anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Systemic inflammation in which lipopolysaccharide (LPS) is released into circulation can cause cognitive dysfunction and we have previously shown that LPS impaired working memory (WM) which refers to the ability to guide incoming behavior by retrieving recently acquired information. However, the mechanism is not very clear, and currently, there is no approved strategy to improve inflammation-induced WM deficit. Notably, epidemiological studies have demonstrated a lower occurrence rate of inflammatory-related diseases in smoking patients, suggesting that inflammation-induced WM impairment may be improved by nicotine treatment. Here, our object is to investigate the effect and potential mechanisms of acute and chronic nicotine treatment on LPS-produced WM deficiency.
METHODS: Delayed alternation T-maze task (DAT) was applied for evaluating WM which includes both the short-term information storage and the ability to correct errors in adult male mice. Immunofluorescence staining and immunoblotting were used for assessing the levels and distribution of CREB-regulated transcription coactivator 1 (CRTC1) and hyperpolarization-activated cation channels 2 (HCN2) in the medial prefrontal cortex (mPFC) and hippocampus. Quantitative PCR and ELISA were employed for analyzing the mRNA and protein levels of TNF-α and IL-1β.
RESULTS: Our results revealed that administration of LPS (i.p.) at a dose of 0.5 mg/kg significantly produced WM impairment in the DAT task accompanied by an increase in IL-1β and TNF-α expression in the mPFC. Moreover, intra-mPFC infusion of IL-1Ra, an IL-1 antagonist, markedly alleviated LPS-induced WM deficiency. More important, chronic (2 weeks) but not acute nicotine (0.2 mg/kg, subcutaneous) treatment significantly alleviated LPS-induced WM deficiency by upregulating CRTC1 and HCN2. Of note, intra-mPFC infusion of HCN blocker ZD7288 produced significant WM deficiency.
CONCLUSIONS: In summary, in this study, we show that chronic nicotine treatment ameliorates acute inflammation-induced working memory deficiency by increasing CRTC1 and HCN2 in adult male mice.
In recent years, the utilization of enterocystoplasty for bladder function enhancement has increased, albeit accompanied by risks such as stone formation, necessitating vigilant follow-up. We report a case of a 60-year-old female with a neobladder who presented with back pain, constipation, and pelvic heaviness, revealing multiple large stones in imaging. Stone analysis showed calcium oxalate and magnesium. Enterocystolithotomy was performed to manage the condition. Enterocystoplasty, a standard treatment for bladder cancer, can lead to stone formation due to factors like urinary stasis and infections. Giant stones are rare but require prompt treatment, often involving neocystolithotomy. Controlling risk factors and selecting appropriate treatment based on stone size and surgical expertise are key to improving patient outcomes.
Pulmonary embolism (PE) is the third most common type of cardiovascular disease and carries a high mortality rate of 30% if left untreated. Although it is commonly known that individuals who suffer heart failure (HF) are more likely to experience a pulmonary embolism, little is known concerning the prognostic relationship between acute PE and HF. This study aims to evaluate the prognostic usefulness of heart failure and pro-BNP in pulmonary embolism cases. A scientific literature search, including PubMed, Medline, and Cochrane reviews, was used to assess and evaluate the most pertinent research that has been published. The findings showed that increased N-terminal brain natriuretic peptide (NT-proBNP) levels could potentially identify pulmonary embolism patients with worse immediate prognoses and were highly predictive of all-cause death. Important prognostic information can be obtained from NT-proBNP and Heart-type Fatty Acid Binding Proteins (H-FABP) when examining individuals with PE. The heart, distal tubular cells of the renal system, and skeletal muscle are where H-FABP is primarily found, with myocardial cells having the highest concentration. Recent studies have indicated that these biomarkers may also help assess the severity of PE and its long-term risk.
Subjects in regimen 2 will start at 150 mg and may stay at 150 mg or increase to 300 mg. This treatment arm increases to 300 mg.
