anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Sepsis and its associated heart failure are among the leading causes of death. Gramine, a natural indole alkaloid, can be extracted from a wide variety of raw plants, and it exhibits therapeutic potential in pathological cardiac hypertrophy. However, the effect of gramine on inflammatory cardiomyopathy, particularly sepsis-induced myocardial injury, remains an unexplored area.
PURPOSE: To determine the role of gramine in sepsis-induced myocardial dysfunction and explore its underlying mechanism.
STUDY DESIGN AND METHODS: In mice, sepsis was established by intraperitoneally injecting lipopolysaccharide (LPS, 10 mg/kg). Subsequently, the effects of gramine administration (50 or 100 mg/kg) on LPS-triggered cardiac dysfunction in mice were investigated. For in vitro studies, isolated primary cardiomyocytes were used to assess the effect of gramine (25 or 50 µM) on LPS-induced apoptosis and inflammation. Additionally, molecular docking, co-immunoprecipitation and ubiquitination analyzes were conducted to explore the underlying mechanisms.
RESULTS: Gramine visibly ameliorated sepsis-induced cardiac dysfunction, inflammatory response, and mortality in vivo. Moreover, it significantly alleviated LPS-induced apoptotic and inflammatory responses in vitro. Furthermore, target prediction for gramine using the SuperPred website indicated that the nuclear factor NF-κB p105 subunit was one of the molecules ranked in priority order with a high model accuracy and a high probability score. Molecular docking studies demonstrated that gramine effectively docked to the death domain of NF-κB p105. Mechanistic studies revealed that gramine suppressed the processing of NF-κB p105 to p50 by inhibiting NF-κB p105 ubiquitination. Additionally, the protective effect of gramine on cardiac injury was almost abolished by overexpressing NF-κB p105.
CONCLUSION: Gramine is a promising bioactive small molecule for treating sepsis-induced myocardial dysfunction, which acts by docking to NF-κB p105 and inhibiting NF-κB p105 ubiquitination, thus preventing its processing to NF-κB p50. Therefore, gramine holds potential as a clinical drug for treating myocardial depression during sepsis.
During the clinical trials and in postmarketing reports, intraventricular access device-related complications were reported (e.g., device leakage, device failure extravasation of CSF fluid, or bulging of the scalp around or above the intraventricular access device) [see Adverse Reactions (6.1)]. For any complications with the implanted intraventricular access device, consult with a neurosurgeon to confirm the integrity or performance of the device. In case of intraventricular access device-related complications, discontinue the BRINEURA infusion and refer to the device manufacturer's labeling for further instructions [see Contraindications (4)].

Material degradation of the intraventricular access device reservoir was reported after approximately 4 years of administration, which may impact the effective and safe use of the device. During benchtop testing such material degradation was recognized after approximately 105 perforations of the intraventricular access device. The intraventricular access device should be replaced prior to 4 years of single-puncture administrations, which equates to approximately 105 administrations of BRINEURA.
BACKGROUND Penetrating traumatic brain injury (TBI) caused by gunshots is a rare type of TBI that leads to poor outcomes and high mortality rates. Conducting a formal neuropsychological evaluation concerning a patient's neurologic status during the chronic recovery phase can be challenging. Furthermore, the clinical assessment of survivors of penetrating TBI has not been adequately documented in the available literature. Severe TBI in patients can provide valuable information about the functional significance of the damaged brain regions. This information can help inform our understanding of the brain's intricate neural network. CASE REPORT We present a case of a 29-year-old right-handed man who sustained a left-hemisphere TBI after a gunshot, causing extensive diffuse damage to the left cerebral and cerebellar hemispheres, mainly sparing the right hemisphere. The patient survived. The patient experienced spastic right-sided hemiplegia, facial hemiparesis, left hemiparesis, and right hemianopsia. Additionally, he had severe global aphasia, which caused difficulty comprehending verbal commands and recognizing printed letters or words within his visual field. However, his spontaneous facial expressions indicating emotions were preserved. The patient received a thorough neuropsychological assessment to evaluate his functional progress following a severe TBI and is deemed to have had a favorable outcome. CONCLUSIONS Research on cognitive function recovery following loss of the right cerebral hemisphere typically focuses on pediatric populations undergoing elective surgery to treat severe neurological disorders. In this rare instance of a favorable outcome, we assessed the capacity of the fully developed right hemisphere to sustain cognitive and emotional abilities, such as language.
