anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Repetitive transcranial magnetic stimulation (rTMS) is an established therapy for treatment-resistant depression. The approved method for treatment is 10Hz stimulation for 40 min over the left dorsolateral prefrontal cortex (L-DLPFC). This methodology has been effective in real world situations. The limitations of this approach include the duration of the treatment (approximately 40 minutes per treatment session, 5 days per week, for 4-8 weeks). Recently, the investigators have pursued modifying the treatment parameters to reduce treatment times with an accelerated treatment paradigm. This study aims to further study the accelerated protocol and examine changes in neuroimaging biomarkers.
Subjects will be asked to exercise 5 days/week for 30 min/day at an intensity of 65-85% of their measured HRmax. Walking will be the main type of exercise. In addition to this training program, subject's will participate in the standard education sessions that are provided to all bariatric surgery patients.
Each subject completed a total of 2 2.8 hr-long clamping sessions.Within each session, procedures differed only by the content of the infusate. In one session, 6% ethanol was infused. In the other session, only vehicle was infused, quantifying the placebo response for every subject. The order of alcohol or placebo sessions was counterbalanced; subjects were blind to which session was which; sessions were scheduled to occur approximately 2 weeks apart. Measures were collected before, and at beginning and end of infusion, and included subjective perceptions, EMG, EEG, stop-signal performance, eye movements, and auditory responses. Design allowed analysis of effect of alcohol vs placebo, initial effect of alcohol and acute tolerance to alcohol.
Reslizumab 3.0 milligrams/kilogram (mg/kg) will be administered by intravenous (IV) infusion, over 20 to 50 minutes, at Baseline (Day 1) of Part 2. PET/CT scan will be done on Weeks 2, 4 and 6. Participants will receive FDG as part of the PET/CT procedures and will provide sputum/blood samples.
The invention discloses a method for purifying body-surface fungal diseases of livestock in a livestock farm at a time. The method is characterized in that fungal disease pathogens in the body surfaces and environments of rabbits are killed at a time by using a medicine to achieve the aim of purifying epidemic diseases in the livestock farm. By virtue of natural infection, artificial infection, observation of infection focuses of baby rabbits, young rabbits and adult rabbits, separation of body-surface and in-vivo pathogenic fungi, observation of the effects of series prevention and treatment methods and analysis of the susceptibility of the rabbits of different day ages, a propagation mode and a propagation medium of body-surface fungal diseases and a body-surface fungal parasitism mechanism are determined; a medicine for purification is screened out, the dosage is determined, and a using method of the medicine is adopted. The cost is equal to the full one-time sterilization cost, and the method is simple and easy to operate. The method is applicable to purification of the body-surface fungal diseases of pigs, cattle, sheep, rabbits, dogs, cats, horses, mules, donkeys and other special animals in the livestock farm. A simple livestock farm of which colony houses are non-standard in design and construction is needed to be repeatedly reinforced when the method is applied, so that the aim of purification can be achieved.
There have been several cases of drug maladministration of intravenous pamidronate disodium in hypercalcemia patients with total doses of 225 mg to 300 mg given over 2 1/2 to 4 days. All of these patients survived, but they experienced hypocalcemia that required intravenous and/or oral administration of calcium. Single doses of pamidronate disodium should not exceed 90 mg and the duration of the intravenous infusion should be no less than 2 hours (see WARNINGS).

In addition, one obese woman (95 kg) who was treated with 285 mg of pamidronate disodium/day for 3 days experienced high fever (39.5°C), hypotension (from 170/90 mmHg to 90/60 mmHg), and transient taste perversion, noted about 6 hours after the first infusion. The fever and hypotension were rapidly corrected with steroids.

If overdosage occurs, symptomatic hypocalcemia could also result; such patients should be treated with short-term intravenous calcium.