PURPOSE: To obtain a new monoclonal antibody useful for discovery of lung cancer at an early stage, reacting on both a glycopeptide derived from a mucin type protein of human tumor cell and human tumor tissue but not on other cancer tissue and normal tissue of the lung. CONSTITUTION: A spleen cell of a mammal (e.g. mouse) immunized against a human lung cancer cell [e.g. established lung cancer cell SK-LU-1 (ATCC No.HTB57), etc] is fused with a cell (myeloma) having self-propagation ability derived from the same kind of an animal as that of the mammal or a different kind of an animal and selectively cultured in a HAT medium to give a hybridoma. Then, an antibody forming clone having reactivity on a human lung cancer cell from the hybridoma and cloned by limiting dilution method. The monoclonal hybridoma is cultured to give the objective new monoclonal antibody reacting on a mucin type protein of human tumor cell but not on an asparagine-bonded glycopeptide, useful for discovering lung cancer at an early stage.
Eligible members are assigned a CareSupport Coordinator who carries a caseload of 25-35 members. A team of 5 Coordinators is supervised by a master's level Social Worker. Community Coordinators work with members to conduct standardized assessments to develop a Care Plan shared with other providers within and outside of SFHP. Coordinators provide members advocacy and navigation across systems of care, to improve coordination focus on treatment goals. Coordinator focus on prevention and early intervention around disease management, advocacy, appointment reminders and accompaniment, home visits, and regular communication with primary care and other providers. Coordinators are encouraged to be accountable for coordinating and following through on all aspects of a member's needs.
Dosing of Ultratrace iobenguane I 131 began at 6.0 mCi/kg and escalated in 1.0 mCi/kg increments in order to establish the MTD. The MTD is the dose immediately below the level at which escalation stops due to dose-limiting toxicity (DLT). An additional 3 patients are to be treated at the MTD, for a total of 6.
The control arm will be populated with claims data for patients with HF and fluid overload who presented to the emergency department and were admitted to the hospital for ≤ 72 hours for the treatment of HF with intravenous diuretics. Patients admitted for diuresis-only will be identified by using diagnostic codes for admittance from a claims database.
ABCG2, also known as breast cancer resistance protein (BCRP), is an ATP-binding cassette (ABC) transporter that has been shown to confer resistance to several drugs, including mitoxantrone and topotecan. Gleevec (imatinib mesylate) has recently been identified as a substrate for ABCG2. The expression of ABCG2 in the human jejunum has been shown to be higher than expression MDR1, which encodes for P-glycoprotein. Therefore, it is plausible that the oral bioavailability of Gleevec could be dependent on the extent of transport. A single nucleotide polymorphism (C421A) has been identified in ABCG2 and has been shown in vitro to result in functional inactivation of this transporter protein. In this study, the relationship between the genotypes of ABCG2 and the pharmacokinetics or side effects will be retrospectively explored in patients with cancer who had been previously enrolled on clinical trials of Gleevec.
One of the hallmarks of chronic kidney disease (CKD) is the development of vascular calcification. Inorganic pyrophosphate is a potent inhibitor of calcification, and previous studies have reported low plasma pyrophosphate levels in hemodialysis patients. A long-term mouse model of CKD-accelerated vascular calcification was developed to study pyrophosphate metabolism and to test whether oral pyrophosphate supplementation attenuates the propensity for arterial calcification. CKD was induced by repeated injections of aristolochic acid in wild-type and Abcc6-/- mice, which tend to develop vascular calcifications. CKD accelerated the development of vascular calcifications in Abcc6-/- mice, in the aorta and small renal arteries, and decreased circulating pyrophosphate levels. Oral pyrophosphate supplementation for 6 months attenuated CKD-induced vascular calcification in this model. These results show that oral pyrophosphate may be of interest in preventing vascular calcification in patients with CKD. KEY MESSAGES: Chronic kidney disease accelerates the development of vascular calcification in pyrophosphate-deficient mice. Oral pyrophosphate supplementation for 6 months attenuates chronic kidney disease-induced vascular calcification in a mouse model. Oral pyrophosphate may be of interest in preventing vascular calcification in patients with chronic kidney disease.
