anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
This study consists of two parts which will be conducted in parallel. In the first part of the study, 14 subjects will be recruited for the Clinically Stable Cohort. Subjects will be asked to provide 1 gm of expectorated sputum and 40-ml of blood. A cell count and differential will be performed on the sputum followed by analysis for IL-17 PMNs by fluorescence-activated cell sorter (FACS). IL-17 PMNs also will be isolated by running the remainder of the cell pellet through a column of magnetic beads designed for this purpose. These neutrophils will be lysed and intracellular cytokines determined. Sputum supernatants will be stored frozen until analyzed for the presence of IL-1β, IL-6, IL-8, IL-17A, TGF-β, TNF-α, and neutrophil elastase. Clinical data will be captured from the subject's clinical outpatient visit including lung function measures and clinical culture results. IL-17 PMNs will be correlated with lung function measures and inflammatory mediators at baseline.

In the second part of this study, 10 subjects will be recruited for the Exacerbation Cohort. Subjects will provide at least 1 gram of expectorated sputum and 40-ml of blood within 72 hours of hospital admission. Sputum and blood will be processed and analyzed as described above. Sputum and blood also will be obtained at the end of treatment (within 72 hours of completion of IV antibiotics) when the subject is at his or her baseline as determined by the managing physician. Clinical data will be captured from the subject's hospitalization records including lung function measures and clinical culture results.
PURPOSE: A composition containing Camellia sinensis assamica extract for preventing and treating diabetic nephropathy is provided to reduce the total amount of albumin and protein. CONSTITUTION: A pharmaceutical composition for preventing and treating diabetic nephropathy contains Camellia sinensis assamica extract as an active ingredient. The Camellia sinensis assamica is fresh leaves or yellow tea. The Camellia sinensis assamica extract is extracted using water, low alcohol of C1-C4, or a mixture solvent thereof. A health food for preventing and treating diabetic nephropathy contains Camellia sinensis assamica extract as an active ingredient. The health food is used in the form of a powder, granule, tablet, capsule, or beverage.
The present invention teaches a convenient way of inducing a broad recognition of dominant and subdominant responses to epitopes of any given antigen of importance for prophylaxis or treatment of a chronic disease by immunizing with pools of overlapping fragments (synthetic peptides e.g. 10-30 mers with 2-20 aa overlap) of the desired antigen in appropriate adjuvants. The T cell repertoire is primed to include not only the immunodominant epitope recognized when the intact molecule is used for immunization and induced by the chronic infection itself, but induce a much broader and balanced response to a number of the subdominant epitopes as well. The resulting T-cell response to subdominant epitopes is important for protection against chronic diseases that on their own induces a response focused only towards immunodominant epitopes. The major advantage of the present invention is that it requires no prior knowledge of the precise localisation and identity of the subdominant epitopes and their recognition in a human population, but expands the T-cell repertoire and thereby the total number of epitopes recognized by specific T cells primed by vaccination from a few immunodominant epitopes to multiple of epitopes of vaccine relevance. For chronic disease controlled by humoral immunity the T helper cell response primed by the peptide mix may conveniently be boosted by the full size protein for maximum induction of an antibody response as well.
The first aim of the current project is to test the precision of AFI in the epidermis of 10 healthy volunteers. For this purpose, a range of nociceptive electrical stimuli with increasing intensities (5Hz @ 0.5mA-1.0mA) and one innocuous control stimulus (2000Hz @1mA) will be delivered to the third finger of each subject. The outcome measure is AFI-intensity, which is the change in autofluorescence intensity compared to baseline (delta F/F). The standard deviation of AFI intensity will be the measure of precision. Pearson's correlation coefficient will be calculated between electrical stimulus intensities and AFI intensity. A linear correlation needs to be confirmed, since this is a general characteristic of AFI. A paired t-tests will be performed to compare AFI intensities following 5Hz @ 1mA stimulation and 2000Hz @ 1mA stimulation. Lidocaine/prilocaine cream will be applied to the fingertips of the subjects and the electrical stimuli will be repeated, to serve as a negative control experiment. A repeated-measures ANOVA will be performed to compare AFI intensities before and after application of lidocaine/prilocaine cream.

