anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
It is known that one cause of TMD symptom development is treatment for head and neck cancer (HNC). The main treatment modalities for HNC include radiotherapy (RT) with or without chemotherapy and surgical intervention, either as a single therapy or a combination therapy. In the head and neck region, the anatomical structures are necessary for essential functions such as speech, swallowing, breathing, smell, and taste. The treatment of head and neck tumours may frequently impair some of these functions, which may result in pain, oral dysfunction, and impaired health-related quality of life.

High intensity laser therapy (HILT) is a non-invasive and painless treatment method. The latest studies have reported the beneficial effects of neodymium-doped yttrium aluminum garnet (Nd: YAG) laser therapy in patients with pain. The advantage of HILT over low level laser therapy (LLLT) is that HILT is able to penetrate and stimulate wider and/or deeper areas; thus, considerably more energy may be transmitted to tissue during HILT therapy compared to LLLT.
In spite of adequate blood pressure control and diet, 30 percent of patients with IgA nephropathy continue to secrete large amounts of protein in the urine and have a high likelihood of progressing to end-stage renal disease over 5-10 years and eventually requiring dialysis or kidney transplant. In IgA nephropathy, the injured kidney tissue secretes a messenger that recruits white blood cells (leukocytes) into the kidney. This messenger is the chemokine, CCL2. As a consequence CCL2 also is excreted into the urine and can be measured as evidence of inflammation in the kidney. This study evaluates the safety of a new potential therapy,CCL2-LPM (leukocyte population modulator), for IgA nephropathy. CCL2-LPM is composed of the messenger chemokine, CCL2, fused to an enzyme that inhibits protein production by the leukocytes and prevents the leukocytes from migrating into the kidney. The CCL2 end of the molecule targets only a small subset of leukocytes that have the corresponding receptor for CCL2 on the surface. After CCL2 binds to its receptor it is drawn inside the cell and carries the enzyme into the cell. The targeted cells are prevented from entering the kidney and causing further damage. Thus, CCL2-LPM may interrupt the ongoing cycle of inflammation that leads to end-stage renal disease.
Gastrointestinal involvement in systemic sclerosis can be severe, reaching the critical point of chronic intestinal pseudo-obstruction, secondary to major disorders of small bowel motility. It is associated with some clinical and biological characteristics, in particular the positivity of anti-fibrillarin/U3RNP antibodies. Chronic intestinal pseudo-obstruction (CIPO) is complicated by a small intestinal bacterial overgrowth that requires cyclic antibiotic therapy. CIPO leads to a reduction of the food intake, due to painful symptoms, nausea and vomiting caused by meals, and ultimately to severe malnutrition. Meal splitting is often transiently effective and patients require exogenous nutritional support, mostly parenteral. Systemic sclerosis is not an obstacle to initiation and long-term continuation of parenteral nutrition and central venous catheter implantation is not associated with an increased risk of cutaneous or infectious complications. However, continuation of long-term parenteral nutrition requires monitoring in an expert nutrition center in order to adapt nutritional volumes and intakes and to limit potentially fatal cardiac and hepatobiliary complications. In addition to nutrition, prokinetic treatments, whose side effects must be known, can be associated. Invasive procedures, whose risk-benefit ratio must be carefully assessed, can also be used to treat symptoms exclusively.
The aryl hydrocarbon receptor (AhR) is a versatile environmental sensor and transcription factor found throughout the body, responding to a wide range of small molecules originating from the environment, our diets, host microbiomes, and internal metabolic processes. Increasing evidence highlights AhR's role as a critical regulator of numerous biological functions, such as cellular differentiation, immune response, metabolism, and even tumor formation. Typically located in the cytoplasm, AhR moves to the nucleus upon activation by an agonist where it partners with either the aryl hydrocarbon receptor nuclear translocator (ARNT) or hypoxia-inducible factor 1β (HIF-1β). This complex then interacts with xenobiotic response elements (XREs) to control the expression of key genes. AhR is notably present in various crucial immune cells, and recent research underscores its significant impact on both innate and adaptive immunity. This review delves into the latest insights on AhR's structure, activating ligands, and its multifaceted roles. We explore the sophisticated molecular pathways through which AhR influences immune and lymphoid cells, emphasizing its emerging importance in managing inflammatory diseases. Furthermore, we discuss the exciting potential of developing targeted therapies that modulate AhR activity, opening new avenues for medical intervention in immune-related conditions.