The invention provides an (aza)indolizine derivative and the pharmaceutical use thereof. Specifically, disclosed is a compound which is useful as a prophylactic or therapeutic agent for diseases or the like caused by abnormal serum urate level. An (aza)indolizine derivative represented by formula (I), said (aza)indolizine derivative having a xanthine oxidase inhibitory activity and being useful as a prophylactic or therapeutic agent for diseases caused by abnormal serum urate level, a prodrug thereof or a salt, etc. of the same. In formula (I), 0 to 2 of X1 to X4 represent a nitrogen atom and the remainder represent CR1; one of T1 and T2 represents cyano while the other represents a group represented by formula (A) [provided that when T1 is cyano, at least one of X1 to X4 represents a nitrogen atom]; R1s independently represent a hydrogen atom, a halogen atom, a hydroxyl group, C1-6 alkyl, C1-6 alkoxy, etc.; the ring U represents a benzene ring, etc.; m is an integer of 0 to 2; and R2s independently represent a fluorine atom, a hydroxyl group, etc.
The aim of this study is to identify the key biomarker of keloid (KD) with significant diagnostic value and to construct the related competing endogenous RNA (ceRNA) network and disease diagnostic model to provide new ideas for the early diagnosis and prevention of KD. Public databases were used to identify the key gene of KD. Enrichment analysis and immune cell infiltration (ICI) analysis revealed its functional and immune characteristics. Then, a ceRNA network was constructed to explore the potential pathways of it. Random forest (RF) analysis was applied to construct a predictive model for the disease diagnosis of KD. Finally, immunohistochemistry (IHC) and RT-qPCR were used to verify the differential expression of key gene. ERRFI1 was identified as a key biomarker in KD and was lowly expressed in KD. The ceRNA network revealed that H0TAIRM1-has-miR-148a-3p-ERRFI1 may be a potential pathway in KD. Finally, a 2-gene diagnostic prediction model (ERRFI1, HSD3B7) was constructed and externally validated and the results suggested that the model had good diagnostic performance. ERRFI1 is a downregulated gene in KD and is expected to be a promising predictive marker and disease diagnostic gene. ICI may play a role in the progression of KD. The ceRNA network may provide new clues to the potential pathogenesis of KD. Finally, the new KD diagnostic model could be an effective tool for assessing the risk of KD development.
An anticarcinogen slow-released membranous bracket is controllable and degradable. The utility model consists of a degradable bracket, an outer anticarcinogen slow-released membranous layer and an inner anticarcinogen slow-released membrane layer. The degradable bracket is equipped with the outer anticarcinogen slow-released membranous layer on the outer layer and the inner anticarcinogen slow-released membranous layer on the inner layer. The curative effect is determined by concentration (C) and time (T); in other words, the curative effect is determined by concentration multiplying time. The technique of anticarcinogen slow-released membranous bracket is the embodiment of the conception and flavors the partial treatment for tumor. The utility model is made up of medical high molecular polymer with good characteristics of physic, chemistry, mechanism and anti-aging. Human body has rejection action to foreign tissue, causing serious consequence. The implanting material of high molecular polymer should adapt to the environment without inflammation, rejection reaction, carcinogenesis, teratogenesis or mutagenicity. The utility model is simple in structure, easy in manipulation and consistent to biologic environment. Moreover, the utility model is safe, reliable, and degradable, without any side effects.
BACKGROUND: Periprosthetic joint infection (PJI) following total hip arthroplasty (THA) is associated with major morbidity. There may be a link between the gut microbiome and an individual's overall immune system. A Clostridium difficile (C. difficile) infection portends poor gut microbiome health and has been previously associated with increased 90-day complication rates in total joint arthroplasty (TJA). The purpose of this study was to determine the effect of a previous history of C. difficile infection within 2 years of undergoing THA on PJI within 2 years postoperatively.
METHODS: Patients undergoing THA from 2010 to 2021 were identified in a patient claims database (n = 770,075). Patients who had active records 2 years before and after THA as well as a history of C. difficile infection within 2 years prior to THA (n = 1,836) were included and propensity matched to a control group using age, sex, and Elixhauser comorbidity index. The primary outcome was the 2-year incidence of postoperative PJI. The exposed C. difficile infection cohort was stratified into 4 groups based on the time proximity of the C. difficile infection. Chi-square tests and logistic regressions were used to compare the groups.
