anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Hyperglycemia-induced oxidative stress is a well-established pathological mediator of vascular complications in diabetes. We assessed plasma oxidant and antioxidant levels in response to acute and chronic hyperglycemia in relation to vascular stiffness and varying degrees of kidney disease in type 1 diabetes individuals.
METHODS: The acute hyperglycemia study included 22 type 1 diabetic individuals with normal albumin excretion rate (AER) and 13 non-diabetic controls. These individuals received an acute glucose challenge during a 120-minute hyperglycemic clamp. The chronic hyperglycemia study included 118 type 1 diabetic individuals with chronically low (n = 60) or high (n = 58) HbA1c concentrations and varying degrees of diabetic kidney disease (DKD) classified as normal, moderate, or severe albuminuria (AER). Levels of malondialdehyde (MDA), reactive oxygen metabolites (ROMs), total antioxidant capacity (TAC), biological antioxidant potential (BAP) and superoxide dismutase (SOD) were measured from plasma or serum samples in the FinnDiane study.
RESULTS: Levels of MDA (p < 0.01) and ROMs (p < 0.01) were elevated in type 1 diabetes individuals compared to non-diabetic controls at baseline. Acute hyperglycemia further increased MDA levels (p < 0.05) and sustained the elevation of ROMs in type 1 diabetes individuals. Acute hyperglycemic challenge impaired TAC in both non-diabetic (p < 0.05) and type 1 diabetes (p < 0.01) individuals compared to baseline whereas BAP was increased (p < 0.05) with no difference observed in non-diabetic controls. There was a positive association between high circulating MDA and AIx (r2 = 0.611, p = 0.05), and between delta ROMs and delta AIx (r2 = 0.955, p = 0.014) in combined analysis of individuals with type 1 diabetes and non-diabetic controls. Type 1 diabetes individuals with varying status of DKD, showed elevated levels of ROMs in those with high HbA1c compared to their counterpart with low HbA1c (p < 0.05). Individuals with severe albuminuria showed elevated ROM levels (p < 0.01) and depressed antioxidant capacity (p < 0.01) compared to those with normal AER of comparable HbA1c concentrations.
CONCLUSIONS: Biomarkers of oxidative stress are associated with vascular stiffness and DKD following acute and chronic hyperglycemic exposure and may provide added value to HbA1c in understanding disease pathology, predicting risk and assessing the status of secondary complications of type 1 diabetes.
Neuromyelitis Optica Spectrum Disorder (NMO-SD) is a recurrent inflammatory demyelinating disease affecting the central nervous system. The disease is clinically recognized by optic neuritis and transverse myelitis and is associated with high risk of mortality. Each attack worsens patients' disability. This means that after 5 years of the disease onset, half of patients need to use wheelchair and approximately 50% of them become blind.

Considering that the disease can be disabling for patients, the maintenance treatment should be applied in addition to treatment of acute attacks, in order to prevent future recurrences. Acute attacks are usually treated with high doses of intravenous corticosteroids. Plasmapheresis is also used when patients fail to response to corticosteroids. B lymphocyte inhibitors are used as the maintenance therapy in these patients. First line therapeutic medications include azathioprine and rituximab which are being recommended for long term therapy and second line medications include methotrexate and mycophenolate mofetil.

