anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
INTRODUCTION: Ventilator-associated pneumonia (VAP) is a hospital-acquired infection with high mortality, and remains a challenge for clinical treatment. Red blood cell distribution width (RDW) was associated with worse outcomes in several diseases. The purpose of this study was to investigate the relationship between mean RDW values, changes in RDW (delta RDW), and in-hospital mortality among patients with VAP.
METHODS: In the present study, we enrolled 1266 VAP patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. All patients were categorized into low group, medium group, and high group according to tertiles of mean RDW values. The primary outcome was all-cause in-hospital mortality. Univariate logistic regression analysis, multivariate logistic regression analysis, and restricted cubic spline (RCS) curve were performed to determine the association between mean RDW values and in-hospital mortality in VAP. Moreover, RCS curve was plotted to explore the dose-response relationship between delta RDW and in-hospital mortality in VAP.
RESULTS: Among the VAP patients included in the study, the in-hospital mortality was 20.85% with 264 non-survivors and 1002 survivors. The non-survivors exhibited significantly higher mean RDW values and delta RDW values compared to survivors. Multivariate logistic regression analysis indicated that mean RDW values were positively associated with in-hospital mortality in VAP after adjusting for relevant covariates. The RCS curve demonstrated a dose-response relationship between mean RDW and the mortality in VAP. Moreover, a linear relationship was observed between delta RDW and in-hospital mortality in VAP.
CONCLUSION: Higher mean RDW values were significantly associated with an increased risk of in-hospital mortality in VAP. Additionally, a linear relationship was found between delta RDW values and in-hospital mortality. These findings suggest that RDW can be used to identify high-risk patients with poorer outcomes in VAP.
Contemporary cardiac injury models in zebrafish larvae include cryoinjury, laser ablation, pharmacological treatment and cardiac dysfunction mutations. Although effective in damaging cardiomyocytes, these models lack the important element of myocardial hypoxia, which induces critical molecular cascades within cardiac muscle. We have developed a novel, tractable, high throughput in vivo model of hypoxia-induced cardiac damage that can subsequently be used in screening cardioactive drugs and testing recovery therapies. Our potentially more realistic model for studying cardiac arrest and recovery involves larval zebrafish (Danio rerio) acutely exposed to severe hypoxia (PO2=5-7 mmHg). Such exposure induces loss of mobility quickly followed by cardiac arrest occurring within 120 min in 5 days post fertilization (dpf) and within 40 min at 10 dpf. Approximately 90% of 5 dpf larvae survive acute hypoxic exposure, but survival fell to 30% by 10 dpf. Upon return to air-saturated water, only a subset of larvae resumed heartbeat, occurring within 4 min (5 dpf) and 6-8 min (8-10 dpf). Heart rate, stroke volume and cardiac output in control larvae before hypoxic exposure were 188±5 bpm, 0.20±0.001 nL and 35.5±2.2 nL/min (n=35), respectively. After briefly falling to zero upon severe hypoxic exposure, heart rate returned to control values by 24 h of recovery. However, reflecting the severe cardiac damage induced by the hypoxic episode, stroke volume and cardiac output remained depressed by ∼50% from control values at 24 h of recovery, and full restoration of cardiac function ultimately required 72 h post-cardiac arrest. Immunohistological staining showed co-localization of Troponin C (identifying cardiomyocytes) and Capase-3 (identifying cellular apoptosis). As an alternative to models employing mechanical or pharmacological damage to the developing myocardium, the highly reproducible cardiac effects of acute hypoxia-induced cardiac arrest in the larval zebrafish represent an alternative, potentially more realistic model that mimics the cellular and molecular consequences of an infarction for studying cardiac tissue hypoxia injury and recovery of function.