The second aim of our study is to validate AFI in experimentally induced small nerve fiber degeneration of the epidermis, by comparing AFI intensities in subjects before and one week after application of a 8% capsaicin patch to the third fingertip. A repeated-measures ANOVA will be performed to compare AFI intensities before and after capsaicin-induced small nerve fiber degeneration. Assuming that all subjects develop epidermal small fiber degeneration following the 8% capsaicin patch, a statistically significant difference in AFI intensity would serve as a proof-of-principle and would provide validity to autofluorescent flavoprotein imaging of epidermal nociceptor activity as a diagnostic test for SFN. Comparing the distributions of before and after capsaicin-induced small nerve fiber degeneration will lead to a probability estimation of having SFN based on the outcome measure, i.e. AFI intensity. In future research, false-positive and false-negative consequences will be evaluated, leading to cut-off values in patients suspected for SFN.
This patent is for a kind of pharmaceutical formulation, used to treat insomnia, consisting of two compounds. The first compound is melatonin or a melatonin receptor agonist. The second is a hypnotic sedative, typically, but not necessarily, one that affects the brain's Gamma-aminobutyric acid A (GABAA) receptors. Examples include zopiclone (a cyclopyrrone), Zolpidem (an imidazopyridine), zaleplon (a pyrazolopyrimidine) and the older benzodiazepine drugs. The formulations are single-dose, meaning that both compounds are ingested at once, though depending on the individual composition, they may be designed to absorb into the bloodstream at differing rates. The melatonin acts by potentiating the second compound and reducing the quantity needed to initiate and maintain sleep. One aim of this is to minimise the dose used of the second compound, since many GABAA-receptor agonists are known to cause physical dependence, and discontinuation after long-term use often requires time-consuming dose reduction. Another aim is to reduce the time of sleep onset caused by the second compound.
Microvascular obstruction (MVO) is linked with adverse clinical outcome in acute coronary syndrome (ACS) patients, therefore, early prediction of MVO with non-invasive peripheral microcirculation is crucial in facilitating optimal treatment. Current study aims to analyze the significance of opisthenar microvessel area (OMA, measured using optical coherence tomography, OCT) in predicting coronary stenosis (Gensini score, GS) and short-term cardiac recovery of ACS patients and the results were compared to those of arterial stiffness parameters (Pulse Wave Velocity, PWV; Ankle-Brachial Index; ABI). Results showed that cardiac functional parameters (e.g. ejection fraction, EF; fractional shortening, FS) and OMA were higher in normal/low risk (GS 0-≤ 20, n = 69) compared to medium/high risk patients (GS > 20, n = 44, P < 0.0001). Furthermore, OMA, EF or FS was negatively associated with the severity of coronary stenosis (P < 0.0001). In addition, OMA was negatively correlated with heart and liver damage parameters (e.g. creatine kinase, CK; creatine kinase muscle brain, CKmB; lactate dehydrogenase, LDH; hydroxybutyrate dehydrogenase, HDBH; aspartate aminotransferase, AST; alanine aminotransferase, ALT) or with inflammatory markers (neutrophil, neutrophil/lymphocyte ratio, NEU, NEU/LYM (NLR); systemic immune inflammation index, SII and system inflammation response index, SIRI), indicating clinical significance of OMA. Conversely, PWV and ABI were not associated with coronary stenosis or organ damage markers. Receiver Operator Characteristic (ROC) analysis showed high specificity and sensitivity of OMA for coronary stenosis (specificity 0.864 or sensitivity 0.87). In conclusion, OMA shows negative associations with the severity of coronary stenosis and adverse clinical parameters indicate that microcirculation measurement from opisthenar possesses prognostic value for severe ACS patients.