Thyroid hormones enhance oxygen consumption by most tissues of the body and increase the basal metabolic rate and the metabolism of carbohydrates, lipids and proteins. In vitro studies indicate that T 3 increases aerobic mitochondrial function, thereby increasing the rates of synthesis and utilization of myocardial high-energy phosphates. This, in turn, stimulates myosin ATPase and reduces tissue lactic acidosis. Thus, thyroid hormones exert a profound influence on virtually every organ system in the body and are of particular importance in the development of the central nervous system. 

While the source of levothyroxine (T 4) and some triiodothyronine (T 3) is via secretion from the thyroid gland, it is now well-established that approximately 80% of circulating T 3 arises predominantly by way of the extrathyroidal conversion of T 4. The membrane-bound enzyme responsible for this reaction is iodothyronine 5’-deiodinase. Activity of the enzyme is greatest in the liver and kidney. A second pathway of T 4 to T 3 conversion occurs via a PTU-insensitive 5’-deiodinase located primarily in the pituitary and central nervous system. 

The prohormone T 4 must be converted to T 3 in the body before it can exert biological effects. During periods of illness or stress, this conversion is often inhibited and can be diverted to the inactive reverse T 3 (rT 3) moiety. Therefore, correction of the hypothyroid condition in patients with myxedema coma is facilitated by the parenteral administration of triiodothyronine (T 3). T 3 is bound much less firmly to serum binding proteins and therefore penetrates into the cells much more rapidly than T 4. Also, the binding of T 3 to a nuclear thyroid hormone receptor seems to initiate most effects of thyroid hormone in tissues. Although most thyroid hormone analogs, both natural and synthetic, will bind to this protein, the affinity of T 3 for this receptor is roughly 10-fold higher than that of T 4. Thus, T 3 is the biologically active thyroid hormone.
FIELD: veterinary biotechnology, virology. SUBSTANCE: invention relates to preparing cell hybrids used in virological and biotechnological researches. The strain of ewe intraspecies hybrid kidney cells is obtained by fusion of mutant strain ПО-ТК -  with ewe splenocytes (ПО-ТК -  x C). Intraspecies hybrid strain (ПО-ТК x C) can be used for culturing the following viruses: infectious rhinotracheitis, latent herpes virus к.р.с, rhinopneumonia and for production of vaccines and diagnosticum. EFFECT: valuable properties of strain. 1 tbl, 1 ex
Sarcopenia is a progressive skeletal muscle disease in which oxidative stress has been proposed as one of the primary markers. The oxidative balance score (OBS) represents the oxidative balance of a person's dietary pattern using the merged intake of anti-oxidants and pro-oxidants. Therefore, the present study assessed the association between OBS and sarcopenia in Iranian older adults. In the current study, 80 people with sarcopenia and 80 without it were considered the case and control groups, respectively. All controls were matched by sex with cases. To confirm sarcopenia, skeletal muscle mass index (SMI), handgrip strength (HGS) measurement, and gait speed were used. Also, body composition was measured by bioelectrical impedance analysis (BIA). A valid and reliable food frequency questionnaire (FFQ) was used to assess all participants' dietary intake of pro-oxidants and anti-oxidants. Conditional logistic regression was applied to assess the association between OBS and sarcopenia. In the bivariate model, we observed lower odds of sarcopenia in the second and last tertile of OBS in comparison to the first tertile (T) (T2 - odds ratio (OR) = 0.414, 95% confidence interval (CI) : 0.186-0.918 and T3 - OR = 0.101, 95% CI: 0.041-0.248). After adjusting for potential confounders, the association was not significant in second and last tertile of OBS in comparision to the first one. The present study's findings demonstrated that overcoming exposure to anti-oxidants over pro-oxidants, as illustrated by a higher OBS, is not related to lower odds of sarcopenia in older adults.