Schizophrenia is a severe mental illness that affects 1% of the population, but accounts for over $60 billion in costs to the national healthcare system. Negative symptoms of schizophrenia, including motivational deficits, are some of the most debilitating aspects of the disorder, being both difficult to treat and representing one of the most significant barriers to functional recovery. One pathophysiologic pathway that may contribute to these alterations in reward circuitry in schizophrenia is inflammation. Increased inflammation has been reliably linked to deficits in reward processing and decreased motivation via effects of inflammatory cytokines on regions of the basal ganglia, including the ventral striatum. Previous findings show that some patients with schizophrenia reliably exhibit elevated concentrations of inflammatory markers and that inflammatory cytokines may be related to negative symptoms including decreased motivation. Relevant to the impact of inflammation on insulin signaling, measures of insulin sensitivity are significantly worse in patients with schizophrenia, including at illness onset. Moreover, antipsychotic medications lead to metabolic syndrome, contributing to risk for insulin resistance and ultimately diabetes. Insulin resistance is believed to be caused by increased inflammation, and in turn can contribute to inflammation through alterations in glucose metabolism.

This study uses an oral glucose tolerance test to test the hypothesis that insulin resistance drives inflammation. The researchers will recruit subjects with a range of insulin resistance, as measured by the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR). This will allow the researchers to investigate the contributions of metabolic dysfunction and inflammation on inflammatory and metabolic markers, brain reward circuitry, motivational deficits, and negative symptoms.
The invention comprises physiologically tolerable, water-insoluble salts of thiamine and pyridoxine with disulphonic acids of alkyl-substituted naphthalenes.  The compounds are prepared by reacting in aqueous solutions hydrochlorides of thiamine and pyridoxine with soluble salts of the disulphonic acids.  In examples, hydrochlorides of thiamine and pyridoxine are reacted with sodium 2,6-di-tert.-butyl -naphthalene-1,5-disulphonic acid.  Pharmaceutical preparations comprise thiamine and pyridoxine salts of disulphonic acids of alkyl-substituted naphthalenes, e.g. 2,6-ditert. -butyl-naphthalene-1,5-di-sulphonic acids. The compositions also may contain 2-diethyl-amino -21,61-acetoxylidide hydrochloride, methyl p-hydroxybenzoate, propy p-hydroxybenzoate, sodium citrate, citric acid, a polyethylene glycol, sorbitan polyoxyethylene monolaurate and distilled water.
The invention belongs to the field of pharmaceutical preparation, and specifically relates to minodronic acid tablets and a preparation method thereof. With large amounts of experiments, proportions of auxiliary materials and hydroxypropyl beta-cyclodextrin are determined, and tablets containing minodronic acid and hydroxypropyl beta-cyclodextrin are prepared. The tablets are composed of minodronic acid, hydroxypropyl beta-cyclodextrin, a filling material, a disintegrating agent, a lubricant, and other pharmaceutically acceptable auxiliary materials. During a preparation process, hydroxypropyl beta-cyclodextrin and minodronic acid are added in a water solution form into mixed powder of the filling material and the disintegrating agent. The dissolution rate of the tablets provided by the invention is substantially improved, such that rapid dissolution and absorption of minodronic acid in gastrointestinal-tract bodily fluids is facilitated. The preparation process is simple, and operation is convenient, such that the method is suitable for industrialized productions.
