anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The antihypertensive agent of the present invention contains a soluble silicon compound. The soluble silicon compound is preferably metasilicic acid or a salt thereof. In one embodiment, the antihypertensive agent of the present invention contains deep sea water containing the soluble silicon compound, or a dried product of such deep sea water. It is preferred that in such embodiment, the antihypertensive agent further contains metasilicic acid or a salt thereof. The amount of silicon present in the deep sea water in the form of silicic acid (SiO 2 —Si) is 25 μM or more. The deep sea water is typically collected at a depth of 300 m or deeper, and preferably at a depth of 600 m or deeper.
OBJECTIVE: This study aimed to investigate the correlation between genetic factors and the occurrence and progression of temporomandibular disorders (TMDs) using a comprehensive review and meta-analysis.
DESIGN: A comprehensive search was conducted using the ScienceDirect, PubMed, Cochrane Library, Dimensions, and Emerald databases. A reviewer selected the study using modified PICO criteria, considering human subjects with TMDs, comparing different genetic factors among TMD and non-TMD patients, and reporting TMD signs and symptoms as outcomes. The methodological standards of the eligible papers were assessed using the Joanna Briggs Institute (JBI) Critical Appraisal Checklist for Non-randomized Experimental Investigations. Information was collected methodically and examined.
RESULTS: The electronic database search yielded 851 articles, 19 of which were included in this study. The data analysis showed a significant influence of genetic factors, such as polymorphisms and gene differences, on the development of TMD signs and symptoms, such as myofascial pain, chronic pain, and disc displacement. In addition, gene polymorphism significantly influenced TMD development, with an odds ratio of 2.46 (1.93-3.14) and p of 0.00001.
CONCLUSIONS: Genetic factors significantly influenced TMD signs and symptoms, and genetic polymorphisms significantly influenced TMD onset and progression. Further research should be conducted in diverse settings with larger sample sizes to verify and validate these findings.
Neomycin sulfate is poorly absorbed from the normal gastrointestinal tract.The small absorbed fraction is rapidly distributed in the tissues and is excreted by the kidney in keeping with the degree of kidney function. The unabsorbed portion of the drug (approximately 97%) is eliminated unchanged in the feces.

Growth of most intestinal bacteria is rapidly suppressed following oral administration of neomycin sulfate, with the suppression persisting for 48-72 hours. Nonpathogenic yeasts and occasionally resistant strains of Enterobacter aerogenes (formerly Aerobacter aerogenes) replace the intestinal bacteria. 

As with other aminoglycosides, the amount of systemically absorbed neomycin transferred to the tissues increases cumulatively with each repeated dose administered until a steady state is achieved. The kidney functions as the primary excretory path as well as the tissue binding site, with the highest concentration found in the renal cortex. With repeated dosings, progressive accumulation also occurs in the inner ear. Release of tissue-bound neomycin occurs slowly over a period of several weeks after dosing has been discontinued.

