anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
OBJECTIVE: The aim of this study is to retrospectively evaluate the presentation of head and neck mucoepidermoid carcinoma at the Royal Melbourne Hospital and identify the significance of AFIP histological grading on the risk of neck metastasis and cancer free survival.
MATERIALS AND METHODS: This study is a retrospective cohort analysis of patients treated for head and neck mucoepidermoid carcinoma at the RMH between 2005 and 2022. Patient demographics, treatment, pathology, in particular the AFIP histological grading of the primary tumour, and outcomes were collected and tabulated. Time to recurrence was recorded, and survival outcomes were calculated with Kaplan-Meier method. Comparisons were made on different histological grading and regional metastases.
RESULTS: Thirty-three patients were identified and thirty met the inclusion criteria. There was an age range of 18-77 years (median 54 years) with no significant sex difference. Our patients had a 94% 5-year survival and an 86% 10-year survival. Thirteen patients had elective neck dissection and 2 out of 13 (15%) of the patients had positive neck disease. Of the two patients with regional metastasis, the primary tumour was graded as intermediate and low grade. No high-grade MEC patients had regional metastasis.
CONCLUSION: Mucoepidermoid carcinoma of the head and neck is associated with a good disease-specific and overall survival despite the presence of regional metastasis. The AFIP histological grading system did not have a statistically significant correlation to the incidence of nodal metastasis.
TQB2930 for injection 20mg/kg combined with TQB3616 capsule 120mg or 150mg or 180mg, and fulvestrant injection. Q2W, 28 days a cycle.
Due to its integrated long-distance telemetry, the implantable pacemaker Philos II DR-T is capable of periodically transmitting data from the pacemaker memory to the BIOTRONIK Service Center via patient device. The BIOTRONIK Service Center decodes the data and presents it to the physician on a password secured internet site. Additionally, in case certain event criteria are met, the most important Home Monitoring information are immediately faxed to the physician as an Event Report. These events can be customised by the physician. Thus, the physician will be able to closely monitor the patient and check the adequacy and efficiency of the pacemaker therapy without requiring the patient to visit the physician. The transmitted data comprise information on atrial and ventricular rhythm, atrioventricular conduction and system status.

The purpose of the national prospective, randomized, multicentric clinical study "COMPArative follow-up Schedule with home monitoring" (COMPAS) described here is to evaluate the benefits of pacemaker follow-up with home monitoring in France. The standard follow-up or therapeutic intervention will be deemed based on faxed event Reports reception and Cardio reports analysis on internet site. During the clinical study, the incidence of serious adverse events (hospitalisation, pacemaker dysfunction, and cardiovascular events), economic impact, safety, and practicability will be analysed. The findings from the ACTIVE group will be compared to those of a group receiving standard of care (CONTROL group). Both patient groups are followed for 18 months and will be followed with Home Monitoring switched on. The data from the CONTROL group will not be presented online to the attending physician, but a retrospective analysis on differences between the two groups will be performed.

The trial will be conducted as a prospective, randomised, open, multicenter, national clinical trial. The enrollment of 400 patients in 50 clinical centres in France is anticipated. The principal inclusion criterion is indication for dual chamber pacemaker/ICD implantation. Main exclusion criteria comprise pacemaker dependency.
MA-TKAs are performed by which the distal femur and proximal tibia cuts are made perpendicular to the mechanical axis, a line connecting the center of the femoral head to the center of the ankle. These cuts are classically described as a 6-degree valgus cut of the distal femur and a 0-degree cut of the proximal tibia in relation to the mechanical axis. MA-TKAs create a 0-degree hip-knee-ankle angle.
The present invention relates to a new human herpesvirus-7, proteins encoded in the genome of the virus, and antibodies specific for the virus and proteins. The virus was isolated from human peripheral blood mononuclear cells following incubation of the cells under conditions promoting T cell activation. Cultures of lymphocytes infected with the virus exhibited a cytopathic effect and electron microscopic analyses revealed a characteristic herpesvirus structure. The new virus is distinct from previously characterized human herpesvirus. The invention also relates to bioassays for the diagnosis of human herpesvirus-7 and the detection of human herpesvirus-7 in a biological sample. It further relates to a vaccine for humans against human herpesvirus-7.
