressive disorder. Prior to this invention, the standard of care left such obese patients untreated or undertreated, delaying resolution of their condition.
Diazepam is a benzodiazepine derivative. Chemically, diazepam is 7-Chloro-1,3-dihydro-1-methyl-5-phenyl-2H-1,4-benzodiazepin-2-one. It is a colorless crystalline compound, and is insoluble in water. The structural formula is represented below: C16H13ClN2O M.W. 284.74

Diazepam Tablets USP 2 mg, 5 mg and 10 mg, for oral administration, contain the following inactive ingredients: anhydrous lactose, magnesium stearate and microcrystalline cellulose.   
Diazepam Tablets USP 5mg also contain D and C Yellow No. 10.  
Diazepam Tablets USP 10 mg also contain FD and C Blue No. 1.