RESULTS: A C. difficile infection anytime within 2 years prior to total hip arthroplasty was independently associated with higher odds of PJI (OR [odds ratio]: 1.49 [95% CI (confidence interval) 1.09 to 2.02, P = .014]). Proximity of C. difficile infection to arthroplasty was associated with increased risk of PJI (infection 0 to 3 months before THA: OR 2.01 [95% CI 1.23 to 3.20], infection 3 to 6 months before THA: OR 1.84 [95% CI 1.06 to 3.04], infection 6 to 12 months before THA: OR 1.10 [95% CI 0.65 to 1.77], infection 1 to 2 years before THA: OR 1.40 [95% CI 0.94 to 2.06]).
CONCLUSIONS: A C. difficile infection prior to THA is an independent risk factor for PJI. Proximity of C. difficile infection is associated with increased risk of PJI. Future investigations should evaluate how to adequately optimize patients prior to THA and pursue strategies to determine appropriate timing for proceeding with THA.
An organ preservation and/or perfusion solution for an isolated tissue or organ is provided. The solution comprises dextran, glucose, calcium ions, a buffer, and water, has a pH of 6.6 to 7.8, and is sterile based on having been subjected to heat sterilization. A method of preparing the solution also is provided. The method comprises combining dextran, glucose, calcium ions, buffer, and water to obtain an initial solution, adjusting the pH of the initial solution to 7.0 to 7.8 if needed, and subjecting the initial solution to heat sterilization, thereby obtaining the organ preservation and/or perfusion solution. A method of preserving and/or perfusing an isolated tissue or organ also is provided. A method for flushing, storage, and/or transportation of an isolated lung after removal from a donor in preparation for eventual transplantation into a recipient also is provided.
###  Risk Summary

There is no information regarding the presence of pretomanid in human milk, or its effects on milk production or the breastfed infant. Pretomanid was detected in rat milk (see Data). When a drug is present in animal milk, it is likely that the drug will be present in human milk. Because of the potential for adverse reactions in nursing infants, the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for Pretomanid Tablets and any potential adverse effects on the breastfed infant from Pretomanid Tablets or from the underlying maternal condition. When Pretomanid Tablets are administered in combination with bedaquiline and linezolid, information on lactation for bedaquiline and linezolid also applies to this combination regimen. Refer to the bedaquiline and linezolid prescribing information for more information on their use during lactation. 

###  Data

#### Animal Data 

In a pre- and postnatal development study in rats treated with pretomanid at doses 0.5 and 2 times the human exposure for a 200 mg dose (AUC) from gestational day 7 through lactation day 20, concentrations in milk on lactation day 14 were 1.4 and 1.6 times higher than the maximum concentration observed in maternal plasma, respectively. The concentration of pretomanid in rat milk does not necessarily predict the concentration of pretomanid in human milk.
The invention relates to a therapeutic polypeptide for increasing resistance to infections and stress and without substantial pyrogenic or antigenic action, recovered from yeast-cell wall material, being substantially free from polypeptides of molecular weight less than 1000, being heat stable at least up to 100 DEG C., being soluble in liquid phenol, in water and in aqueous bases, being precipitatable from aqueous solution by phosphotungstic acid and sulphosalicylic acid, showing a yellow-green fluorescence and containing the following amino acids in polypeptide form namely glutamic and aspartic acids, argimine, lysine, alanine serine, valine, leucine, isoleucine, glycine, phenylalanine histidine, proline, tyrosine and threobine, being substantially free from combined phosphorus exhibiting a positive anthrone and biuret reaction and having an antimitotic effect against He La and Chang cells.  Preferably the polypeptide is free from polypeptides having a molecular weight less than 8000.  It may be isolated from zymosan, a substantially protein-and carbohydrate-free water-insoluble yeast cell-wall product, by extraction with 90% aqueous phenol at 37 DEG C., followed by treatment of the extract with water-ether, separation of the water layer, addition of NH40H to solubilize any insolubles, treatment with ether to remove traces of phenol and freeze-drying. Alternatively, zymosan may be treated with NaOH for 24 hours, the supernatant separated and neutralized, concentrated and filtered. The solution was purified by fractionation or a Sephadex G50 column equilibrated with water-containing 0.3% cresol.  Further purification may be by dialysis and ultrafiltration.  The therapeutic polypeptide may be formulated into compositions for oral, parenteral, topical and rectal administration.