Lower eyelid reconstruction using skin flaps sometimes results in undesirable deformities due to postoperative flap drooping. We aimed to examine the effectiveness of a novel procedure for reconstructing the skin-tarsoligamentous sling of the lower eyelid. We included 37 patients who underwent anterior lamellar reconstruction with a cheek rotation flap for full-thickness lower eyelid defect. They were divided into two groups: Group A included 19 patients who underwent tarsoligamentous sling reconstruction with a fascia lata strip and buccal mucosa grafting, and Group B comprised 18 patients who underwent skin-tarsoligamentous sling reconstruction using an additional combination of a periosteal flap and de-epithelialized triangular flap at the lateral canthal region, representing our novel approach. To evaluate the severity of postoperative deformities, we used the drooping index, the ratio of drooping compared to the healthy side, along with the angular difference in canthal tilt, obtained between the reconstructed and healthy sides, using photographs taken ≥6 months post-reconstruction. Group B demonstrated superior outcomes, with mean drooping indices of 1.13 compared to 1.33 in Group A (P = 0.031) and mean angular differences in canthal tilt of -0.73° compared to -2.45° in Group A (P = 0.021). Patient satisfaction was significantly higher in Group B than in Group A (P = 0.042). Furthermore, patients with drooping index <1.2 and an angular difference in canthal tilt ≥-1.0° exhibited higher satisfaction scores. Our novel approach to lower eyelid reconstruction using a skin-tarsoligamentous sling yielded improved aesthetic outcomes, fewer complications, and higher patient satisfaction.
Mice with cardiac-specific overexpression of adenylyl cyclase (AC) type 8 (TGAC8) are under a constant state of severe myocardial stress. They have a remarkable ability to adapt to this stress, but they eventually develop accelerated cardiac aging and experience reduced longevity. We have previously demonstrated through bioinformatics that constitutive adenylyl cyclase activation in TGAC8 mice is associated with the activation of inflammation-related signaling pathways. However, the immune response associated with chronic myocardial stress in the TGAC8 mouse remains unexplored. Here we demonstrate that chronic activation of adenylyl cyclase in cardiomyocytes of TGAC8 mice results in activation of cell-autonomous RelA-mediated NF-κB signaling. This is associated with non-cell-autonomous activation of proinflammatory and age-associated signaling in myocardial endothelial cells and myocardial smooth muscle cells, expansion of myocardial immune cells, increase in serum levels of inflammatory cytokines, and changes in the size or composition of lymphoid organs. All these changes precede the appearance of cardiac fibrosis. We provide evidence indicating that RelA activation in cardiomyocytes with chronic activation of adenylyl cyclase is mediated by calcium-protein Kinase A (PKA) signaling. Using a model of chronic cardiomyocyte stress and accelerated aging, we highlight a novel, calcium/PKA/RelA-dependent connection between cardiomyocyte stress, myocardial inflammation, and systemic inflammation. These findings suggest that RelA-mediated signaling in cardiomyocytes might be an adaptive response to stress that, when chronically activated, ultimately contributes to both cardiac and systemic aging.
<P>PROBLEM TO BE SOLVED: To provide a resin cement comprising acid functionality and water, but not comprising an acid reactive filler.  <P>SOLUTION: Dental resin cement material having unique handling properties comprises (a) filler, (b) polymerizable resin, and (c) a polymeric handling modifier that is dispersed in the polymerizable resin at 25°C and that has a molecular weight of about 500-100,000. The components (a), (b), and (c) are present in an amount effective to achieve a viscosity-shear rate curve satisfying a power law of F(x)=Ax<SP>B</SP>. The correlation value of the material to the curve is greater than 0.85 for both the increasing and decreasing shear rate curves, and the value of B is smaller than about -0.01. Such cements are self-etching, thereby avoiding the need to carry out a separate acid etch step.  <P>COPYRIGHT: (C)2010,JPO&INPIT
Different etiologies can lead to chronic liver disease, and common causes include non-alcoholic fatty liver disease (NAFLD), hepatitis B virus (HBV), hepatitis C virus (HCV), alcohol-related liver disease (ALD), primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH). In recent years, with the popularization of HBV vaccination and the advancement of drugs for the treatment of viral hepatitis, the incidence of cirrhosis has been curbed in many countries, but obesity, metabolic syndrome and alcohol abuse have led to an increase in the incidence of NAFLD and ALD recently. The large number of patients with cirrhosis causes loss of social workforce and depletion of medical resources, as well as increased family stress and reduced quality of life. As a result of that, cirrhosis remains a public health problem that cannot be ignored.

To better understand the natural course and clinical characteristics of chronic liver disease due to different etiologies, this study proposes to establish a multicenter, large sample, long-term follow-up cohort of patients with chronic liver disease to improve the clinical data related to chronic liver disease in China. This cohort study will help us to better manage patients with chronic liver disease and build on this foundation for epidemiology, interventions, and prognosis of chronic liver disease. The cohort and experience generated from this study serves as a support for a series of future studies to focus on clinical issues such as low-level viremia, other complications of cirrhosis, liver failure, end-stage liver disease, and liver cancer.