PURPOSE:To obtain a paste for synthetic dental calculus having excellent adhesiveness to the teeth of model and excellent similarity in properties of synthetic dental calculus, sense in removal and characteristics to really occurring dental calculus, containing glass powder and a polymerizable and curable organic compound. CONSTITUTION:100pts.wt. polymerizable and curable organic compound such as preferably dimethacrylate monomer, especially diglycidyl methacrylate or polyethylene glycol is blended with 150-350pts.wt., preferably 230-280pts.wt glass powder, preferably glass powder having <=100 meshes and containing a small amount of colored component (e.g. organic metallic oxide). A curable composition paste comprising a polymerizable and curable compound, a polymerization promoter (e.g. tertiary amine) and glass powder and a curing agent composition paste containing a polymerization initiator, an organic solvent and glass powder are prepared and both the pastes are blended, applied to the teeth of model and cured.
An acellular soft tissue-derived matrix includes a collagenous tissue that has been delipidated and decellularized. Adipose tissue is among the soft tissues suitable for manufacturing an acellular soft tissue-derived matrix. Exogenous tissuegenic cells and other biologically-active factors may be added to the acellular matrix. The acellular matrix may be provided as particles, a slurry, a paste, a gel, or in some other form. The acellular matrix may be provided as a three-dimensional scaffold that has been reconstituted from particles of the three-dimensional tissue. The three-dimensional scaffold may have the shape of an anatomical feature and serve as a template for tissue repair or replacement. A method of making an acellular soft tissue-derived matrix includes steps of removing lipid from the soft tissue by solvent extraction and chemical decellularization of the soft tissue.
Intensive support measures should be instituted and individual symptoms treated as they arise. The airway should be secured and adequate respiratory exchange established. Since nausea and vomiting are likely to be present, gastric lavage within the first 2 to 3 hours after ingestion is probably preferable to induction of emesis. Following evacuation of the gastric contents, the instillation of activated charcoal slurry into the stomach may help absorb any remaining drug from the gastrointestinal tract. Antiemetic medication may be required to control severe nausea and vomiting. 

Active diuresis (with measured intake and output) will help promote excretion of the drug. For severe cases, extracorporeal hemodialysis may be required. If this is not available, peritoneal dialysis can be used along with forced diuresis.
BACKGROUND: Increasing evidence suggests an association between childhood obstructive sleep apnea (OSA) and metabolic syndrome, with more research available on the potential impacts of positive airway pressure (PAP) on metabolic markers in children. The purpose of this systematic review is to provide a systematic synthesis of the evidence on the effect of PAP use on metabolic markers in children with OSA.
METHODS: A search strategy with terms for "OSA" and metabolic markers in pediatrics was run to systematically assess 5 databases until August 26, 2022. Two reviewers independently screened eligible articles, extracted data, and conducted quality appraisal. Meta-analysis was done using random-effects models. Body mass index (BMI), glycemic, lipid, cardiovascular, and other metabolic and inflammatory markers were reported.
RESULTS: Sixteen studies (N = 1,213) were included, 15 observational studies and 1 randomized controlled trial (RCT); most reported outcomes in children with obesity. Meta-analysis of 4 studies found no changes in BMI at median average follow-up of 12 months after PAP initiation. A reduction in heart rate and blood pressure parameters was demonstrated in several studies in children with OSA with and without obesity at a median average follow-up of 4.9 months after PAP initiation. Research in echocardiographic outcomes is limited, including one RCT in children with Down syndrome and OSA showing no changes in heart rate variability parameters. Evidence of improvements in glycemic and/or lipid control, liver enzymes, and inflammatory markers with PAP therapy is even more limited and of limited clinical importance. Risk of bias was moderate to critical and outcome evidence very low.
CONCLUSIONS: Although evidence on effects of PAP on metabolic markers in children with OSA is encouraging, available literature is limited. Longitudinal studies are still required to further assess the long-term influence of PAP on metabolic and inflammatory markers, particularly in children with obesity.
OBJECTIVE: This study examines the therapeutic potential of monotropein (Mon) in a rat model of acute pulmonary embolism (APE), aiming to elucidate its mechanistic role and provide new insights for APE treatment.
METHODS: Thirty Sprague Dawley (SD) rats were randomly assigned to five groups (n = 6 per group): sham, Mon (40 mg/kg), APE, APE + 20 mg/kg Mon, and APE + 40 mg/kg Mon. APE was induced via autologous thrombus infusion in all groups except sham and Mon-only groups. We assessed blood gas parameters, lung wet/dry weight (W/D) ratio, and oxidative stress markers. Additionally, excised lung tissues underwent evaluation for serum inflammatory factors via ELISA, apoptotic cells via TUNEL assay, and protein expression via Western blot.