Preparations comprising an enriched population of extracellular vesicles (nEVs) having a negatively charged surface, and that are CD81+ and CD9-, are provided. Improved processes and methods for producing an enriched population of nEVs from non-murine cells, especially human origin cells and/or tissues, are disclosed. Therapeutic methods for using the preparations, including for reducing brain inflammation and treatment of various pathologies associated with brain inflammation, such as by intravenous or intranasal administration, are also described. Methods and preparations for reducing brain inflammation associated with traumatic brain injury (TBI) are also disclosed. A method for treating a patient having suffered a mild traumatic injury (mTMI), or concussion, such as a sports-related head injury, is also disclosed. The nEVs are also demonstrated to reduce the expression level of IL-Ιβ in brain tissue of an animal having had traumatic brain injury. Methods for improving cognitive function and performance in animals after a traumatic brain injury is also demonstrated using the preparations of nEVs disclosed herein.
NEW MATERIAL:3-l-Menthoxypropane-1,2-diol of formulaI. USE:An almost odorless widely utilizable liquid, having low volatility, useful as a cold feeling agent, and capable of being easily synthesized from an easily available raw material and assistant in a short step without the difficulty in operations. PROCESS:l-Menthol of formula II is a raw material is heated in a solvent, e.g. toluene, in the presence of metallic sodium, etc. An allyl halide, e.g. allyl chloride, is then added to and reacted with the l-menthol to give 3-l-3-menthoxypropan-1-ene of formula III, which is then oxidized with an organic peracid to give an oxide. The resultant oxide is further hydrolyzed to afford the compound of formulaI.
Colchicine is an alkaloid obtained from the plant colchicum autumnale. 

The chemical name for colchicine is ( S)-N-(5,6,7,9- tetrahydro-1,2,3,10-tetramethoxy-9 oxobenzol[a]heptalen-7-yl) acetamide. The structural formula is represented below: 

Colchicine consists of pale yellow scales or powder; it darkens on exposure to light. Colchicine is soluble in water, freely soluble in alcohol, and slightly soluble in ether.

Colchicine capsules are supplied for oral administration. Each capsule contains 0.6 mg colchicine, USP and the following inactive ingredients: colloidal silicon dioxide, lactose anhydrous, magnesium stearate, microcrystalline cellulose, and sodium starch glycolate. The capsule shell contains gelatin, purified water, titanium dioxide, erythrosine, Brilliant Blue FCF, and may contain D&C Red No. 28, FD&C Red No. 40 and Quinoline Yellow.
FIELD: organic chemistry, biochemistry. SUBSTANCE: invention relates to poly-(para-dihydroxy-para-phenylene)-thiosulfoacid sodium salt of the general formula (I)   eliciting superoxidase activity. Indicated compound provides to broaden the spectrum of substances which are able to carry out the reaction of dismutation of O 2  and they can be used as antioxidants in biology, microbiology and medicine. Invention describes also method of synthesis of said compound that involves the interaction of para-benzoquinone with sodium thiosulfate in an aqueous medium in the mole ratio of components from 3:1 to 10:1. EFFECT: improved method of synthesis, broadened spectrum of antioxidants. 4 cl, 5 dwg, 3 ex
Patients receive docetaxel IV over 1 hour and carboplatin IV over 30 minutes on day 1. Courses repeat every 21 days in the absence of disease progression or unacceptable toxicity.
Participants randomized to the control group will receive Treatment As Usual (TAU). TAU is defined as comprising at least 12 monthly individual supportive sessions provided by non-MBT trained mental health professionals in the Department of Child and Adolescent Psychiatry in Region Zealand. Additional supportive sessions or other types of intervention may be offered to the patients according to the needs of the patients as evaluated by mental health professionals responsible for his/hers treatment. Hence, TAU may vary considerably in number and type of intervention across clinics and patients. All mental health services delivered during the treatment period to patients in the TAU group will be monitored and registered.
MOTIVATION: Identifying causal relations between diseases allows for the study of shared pathways, biological mechanisms, and inter-disease risks. Such causal relations can facilitate the identification of potential disease precursors and candidates for drug re-purposing. However, computational methods often lack access to these causal relations. Few approaches have been developed to automatically extract causal relationships between diseases from unstructured text, but they are often only focused on a small number of diseases, lack validation of the extracted causal relations, or do not make their data available.