Excessive elevation or reduction of soluble uric acid (sUA) levels has been linked to some of pathological states, raising another subject that sUA at physiological levels may be essential for the maintenance of health. Yet, the fundamental physiological functions and molecular targets of sUA remain largely unknown. Using enzyme assays and in vitro and in vivo metabolic assays, we demonstrate that sUA directly inhibits the hydrolase and cyclase activities of CD38 via a reversible non-competitive mechanism, thereby limiting nicotinamide adenine dinucleotide (NAD+) degradation. CD38 inhibition is restricted to sUA in purine metabolism, and a structural comparison using methyl analogs of sUA such as caffeine metabolites shows that 1,3-dihydroimidazol-2-one is the main functional group. Moreover, sUA at physiological levels prevents crude lipopolysaccharide (cLPS)-induced systemic inflammation and monosodium urate (MSU) crystal-induced peritonitis in mice by interacting with CD38. Together, this study unveils an unexpected physiological role for sUA in controlling NAD+ availability and innate immunity through CD38 inhibition, providing a new perspective on sUA homeostasis and purine metabolism.
INTRODUCTION: Ventricular septal rupture (VSR) following acute myocardial infarction (AMI) is a rare but serious complication often causing cardiogenic shock (CS). The timing of surgery is a difficult problem for surgeons because of high mortality and surgical complexity. We present a case of successful use of extracorporeal membrane oxygenation (ECMO) for maintaining haemodynamic stability preoperative and delaying surgical repair of VSR patient in severe CS.
CASE REPORT: A 57-year-old man with AMI complicated by severe CS due to an massive VSR. Emergency surgery was considered a too high mortality risk. The patient was implanted with a percutaneous veno-arterial ECMO (VA-ECMO) system as a bridge to surgery for stabilizing general condition. On the 31th day after ECMO implantation, the ventricular septal defect was successfully repaired and weaning from the ECMO.
DISCUSSION: This case study illustrates that it may be considered to use long term ECMO preoperative to delayed surgery which leads to higher survival in cases of massive VSR patient after AMI in hemodynamically compromised patients. Still the optimal duration of mechanical circulatory support and the optimal timing for surgery need more research to define.
CONCLUSION: This case indicates the feasibility of preoperative using of a long term VA-ECMO as a bridge to surgical repair of VSR patient after AMI in severe CS. The optimal duration of mechanical circulatory support and the optimal timing for surgery still require further investigation.
BACKGROUND: Recent advancements in animal studies have demonstrated the potential of normobaric hyperoxia (NBO) as a promising intervention for preserving the integrity of the blood-brain barrier (BBB). However, there is still limited understanding of the effects of NBO on BBB function in patients with clinical stroke. Therefore, the objective of this study was to investigate the efficacy of NBO therapy in attenuating BBB damage and reducing brain injury in individuals undergoing endovascular treatment (EVT) for acute stroke.
METHODS AND RESULTS: This study enrolled patients from the OPENS-1 (Normobaric Hyperoxia Combined With Reperfusion for Acute Ischemic Stroke) study, with 43 patients receiving NBO combined with EVT and 43 patients receiving EVT alone. The main outcome measures included serum levels of occludin, MMP-9 (matrix metalloproteinase-9), NSE (neuron-specific enolase), and S100b at 24 hours and 7 days, as well as the intracranial extravasation rate at 24 hours. Serum markers were assessed using ELISA, and intracranial contrast extravasation was visualized using dual-energy computed tomography scan. We analyzed a total of 86 patients and found that the 24-hour serum markers levels of BBB damage and brain injury were significantly lower in the group receiving NBO therapy combined with EVT compared with the group receiving EVT alone. Similarly, at 7 days, the levels of occludin, MMP-9, and NSE were lower in the NBO+EVT group. We also found that the 24-hour serum levels of occludin and MMP-9 were correlated with intracranial contrast extravasation. Additionally, the incidence of intracranial contrast extravasation was lower in the NBO+EVT group compared with the EVT group (35.9% versus 60.5%, P=0.031).
CONCLUSIONS: This study offers valuable insights into the positive impact of NBO on maintaining BBB integrity and reducing brain injury in patients with acute stroke undergoing EVT.