RESULTS: Compared to the sham group, APE-induced rats exhibited significantly elevated blood oxygen levels and increased pro-inflammatory factors, including interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-8. Mon treatment effectively mitigated these APE-induced changes, reducing blood oxygen concentration and downregulating IL-1β and TNF-α levels. Furthermore, Mon demonstrated anti-apoptotic effects by decreasing cleaved caspase-3 and Bax protein levels while upregulating Bcl-2 expression. Mon also suppressed nuclear factor-κB (NF-κB) activation by inhibiting the phosphorylation levels of p65/RelA and IκBα proteins, while the total protein level of IκBα was increased with Mon treatment.
CONCLUSION: Mon effectively ameliorated lung tissue injury in APE rats by inhibiting apoptosis, attenuating inflammatory responses, and alleviating oxidative stress. These beneficial effects appear to be mediated through modulation of the NF-κB pathway, suggesting Mon as a promising therapeutic candidate for APE treatment.
Pre-test measures: Interested participants will be invited to the Physical Activity and Diabetes Laboratory on the main campus of the University of Alberta. They will be asked questions related to their menstrual cycle, physical activity levels and medication. Blood pressure will also be measured to assess their eligibility. Where participants are eligible, anthropometric characteristics will be measured using standard protocols. A blood sample will be drawn for assessment of HbA1c. Participants will perform an incremental treadmill test to volitional exhaustion. Indirect calorimetry will be used to assess oxygen consumption and carbon dioxide production to determine the participant's aerobic capacity.

Testing sessions: Participants will perform two testing sessions separated by at least 5 days. One session will take place during the last week of active pill consumption of monophasic hormonal contraceptives. The second session will take place during the placebo pill consumption phase (i.e. menses). Participants will be asked to arrive at the lab at around 4:00 pm for both sessions, which will be randomly assigned. During the sessions, participants will be asked to perform 45 minutes of aerobic exercise on an ergonomic cycle ergometer at 60% of the participant's pre-determined aerobic capacity. Blood samples will be drawn at baseline, at the end of exercise, and an hour post-exercise via an IV catheter. Participants will be asked to match their daily food and insulin intake as closely as possible from one testing session to the next for the day before, day of and day after the testing session. They will also be asked to avoid strenuous exercise and alcohol intake.

A continuous glucose monitor (CGM) sensor will be subcutaneously inserted by one of the investigators (trained by a group from the CGM manufacturer) into the anterior abdominal area of the participant in the morning of the day prior to each testing session. The participant will wear the CGM for at least 24 hours before the exercise session, and at least 24 hours after the exercise session.
Rabies is caused by rabies virus with a 100% mortality rate in humans. An estimated 59000 human deaths and over 3.7 million disability-adjusted life years lost every year. Most of cases occur in Africa and Asia, mainly in underserved populations, with approximately 40% of cases in children aged \<15 years. WHO and its partners have endorsed a target of Zero Human Rabies Deaths from dog-transmitted rabies by 2030 (Zero by 30). Fortunately, rabies is a vaccine-preventable disease in both humansand animals.

At present, chicken embryo cell vaccine, Vero cell vaccine, hamster kidney cell vaccine, and human diploid cell (HDC) rabies vaccine (HDCV) have been approved. The WHO clearly states that HDCV is the "gold standard" rabies vaccine. Because HDCs are normal karyotype cells without carcinogenicity, the HDCV does not contain any foreign animal impurity or neurotoxicity factor. Furthermore, there are fewer injections required and mild adverse reactions and it is safe and efficacious; thus, it is recommended by the WHO as the "nearly ideal human vaccine." Although HDCV was primarily used in developed countries prior to 2015, China does not approve the import of foreign HDCV. Meanwhile, domestic diploid rabies vaccine for human use is insufficiency and in this regard, Minhai Biothechnology Co., Ltd in China has overcome technical difficulties for the large-scale developing of a lyophilized and purified HDCV. This clinic trial was to assess the immunogenicity and safety of HDCV in healthy population vaccinated according to the Essen and Zagreb post-exposure immunization schedule, exploring the appropriate immunization procedures.