Type 1 diabetes (T1D) results from a complex interplay of genetic predisposition, immunological dysregulation, and environmental triggers, that culminate in the destruction of insulin-secreting pancreatic β cells. This review provides a comprehensive examination of the multiple factors underpinning T1D pathogenesis, to elucidate key mechanisms and potential therapeutic targets. Beginning with an exploration of genetic risk factors, we dissect the roles of human leukocyte antigen (HLA) haplotypes and non-HLA gene variants associated with T1D susceptibility. Mechanistic insights gleaned from the NOD mouse model provide valuable parallels to the human disease, particularly immunological intricacies underlying β cell-directed autoimmunity. Immunological drivers of T1D pathogenesis are examined, highlighting the pivotal contributions of both effector and regulatory T cells and the multiple functions of B cells and autoantibodies in β-cell destruction. Furthermore, the impact of environmental risk factors, notably modulation of host immune development by the intestinal microbiome, is examined. Lastly, the review probes human longitudinal studies, unveiling the dynamic interplay between mucosal immunity, systemic antimicrobial antibody responses, and the trajectories of T1D development. Insights garnered from these interconnected factors pave the way for targeted interventions and the identification of biomarkers to enhance T1D management and prevention strategies.
An aspect is a method of improving sleep quality and/or subsequent behavioural outcomes. Another aspect is amethod of treating, preventing, and/or reducing at least one of risk, incidence or severity of at least one condition for which improved sleep quality is beneficial. The methods include orally administering a composition to an individual at a predetermined time before consumption of a meal and/or concurrently with consumption of a meal. The combination of the composition and the meal has a glycemic load that is lower than that of the meal and about 0.0 to about 45.0. Preferably the meal is a balanced evening meal, and the composition is a food, a supplement, or a liquid beverage, for example a ready to drink beverage or a beverage reconstituted from a powder. The composition can contain one or more of tryptophan, a glucosidase inhibitor, arginine-proline (AP) dipeptide, a fiber, a resistant starch, a beta-glucan, A-cyclodextrin, glucosidase, a polyphenol, or an amylase inhibitor..
PROBLEM TO BE SOLVED: To obtain a kneaded composition by blending a specific resin with powder or further adding alkali water, providing highly pigment dispersing effect without damaging characteristics such as adhesiveness, film strength, etc., of a product, useful as a cosmetic. SOLUTION: This kneaded composition is obtained by blending an anionic acrylic resin (especially preferably one having 30-350 acid value) with powder. The resin is a copolymer composed of acrylic acid, methacrylic acid or their alkyl ester. Talc, kaolin, nylon powder, titanium oxide, etc., may be cited as the power. The blending ratio of the anionic acrylic resin and powder is 5-90wt.%, especially 10-80wt.% of the resin and 10-95wt.%, especially 20-90wt.% of the powder. When a volatile base such as ammonia is used as alkali water, preferably the composition has water resistance. The composition is adjusted to pH5 to pH9. The amount of the composition added to a cosmetic is 0.01-60wt.%, especially about 0.1-40wt.%.