RESULTS: We automatically mined statements asserting a causal relation between diseases from the scientific literature by leveraging lexical patterns. Following automated mining of causal relations, we mapped the diseases to the International Classification of Diseases (ICD) identifiers to allow the direct application to clinical data. We provide quantitative and qualitative measures to evaluate the mined causal relations and compare to UK Biobank diagnosis data as a completely independent data source. The validated causal associations were used to create a directed acyclic graph that can be used by causal inference frameworks. We demonstrate the utility of our causal network by performing causal inference using the do-calculus, using relations within the graph to construct and improve polygenic risk scores, and disentangle the pleiotropic effects of variants.
AVAILABILITY AND IMPLEMENTATION: The data are available through https://github.com/bio-ontology-research-group/causal-relations-between-diseases.
Patients will be randomized 1:1 to receive the intervention at study start or delayed appointment 6 months later. The intervention includes initial baseline data collection from the patient including data on demographics, medications, and illness characteristics. The patient will then attend an appointment with a pharmacist to review medications appropriate for discontinuation/dose reduction, after which the patient will meet with his/her family physician to discuss patient preferences for discontinuation/dose reduction. Follow up appointments will take place at one week, 3 months and 6 months (study end). Questionnaires and a semi-structured interview will take place at the 6 month appointment. After six months, the control group will be offered the intervention.
Each subject will receive a single dose of Treatment E (DTG/RPV 50 mg/25 mg: Product Code AK), Treatment D (DTG/RPV 50 mg/25 mg: Product Code AQ) and Treatment A (DTG 50 mg tablet plus RPV 25 mg tablet), in period 1, period 2 and period 3 respectively with a washout period of \>=9 days between doses of study medication. All treatments will be administered in fed state.
Benzo(a)pyrene (BaP) can be detected in the human placenta. However, little is known about the effects of BaP exposure on different placental cells under various conditions. In this study, we aimed to investigate the effects of BaP on mitochondrial function, pyrin domain-containing protein 3 (NLRP3) inflammasome, and apoptosis in three human trophoblast cell lines under normoxia, hypoxia, and inflammatory conditions. JEG-3, BeWo, and HTR-8/SVneo cell lines were exposed to BaP under normoxia, hypoxia, or inflammatory conditions for 24 h. After treatment, we evaluated cell viability, apoptosis, aryl hydrocarbon receptor (AhR) protein and cytochrome P450 (CYP) gene expression, mitochondrial function, including mitochondrial DNA copy number (mtDNAcn), mitochondrial membrane potential (ΔΨm), intracellular adenosine triphosphate (iATP), and extracellular ATP (eATP), nitric oxide (NO), NLPR3 inflammasome proteins, and interleukin (IL)-1β. We found that BaP upregulated the expression of AhR or CYP genes to varying degrees in all three cell lines. Exposure to BaP alone increased ΔΨm in all cell lines but decreased NO in BeWo and HTR-8/SVneo, iATP in HTR-8/SVneo, and cell viability in JEG-3, without affecting apoptosis. Under hypoxic conditions, BaP did not increase the expression of AhR and CYP genes in JEG-3 cells but increased CYP gene expression in two others. Pro-inflammatory conditions did not affect the response of the 3 cell lines to BaP with respect to the expression of CYP genes and changes in the mitochondrial function and NLRP3 inflammasome proteins. In addition, in HTR-8/SVneo cells, BaP increased IL-1β secretion in the presence of hypoxia and poly(I:C). In conclusion, our results showed that BaP affected mitochondrial function in trophoblast cell lines by increasing ΔΨm. This increased ΔΨm may have rescued the trophoblast cells from activation of the NLRP3 inflammasome and apoptosis after BaP treatment. We also observed that different human trophoblast cell lines had cell type-dependent responses to BaP exposure under normoxia, hypoxia, or pro-inflammatory conditions.
Patients with a clinical diagnosis of haemorrhagic stroke on CT imaging within 48 hours of onset (for patients waking with a stroke, time of onset will be taken to be the time when the patient was last asymptomatic). This is a non-intervention study so no intervention will be given. However, the investigators will observe changes in cerebral haemodynamics of this group within 48 hours of stroke onset and within 3-7 days post-onset.