In the presence of high environmental temperature, heat prostration can occur with drug use (fever and heat stroke due to decreased sweating). Diarrhea may be an early symptom of incomplete intestinal obstruction, especially in patients with ileostomy or colostomy. In this instance, treatment with this drug would be inappropriate and possibly harmful. Like other anticholinergic agents, hyoscyamine sulfate may produce drowsiness, dizziness or blurred vision. In this event, the patient should be warned not to engage in activities requiring mental alertness such as operating a motor vehicle or other machinery or to perform hazardous work while taking this drug.

Psychosis has been reported in sensitive individuals given anticholinergic drugs. CNS signs and symptoms include confusion, disorientation, short term memory loss, hallucinations, dysarthria, ataxia, coma, euphoria, anxiety, fatigue, insomnia, agitation and mannerisms, and inappropriate affect. These CNS signs and symptoms usually resolve within 12 to 48 hours after discontinuation of the drug.
Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by inflammation, demyelination, gliosis, and neuronal loss. Neurological symptoms may include visual disturbances, numbness and tingling, focal weakness, bladder and bowel incontinence, and cognitive impairment. Some previous studies have indicated that the NeuroBiofeedback (NBF) technique could be a promising new treatment for the rehabilitation of many neurological disorders and neurodegenerative diseases, including MS. Several studies have investigated the beneficial effects of this technique on the motor and cognitive outcomes of MS, mainly aiming to evaluate motor performance, fatigue and chronic pain. Few studies have focused on the evaluation and treatment of cognitive processes with NBF, except for one study on information processing speed. Specifically, regarding the application of NBF techniques in MS, recent literature has demonstrated that modulation of the alpha-theta rhythm has led to an improvement in attentional processes with consequent reduction in anxiety. Therefore, the objective of this study is to verify the effectiveness of NBF training on the modulation of cortical activity and physiological responses through the exposure of subjects with MS to cognitive tasks and training for mood regulation.

Patients will not undergo an experimental procedure as foreseen by the study; the clinical and neuropsychological variables that will be collected for the study are those that are commonly collected by the neuropsychologist, in particular the main neuro-cognitive functions (memory, language, attention and executive functioning) and emotional abilities (meta cognition) will be considered. After enrollment, the clinical background and baseline characteristics of patients will be assessed. Enrolled patients will be randomly assigned to IG and SG. After randomization, patients will undergo instrumental examinations and neuropsychological evaluation, as required by the protocol. Patients in both groups will undergo 2 neurofeedback training sessions. All recruited subjects will be evaluated at two time-points: a first evaluation at baseline (T0) and at the end of the training (T1). Patients will undergo stimulation training via NBF 2 times a week for two months, for a total of 16 sessions. The procedure and execution of the training requires that the subjects are connected to a series of electrodes that will record the cortical electrical activity. During each session, IG patients will view their recorded brain waves and physiological responses in front of a computer screen, while a professional will explain to them what they need to do to intervene on what they see, in order to correctively modify their brain waves. While SG patients will be provided with irrelevant information (recorded data from other patients) and therefore will not be able to modulate their cortical activation
Wear the pulse-oxygen monitoring finger set of the medical monitor while wearing the Huami Smart Wearable device on the ipsilateral wrist according to the instructions for use. The medical monitor displays a steady pulse oximetry level for at least 30 seconds, starts the first measurement, slides the main dial page of the wearable device to the "Oxygen Saturation" measurement interface, clicks the measurement button to start the single measurement of blood oxygen saturation. Record the pulse oximetry and pulse rate values measured at the same time by the medical monitor and the Huami Smart Wearable Pulse Oximetry Device, respectively. After an interval of 30 seconds, repeat the above steps to start the second measurement and record the measured value. After an interval of 30 seconds, repeat the above steps to start the third measurement and record the measured value. The average of three measurements was taken as data for the test group.