Azathioprine is an immune-modulatory agent which is available in the oral form and don't require hospitalization to be administered, however, because of side effects such as bone marrow suppression and hepatotoxicity, periodic check of blood cells and liver enzymes are needed. Rituximab is a cluster of differentiation antigen 20 inhibitor which leads to decreased B lymphocytes and antibody in patients. This medication is only available in the injectable form and needs hospitalization to be administered. Close monitory is needed during the administration considering severe side effects such as allergic reactions and respiratory distress. However, laboratory tests are not needed in patients taking rituximab although it is more expensive than azathioprine. No clinical trial has been performed previously to compare clinical efficacy of these two drugs in NMO-SD patients. Therefore, we aimed to compare their efficacy through a randomized clinical trial.
The present invention relates to dual activation of Akt/NF.kappa.3 pathway by DMA (5-(4-methylpiperazin- 1 -yl)-2- [2' -(3 ,4-dimethoxyphenyl)-5 ' - benzimidazolyl]benzimidazole) to render radioprotection both in mammalian cells and in Balb/c mice. Further it selectively protects normal cells overs tumor tissues against lethal total body irradiation (TBI) and there was no activation of Akt/NF.kappa.B pathway by DMA in response to radiation in tumor tissues. A single dose of DMA before TBI protect mice from GI and HP acute radiation syndrome (ARS) and offered radioprotection through oral, i.v., i.p., and .s.c route of administration. The half life of DMA in plasma is 3.5h at oral dose and 90% clearance was observed in 16h. DMA accumulates in high concentration in intestine, liver, kidney and spleen tissues, justifying the observed radioprotection to normal tissue even at single dose. This data provide molecular rationale that DMA is selective radioprotector to normal tissue and has the potential to improve clinical outcome of radiotherapy, valuable as adjuvants in cancer therapy and management of radiation emergencies.
A pouch for internal mixture of segregated reactants includes an outer containment envelope with a sealed reactant compartment inside. A middle shear strip and two outer strips, together defining two shear lines, are connected to the reactant compartment. The outer strips are folded under the reactant compartment with their tips anchored to the containment envelope. The middle strip extends away from the reactant compartment and through a slit in the containment envelope. Pulling on the middle strip causes the shear lines to lengthen until the reactant compartment is shorn open to release a reactant. A permeable second reactant compartment containing a second reactant may also be disposed inside the containment envelope, and may include a slit through which the middle strip passes. The reaction in the pouch may be exothermic and the pouch may be applied to any object to be heated such as a wet wipes dispenser.
All patients seen with suspected mTBI will undergo standard TBI assessment per institutional standard operating procedure. Mild TBI will be defined by Department of Defense/Department of Veterans Affairs Consensus- based Classification of Closed TBI Severity. This project will leverage several existing TBI clinics/programs and benefits from the clinical and technical knowledge gained from each. All participants will undergo the same screening, eligibility assessment, informed consent, baseline history/physical, statement of negative pregnancy status (if applicable), survey questionnaires, VOMS, BESS, King-Devick and abbreviated neurocognitive testing once. Participants will undergo research MRI twice at time points \> 2 weeks apart and one clinical MRI. Blood samples will be collected at each study visit. The research blood specimens will be processed immediately, frozen and sent to the WRNMMC Research Laboratory for future biomarker and genomic analysis.

MRI imaging findings (common data elements or newer imaging biomarkers discovered during the initial two-year technical development phase) will be analyzed to determine the most relevant biomarkers indicative of mTBI injury and/or prognosis for recovery. More advanced correlation analysis and relative risk regression will be performed to correlate mTBI and PTSD and their comorbid associations (e.g., depression, anxiety), Statistical tests will be corrected for multiple comparisons as appropriate.
PURPOSE:To adjust the pH of an aq. soln. of a high-molecular material to the desired value without causing lowering in the viscosity thereof, by using a high- molecular acid. CONSTITUTION:In adjusting the pH of an aq. soln. of a high-molecular material (e.g. an aq. polysodium acrylate soln. having a pH of 8-9.5) used for cosmetics, wetting agent for massage, agent for wet pack, mucosa-protecting agent, etc. to 5.5-6.5 by the addition of an acid to moderate skin irritation, a high-molecular acid such as a (co)polymer of (meth)acrylic, maleic or citraconic acid is used.
Overdose of acetaminophen may cause dose-dependent potentially fatal hepatic toxicity. Early symptoms within 24 hours after the overdose may include anorexia, nausea, vomiting, diaphoresis, general malaise, and abdominal pain. The patient may then present no symptoms, but evidence of liver dysfunction may become apparent up to 72 hours after ingestion, with elevated serum transaminase and lactic dehydrogenase levels, an increase in serum bilirubin concentrations, and a prolonged prothrombin time. Death from hepatic failure may result 3 to 7 days after overdosage. 

Because clinical and laboratory evidence of hepatic toxicity may not be apparent until 48 to 72 hours post-ingestion, liver function studies should be obtained initially and repeated at 24-hour intervals. 