Eligible patients must have undergone standard radiation (typically 60Gy in 30 fractions), with or without concurrent drug therapy, and have MRI findings consistent with tumor progression and/or pseudoprogression within 24 weeks after completion of radiation. Eligible patients will undergo an 11C-CH PET study within 2 weeks of the standard of care MRI that shows changes concerning for tumor progression vs. pseudoprogression. All patients will then be followed with surveillance brain MRI with and without contrast as per standard of care for a period of 11 months, to assess further progression or stabilization of the lesion. Initial MRI changes are considered to represent pseudoprogression/treatment related changes if the lesion stabilizes or becomes smaller without a change in tumor-related therapy. Otherwise, it will be considered a recurrence should there be progessive radiographic changes.
In RA Safety Study 1, RA patients who were 50 years of age and older with at least one cardiovascular risk factor treated with XELJANZ 5 mg twice daily or XELJANZ 10 mg twice daily had a higher rate of major adverse cardiovascular events (MACE) defined as cardiovascular death, non-fatal myocardial infarction (MI), and non-fatal stroke, compared to those treated with TNF blockers. The incidence rate of MACE per 100 patient-years was 0.91 for XELJANZ 5 mg twice a day, 1.11 for XELJANZ 10 mg twice a day, and 0.79 for TNF blockers. The incidence rate of fatal or non-fatal myocardial infarction per 100 patient-years was 0.36 for XELJANZ 5 mg twice a day, 0.39 for XELJANZ 10 mg twice a day, and 0.20 for TNF blockers [see Clinical Studies (14.6)]. Patients who are current or past smokers are at additional increased risk.

Consider the benefits and risks for the individual patient prior to initiating or continuing therapy with XELJANZ/XELJANZ XR/XELJANZ Oral Solution, particularly in patients who are current or past smokers and patients with other cardiovascular risk factors. Patients should be informed about the symptoms of serious cardiovascular events and the steps to take if they occur. Discontinue XELJANZ/XELJANZ XR/XELJANZ Oral Solution in patients that have experienced a myocardial infarction or stroke. A XELJANZ/XELJANZ Oral Solution 10 mg twice daily (or a XELJANZ XR 22 mg once daily) dosage is not recommended for the treatment of RA or PsA [see Dosage and Administration (2.2)].
The present invention demonstrates that epibatidine binds to nicotinic receptors on leukocytes. Epibatidine is a sensitive detector of increases in the number of nicotinic receptors expressed by a cell. Epibatidine binds to the leukocytes of smokers, but does not bind to the leukocytes of non-smokers. Both in vivo and ex vivo nicotine exposure induces epibatidine receptor expression. Epibatidine binding to leukocytes reflects epibatidine binding in the central nervous system, which in turn reflects nicotine-induced effects on the central nervous system. Epibatidine binding assays in peripheral blood leukocytes can be used to evaluate an individual's exposure to, and dependence on, nicotine.
PROBLEM TO BE SOLVED: To obtain a pretreating agent for hair, capable of promoting and enhancing dyeing action by an acidic dyeing agent and exceeding in fastness to hair washing and color tone, comprising an organic solvent and an organic acid or an inorganic acid. SOLUTION: This pretreating agent for hair comprises 1-50wt.% of an organic solvent and an organic acid or an inorganic acid so as to adjust pH1-5 and 1-20 normal acidity. Benzyl alcohol, etc., are used as the organic solvent and citric acid, etc., as the organic acid or the inorganic acid. They may be used alone. In order to satisfy both pH and acidity, buffering action can be utilized by using an alkali such as sodium hydroxide. The hair pretreating agent for hair dyeing is applied to hair, allowed to stand at 30-60 deg.C for 5-30 minutes and the hair is washed with water and can be readily dyed with an acidic hair dyeing agent.