BACKGROUND: Previous observational studies have reported sarcopenia can affect the structure and function of brain cortical structure. However, the causality inferred from those studies was subjected to residual confounding and reverse causation. Herein, we use a two-sample Mendelian randomization (MR) analysis to illustrate the causal effect of sarcopenia-associated traits on brain cortical structure.
METHODS: We selected appendicular lean mass (ALM), hand grip strength (left and right) (HGSL and HGSR), and usual walking pace (UWP) to symbolize sarcopenia. The definition of brain cortical structure is human brain cortical surface area (SA) and cortical thickness (TH) globally and in 34 functional regions measured by magnetic resonance imaging. Instrumental variables at the genome-wide significance level were obtained from publicly available datasets, and inverse variance weighted as the primary method was used for MR analysis.
RESULT: At the global level, we found ALM (β=2604.68, 95 % confidence interval (CI): 1886.17 to 3323.19, P = 1.20 × 10-12) and HGSR (β=4733.05, 95 % CI: 2245.08 to 7221.01, P = 1.93 × 10-4) were associated with increased SA. At the region level, the SA of 25 functional gyrus without global weighted was influenced by ALM. The HGSR significantly increased SA of medial orbitofrontal and precentral gyrus without global weighted and ALM was associated with decrease of TH of lateral occipital gyrus with global weighted. No pleiotropy was detected.
CONCLUSION: This was the first MR study investigated the causal effect of sarcopenia-associated traits on brain cortical structure. In our study, we revealed genetically predicted sarcopenia-associated traits including ALM and HGSR could affect brain cortical structure.
The SystemCHANGE™ intervention will be delivered over a six-month period involving 12 face-to-face group sessions (1.5 to 2 hours each) held weekly for three months, followed by three monthly "booster calls." Intervention groups include \~10 to 15 patients, and friends and family members are encouraged to attend. Intervention sessions consist of 30-min to 60-min of behavior change activities and 60-min focused on healthy behaviors.
The present invention relates to an application of pickle juice in preparing for medicine preventing and remedying the diarrhea of chicken and a feed additive. The pickle juice is obtained from the curing process of pickle. In the process of making the pickle, various vegetables are fermented by pickle lactobacillus. The pickle is all cured under 1 to 40 DEG C for 5 to 60 days since being prepared or till that the pH value reaches 3.0. The prepared pickle juice, pickle juice condensed liquid, pickle juice dry substance or mixture are respectively applied to the medicine preventing and remedying the diarrhea in chicken and the feed additive. The pickle lactobacillus in the pickle juice is one of leuconostoc lactobacillus, milk globule lactobacillus, lactobacilli lactobacillus and bifidobacterium lactobacillus. The present invention applies the pickle juice for remedying the diarrhea in chicken effectively, more particularly, for the symptomatic treatment of secondary bacterial infection caused by the chicken virosis, thus relieving the symptom of the diarrhea of chicken, improving immunity obviously, retarding stress reaction and improving and maintaining gastrointestinal tract flora balance. The application of the pickle juice has good curative effect, low cost, no drug resistance, no residual drug and no toxic and side effect, which is a green environment-friendly natural active substance.
This will be an open-label, clinical study in male and female patients with NASH (n=10) and healthy volunteers (n=10) of any race and ethnicity investigating the effect of liver disease on the pharmacokinetics of 99mTechnetium-mebrofenin. The use of the gamma emitter 99m Tc- labeled mebrofenin will allow real-time assessment of hepatic exposure. To determine the differences between healthy subjects and patients with NASH, blood and hepatic concentrations will be analyzed by non-compartmental analysis. Additionally, serum bile acid samples and fibroscan data will be collected to determine whether the bile acid profile and/or fibroscan readings are different between healthy subjects and patients with NASH. Changes in 99mTc-mebrofenin will be correlated with the patient specific bile acid profile and fibroscan data. This study will increase our understating of the effect of liver disease on the disposition of medications that undergo transporter-mediated hepatic clearance.