Abdominal ultrasound is a key non-invasive imaging method for diagnosing liver, kidney, and gallbladder diseases, despite its clinical significance, not all individuals can undergo abdominal ultrasonography during routine health check-ups due to limitations in equipment, cost, and time. This study aims to use basic physical examination data to predict the risk of diseases of the liver, kidney, and gallbladder that can be diagnosed via abdominal ultrasound. Basic physical examination data contain gender, age, height, weight, BMI, pulse, systolic blood pressure (SBP), diastolic blood pressure (DBP), high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol, triglycerides, fasting blood glucose (FBG), and uric acid-we established seven single-label predictive models and one multi-label predictive model. These models were specifically designed to predict a range of abdominal diseases. The single-label models, utilizing the XGBoost algorithm, targeted diseases such as fatty liver (with an Area Under the Curve (AUC) of 0.9344), liver deposits (AUC: 0.8221), liver cysts (AUC: 0.7928), gallbladder polyps (AUC: 0.7508), kidney stones (AUC: 0.7853), kidney cysts (AUC: 0.8241), and kidney crystals (AUC: 0.7536). Furthermore, a comprehensive multi-label model, capable of predicting multiple conditions simultaneously, was established by FCN and achieved an AUC of 0.6344. We conducted interpretability analysis on these models to enhance their understanding and applicability in clinical settings. The insights gained from this analysis are crucial for the development of targeted disease prevention strategies. This study represents a significant advancement in utilizing physical examination data to predict ultrasound results, offering a novel approach to early diagnosis and prevention of abdominal diseases.
The invention relates to a medicine for treating gall-stone and muddy gall-stone. The medicine is prepared from 15-20g of herba glechomae longitubae, 10-15g of carapax trionycis, 15-20g of endothelium corneum gigeriae galli, 15-20g of radix seu cortex acanthopanacis trifoliati, 30-50g of corn stigma, 30-50g of herba lysimachiae and 20-30g of radix clematidis by crushing and mixing. The medicine is obtained by matching of the pure natural medicinal materials and has functions of removing toxins and relieving swelling, clearing heat and draining dampness, thawing stone, benefiting gallbladder and expelling stone. The medicine can promote full dredging of bile stasis, eliminate bacterial infection and change bile components. Through use of the medicine, whatever a disease cycle is long or short, the gall-stone and muddy gall-stone can be eliminated and a recurrence rate is zero. The medicine has a short treatment course and produces effects fast. The medicine does not produce adverse action on stomach and kidney functions and avoids operation pain.
An apparatus for predicting a physiological indicator is disclosed. The apparatus comprises a processor and a memory communicatively connected to the at least a processor. The memory instructs the processor to receive a time series input from a user. The memory instructs the processor to predict a physiological indicator as a function of the time series input using a prediction machine learning model. The memory instructs the processor to generate an uncertainty metric as a function of the physiological indicator. Wherein determining the physiological indicator includes receiving a plurality of prediction training data. Determining the physiological indicator includes fitting the plurality of prediction training data with a kernel density estimate. Determining the physiological indicator additionally includes training the prediction machine learning model using a plurality of prediction training data. Training the prediction machine learning model includes, using the kernel density estimate, assigning a weight to each time series input.
Metabolic acidosis is a frequent complication of chronic kidney disease and is associated with a number of adverse outcomes, including worsening kidney function, poor musculoskeletal health, cardiovascular events, and death. Mechanisms that prevent metabolic acidosis detrimentally promote further kidney damage, creating a cycle between acid accumulation and acid-mediated kidney injury. Disrupting this cycle through the provision of alkali, most commonly using sodium bicarbonate, is hypothesized to preserve kidney function while also mitigating adverse effects of excess acid on bone and muscle. However, results from clinical trials have been conflicting. There is also significant interest to determine whether sodium bicarbonate might improve patient outcomes for those who do not have overt metabolic acidosis. Such individuals are hypothesized to be experiencing acid-mediated organ damage despite having a normal serum bicarbonate concentration, a state often referred to as subclinical metabolic acidosis. Results from small- to medium-sized trials in individuals with subclinical metabolic acidosis have also been inconclusive. Well-powered clinical trials to determine the efficacy and safety of sodium bicarbonate are necessary to determine if this intervention improves patient outcomes.