Chronic suppurative otitis media (CSOM) is a leading global cause of potentially preventable hearing loss in children and adults, associated with socioeconomic deprivation. There is an absence of consensus on the definition of CSOM, which complicates efforts for prevention, treatment, and monitoring. CSOM occurs when perforation of the tympanic membrane is associated with severe or persistent inflammation in the middle ear, leading to hearing loss and recurrent or persistent ear discharge (otorrhoea). Cholesteatoma, caused by the inward growth of the squamous epithelium of the tympanic membrane into the middle ear, can also occur. The optimal treatment of discharge in CSOM is topical antibiotics. In resource-limited settings where topical antibiotics might not be available, topical antiseptics are an alternative. For persistent disease, surgery to repair the tympanic membrane or remove cholesteatoma might offer long-term resolution of otorrhoea and potential improvement to hearing. Recent developments in self-fitted air-conduction and bone-conduction hearing aids offer promise as new options for rehabilitation.
Lanthanide-doped upconversion nanoparticles (Ln-UCNPs) have been considered promising materials for various fields, such as biomedical and industrial applications. However, data and reports regarding its toxicity and environmental risks are scarce. Under these circumstances, data must be obtained to fully understand potential toxicity and adverse outcome pathways. In the present study, the toxicity of uncoated Ln-UCNP cores (NaYF4:Yb, Er) was systematically assessed in zebrafish embryos during early developmental stages. Ln-UCNPs were found to have multiple toxic effects, such as effects on survival rates, delayed hatching times, shorter body lengths, altered heart rates and blood circulation (significantly reduced), and neurobehavioral impairments in response to photoperiod stimulation. Bioimaging showed that Ln-UCNPs were distributed on the chorion, eyes, and skin at 72 hpf. However, it accumulates in the pharynx, esophagus, and intestine after oral administration. Ln-UCNPs disrupt the diversity and abundance of host-associated microorganisms (gut microbiota) leading to an increase in the prevalence of harmful bacteria in zebrafish. Transcriptomic and Ingenuity Pathway Analysis (IPA) predicted Interleukin-8 (IL-8) signaling, neuroinflammation, cardiac hypertrophy signaling pathways, immune and inflammation-related response interferon-gamma (ifnγ), and miR-155 as key mediators in regulatory effects. Based on this, a causal network was built showing the strong links between the induced gene expression of differentially expressed genes (DEGs), such as nitric oxide synthase 2 (nos2) and tumor necrosis factor (tnf) upon Ln-UCNPs treatment, and with the downstream adverse outcomes, in particular, the promotion of apoptosis, liver damage, and inflammatory response. Finally, RT-qPCR analysis confirmed the up-regulated expression of nos2 and tnf in the exposed larvae, consistent with the observation of an increased number of fluorescence-labelled neutrophils and macrophages in lyz: DsRed transgenic zebrafish until 120 hpf exposure, which together demonstrated the proinflammatory effects of Ln-UCNPs on organisms. In conclusion, we illustrated the developmental toxicity, disruption of gut-microbiome, and proinflammatory effects of Ln-UCNP cores on zebrafish, and the causal network from IPA analysis may help further elucidate the adverse outcome pathway of Ln-UCNPs.