A medical data authentication system, a medical data authentication method, and a computer program product thereof are disclosed. The medical data authentication system includes a data establishment module, a signature module, a blockchain establishment module, and an authorization code generation module. The data establishment module is used for establishing a medical data. The signature module is used for receiving the medical data to obtain a medical digital signature. The blockchain establishment module is used for uploading the medical digital signature to a medical blockchain. The authorization code generation module is used for obtaining the medical digital signature from the medical blockchain to generate a corresponding authentication authorization code.
Cohort 2 will consist of the remaining target size population of 230 patients for H1 Hip Resurfacing Arthroplasty. They will undergo the same intervention as previously described for Cohort 1, but will not undergo metal-ion testing and reduced frequency CT-scans.
In the Experimental Group, Mirror Therapy will be applied by covering any birthmarks or scars on the less affected lower extremity (LE) if they obstruct the child's view. The therapy will take place in a distraction-free environment to help each child maintain focus and concentration. A mirror, at least 35 × 25 inches in size, will be placed between both LEs, with the more affected LE concealed behind a black curtain, allowing a clear reflection of the less affected LE. The child will be instructed to observe the mirror image of their more affected LE for one to two minutes. To begin, the therapist will visually demonstrate the technique.
Skeletal muscle unloading occurs during a wide range of conditions, from space flight to bed rest. The unloaded muscle undergoes negative functional changes, which include increased fatigue. The mechanisms of unloading-induced fatigue are far from complete understanding and cannot be explained by muscle atrophy only. In this review, we summarize the data concerning unloading-induced fatigue in different muscles and different unloading models and provide several potential mechanisms of unloading-induced fatigue based on recent experimental data. The unloading-induced changes leading to increased fatigue include both neurobiological and intramuscular processes. The development of intramuscular fatigue seems to be mainly contributed by the transformation of soleus muscle fibers from a fatigue-resistant, "oxidative" "slow" phenotype to a "fast" "glycolytic" one. This process includes slow-to-fast fiber-type shift and mitochondrial density decline, as well as the disruption of activating signaling interconnections between slow-type myosin expression and mitochondrial biogenesis. A vast pool of relevant literature suggests that these events are triggered by the inactivation of muscle fibers in the early stages of muscle unloading, leading to the accumulation of high-energy phosphates and calcium ions in the myoplasm, as well as NO decrease. Disturbance of these secondary messengers leads to structural changes in muscles that, in turn, cause increased fatigue.
The usual adult dose is one amoxicillin and clavulanate potassium tablet, 500 mg/125 mg every 12 hours or one amoxicillin and clavulanate potassium tablet, 250 mg/125 mg every 8 hours. For more severe infections and infections of the respiratory tract, the dose should be one amoxicillin and clavulanate potassium tablet, 875 mg/125 mg every 12 hours or one amoxicillin and clavulanate potassium tablet, 500 mg/125 mg every 8 hours. Adults who have difficulty swallowing may be given the 125 mg/5 mL or 250 mg/5 mL suspension in place of the 500 mg/125 mg tablet. The 200 mg/5 mL suspension or the 400 mg/5 mL suspension may be used in place of the 875 mg/125 mg tablet. 

Two 250 mg/125 mg tablets of amoxicillin and clavulanate potassium should not be substituted for one 500 mg/125 mg tablet of amoxicillin and clavulanate potassium. Since both the 250 mg/125 mg and 500 mg/125 mg tablets of amoxicillin and clavulanate potassium contain the same amount of clavulanic acid (125 mg, as the potassium salt), two 250 mg/125 mg tablets are not equivalent to one 500 mg/125 mg tablet of amoxicillin and clavulanate potassium. 

The 250 mg/125 mg tablet of amoxicillin and clavulanate potassium and the 250 mg/62.5 mg chewable tablet should not be substituted for each other, as they are not interchangeable. The 250 mg/125 mg tablet of amoxicillin and clavulanate potassium and the 250 mg/62.5 mg chewable tablet do not contain the same amount of clavulanic acid (as the potassium salt). The 250 mg/125 mg tablet of amoxicillin and clavulanate potassium contains 125 mg of clavulanic acid, whereas the 250 mg/62.5 mg chewable tablet contains 62.5 mg of clavulanic acid.
