anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PROBLEM TO BE SOLVED: To provide a bath preparation high in dispersibility in a bath water and not only exhibiting neat milky white color but also slight in milkiness deterioration even if it absorbed moisture when left to stand in a bathroom or the like. SOLUTION: This bath preparation contains a milkiness agent which is prepared by coating the surface of titanium oxide 0.2-0.7 μm in average particle size with 5-40 pts.wt. of a nonionic surfactant >=11 in HLB number, 5-40 pts.wt. of a stearic alkali metal salt and 5-40 pts.wt. of a fatty acid soap other than the stearic alkali metal salt, each based on 100 pts.wt. of the titanium oxide.
BACKGROUND: The heme oxygenase (HO) system plays a significant role in neuroprotection and reduction of neuroinflammation and neurodegeneration. The system, via isoforms HO-1 and HO-2, regulates cellular redox balance. HO-1, an antioxidant defense enzyme, is highlighted due to its association with depression, characterized by heightened neuroinflammation and impaired oxidative stress responses.
METHODOLOGY: We observed the pathophysiology of HO-1 and phytochemicals as its modulator. We explored Science Direct, Scopus, and PubMed for a comprehensive literature review. Bibliometric and temporal trend analysis were done using VOSviewer.
RESULTS: Several phytochemicals can potentially alleviate neuroinflammation and oxidative stress-induced depressive symptoms. These effects result from inhibiting the MAPK and NK-κB pathways - both implicated in the overproduction of pro-inflammatory factors - and from the upregulation of HO-1 expression mediated by Nrf2. Bibliometric and temporal trend analysis further validates these associations.
CONCLUSION: In summary, our findings suggest that antidepressant agents can mitigate neuroinflammation and depressive disorder pathogenesis via the upregulation of HO-1 expression. These agents suppress pro-inflammatory mediators and depressive-like symptoms, demonstrating that HO-1 plays a significant role in the neuroinflammatory process and the development of depression.
This study builds on preliminary data from this population based on over 1,000 Airmen. We have developed and validated a Brief Tobacco Intervention (BTI) that is currently being implemented as part of Technical Training. We found that a motivational interviewing based, 40 minute BTI was efficacious in increasing perceived harm and decreasing intentions to use tobacco in a sample of 1055 Air Force trainees. Although we obtained significant positive changes that are predictive of future tobacco use in self-reported intent to use (decreased) and self-reported perceived harm (increased), we did not obtain measures of actual tobacco resumption following the tobacco use ban in Air Force training. This study will obtain and analyze data on these measures.