Protein binding studies have shown that the degree of aminoglycoside protein binding is low and, depending upon the methods used for testing, this may be between 0% and 30%.
Methods of degrading a polymer are provided. The methods may include incubating the polymer with  Pseudomonads  and/or  Bacillus  species and/or bacterial consortia thereof. Kits for degrading a polymer are also provided. The kits may include  Pseudomonads  and/or  Bacillus  species and/or bacterial consortia thereof. The kits may also include an incubator for culturing the  Pseudomonads  and/or the  Bacillus  species and/or bacterial consortia thereof. Compositions for degrading a polymer-containing substrate including the  Pseudomonads  and/or  Bacillus  species and/or bacterial consortia thereof are also provided.
A medical network service can replace or supplement some or all of an expensive internally staffed clinical facility network with a cloud-based networking service. The medical network service in certain embodiments can provide networking services via software as a service technologies, platform as a service technologies, and/or infrastructure as a service technologies. The medical network service can provide these services to large existing clinical facilities such as metropolitan hospitals as well as to smaller clinical facilities such as specialized surgical centers. The medical network service can replace and/or supplement existing IT networks in hospitals and other clinical facilities and can therefore reduce costs and increase security and reliability of those networks. In addition, the medical network service can provide synergistic benefits that can improve patient outcomes and patient care. In addition, a medical edge router can provide redundant communications features for transmitting patient data to the medical network service.
Heavy metals are environmental pollutants that can harm animals and humans even at low concentrations. Cadmium (Cd) is known for its serious health effects on different organs and its toxicity is associated with oxidative stress (OS) and inflammation. Farnesol (FAR), a sesquiterpene alcohol found in many vegetables and fruits, possesses promising anti-inflammatory and antioxidant activities. This study evaluated the effect of FAR on Cd-induced kidney injury, pinpointing its effect of the redox status, inflammation, fibrosis and necroptosis. Rats in this study received FAR for 14 days and Cd on day 7. Elevated serum creatinine, urea and uric acid, and several kidney histopathological alterations were observed in Cd-administered rats. Cd increased MDA, decreased antioxidants, downregulated PPARγ and upregulated NF-κB p65, IL-6, TNF-α, and IL-1β. Necroptosis mediators (RIP1, RIP3, MLKL, and caspase-8) and α-SMA were upregulated, and collagen deposition was increased in Cd-administered rats. FAR ameliorated kidney injury markers and tissue damage, attenuated OS, suppressed NF-κB and inflammatory mediators, and enhanced antioxidants. In addition, FAR suppressed RIP1, RIP3, MLKL, caspase-8, and α-SMA, and enhanced kidney cytoglobin and PPARγ. In conclusion, FAR protects against Cd nephrotoxicity by suppressing OS, inflammatory response and necroptosis, effects associated with enhanced antioxidants, cytoglobin, and PPARγ.
Deferasirox is an iron-chelating agent provided as a tablet for oral use. Deferasirox is designated chemically as 4-[3,5-bis(2-hydroxyphenyl)-1H-1,2,4-triazol-1-yl]benzoic acid and has the following structural formula:

Deferasirox is a white to slightly yellow color powder. It has a molecular formula C21H15N3O4 and molecular weight of 373.36 g/mol. It is freely soluble in dimethyl formamide, sparingly soluble in dimethylsulfoxide and practically insoluble in water with a pH of suspension of 4.1. 

Each deferasirox tablet contains 90 mg, 180 mg or 360 mg deferasirox and contains following Inactive ingredients: colloidal silicon dioxide, croscarmellose sodium, hypromellose, polyethylene glycol, magnesium stearate, microcrystalline cellulose, povidone K30, poloxamer 407, talc and titanium dioxide.