Acute renal failure may accompany the hepatic dysfunction and has been noted in patients who do not exhibit signs of fulminant hepatic failure. Typically, renal impairment is more apparent 6 to 9 days after ingestion of the overdose.
Juvenile Primary Fibromyalgia Syndrome (JPFS) is a debilitating chronic pain condition that occurs in adolescence and is characterized by persistent pain, multiple tender points, sleep difficulty, and fatigue. The cause of JPFS is unknown and there is no known cure. Children and adolescents with JPFS have difficulty with daily functioning, miss a great deal of school, and experience increased emotional distress compared to their peers. Fibromyalgia syndrome appears to be resistant to treatment in adulthood, so early behavioral treatment for JPFS with long-term beneficial effects would be useful. This study will evaluate the efficacy of coping skills training (CST) when combined with usual medical care in reducing functional disability, pain intensity, and depressive symptoms in adolescents with JPFS. This study will also determine whether improvements can be sustained long-term.

This study will last 34 weeks. Participants will be recruited from three pediatric rheumatology clinics. Patients will be randomly assigned to one of two groups: CST plus usual medical care or education plus usual medical care. There will be 6 medical visits, spaced 4 to 5 weeks apart. In addition, patients will attend 8 individual sessions of CST or education over the first 8 weeks of the study. CST sessions will include training in cognitive-behavioral techniques of pain management for the adolescent and behavioral management techniques for their parents. Education sessions will include education on fibromyalgia and discussion about lifestyle issues, but no training in pain management procedures.

Patients will be evaluated at Week 9 and will be followed for an additional 6-month maintenance phase. During this maintenance phase, adolescents will continue to receive their usual medical care and will attend 2 additional sessions of CST or education. There will be one final evaluation at the end of the maintenance phase.
The combination of a HMG CoA reductase inhibitor like a statin, such as simvastatin, with a pFox inhibitor such as trimetazidine (“Simetazidine”) is particularly advantageous for treatment of end-stage complications, such as acute coronary syndrome (ACS) and chronic angina, especially in type II diabetics. The combination therapy is also useful in the treatment and/or prevention of chronic heart failure (CHF) and peripheral arterial disease (PAD). The combination of a nitric oxide (NO) mechanism with increased NO production with pFox inhibition simultaneously treats both the effect and the cause of angina. One or more oral hypoglycemic compounds (biguanides, insulin sensitizers, such as thiazolidinediones, α-glucosidase inhibitors, insulin secretagogues, and dipeptidyl peptidase IV inhibitors), protein kinase C (PKC) inhibitors, and acetyl-CoA carboxylase inhibitors can also be used in combination with the HMG CoA reductase inhibitors and/or pFox inhibitors, especially in type II diabetics, to control glucose levels and treat endothelial dysfunction. The drugs can be given in combination (e.g. a single tablet) or in separate dosage forms, administered simultaneously or sequentially. In the preferred form the statin is given in a dose of between 5 and 80 mg/day in two separate doses, and the pFox inhibitor is administered in a sustained or extended dosage formulation at a dose of 20 mg three times a day or 35 mg two times a day. The dose of the oral hypoglycemic, PKC inhibitor, or acetyl-CoA carboxylase inhibitor varies with the type of drug used.
AZILECT is a selective inhibitor of monoamine oxidase (MAO)-B at the recommended doses of 0.5 or 1 mg daily. AZILECT should not be used at daily doses exceeding 1 mg/day (or 0.5 mg/day for patients with mild hepatic impairment or in patients using concomitant ciprofloxacin or another CYP1A2 inhibitor) because of the risks of hypertensive crisis and other adverse reactions associated with nonselective inhibition of MAO [see Dosage and Administration (2), Drug Interactions (7.9), and Clinical Pharmacology (12.3)]. 

Dietary tyramine restriction is not ordinarily required with ingestion of most foods and beverages that may contain tyramine, during treatment with recommended doses of AZILECT. However, certain foods (e.g., aged cheeses, such as Stilton cheese) may contain very high amounts (i.e., > 150 mg) of tyramine and could potentially cause a hypertensive "cheese" reaction in patients taking AZILECT even at the recommended doses due to mild increased sensitivity to tyramine. Patients should be advised to avoid foods (e.g., aged cheese) containing a very large amount of tyramine while taking recommended doses of AZILECT because of the potential for large increases in blood pressure. Selectivity for inhibiting MAO-B diminishes in a dose-related manner as the dose is progressively increased above the recommended daily doses. 