OBJECTIVE: Steatotic livers exhibit higher susceptibility to ischemia reperfusion (IR) injury, which increase the risk of primary graft non-function following liver transplantation. S100A9 is identified as a pivotal innate immune sensor that regulates the progression of liver diseases. However, its significance in steatotic liver IR injury remains under-investigated.
METHODS: In mice model, we generated S100A9 knockout (S100A9 KO) mice to investigate the role of S100A9 in IR-stimulated steatotic livers. In vitro, primary bone marrow-derived macrophages were utilized to explore the effect of S100A9 in regulating macrophage polarization and inflammation.
RESULTS: S100A9 expression was markedly increased in steatotic livers of mice subjected to IR insult. S100A9 deletion significantly attenuated liver inflammatory injury, as evidenced by the diminished infiltration of both monocytes/macrophages and neutrophils (p < 0.05). The expression of proinflammatory factors was reduced (p < 0.05) at the same time. Additionally, S100A9-deficient livers demonstrated M1 polarization decrease and Toll-like receptor 4 (TLR4) suppression (p < 0.05). In vitro, genetic TLR4 inhibition led to nuclear factor kappa B (NF-κB) inactivation and subsequent M1 polarization decrease (p < 0.05) in macrophages treated with recombinant S100A9. Conclusion In this study, we highlight the pivotal role of TLR4/NF-κB as a critical mediator of S100A9 in inducing M1 macrophage polorization- dependent inflammation in steatotic livers IR injury.
A double compound of calcium oxychloride and asparagine is prepared by adding the oxychloride to a solution of asparagine in hot water. Similarly, compounds of calcium chloride with urea, and of calcium lactate with quinine, may be prepared.ALSO:Assimilable calcium-containing preparations having only a slight calcereous taste are obtained by mixing at least two per cent of a soluble organic compound of calcium with a liquid which does not combine therewith to form crystal aggregates and is such that the proportion of the electric conductivity of the preparation due to calcium ions is very much less than the conductivity of an equivalent solution of the calcium compound dissolved in water, on account of low electrolytic dissociation or low ionic mobility or both.  The liquid should preferably be viscous and contain less than 30 per cent of free water.  Examples of suitable liquids are: iso-stable lyophylic colloids such as glucose syrup, kitchen syrup and dextrin solution, and emulsions of oil in water or water in oil.  The calcium compound used may be calcium lactate, calcium sodium lactate, calcium gluconate, or double compounds formed between calcium compounds and organic nitrogen-containing substances, for instance, calcium chloride-urea, calcium lactate-quinone, or calcium oxychloride - asparagine.  Each double compounds may be added as such or may be formed in situ by adding the separate ingredients.  The taste of the preparations may be further reduced by addition of other electrolytes.  According to an example, a mayonnaise may contain groundnut oil or olive oil, vinegar, egg yolk, calcium lactate and water, with or without a colloid such as gelatine.  Mixtures of calcium compounds with gelatine solution alone, or with saccharose solution alone are stated to be unsuitable.
For the relief of signs and symptoms of rheumatoid arthritis or osteoarthritis the recommended dose is 400 mg to 600 mg given orally, 3 or 4 times a day. The dose should be tailored to the needs of the patient and may be increased or decreased depending on the severity of the symptoms. Dosage adjustments may be made after initiation of drug therapy or during exacerbations of the disease. Total daily dosage should not exceed 3200 mg.