SARS-CoV-2 infection is associated with excessive inflammation and cytokine storm that can result in lung damage and potentially severe disease. SP16 is an anti-inflammatory and homeostatic drug that rebalances innate immune responses potentially resulting in mitigation of inflammation and lung damage without immunosuppressive effects. SP16's mechanism of action is through targeting LRP1, a receptor that regulates a variety of physiological processes that contribute to inflammation and tissue injury, particularly in the lung. The main objective of this study is to determine the safety and tolerability, and effects on inflammation of SP16 administered subcutaneously at a dose of 6 mg (0.1 mg/kg) or 12 mg (0.2 mg/kg). SP16 has previously been well tolerated in both healthy individuals and heart attack patients at a dose of 0.2 mg/kg. The study will also evaluate improvements in clinical parameters such as patients requiring ventilation, improvement in blood oxygen levels (as defined by both SpO2 \> 95% and respiratory rate ≤ 20/minute) and duration of hospitalization or time spent in the Intensive Care Unit (ICU).
FIELD: medicine. SUBSTANCE: agent is an oligomeric product of chitin deacetylation or their pharmaceutically acceptable salts. Preferable polymerization degree of oligomeric products is 4-8. Agent can contain additionally pharmaceutically acceptable special additions and biologically active substances of other effect. Agent shows effective and nontoxic product producing from natural raw and can be used for treatment of patients with bronchial asthma and diseases where leukocytes take part an essential role in pathogenesis process. EFFECT: enhanced effectiveness of an agent. 4 cl, 1 tbl, 1 dwg, 7 ex
Cardiogenic shock (CS) is characterized by impaired cardiac function, very high mortality, and limited treatment options. The proinflammatory signaling during different phases of CS is incompletely understood. We collected serum and plasma (n = 44) as well as freshly isolated peripheral blood mononuclear cells (PBMCs, n = 7) of patients with CS complicating acute myocardial infarction on admission and after revascularization (24, 48, and 72 h) and of healthy controls (serum and plasma, n = 75; PBMCs, n = 12). PBMCs of patients with CS had increased gene expression of NLRP3, CASP1, PYCARD, IL1B, and IL18 and showed increased rates of pyroptosis (control, 4.7 ± 0.3 vs. 9.9 ± 1.7% in patients with CS, P = 0.02). Serum interleukin (IL)-1β levels were increased after revascularization. IL-18 and IL-6 were higher in patients with CS than in healthy controls but comparable before and after revascularization. Proinflammatory apoptosis-associated speck-like proteins containing CARD (ASC) specks were elevated in the serum of patients with CS on admission and increased after revascularization (admission, 11.1 ± 4.4 specks/µL; after 24 h, 19.0 ± 3.9, P = 0.02). ASC specks showed a significant association with 30-day mortality in patients with CS (P < 0.05). The estimated regression coefficients and odds ratios indicated a positive relationship between ASC specks and mortality (odds ratio: 1.029, 95% confidence interval, 1.000 to 1.072; P = 0.02). Pyroptosis and circulating ASC specks are increased in patients with CS and are particularly induced after reperfusion. This underscores their potential role as a biomarker for poor outcomes in patients with CS. ASC specks represent promising new therapeutic targets for patients with CS with high inflammatory burden.NEW & NOTEWORTHY The expression of NLR family pyrin domain containing-3 (NLRP3) inflammasome-related genes and the rate of pyroptosis are increased in PBMCs from patients with CS. Furthermore, patients with CS are characterized by higher serum concentrations of ASC specks and IL-1β, IL-6, and IL-18. This current study adds circulating ASC specks to the portfolio of biomarkers for the identification of patients with a high inflammatory burden paving the way for precision medicine approaches to improve clinical outcomes.
General practitioners (n = 10), outpatient psychiatrists and psychologists (n = 10) and their patients (n = 20) will be involved. First, partly structured interviews will be conducted with the general practitioners and the psychiatric/psychological professionals as well as the patients they treat in order to record their perspectives on digital health services and the role of digital navigators. In parallel, focus groups will be organized with all three main groups to understand their opinions, concerns and expectations regarding the use of digital health applications and digital navigators. The data collection for the preliminary study extends over a period of 3 months (October - December 2024).