Additionally, each 180 mg and 360 mg tablet contains FD&C blue # 2/Indigo Carmine Aluminum Lake; each 180 mg tablet contains iron oxide yellow and each 360 mg tablets contain D&C red #27/Phloxine Aluminum Lake.
BACKGROUND: Microplastics (MPs) have become a global environmental problem, emerging as contaminants with potentially alarming consequences. However, long-term exposure to polystyrene microspheres (PS-MS) and its effects on diet-induced obesity are not yet fully understood.
OBJECTIVES: We aimed to investigate the effect of PS-MS exposure on high-fat diet (HFD)-induced obesity and underlying mechanisms.
METHODS: In the present study, C57BL/6J mice were fed a normal diet (ND) or a HFD in the absence or presence of PS-MS via oral administration for 8 wk. Antibiotic depletion of the microbiota and fecal microbiota transplantation (FMT) were performed to assess the influence of PS-MS on intestinal microbial ecology. We performed 16S rRNA sequencing to dissect microbial discrepancies and investigated the dysbiosis-associated intestinal integrity and inflammation in serum.
RESULTS: Compared with HFD mice, mice fed the HFD with PS-MS exhibited higher body weight, liver weight, metabolic dysfunction-associated steatotic liver disease (MASLD) activity scores, and mass of white adipose tissue, as well as higher blood glucose and serum lipid concentrations. Furthermore, 16S rRNA sequencing of the fecal microbiota revealed that mice fed the HFD with PS-MS had greater α-diversity and greater relative abundances of Lachnospiraceae, Oscillospiraceae, Bacteroidaceae, Akkermansiaceae, Marinifilaceae, Deferribacteres, and Desulfovibrio, but lower relative abundances of Atopobiaceae, Bifidobacterium, and Parabacteroides. Mice fed the HFD with PS-MS exhibited lower expression of MUC2 mucin and higher levels of lipopolysaccharide and inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β, and IL-17A] in serum. Correlation analyses revealed that differences in the microbial flora of mice exposed to PS-MS were associated with obesity. Interestingly, microbiota-depleted mice did not show the same PS-MS-associated differences in Muc2 and Tjp1 expression in the distal colon, expression of inflammatory cytokines in serum, or obesity outcomes between HFD and HFD + PS-MS. Importantly, transplantation of feces from HFD + PS-MS mice to microbiota-depleted HFD-fed mice resulted in a lower expression of mucus proteins, higher expression of inflammatory cytokines, and obesity outcomes, similar to the findings in HFD + PS-MS mice.
CONCLUSIONS: Our findings provide a new gut microbiota-driven mechanism for PS-MS-induced obesity in HFD-fed mice, suggesting the need to reevaluate the adverse health effects of MPs commonly found in daily life, particularly in susceptible populations. https://doi.org/10.1289/EHP13913.
Global estimates exhibit that one million people have end-stage renal disease, a disease-state characterized by irreversible loss of kidney structure and function, thus necessitating renal replacement therapy. The disease-state, oxidative stress, inflammatory responses, as well as the treatment procedure can have damaging effects on the genetic material. Therefore, the present study was carried out to investigate DNA damage (basal and oxidative) using the comet assay in peripheral blood leukocytes of patients (n = 200) with stage V Chronic Kidney Disease (on dialysis and those recommended but yet to initiate dialysis) and compare it to that in controls (n = 210). Basal DNA damage was significantly elevated (1.13x, p ≤ 0.001) in patients (46.23 ± 0.58% DNA in tail) compared to controls (40.85 ± 0.61% DNA in tail). Oxidative DNA damage was also significantly (p ≤ 0.001) higher in patients (9.18 ± 0.49 vs. 2.59 ± 0.19% tail DNA) compared to controls. Twice-a-week dialysis regimen patients had significantly elevated % tail DNA and Damage Index compared to the non-dialyzed and to the once-a-week dialysis group implying dialysis- induced mechanical stress and blood-dialyzer membrane interactions as probable contributors to elevated DNA damage. The present study with a statistically significant power implies higher disease-associated as well as maintenance therapy (hemodialysis)-induced basal and oxidatively damaged DNA, which if not repaired has the potential to initiate carcinogenesis. These findings mark the need for improvement and development of interventional therapies for delaying disease progression and associated co-morbidities so as to improve life expectancy of patients with kidney disease.
Aducanumab, intravenous infusion, every 4 weeks for up to Week 52 during the randomized treatment period. The dose will be titrated to a desirable dose. Participants will be managed for drug continuation and suspension. Following a 4-week follow-up period, eligible participants will continue to receive aducanumab, intravenous infusion, every 4 weeks for an additional 104 weeks in the long-term extension period.
Isotretinoin must not be used by patients who are or may become pregnant. There is an extremely high risk that life-threatening birth defects will result if pregnancy occurs while taking isotretinoin in any amount, even for short periods of time. Potentially any fetus exposed during pregnancy can be affected. There are no accurate means of determining whether an exposed fetus has been affected.

Birth defects which have been documented following isotretinoin exposure include abnormalities of the face, eyes, ears, skull, central nervous system, cardiovascular system, and thymus and parathyroid glands. Cases of IQ scores less than 85 with or without other abnormalities have been reported. There is an increased risk of spontaneous abortion, and premature births have been reported.

Documented external abnormalities include: skull abnormality; ear abnormalities (including anotia, micropinna, small or absent external auditory canals); eye abnormalities (including microphthalmia); facial dysmorphia; cleft palate. Documented internal abnormalities include: CNS abnormalities (including cerebral abnormalities, cerebellar malformation, hydrocephalus, microcephaly, cranial nerve deficit); cardiovascular abnormalities; thymus gland abnormality; parathyroid hormone deficiency. In some cases death has occurred with certain of the abnormalities previously noted.   


If pregnancy does occur during treatment of a patient who is taking isotretinoin, isotretinoin must be discontinued immediately and the patient should be referred to an Obstetrician-Gynecologist experienced in reproductive toxicity for further evaluation and counseling.   