Fenoprofen calcium tablets may be administered with meals or with milk. Although the total amount absorbed is not affected, peak blood levels are delayed and diminished.

Patients with rheumatoid arthritis generally seem to require larger doses of fenoprofen calcium tablets than do those with osteoarthritis. The smallest dose that yields acceptable control should be employed.

Although improvement may be seen in a few days in many patients, an additional 2 to 3 weeks may be required to gauge the full benefits of therapy.
Ophthalmic compositions, particularly for use with an applanation tonometer and in the location of foreign bodies in the eye, comprise (a), as local anaesthetic, 0.1 to 2% by weight of proparacaine, parethoxycaine, benoxinate, or tetracaine (in the form of a non-toxic, water-soluble salt, e.g. hydrochloride), (b) as disclosing agent, 0.05% to 0.3% by weight of fluorescein sodium and (c) 5 to 15% by weight of polyvinylpyrrolidone as complexing and solubilizing agent, the percentages being based on the total weight of the composition, and the balance of the composition being water and a non-toxic acid to bring the pH of the composition to 4.5 to 5.5.  The non-toxic acid may be citric or preferably boric acid.  The compositions may also contain an antimicrobial agent (e.g. chlorobutanol \sB phenyl mercuric acetate) and a chelating agent (e.g. disodium ethylene diamine tetra acetic acid).
Epiretinal membrane (ERM) is a frequent, sight-threatening eye condition occurring in 1.02% - 28.9% of eyes in persons aged 40 years or older. \[1\] While often idiopathic in nature, ERM formation has been associated with retinal tears, possibly due to a breakdown of the blood-retinal barrier \[1-3\]. Pathological analysis of ERM content shows inflammatory mediators such as cytokines, growth factors and interleukins, which can promote fibroblast remodelling that leads to a contractile scar formation on the retinal surface. \[1, 4-8\] For this reason, ERM formation has been suggested to be an aberrant tissue repair or wound-healing process driven by inflammatory reactions. Since corticosteroids inhibit the inflammatory cascade and fibroblast transdifferentiation, administration of a corticosteroid following retinal tears should theoretically reduce the risk of ERM formation. \[9-10\] In this study, we aim to assess whether administration of a topical corticosteroid would attenuate ERM formation following laser retinopexy of retinal tears.
LN-145-S1 therapy as a single agent in patients with Stage IIIC or Stage IV unresectable or metastatic melanoma, who have previously received systemic therapy with a PD-1 blocking antibody. If the tumor is proto-oncogene B-Raf (BRAF) V600 mutation positive, patients must have received a BRAF inhibitor with or without a mitogen-activated extracellular signal-related kinase (MEK) inhibitor.
FOLFOX\* + BEVACIZUMAB CHEMOTHERAPY: Patients receive oxaliplatin IV over 2 hours, leucovorin calcium IV over 2 hours, fluorouracil IV continuously over 46-48 hours, and bevacizumab IV over 30-90 minutes. Treatment repeats for up to 12 courses in the absence of disease progression or unacceptable toxicity. RIT: Within 4-12 weeks after completion of post-hepatic resection therapy chemotherapy, patients receive yttrium Y 90 DOTA anti-CEA monoclonal antibody M5A IV over 25 minutes. Treatment repeats every 6-10 weeks for 2 courses in the absence of disease progression or unacceptable toxicity. NOTE:\*Patients previously failing oxaliplatin regimen receive FOLIFIRI chemotherapy comprising irinotecan hydrochloride IV over 90 minutes, leucovorin calcium over 2 hours, fluorouracil IV continuously over 46-48 hours, and bevacizumab IV over 30-90 minutes. Treatment repeats for up to 6 courses in the absence of disease progression or unacceptable toxicity.
PURPOSE: The study aimed to evaluate the factors influencing recombinant human growth hormone (rhGH) treatment in Chinese children with short stature born small for gestational age (SGA).
METHODS: A single-centre, real-world retrospective study was conducted in short stature children born SGA in China. Outcomes were observed at 6, 12, 18, 24, 30, and 36 months. Outcome measures included height standard deviation score (HTSDS), height, growth velocity (GV), and change of HTSDS (ΔHTSDS). The study used the generalized estimating equation (GEE) to identify potential influencing factors, such as rhGH treatment duration, age at rhGH initiation, sex, 11p15 hypomethylation, GH secretion, and birth weight. A subgroup analysis was conducted to investigate the impact of 11p15 hypomethylation related to SGA or impaired GH secretion.
RESULTS: Of all 101 SGA patients included in the screening, 41 were eligible for inclusion in the study. The mean age at rhGH initiation was 5.6 ± 2.4 years. The results of the GEE analysis showed a significant association between time after rhGH initiation and HTSDS, height, GV, and ΔHTSDS. GV increased after treatment, with the highest increase observed in the first six months. Additionally, the study found negative correlations between 11p15 hypomethylation and GV, as well as between birth weight and both GV and ΔHTSDS. The study found a positive correlation between impairment in GH secretion and both GV and ΔHTSDS. No statistically significant difference was observed in the comparison of GV or ΔHTSDS between the initiation age of GH treatment and 11p15 hypomethylation. After 24 and 30 months of rhGH treatment, patients with impaired GH secretion had significantly higher ΔHTSDS scores.
CONCLUSIONS: In short stature Chinese children born SGA, those without SGA-related 11p15 hypomethylation or with impaired GH secretion showed better response to rhGH treatment. These findings highlight the importance of pre-treatment evaluation, including genetic and endocrine assessments.
Chlorthalidone should be used with caution in severe renal disease. In patients with renal disease, chlorthalidone or related drugs may precipitate azotemia. Cumulative effects of the drug may develop in patients with impaired renal function.

Chlorthalidone should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.

Sensitivity reactions may occur in patients with a history of allergy or bronchial asthma.