Crystalline silica (CS) particle exposure leads to silicosis which is characterized as progressive fibrosis. Fibroblasts are vital effector cells in fibrogenesis. Emerging studies have identified immune sentinel roles for fibroblasts in chronic disease, while their immune-modulatory roles in silicosis remain unclear. Herein, we show that group 2 innate lymphoid cell (ILC2) conversion to ILC1s is closely involved in silicosis progression, which is mediated by activated fibroblasts via interleukin (IL)-18. Mechanistically, Notch3 signaling in mechanics-activated fibroblasts modulates IL-18 production via caspase 1 activity. The mouse-specific Notch3 knockout in fibroblasts retards pulmonary fibrosis progression that is linked to attenuated ILC conversion. Our results indicate that activated fibroblasts in silicotic lungs are regulators of ILC2-ILC1 conversion, associated with silicosis progression via the Notch3-IL-18 signaling axis. This finding broadens our understanding of immune-modulatory mechanisms in silicosis, and indicates potential therapeutic targets for lung fibrotic diseases.
Eating and sleeping behaviour are known to interact with each other, yet research is limited in the context of menopausal women. The aim of this study was to examine whether menopausal status is associated with perceived problems in sleeping. Furthermore, we studied different aspects of eating behaviour as potential risk factors for poor sleep in menopausal women. The present study is exploratory in nature, thus the results should be interpreted as hypothesis-generating. We analysed the sleeping and eating behaviour of 1098 women aged 47-55 years and represented different menopausal statuses with regression analyses. Over 20% of them reported fairly poor or poor perceived sleep quality. A higher number of postmenopausal women reported experiencing at least fairly poor sleep quality compared with the other menopausal groups. However, in regression models controlled for several confounding factors menopausal status was not associated with measures of sleep. Women who reported more snacking-type eating behaviour were more likely to report shorter sleep duration, and more daytime tiredness. Externally cued eating was associated with shorter sleep duration and emotional eating was associated with experiencing daytime tiredness. However, after adjusting for multiple testing, it appears that eating behaviour is associated only with daytime tiredness. Menopausal women with sleeping problems may benefit from nutritional interventions targeting eating behaviour.
Isatuximab will be administered in combination with carfilzomib and dexamethasone. Isatuximab will be administered via OBDS from Cycle 1 to 3. For Cycle 4 to 6, the method of administration will be switched for each participant from OBDS to manual administration. From Cycle 7 and onwards, participants can choose manual or OBDS. Participants may receive other treatments as rescue medication or background medication.
Ubiquitin modifications alter protein function and stability, thereby regulating cell homeostasis and viability, particularly under stress. Ischemic stroke induces protein ubiquitination at the ischemic periphery, wherein cells remain viable, however the identity of ubiquitinated proteins is unknown. Here, we employed a proteomics approach to identify these proteins in mice undergoing ischemic stroke. The data are available in a searchable web interface ( https://hochrainerlab.shinyapps.io/StrokeUbiOmics/ ). We detected increased ubiquitination of 198 proteins, many of which localize to the postsynaptic density (PSD) of glutamatergic neurons. Among these were proteins essential for maintaining PSD architecture, such as PSD95, as well as NMDA and AMPA receptor subunits. The largest enzymatic group at the PSD with elevated post-ischemic ubiquitination were kinases, such as CaMKII, PKC, Cdk5, and Pyk2, whose aberrant activities are well-known to contribute to post-ischemic neuronal death. Concurrent phospho-proteomics revealed altered PSD-associated phosphorylation patterns, indicative of modified kinase activities following stroke. PSD-located CaMKII, PKC, and Cdk5 activities were decreased while Pyk2 activity was increased after stroke. Removal of ubiquitin restored kinase activities to pre-stroke levels, identifying ubiquitination as the responsible molecular mechanism for post-ischemic kinase regulation. These findings unveil a previously unrecognized role of ubiquitination in the regulation of essential kinases involved in ischemic injury.