Special Prescribing Requirements   


Because of isotretinoin's teratogenicity and to minimize fetal exposure, isotretinoin is approved for marketing only under a special restricted distribution program approved by the Food and Drug Administration. This REMS is called iPLEDGE®. Isotretinoinmust only be prescribed by prescribers who are enrolled and activated with the iPLEDGE REMS. Isotretinoinmust only be dispensed by a pharmacy enrolled and activated with iPLEDGE, and must only be dispensed to patients who are enrolled and meet all the requirements of iPLEDGE (see PRECAUTIONS).
The disclosure provides a pharmaceutical composition for fistula treatment of children. The pharmaceutical composition includes a fibrinogen and a thrombin. Wherein a dose of the fibrinogen is between 20 mg/mL and 200 mg/mL. A dose of the thrombin is between 1 IU/mL and 20 IU/mL. The disclosure further provides a use of the fibrinogen and the thrombin for manufacturing the pharmaceutical composition for fistula treatment of children. The application of the pharmaceutical composition and the use of the present invention are advantageous for fistula treatment of children.
OBJECTIVE: The overall 5-year survival for oral squamous cell carcinoma (OSCC) has not changed in the last 20 years despite advances in treatment. Lymphovascular invasion (LVI) has been shown to be a negative prognostic factor in other cancers, however its role in the prognosis of OSCC remains unclear. This study aims to determine if LVI is a predictor of cervical lymph node metastasis and/or recurrence in OSCC.
METHODS: We conducted a retrospective cohort review of patients from our institutional cancer registry who were treated for OSCC between 2004 and 2018. Patient demographics, surgical pathology results, and clinical outcome data were collected. A multivariable logistic regression analysis was performed to determine if LVI was an independent predictor of cervical lymph node metastasis and/or recurrence.
RESULTS: 442 patients were included, 32.8% were female and median age at time of diagnosis was 61.2 years. LVI was present in 32.8% of patients. When controlled for age, sex, t-classification, perineural invasion, depth of invasion (DOI), and margin status, LVI was a significant predictor of the presence of cervical node metastasis (OR: 3.42, CI: 2.17-5.39, P < .001). There was no significant association found between LVI and local recurrence (OR: 1.03, CI: 0.57-1.84, P = .92), regional recurrence (OR: 1.10, CI: 0.57-2.11, P = .78), or distant recurrence (OR: 1.59, CI: 0.87-2.94, P = .13).
CONCLUSION: The results of this study suggest that LVI is a significant predictor of the presence of cervical lymph node metastasis at presentation independent of other known prognostic factors. LVI, however, was not found to be a significant independent predictor of locoregional or distant recurrence.Level of Evidence: Level III.
Navigating the evaluation and management of pain in long-term care homes is a complex task. Despite an extensive body of literature advocating for a paradigm shift in pain assessment and management within long-term care homes, much more remains to be done. The assessment of pain in long-term care is particularly challenging, given that a substantial proportion of residents live with some degree of cognitive impairment. Individuals living with dementia may encounter difficulties articulating the frequency and intensity of their pain, potentially resulting in an underestimation of their pain. In Canada and in the United States, the interRAI Minimum Data Set 2.0, Minimum Data Set 3.0, and the interRAI Long-Term Care Facilities assessments are administered to capture the presence and intensity of pain. These assessment instruments are used both on admission and quarterly, offering a reliable and validated method for comprehensive assessment. Nonetheless, the daily assessment and documentation of pain across long-term care homes, which is used to inform the interRAI Pain Scale, is not always consistent. The reality is that assessing pain can be inaccurate for several reasons, including the fact that it is rated by long-term care staff with diverse levels of expertise, resources, and education. This call for action explores the current approaches used in pain assessment and management within long-term care homes. The authors not only bring attention to the existing challenges but also emphasize the necessity of considering a more comprehensive assessment approach.
Participants are referred to lung cancer screening educational materials. Participants also complete questionnaires at 1 week and 6 months after referral to educational materials.
Each subject will provide a fresh urine sample in an empty sterile plastic cup. Urinalysis will be performed to check for macro- or micro-hematuria or signs of infection. We will take 10mL of the urine sample and add 1mL of transparent (colorless) household bleach (≤5% sodium hypochlorite). The color of the urine before and 5 minutes after adding the bleach will be recorded.