A fish toxicant composition comprises a fish toxicant, a water-immiscible organic solvent for the fish toxicant, an emulsifier and an organic acid, acid anhydride or acid chloride which is soluble in the water-immiscible solvent to the extent of at least 1% by weight and has a water-solubility of less than 1% by weight and a dissociation constant in water greater than k=10-6.  Specified fish toxicants are rotenone and other rotenoids, toxaphene strobane, chlordane, D.D.T. and dieldrin.  If the fish toxicant is a rotenoid the composition may contain a synergist therefor, e.g. piperonyl butoxide, n-octyl sulphoxide of isosafrote or di-n-propyl, 6,7 - methylenedioxy - 3 - methyl-1,2,3,4-tetrahydronaphthalene.  The emulsifier may be a non-ionic or anionic surfactant.  Specified acids, acid anhydrides and acid chlorides are maleic, malonic, malic, fumaric, adipic, succinic, pimelic, sebacic, benzoic, salicylic, toluic, phthalic and cinnamic acids and the chlorinated derivatives of the specified aromatic acids; and their anhydrides and acid chlorides. Suitable water-immiscible organic solvents are petroleum fractions, acetone, aromatic hydrocarbons, e.g. methylated naphthalenes, chlorinated hydrocarbons, e.g. ethylene dichloride and perchlorethylene and those whose density approximates to that of water.  The compositions are used for treating thermally stratified water to kill fish therein.  The compositions may contain a carrier, e.g. a dispersible powder.
Prospective randomized outcome study. Patients will be randomized either into the control group (Group A) or the study group (Group B) based on a computer generated randomization table. Both groups will undergo an identical surgical protocol, as outlined below. The only difference is that patients in Group A will have a range of motion external brace placed following surgery, while patients in Group B will have a CKH placed. The rehabilitation protocol for the two groups will be identical, as outlined below. Both groups will undergo an Anterior Cruciate Ligament (ACL) reconstruction on a delayed basis two months following surgery, if the ACL was torn during the knee dislocation. The ACL reconstruction will be delayed in both groups if a minimum range of motion of 10-90 degrees has not been attained.

Surgical Protocol : Approximately 10 - 21 days following the injury, patients will undergo the first surgical procedure on their knee dislocation. During the first procedure, they will have a Posterior Cruciate Ligament (PCL) reconstruction using an achilles tendon allograft, with the direct onlay, two bundle technique. Additionally, any damage to either the posterior medial or posterior lateral corner will be repaired (not reconstructed), and any meniscus pathology will be addressed. The final step of this first procedure will be applying the CKH to patients randomized to the compass group (the alignment pins will be placed prior to repair of the corner). Patients will undergo an ACL reconstruction (if necessary) approximately 8 weeks following the initial surgery, when the CKH will be removed. Additional surgeries will be performed on patients to treat motion problems/arthrofibrosis as well as recurrent instability on an "as-needed basis."

Rehabilitation Protocol - aggressive rehabilitation will be started on the day following surgery. Patients will be placed in Continuous Passive Motion (CPM) machines with an initial range of motion of 0 - 30 degrees. The hinge will be locked into full extension for at least 4 hours per day. We will continue CPM for two weeks, with a goal of increasing by at least 10 degrees per day to 90 degrees of flexion. Weightbearing will be allowed as tolerated with the hinge locked in extension.
BACKGROUND: In revision total knee arthroplasty (TKA), there is little information on the magnitude of potential limb lengthening, risk factors for lengthening, or its impact on patient-reported outcome measures. We aimed to quantify limb length alteration during revision TKA and assess risk factors for lengthening.
METHODS: We identified 150 patients over a 3-year period who underwent revision TKA and had preoperative and postoperative EOS hip-to-ankle standing radiographs. The average patient age was 64 years, 51% were women; 68% had a preoperative varus deformity and 21% had a preoperative valgus deformity. Outcomes assessed included change in functional and anatomic limb length, risk factors for lengthening, and clinical outcome scores, including the Knee Osteoarthritis Outcome Score Joint Replacement, and the Veterans RAND 12-item Physical and Mental Scores.
RESULTS: There were 124 patients (83%) who had functional limb lengthening, and 108 patients (72%) had anatomic limb lengthening. Patients had an average functional limb lengthening of 7 mm (range, -22 to 35) and an average anatomic limb lengthening of 5 mm (range, -16 to 31). Patients undergoing revision for instability experienced significantly greater anatomic lengthening (7.6 versus 4.6, P = .047). Patients who had ≥ 10° of deformity were more likely to be functionally lengthened (91 versus 79%) and had significantly greater average functional lengthening (12 versus 6 mm; P = .003). There was no significant change in clinical outcome scores at 6 weeks and 1 year for patients lengthened ≥ 5 or 10 mm compared to those not lengthened as substantially.
CONCLUSIONS: There is major potential for functional and anatomic limb lengthening following revision TKA, with greater preoperative deformity and revision for instability being risk factors for lengthening.