Airmen will be consented in the presence of an Ombudsman and randomly assigned to either (1) BTI + The Airman's Guide to Remaining Tobacco Free at the beginning of Technical Training, (2) The Airman's Guide to Remaining Tobacco Free (no BTI), or (3) the standard smoking cessation pamphlet (no BTI). All interventions in this study are command-directed interventions provided to all Technical Training students in the 37th Training Group. Airmen who are willing to participate in the study will be consented before the administration of the brief assessment of the BTI. Immediately following the intervention, consented Airmen will receive another assessment to evaluate any immediate changes in several important cognitive constructs (e.g., perceived harm, self-efficacy, perceived behavioral control, subjective norms, attitudes, intentions). At the end of Technical Training (3 months), consented Airmen will complete a final assessment to determine tobacco abstinence.
Cardiovascular disease (CVD) remains a major health burden despite significant therapeutic advances accomplished over the last decades. It is widely and increasingly recognized that systemic inflammation not only represents a major cardiovascular risk and prognostic factor but also plays key pathogenic roles in CVD development and progression. Despite compelling preclinical evidence suggesting large potential of anti-inflammatory pharmacological interventions across numerous CVDs, clinical translation remains incomplete, mainly due to (1) yet undefined molecular signaling; (2) challenges of safety and efficacy profile of anti-inflammatory drugs; and (3) difficulties in identifying optimal patient candidates and responders to anti-inflammatory therapeutics, as well as optimal therapeutic windows. Randomized controlled trials demonstrated the safety/efficacy of canakinumab and colchicine in secondary cardiovascular prevention, providing confirmation for the involvement of a specific inflammatory pathway (NLRP3 [NACHT, LRR, and PYD domain-containing protein 3] inflammasome/IL [interleukin]-1β) in atherosclerotic CVD. Colchicine was recently approved by the US Food and Drug Administration for this indication. Diverse anti-inflammatory drugs targeting distinct inflammatory pathways are widely used for the management of other CVDs including myocarditis and pericarditis. Ongoing research efforts are directed to implementing anti-inflammatory therapeutic strategies across a growing number of CVDs, through repurposing of available anti-inflammatory drugs and development of novel anti-inflammatory compounds, which are herein concisely discussed. This review also summarizes the main characteristics and findings of completed and upcoming randomized controlled trials directly targeting inflammation in CVDs, and discusses major challenges and future perspectives in the exciting and constantly expanding landscape of cardioimmunology.
FIELD: medicine. SUBSTANCE: method involves preparing oral cavity after removing background oral fluid by rinsing with water to bring the oral cavity to standard state and exclude other influence exerted over samples. Initial level of activity of leucine aminopeptidase enzyme being pathognomonic factor of living activity. Action of preventive medication under test is shown for 2-4 min on the above background and microorganisms inhibition effectiveness in deactivating leucine aminopeptidase enzyme is checked. The like studies are carried out in 1, 3, 7 days and mean value of leucine aminopeptidase activity drop coefficient is determined. The drop being equal to or greater than 45%, the preparation under test is considered to be highly effective. The value being equal to 30-44%, the preparation is considered to be medium effective. Enzyme activity drops for less than 30%, the preparation is considered to possess low effectiveness. EFFECT: enhanced selectivity and sensitivity of the method. 1 tbl
The present invention relates to antibodies that specifically bind to CD 3. The present invention relates to antibodies that specifically bind PSMA. The present invention relates to antibodies that specifically bind CD3 and PSMA. The present invention relates to antibodies that specifically bind IL1 RAP. The present invention relates to antibodies that specifically bind to CD 33. The present invention relates to antibodies that specifically bind CD3 and IL1 RAP. The present invention relates to antibodies that specifically bind to CD3 and CD 33. The present invention relates to antibodies that specifically bind TMEFF 2. The present invention relates to antibodies that specifically bind to CD3 and TMEFF 2. The present invention relates to fragments of the antibodies, polynucleotides encoding the antibodies or fragments thereof, and methods of making and using the antibodies.
PURPOSE:To use 2-[2-phenyl-2-(2-pyridyl)]ethylamidazolin, or its acid addition salt well-known as a diabetic drug as a remedy for retinopathy by its improved inhibitory action on the whole blood aggregation. CONSTITUTION:A remedy for retinopathy containing 2-[2-phenyl-2-(2- pyridyl)]ethylimidazolin, or its acid addition salt (this compound for short). The blood sugar lowering action and inhibitory action on blood platelet aggregation of this compound are well-known. The remedying effect of retinopathy accompanying diabetes is not directly linked to the inhibitory action of blood platelet aggregation, but greatly affected by inhibitory action on the whole blood aggregation. This compound shows improved inhibitory action on the whole blood aggregation, and is useful as a remedy for retinopathy. Dosage is usually performed by orally, and a dose is preferably 300-900mg/day. This compound has high safety.
To date, PS is not recommended to adult and pediatric ARDS. Meantime, systematic review indicates that PS does not demonstrate statistically significant beneficial effects on reducing the mortality and the rate of BPD in term and late preterm infants with meconium aspiration syndrome(MAS). Therefore, a reasonable speculation is that preterm infants with NARDS do not benefit from one dose of PS. And the speculation can explain why not all preterm infants with respiratory distress can be beneficial from PS. In the era of pre-NARDS, the preterm infants fulfilling the definition of NARDS may have been considered as NRDS in the first three days after birth.