LPS will be administered twice on days 1 and 7. In between GM-CSF will be administered on days 2, 4 and 6 subcutaneously.
AIM: To determine whether recent repeated exposure to real-life hypoglycaemia affects the pro-inflammatory response during a hypoglycemia episode.
MATERIALS AND METHODS: This was a post hoc analysis of a hyperinsulinaemic normoglycaemic-hypoglycaemic clamp study, involving 40 participants with type 1 diabetes. Glucose levels 1 week before the clamp were monitored using a Freestyle Libre 1. Blood was drawn during normoglycaemia and hypoglycaemia, and 24 hours after resolution of hypoglycaemia for measurements of inflammatory responses and counterregulatory hormone levels. We determined the relationship between the frequency and duration of spontaneous hypoglycaemia, and time below range (TBR) and the inflammatory response to experimental hypoglycaemia.
RESULTS: On average, participants experienced 0.79 (0.43, 1.14) hypoglycaemia episodes per day, with a duration of 78 (47, 110) minutes and TBR of 5.5% (2.8%, 8.5%). TBR and hypoglycaemia frequency were inversely associated with the increase in circulating granulocyte and lymphocyte counts during experimental hypoglycaemia (P < .05 for all). A protein network consisting of DNER, IF-R, uPA, Flt3L, FGF-5 and TWEAK was negatively associated with hypoglycaemia frequency (P < .05), but not with the adrenaline response. Neither other counterregulatory hormones, nor hypoglycaemia awareness status, was associated with any of the inflammatory parameters markers.
CONCLUSIONS: Repeated exposure to spontaneous hypoglycaemia is associated with blunted effects of subsequent experimental hypoglycaemia on circulating immune cells and the number of inflammatory proteins.
The no treatment control arm did not receive the intervention during the first six-month period. However the intervention, which has been proven to be beneficial, was administered to the control arm immediately following the 6 month assessment.
NIH 0 NH HN 0 N N I. Amid linkage H Hu- R R R 1l. Unsubstituted metal binding enterobachn I triscatecholate sideropohre 2 (R= H or Ac) oran Trarsaportdiated Dug D9eivery C IiV ~)OI~t dd(~II~ Am#001Ad snd AmaxkUiln Affdn~p@WrIJIn Cooqiupaieo Ahfi'psuadomomi V10,f 00 MRl And-psadimww KMCm4O54JO p Figure 1 An artificial tris-catecolate siderophore with a tripodal backbone and its conjugates with ampicillin and amoxicillin were synthesized. Both conjugates exhibited significantly enhanced in vitro antibacterial activities against Gram-negative species compared to the parent drugs, especially against P. aeruginosa. The conjugates appear to be assimilated by an induced bacterial iron transport process as their activities were inversely related to iron concentration. The easily synthesized tris catecolate siderophores can be used with a variety of drugs as conjugates to target antibiotic-resistant Gram-negative bacteria.
Inflammatory reaction plays a key role in the pathogenesis of hypoxic-ischemic encephalopathy (HIE) in neonates. Microglia are resident innate immune cells in the central nervous system and are profoundly involved in neuroinflammation. Studies have revealed that atorvastatin exerts a neuroprotective effect by regulating neuroinflammation in adult animal models of brain stroke and traumatic brain injury, but its role regarding damage to the developing brain remains unclear. This study aimed to clarify the effect and mechanism of atorvastatin on the regulation of microglia function in neonatal hypoxic-ischemic brain damage (HIBD). The oxygen glucose deprivation (OGD) of microglia and neonatal rat HIBD model was established. Atorvastatin, recombinant sclerostin protein (SOST), and XAV939 (degradation of β-catenin) were administered to OGD microglia and HIBD rats. The pathological changes of brain tissue, cerebral infarction volume, learning and memory ability of rats, pro-inflammatory (CD16+/Iba1+) and anti-inflammatory (CD206+/Iba1+) microglia markers, inflammation-related indicators (Inos, Tnfα, Il6, Arg1, Tgfb, and Mrc1), and Wnt/β-catenin signaling molecules were examined. Atorvastatin reduced OGD-induced pro-inflammatory microglia and pro-inflammatory factors, while increasing anti-inflammatory microglia and anti-inflammatory factors. In vivo, atorvastatin attenuated hypoxia-ischemia (HI)-induced neuroinflammation and brain damage. Mechanistically, atorvastatin decreased SOST expression and activated the Wnt/β-catenin signaling pathway, and the administration of recombinant SOST protein or XAV939 inhibited Wnt/β-catenin signaling and attenuated the anti-inflammatory effect of atorvastatin. Atorvastatin promotes the pro/anti-inflammatory phenotypic transformation of microglia via the Wnt/β-catenin pathway in HI neonatal rats. Atorvastatin may be developed as a potent agent for the treatment of HIE in neonates.