There were no cases of hypertensive crisis in the clinical development program associated with 1 mg daily rasagiline treatment, in which most patients did not follow dietary tyramine restriction. 

Rare cases of hypertensive crisis have been reported in the post-marketing period in patients after ingesting unknown amounts of tyramine-rich foods while taking recommended doses of AZILECT.
There is provided a system architecture including a PPG hardware module and a MEMS hardware module. The PPG hardware module processes PPG raw data, which is generally composed of analog signals or digital signals. The PPG hardware module filters the raw data for later digital calculation to, for example, find out frequency signals with higher peak values. The PPG hardware module then outputs the selected frequency signals to an MCU for heart rate calculation. The MEMS hardware module receives MEMS raw data from a motion detector made of MEMS elements. The MEMS raw data represents motion status of a user that could possibly affect the heart rate determination result. The MEMS hardware module filters the raw data for later digital calculation to find out frequency signals with higher peak values caused by motion.
Doxorubicin (Dox) use is limited by Dox-induced cardiotoxicity. TANK-blinding kinase 1 (TBK1) is an important kinase involved in the regulation of mitophagy, but the role of TBK1 in cardiomyocytes in chronic Dox-induced cardiomyopathy remains unclear. Cardiomyocyte-specific Tbk1 knockout (Tbk1CKO) mice received Dox (6 mg/kg, injected intraperitoneally) once a week for 4 times, and cardiac assessment was performed 4 weeks after the final Dox injection. Adenoviruses encoding Tbk1 or containing shRNA targeting Tbk1, or a TBK1 phosphorylation inhibitor were used for overexpression or knockdown of Tbk1, or inhibit phosphorylation of TBK1 in isolated primary cardiomyocytes. Our results revealed that moderate Dox challenge decreased TBK1 phosphorylation (with no effect on TBK1 protein levels), resulting in compromised myocardial function, obvious mortality and overt interstitial fibrosis, and the effects were accentuated by Tbk1 deletion. Dox provoked mitochondrial membrane potential collapse and oxidative stress, the effects of which were exacerbated and mitigated by Tbk1 knockdown, specific inhibition of phosphorylation and overexpression, respectively. However, Tbk1 (Ser172A) overexpression did not alleviate these effects. Further scrutiny revealed that TBK1 exerted protective effects on mitochondria via SQSTM1/P62-mediated mitophagy. Tbk1 overexpression mediated cardioprotective effects on Dox-induced cardiotoxicity were cancelled off by Sqstm1/P62 knockdown. Moreover, TBK1-mitophagy-mitochondria cascade was confirmed in heart tissues from dilated cardiomyopathy patients. Taken together, our findings denoted a pivotal role of TBK1 in Dox-induced mitochondrial injury and cardiotoxicity possibly through its phosphorylation and SQSTM1/P62-mediated mitophagy.
To provide formulations of nanostructured gels for increased agent loading and adhesion.SOLUTION: A gel formulation has been developed which provides high loading, e.g., between about 5% wt./wt. agent/total gel weight and about 50% wt./wt. agent/total gel weight, of a wide range of agents, especially amine-containing compounds such as local anesthetic agents that are known to be difficult to encapsulate, and which adhere to charged surfaces. Examples of pharmaceutically important amines include anesthetics, such as lidocaine. Tuning the ionic strength of an aqueous medium during preparation, suspension, and dialysis purification of the hydrogel composition allows for retention and/or control of agent loading contents, as well as a high capacity for adhesion to charged surfaces mimicking inflamed tissue. In some instances, the rheological properties of the gel can be tuned such as to impart thixotropic properties to the gels formed.SELECTED DRAWING: None
In patients with acute ST-elevation myocardial infarction (STEMI) primary percutaneous coronary intervention (PCI) is the preferred reperfusion regimen, if performed by experienced operators in a timely manner. Nevertheless, myocardial damage is not immediately terminated after successful epicardial reperfusion by primary PCI. Current strategies are directed to improve myocardial tissue perfusion, which is impaired in approximately 50% of patients and which has prognostic impact. Adjunctive intravenous abciximab administration is an established therapy to improve coronary microcirculation and reduce major cardiac adverse events.5-10 In randomized clinical trials intravenous abciximab administration has been studied. Clinical trials have shown that earlier administration results in higher preinterventional TIMI-flow with subsequent improved perfusion post PCI. However, in a pooled analysis there was no effect on mortality. As door-to-balloon-times getting shorter in current trials, earlier abciximab administration requires treatment in the prehospital setting, which poses substantial logistic obstacles. Another option might be intracoronary abciximab bolus administration which results in very high local platelet inhibitor concentrations. This might be favorable in dissolution of thrombi and microemboli with subsequent improved myocardial microcirculation, reduction of no-reflow, and infarct size. Currently, there is only limited clinical experience on the efficacy of intracoronary abciximab administration mainly restricted to case reports, retrospective registries or small randomized trials. In a recently published randomized clinical trial, we were able to show that intracoronary versus intravenous abciximab bolus administration has beneficial effects on the occurrence of no-reflow and infarct size assessed by contrast-enhancement magnetic resonance imaging. This led to a trend towards improved clinical outcome. The composite major adverse cardiac event rate, defined as death, reinfarction, target vessel revascularization, and new congestive heart failure, at 30 day follow-up was 15.6% after intravenous and 5.2% after intracoronary abciximab administration (relative risk 3.00; 95% confidence intervals 0.94-10.80; p=0.06).