According to the diagnostic criteria of NARDS, a key procedure for diagnosis of NARDS is to exclude the newborn infants with NRDS. But no detailed procedures are available to differentiate NRDS from NARDS.
Patient simulation is a new and expanding technology that has proven effective as a teaching tool in various clinical settings, but data on pediatric simulation is lacking. Mock resuscitation scenarios have been shown in prior studies to be effective for improving knowledge, skill, and confidence in pediatric housestaff. Our objective is to assess the utility of a training program utilizing a human patient simulator of an infant as a teaching tool for pediatric housestaff training in resuscitation skills. We hypothesize that mock resuscitation exercises performed by pediatric housestaff on a patient simulator will result in improved performance on test scenarios when compared to the same training on a standard manikin.

We propose a randomized trial of pediatric residents of identical training levels from three children's hospitals. Participants will be assigned to a control group or an intervention group. The control group will undertake mock resuscitation scenarios on a standard manikin; the intervention group will perform the same exercises on a simulator. A test scenario will be administered at the end of each set of training scenarios and frequency and timing of a predetermined list of critical clinical assessments and interventions will be recorded. Analysis will consist of a comparison between control and intervention groups for success rates and time to completion for clinical assessments and interventions.
Mitogen-activated protein kinase (MAPK) signalling cascades are functionally important signalling modules in eukaryotes. Transcriptome reprogramming of immune-related genes is a key process in plant immunity. Emerging evidence shows that plant MAPK cascade is associated with processing (P)-body components and contributes to transcriptome reprogramming of immune-related genes. However, it remains largely unknown how this process is regulated. Here, we show that OsMPK12, which is induced by Magnaporthe oryzae infection, positively regulates rice blast resistance. Further analysis revealed that OsMPK12 directly interacts with enhancer of mRNA decapping protein 4 (OsEDC4), a P-body-located protein, and recruits OsEDC4 to where OsMPK12 is enriched. Importantly, OsEDC4 directly interacts with two decapping complex members OsDCP1 and OsDCP2, indicating that OsEDC4 is a subunit of the mRNA decapping complex. Additionally, we found that OsEDC4 positively regulates rice blast resistance by regulating expression of immune-related genes and maintaining proper mRNA levels of some negatively-regulated genes. And OsMPK12 and OsEDC4 are also involved in rice growth and development regulation. Taken together, our data demonstrate that OsMPK12 positively regulates rice blast resistance via OsEDC4-mediated mRNA decay of immune-related genes, providing new insight into not only the new role of the MAPK signalling cascade, but also posttranscriptional regulation of immune-related genes.
Women who receive surgery(staging or cytoreductive surgery) for endometrial cancer. We will obtain one 5\*5 cm omental fat and one 3\*3 cm subcutaneous adipose tissue during surgery.
Women with thrombophilia, i.e. carriage of a factor V leiden mutation, a factor II prothrombin G20210A mutation or a reduced amount of antithrombin III, protein C or protein S, are at elevated risk for thrombosis and related sequelae. Specifically, pregnant women with thrombophilia are at risk for pregnancy-associated thrombosis, pregnancy-associated thromboembolism as well as early miscarriage (until 20 weeks gestation) late miscarriage (after 20 weeks gestation), preeclampsia, and intrauterine growth retardation \<10th percentile. Uncontrolled retrospective and prospective studies indicate that a therapy with unfractionated heparin or low molecular weight heparin in pregnancy significantly reduces these pregnancy complications and improves maternal and fetal outcome. The use of low molecular weight heparin in pregnancy is safe with complication rates between 1% and 3%, mainly thrombocytopenia and bleeding complications. Randomized trials to adequately assess the safety and efficacy of heparin in pregnant women with thrombophilia are not available to date. Thus, we intend to randomize pregnant women with thrombophilia during weeks of gestation 11 to 14 into a therapy with nadroparin calcium (fraxiparin®) 0.3 mL daily during pregnancy and six weeks post partum and usual care. The primary end point of this study is a composite endpoint of pregnancy-associated thrombosis, pregnancy-associated thromboembolism, early miscarriage (until 20 weeks gestation) late miscarriage (after 20 weeks gestation), preeclampsia, and intrauterine growth retardation \<10th percentile. We hypothesize that a prophylactic therapy with nadroparin calcium will significantly reduce pregnancy complications in pregnant women with thrombophilia.
The synthesis and application of film targeting naphthalene endoperoxide belongs to the field of biomedicine technology. Coupling long alkyl side chains at the 1,4 positions of naphthalene results in highly lipophilic target compounds. These endoperoxides have a strong membrane targeting. Their cytotoxic activity against cancer cells is the killing of cancer cells by the release of singlet oxygen and is highly dependent on the length of the alkyl chain. We demonstrate through a series of experiments that the orientation and localization of peroxides within the cell membrane is a critical issue in determining its toxicity. The target compounds can effectively kill cancer cells by targeting cell membranes.
Following oral administration of perphenazine tablets, mean peak plasma perphenazine concentrations were observed between 1 to 3 hours. The plasma elimination half-life of perphenazine was independent of dose and ranged between 9 and 12 hours. In a study in which normal volunteers (n=12) received perphenazine 4 mg q8h for 5 days, steady-state concentrations of perphenazine were reached within 72 hours. Mean (%CV) Cmax and Cmin values for perphenazine and 7-hydroxyperphenazine at steady-state are listed below:

  


Peak 7-hydroxyperphenazine concentrations were observed between 2 to 4 hours with a terminal phase half-life ranging between 9.9 to 18.8 hours. Perphenazine is extensively metabolized in the liver to a number of metabolites by sulfoxidation, hydroxylation, dealkylation, and glucuronidation. The pharmacokinetics of perphenazine covary with the hydroxylation of debrisoquine which is mediated by cytochrome P450 2D6 (CYP 2D6) and thus is subject to genetic polymorphism – i.e., 7% to 10% of Caucasians and a low percentage of Asians have little or no activity and are called “poor metabolizers.” Poor metabolizers of CYP 2D6 will metabolize perphenazine more slowly and will experience higher concentrations compared with normal or “extensive” metabolizers.
The mechanosensitivity of inflammation can alter cellular mechanotransduction. However, the underlying mechanism remains unclear. This study aims to investigate the metabolic mechanism of inflammation under mechanical force to guide tissue remodeling better. Herein, we found that inflammation hindered bone remodeling under mechanical force, accompanied by a simultaneous enhancement of oxidative phosphorylation (OXPHOS) and glycolysis. The control of metabolism direction through GNE-140 and Visomitin revealed that enhanced glycolysis might act as a compensatory mechanism to resist OXPHOS-induced osteoclastogenesis by promoting osteogenesis. The inhibited osteogenesis induced by inflammatory mechanical stimuli was concomitant with a reduced expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). PGC-1α knockdown impeded osteogenesis under mechanical force and facilitated osteoclastogenesis by enhancing OXPHOS. Conversely, PGC-1α overexpression attenuated the impairment of bone remodeling by inflammatory mechanical signals through promoting glycolysis. This process benefited from the PGC-1α regulation on the transcriptional and translational activity of lactate dehydrogenase A (LDHA) and the tight control of the extracellular acidic environment. Additionally, the increased binding between PGC-1α and LDHA proteins might contribute to the glycolysis promotion within the inflammatory mechanical environment. Notably, LDHA suppression effectively eliminated the bone repair effect mediated by PGC-1α overexpression within inflammatory mechanical environments. In conclusion, this study demonstrated a novel molecular mechanism illustrating how inflammation orchestrated glucose metabolism through glycolysis and OXPHOS to affect mechanically induced bone remodeling.
Age-related macular degeneration (AMD) is a prominent cause of vision loss, characterized by two different types, dry (atrophic) and wet (neovascular). Dry AMD is distinguished by the progressive deterioration of retinal cells, which ultimately causes a decline in vision. In contrast, wet AMD is defined by the abnormal development of blood vessels underneath the retina, leading to a sudden and severe vision impairment. The course of AMD is primarily driven by chronic inflammation and pathological angiogenesis, in which the NF-κB signaling pathway plays a crucial role. The activation of NF-κB results in the generation of pro-inflammatory cytokines, chemokines, and angiogenic factors like VEGF, which contribute to inflammation and the formation of new blood vessels in AMD. This review analyzes the intricate relationship between NF-κB signaling, inflammation, and angiogenesis in AMD and assesses the possibility of using NF-κB as a target for therapy. The evaluation involves a comprehensive examination of preclinical and clinical evidence that substantiates the effectiveness of NF-κB inhibitors in treating AMD by diminishing inflammation and pathological angiogenesis.
A simple model is used to simulate seizures in a population of spiking excitatory neurons experiencing a uniform effect from inhibitory neurons. A key feature is introduced into the model, i.e., a mechanism that weakens the firing thresholds. This weakening mechanism adds memory to the dynamics. We find a seizure-prone state in a "mode-switching" phase. In this phase, the system can suddenly switch from a "healthy" state with small scale-free avalanches to a "seizure" state with almost periodic large avalanches ("seizures"). Simulations of the model predict statistics for the average time spent in the seizure state (the seizure "duration") that agree with experiments and theoretical examples of similar behavior in neuronal systems. Our study points to. different connections between seizures and fracture and also offers an alternative view on the type of critical point controlling neuronal avalanches.
Teratogenic Effects: Pregnancy Category D [see WARNINGS AND PRECAUTIONS (5.1)]