Buffered Pfizerpen (Penicillin G Potassium for Injection, USP) is a sterile, pyrogen-free powder for reconstitution. Buffered Pfizerpen for Injection is an antibacterial agent for intramuscular, continuous intravenous infusion, intrapleural or other local infusion, and intrathecal administration.

Each million units contains approximately 6.8 milligrams of sodium (0.3 mEq) and 65.6 milligrams of potassium (1.68 mEq). Buffered Pfizerpen (Penicillin G Potassium for Injection, USP) is supplied in vials equivalent to 5,000,000 units (5 million units) or 20,000,000 units (20 million units) of penicillin G as the potassium salt.

Chemically, Pfizerpen is monopotassium 3,3-dimethyl-7-oxo-6-(2-phenylacetamido)-4-thia-1-azabicyclo (3.2.0) heptane-2-carboxylate. It has a molecular weight of 372.48 and the following chemical structure:

Penicillin G potassium is a colorless or white crystal, or a white crystalline powder which is odorless, or practically so, and moderately hygroscopic. Penicillin G potassium is very soluble in water. The pH of the reconstituted product is between 6.0–8.5.
In five prospective randomized controlled clinical trials involving 3711 patients with non-rheumatic AF, warfarin significantly reduced the risk of systemic thromboembolism including stroke (See Table 2). The risk reduction ranged from 60% to 86% in all except one trial (CAFA: 45%) which stopped early due to published positive results from two of these trials. The incidence of major bleeding in these trials ranged from 0.6 to 2.7% (see table 2). Meta-analysis findings of these studies revealed that the effects of warfarin in reducing thromboembolic events including stroke were similar at either moderately high INR (2.0-4.5) or low INR (1.4-3.0). There was a significant reduction in minor bleeds at the low INR. Similar data from clinical studies in valvular atrial fibrillation patients are not available.
After ethics committee approval and informed consent from legal guardians and fulfilling inclusion criteria, critically ill paediatric patients scheduled for weaning will be randomized (in 1:1 allocation) to NPV (interventional group) or standard approach (without NPV) after extubation. NPV in paediatric patients after extubation could be associated with reduced incidence of weaning failure. The initial setting on NPV will be: negative pressure set to -10cmH2O and will proceed for minimal time of 60 minutes after extubation (will proceed longer in case of good tolerance). In case of hypoxaemia, additional oxygentherapy will be administered according to the patients condition Primary outcome will be defined as postextubation failure incidence at 60 minutes after extubation (defined as need of noninvasive positive pressure ventilation, intubation, or high-flow oxygen therapy) and the overall incidence of weaning failure during initial 24 hour after extubation. The secondary outcome will be the dynamics of blood gases (arterial or capillary blood sample) during initial 60 minutes after extubation (1. extubation, 2. 60 minutes after extubation) and the need of and amount of artificial oxygentherapy (litres of oxygen per minute, pulse oximetry). Another outcome will be the overall cuirass tolerance after 60 minutes and after 24 hours defined by incidence of skin lesions.
Acne vulgaris is a common, often chronic inflammatory disease that can affect all ages and skin tones. Beyond acute lesions, the sequelae of acne - specifically scarring and dyspigmentation - can be long-lasting, challenging to treat and have substantial psychosocial impact on affected individuals. For acne scarring, treatment modalities include topical, physical, and laser and light therapies, with combination approaches typically yielding optimal outcomes. Trifarotene is a novel fourth generation retinoid with targeted action towards retinoid acid receptor gamma (RAR-γ), the most common isotype found in the epidermis, that has previously been approved for the management of moderate-to-severe facial and truncal acne in individuals over the age of 12 years. Recently, data on trifarotene supports its application in acne scarring. Herein, we provide a succinct review on various treatments for acne scarring and explore how trifarotene and its mechanism of action present an additional topical approach to target atrophic acne scarring.