INTRODUCTION: Previous studies have demonstrated that abnormal body mass index (BMI) is associated with adverse pregnancy outcomes in frozen-thawed embryo transfer cycles. However, the relationship between BMI and pregnancy and perinatal outcomes in patients with polycystic ovary syndrome (PCOS) remains unclear. Furthermore, whether a diagnosis of PCOS could result in adverse pregnancy and perinatal outcomes in women with different BMIs remains unknown.
MATERIAL AND METHODS: A historical cohort study included 1667 women with PCOS and 12 256 women without PCOS after a freeze-all policy between January 2016 and December 2020. The outcomes encompassed both pregnancy and perinatal outcomes. Multivariate logistic regression analysis and restricted cubic spline models were performed to eliminate confounding factors when investigating the relationship between BMI and different outcomes.
RESULTS: After controlling for covariates, pregnancy outcomes were comparable between underweight women with PCOS and normal weight women with PCOS. However, overweight patients had a lower clinical pregnancy rate and an overall live birth rate. Furthermore, patients with obesity had a lower rate of multiple pregnancies but a higher rate of biochemical pregnancy than in the normal BMI group. Additionally, the restricted cubic spline models showed that as maternal BMI increased to 32 kg/m2, the clinical pregnancy rate and live birth rate after blastocyst transfer decreased, but the risks of preterm birth, gestational diabetes mellitus, macrosomia, large-for-gestational age (LGA) and very LGA increased in patients with PCOS after a freeze-all strategy. Moreover, a diagnosis of PCOS resulted in a higher clinical pregnancy rate and live birth rate and a higher risk of small-for-gestational age in the normal weight group. However, women with PCOS in the overweight group exhibited higher risks of very preterm birth and gestational diabetes mellitus compared with women without PCOS.
CONCLUSIONS: This study showed that a higher BMI had a detrimental impact on the pregnancy and perinatal outcomes of PCOS patients undergoing a freeze-all strategy. However, it was only statistically significant in the overweight group. A diagnosis of PCOS had a higher clinical pregnancy rate and live birth rate in normal weight women but higher risks of perinatal complications in normal weight and overweight women.
Altered nociception, a key feature of nociplastic pain, often involves central sensitization. We previously found that central sensitization underlying a nociplastic pain state in female mice depends on the ongoing activity of TRPA1 agonist-responsive afferents. Here, we investigated how the activity of these afferents induces and maintains central sensitization at the spinal level. We hypothesized that, in the superficial dorsal horn where somatostatin (SST) is expressed in excitatory interneurons and the SST2A receptor (SST2A-R) in GABAergic inhibitory interneurons (GABAn), TRPA1 agonist-responsive afferents stimulate SST-expressing excitatory interneurons (SSTn), leading to GABAn suppression through SST2A-R and resulting in altered nociception. We tested this hypothesis using ex vivo Ca2+ imaging of dorsal root-attached spinal cord slices expressing GCaMP6f in either SSTn or GABAn and in vivo assessment of mechanical hypersensitivity. The dorsal root was chemically (with allyl isothiocyanate [AITC]) and electrically stimulated to activate TRPA1-expressing nociceptors and all afferents, respectively. The stimulation of dorsal root with AITC excited SSTn. During activation of AITC-responsive afferents, a subset of SSTn showed potentiated responses to both low- and high-threshold afferent inputs, whereas a subset of GABAn showed suppressed responses to those afferents in an SST2A-R-dependent manner. Intrathecally administered SST2A-R antagonist inhibited the development of mechanical hypersensitivity by intraplantar AITC injection and alleviated persistent mechanical hypersensitivity in the murine model of nociplastic pain. These results suggest that the activity of TRPA1 agonist-responsive afferents induces and maintains central sensitization by activating dorsal horn SSTn and suppressing GABAn via SST2A-R, resulting in altered nociception that manifests as mechanical hypersensitivity. PERSPECTIVE: This article presents experimental evidence that TRPA1 agonist-responsive afferents induce and maintain central sensitization at the spinal level by activating SST-expressing excitatory interneurons and suppressing GABAergic inhibitory interneurons via SST2A-R. Spinal SST2A-R may represent a promising target for treating mechanical pain hypersensitivity due to central sensitization by TRPA1 agonist-responsive afferents.