Minocycline hydrochloride extended-release tablets should not be used during pregnancy. If the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus and stop treatment immediately.

There are no adequate and well-controlled studies on the use of minocycline in pregnant women. Minocycline, like other tetracycline-class drugs, crosses the placenta and may cause fetal harm when administered to a pregnant woman.

Rare spontaneous reports of congenital anomalies including limb reduction have been reported with minocycline use in pregnancy in post-marketing experience. Only limited information is available regarding these reports; therefore, no conclusion on causal association can be established.

Minocycline induced skeletal malformations (bent limb bones) in fetuses when administered to pregnant rats and rabbits in doses of 30 mg/ kg/day and 100 mg/kg/day, respectively, (resulting in approximately 3 times and 2 times, respectively, the systemic exposure to minocycline observed in patients as a result of use of minocycline hydrochloride extended-release tablets). Reduced mean fetal body weight was observed in studies in which minocycline was administered to pregnant rats at a dose of 10 mg/kg/day (which resulted in approximately the same level of systemic exposure to minocycline as that observed in patients who use minocycline hydrochloride extended-release tablets).

Minocycline was assessed for effects on peri- and post-natal development of rats in a study that involved oral administration to pregnant rats from day 6 of gestation through the period of lactation (postpartum day 20), at dosages of 5, 10, or 50 mg/kg/day. In this study, body weight gain was significantly reduced in pregnant females that received 50 mg/kg/day (resulting in approximately 2.5 times the systemic exposure to minocycline observed in patients as a result of use of minocycline hydrochloride extended-release tablets). No effects of treatment on the duration of the gestation period or the number of live pups born per litter were observed. Gross external anomalies observed in F1 pups (offspring of animals that received minocycline) included reduced body size, improperly rotated forelimbs, and reduced size of extremities. No effects were observed on the physical development, behavior, learning ability, or reproduction of F1 pups, and there was no effect on gross appearance of F2 pups (offspring of F1 animals).