Previous studies indicate a strong correlation between the incidence of chronic kidney disease (CKD) and lower economic status. However, these studies often struggle to delineate a clear cause-effect relationship, leaving healthcare providers uncertain about how to manage kidney disease in a way that improves patients' financial outcomes. Our study aimed to explore and establish a causal relationship between CKD and socioeconomic status, identifying critical influencing factors. We utilized summary meta-analysis data from the CKDGen Consortium and UK Biobank. Genetic variants identified from these sources served as instrumental variables (IVs) to estimate the association between CKD and socioeconomic status. The presence or absence of CKD, estimated glomerular filtration rate (eGFR), and albuminuria were used as exposures, while income and regional deprivation were analyzed as outcomes. We employed the R packages 'TwoSampleMR' and 'Mendelianrandomization' to conduct both univariable and multivariable Mendelian randomization (MR) analyses, assessing for potential pleiotropy and heterogeneity. Our univariable MR analysis revealed a significant causal relationship between high levels of albuminuria and lower income (OR = 0.84, 95% CI: 0.73-0.96, p = 0.013), with no significant pleiotropy detected. In the multivariable MR analysis, both CKD (OR = 0.867, 95% CI: 0.786-0.957, p = 0.0045) and eGFR (OR = 0.065, 95% CI: 0.010-0.437, p = 0.0049) exhibited significant effects on income. This study underscores that higher albuminuria levels in CKD patients are associated with decreased income and emphasizes the importance of effective management and treatment of albuminuria in CKD patients to mitigate both social and personal economic burdens.
NEW MATERIAL:A compound of formula I [R is a group of formula II or III (R' is 10-20C aliphatic group; X, Y are halogen, alkyl, cyano, nitro, amino, carboxyl or alkoxy; m, n are 0-4)]. EXAMPLE:2,4-Diamino-6-(p-octadecyloxyphenyl)-1,3,5-triazine. USE:A component for preparing thin films such as liposomes, LB films, single molecular films or casted films. A physiological substance is combined with the film structure regular at a molecular level and released from the thin film at a constant time interval. PREPARATION:A cyanophenol derivative is reacted with a long chain alkylating agent (e.g. stearyl bromide) in the presence of an alkali (e.g. KOH) and the prepared long chain alkyl cyano product is reacted with dicyandiamide in the presence of an alkali to provide the compound of formula I.
In a drug-drug interaction study with ANNOVERA and the concurrent use of three different formulations of vaginal miconazole, the use of water-based vaginal miconazole cream resulted in no change in exposure to EE or SA from the vaginal system. However, the use of either the 1- day or the 3-day oil-based miconazole suppository was associated with an overall increase in exposure up to 67% for EE and 32% for SA. Considering the potential long-term effect on vaginal system performance, concurrent use of oil-based vaginal suppositories should not occur with ANNOVERA use. If there is a need to treat a vaginal condition, water-based vaginal cream or oral therapy may be used concurrently with the vaginal system [see Clinical Pharmacology (12.3)]. 

Lubricants: Water-based vaginal lubricants have no effect on ANNOVERA; however, oil-based (including silicone-based) vaginal lubricants will alter the vaginal system and/or exposure to EE and SA and should not be used. 

ANNOVERA use is compatible with male condoms made with natural rubber latex, polyisoprene, and polyurethane. 

The effect of tampon use on the systemic exposure of SA and EE from ANNOVERA has not been studied.
The genetic heterogeneity has been a barrier to broad natural history efforts, with prior investigations often limited to single gene mutations. Much attention is paid to the variability within individual mutations (e.g. distal presentations), as opposed to defining the best strategy for measuring change in overall LGMD disease burden. This presents a major dilemma for LGMD rare disease research: how to balance diverse genes leading to overlapping phenotypes, versus variants in the same gene leading to divergent phenotypes. What is clear, is as a group, LGMDs are chronic and progressive leading to significant lifetime morbidity and represent a large unmet clinical need.

Recent developments in the investigator's genetic understanding of LGMD and molecular approaches to therapy have led to proposed gene replacement therapies for at least three of the LGMD mutations. Several of these gene replacement therapies are currently in pre-clinical/phase 1 testing, leading to an urgent need for natural history data. In addition, non-specific therapies which target muscle mass or function are being tested in other muscular dystrophies and may prove beneficial for LGMD.