Currently, there is no adequately powered clinical trial to assess the effects of intracoronary bolus in comparison to standard intravenous abciximab administration. Due to its general availability and its ease of intracoronary administration this treatment has overwhelming potential in clinical practice, which is much easier to achieve than a logistically cumbersome prehospital or interhospital transfer administration.

In the era of evidence-based medicine, such a trial is of paramount importance to achieve a break-through in abciximab use and a reduction of the high associated morbidity and mortality of STEMI patients.
Dutasteride inhibits the conversion of testosterone to DHT. DHT is the androgen primarily responsible for the initial development and subsequent enlargement of the prostate gland. Testosterone is converted to DHT by the enzyme 5 alpha-reductase, which exists as 2 isoforms, type 1 and type 2. The type 2 isoenzyme is primarily active in the reproductive tissues, while the type 1 isoenzyme is also responsible for testosterone conversion in the skin and liver. 

Dutasteride is a competitive and specific inhibitor of both type 1 and type 2 5 alpha-reductase isoenzymes, with which it forms a stable enzyme complex. Dissociation from this complex has been evaluated under in vitro and in vivo conditions and is extremely slow. Dutasteride does not bind to the human androgen receptor.
Subjects will be followed and assessed for depressive symptoms at monthly time intervals similar to the active treatment arm using QIDS and PHQ9. This group does not receive TMS treatment.
AIM: An excessively activated or dysregulated complement system has been proven to be a vital contributor to the pathogenesis of periodontitis. It has been previously hypothesized that inhibiting the activity of complement component C5 by targeting the C5a receptor is a powerful candidate for treating periodontitis. Here, we apply the drug target instrumental variable (IV) approach to investigate the therapeutic effect of genetically proxied inhibition of C5 on periodontitis.
METHOD: In our primary analysis, we used 26 independent 'cis' single nucleotide polymorphisms as IVs from the vicinity of the encoding locus of C5 that are associated with plasma C5 levels. In a secondary analysis, we assess the validity of our primary findings, exploring the involvement of alternative downstream biomarkers, interleukin 17 (IL-17), interleukin 1β (IL-1β), and tumor necrosis factor (TNF). Summary statistics of plasma levels (C5, IL-17, IL-1β, and TNF) were obtained from a genome-wide association study (GWAS) of 35,559 European descent individuals. We extracted association statistics from a GWAS of 17,353 clinical periodontitis cases and 28,210 European controls. Wald ratios were combined using inverse-variance weighted meta-analysis.
RESULTS: In our primary approach, inhibiting C5 reduced the risk of periodontitis (Odds ratio 0.89 per 1 standard deviation reduction in C5; 95% confidence Interval 0.80-0.98, p value=0.022). Our secondary analysis suggests an involvement of IL-17 within the potential causal pathway, but was inconclusive for other biomarkers.
CONCLUSIONS: The findings from our study suggest that C5 inhibition may reduce the risk of periodontitis, prioritizing C5 inhibitors as a potential adjunctive therapeutic intervention in this disease.