The possibility of exacerbation or activation of systemic lupus erythematosus has been reported with thiazide diuretics, which are structurally related to chlorthalidone. However, systemic lupus erythematosus has not been reported following chlorthalidone administration.
Provided are methods and compositions for treating an individual who has a medulloblastoma. Methods for treating an individual who has a medulloblastoma tumor can include a step of administering to the individual, at a dose sufficient to reduce the size and/or growth rate of the medulloblastoma tumor, a composition that includes a casein kinase II (CK2) inhibitor (e.g., a CK2-selective inhibitor such as CX-4945). In some cases, the medulloblastoma tumor is a hedgehog-dependent medulloblastoma tumor. In some cases, the medulloblastoma tumor is a hedgehog-independent medulloblastoma tumor. In some cases, the medulloblastoma tumor is smoothened inhibitor-resistant (SMO inhibitor-resistant). In some cases, the medulloblastoma is resistant to treatment with 4,5,6,7-tetrabromo-2H-benzotriazole (TBB). In some cases, the dose is sufficient to cause long term regression of the medulloblastoma tumor, and in some cases, the dose is sufficient to increase the chance of survival of the individual.
This is a single dose, parallel group, open-label, 2 center pharmacokinetic study, consisting of a pretreatment (screening) period of between 1 and 3 weeks, an open label treatment period (single dose of ER OROS paliperidone on Day 1 only, and with end of study procedures and discharge ending on Day 6). All patients will be screened between Day 21 and Day 1 for renal function. On Day 1, all patients will receive a single oral dose of 3 mg ER OROS paliperidone and undergo a 120 hour follow up with serial blood collections for pharmacokinetics, safety and tolerability assessments. Patients will be discharged after giving a pharmacokinetic blood sample and completing end of study assessments in the morning of Day 6. Group matching will be applied to the renal function groups to reduce bias and increase comparability of age, weight, gender, and ethnicity. This study is aimed to compare the pharmacokinetics and safety profile of ER OROS paliperidone in patients with varying degrees of renal impairment with that of normal patients. 3 mg oral ER OROS paliperidone
Alcohol abuse inflicts enormous physical, emotional, and financial burdens on the individual and society at large. Knowing who is at risk for alcohol abuse, and why, is crucial for the development of effective prevention and treatment strategies. Alcohol abuse has been traditionally considered a male-oriented problem and as a consequence research on risk factors specific to women has been minimal. However, the sex gap in substance abuse is closing rapidly, and findings from both animal and human studies suggest that females are actually more vulnerable to drug use than males. As such, there is an urgent need to identify sex differences in risk factors for alcohol abuse in order to develop sex-specific prevention and treatment efforts. One clear candidate risk factor is poor inhibitory control, both in terms of baseline levels of inhibition and sensitivity to the disinhibiting effects of alcohol. Recent studies suggest that sex hormones affect inhibitory control in drug-free individuals, potentially contributing to sex differences in baseline levels of inhibition. However, the degree to which fluctuations in sex hormones influence sex differences in inhibition-related brain function in sober and intoxicated individuals is not known. The proposed project will determine the neural and hormonal mechanisms underlying sex differences in sensitivity to the disinhibiting effects of alcohol in heavy drinkers.

The overall objective of the research is to identify hormonal determinants of alcohol effects on brain activation during response inhibition (BARI) in young adult female and male drinkers. BARI will be assessed using functional magnetic resonance imaging (fMRI) during performance of the stop signal task. This task reliably activates right-lateralized prefrontal regions implicated in inhibitory control. This study will assess BARI during IV alcohol (60mg%) and saline infusion in women during the early follicular and mid-luteal phases and in men at matched intervals.
Compositions and methods are provided for preparing nanosized biologically active agents, including agents formulated for target specific drug delivery. The nanosized agents are prepared with supercritical carbon dioxide as an antisolvent, providing nanoparticles whose size, shape, and surroundings are well-controlled. The nanoparticles are made of small molecules, e.g. drugs, anti-oxidants, luciferin, polypeptides, e.g. oligopeptides; polynucleotides, e.g. siRNA, antisense oligonucleotides, etc. In some embodiments, the nanoparticles comprise a polymer coating, which can provide for controlled delivery, targeting, controlled release, and the like. In other embodiments, the nanoparticles comprise a target specific tag for targeting the nanoparticles to a site of interest, e.g. tissue, cell, etc.
Elevations of ALT or AST (three or more times the upper limit of normal [ULN]) have been reported in approximately 1% of NSAID-treated patients in clinical trials. In addition, rare, sometimes fatal, cases of severe hepatic injury, including fulminant hepatitis, liver necrosis, and hepatic failure have been reported.

Elevations of ALT or AST (less than three times ULN) may occur in up to 15% of patients treated with NSAIDs including naproxen.

Inform patients of the warning signs and symptoms of hepatotoxicity (e.g., nausea, fatigue, lethargy, diarrhea, pruritus, jaundice, right upper quadrant tenderness, and "flu-like" symptoms). If clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, etc.), discontinue NAPROSYN Tablets, EC-NAPROSYN, or ANAPROX DS immediately, and perform a clinical evaluation of the patient.
The extensive arm will consist of a comprehensive training program, involving five to eight sessions (each approximately 60 minutes in duration), which have to be completed in a period of 12 weeks. After the first session, each further session in the extensive group involves tailored therapy guidance . Cognitive strategy modules will be assigned by the therapist depending on the participants' cognitive profile and personal treatment goals.