anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
A premature ventricular complex is frequently observed in routine clinical practice and patients without structural heart disease occasionally have benign outcomes. The initial therapy of symptomatic premature ventricular complex is medical treatment with beta-blocker, calcium channel blocker or antiarrhythmic agents. However, no large prospective study has been performed to identify the difference in the efficacy between drugs. The current study was designed to compare the efficacy between beta-blocker and class Ic antiarrhythmic agent. Patient with symptomatic PVC more than 6000 episode per 24 hours is included. Exclusion criteria are evidence of structural heart disease, coronary heart disease, significant bradycardia or use of a concomitant antiarrhythmic agent. Patients are randomized into beta-blocker group (propranolol) and Ic antiarrhythmic agent group (propafenone). Response to the drug is evaluated after 2 months from randomization by 24 hours Holter and questionnaire. The primary endpoint is more than 80% PVC reduction or PVC burden less than 300 beats per 24 hours. The secondary endpoint is patient's symptom evaluated by questionnaire and the number of PVCs measured in 24 hours Holter.
The 1st vaccine was prepared using healthy but strongly irritated in vivo and in vitro human epithelial and mucosal cells, namely: 1) multiple physical/chemical irritation of the cells in vivo and in vitro; 2) separation and selection of the antigens using special filters, 3) simultaneous inoculation of the non-specific vaccine in the same zone as the former, 4) association with biolymphotherapy invented ex novo by myself, 5) other authors instead use cancer cells which are in fact poorly antigenic. The 2nd vaccine was prepared using special strains of streptococci and/or erysipelototrix in multiple scarring in order to obtain local third grade reactions. In this way either complete remission of the malignant neoplasm in some cases or arrest followed by definitive regression was obtained, a type of "fulmination" of the tumoural foci. Ref: 1) other authors use the said microorganisms or other dead or very much attenuated microorganisms which are really so inefficient! All their toxins are really not very active, 2) the multiple physical/chemical irritations increase the virulence and tropism of the microorganisms, 3) the ex novo invention of the irritative vector plate capable of delivering the microorganisms, 5) the brilliant idea of diffusive transfer in the case of reactions localized in the scarring zone, 6) the discovery of biolymph, which is wholly original in the preparation and in the composition, which is essential in the method of action of the two vaccines, these, the biolymph and the plates being four essential systems, their relationship can be revealed by the following statement: "the first vaccine joins the second in a ring which is the plate and altogether are fed to the biolymph". I carried out the tests first on plants and then on animals, and then on myself, 700 tests in all; finally I satisfactorily treated 45 patients suffering from advanced phase malignant neoplasms and 65 healthy volunteers of adult age are receiving prophylactic treatment. <IMAGE>
NEW MATERIAL:The titled compound of formulaI(R is lower alkanoyl, lower alkoxycarbonyl, furoyl, lower alkanesulfonyl, etc.; A is lower alkylene; the C- bond between the 3- and 4-positions of the carbostyril skeleton is single or double) and its salt. EXAMPLE:6-[4-(3,4,5-Trimethoxybenzoyl)-1-piperazinylacetyl]-3,4-dihydr ocarbostyril.monohydrochloride.3/2-hydrate. USE:A cardiotonic drug useful for the remedy of cardiac diseases such as congestive heart failure, etc. It has high positive inotropic activity and coronary vessel flow increasing activity, and nevertheless has weak activity to increase the heart rate. PROCESS:The compound of formulaIcan be prepared e.g. by reacting 3,4-dihydrocarbostyril with the compound of formula III (X and X' are halogen) in a solvent in the presence of a Lewis acid, and reacting the resultant compound of formula IV with the piperazine derivative of formula V in the absence of a solvent or in an inert solvent.
PURPOSE:To obtain a hair tonic and growing agent capable of manifesting remarkably improved antiinflammatory action, simultaneously providing good hair tonic, growing and alopecia preventing actions and exhibiting high safety for a long period by using an extract separated from Hypericum erectum Thunb. and an antiinflammatory agent in combination. CONSTITUTION:The hair tonic and growing agent is obtained by using an extract prepared by pulverizing any of the whole herb, a leaf, a stem, a root, a fruit, a seed and a flower of Hypericum erectum Thunb. belonging to the family Guttiferae and extracting the pulverized material with a solvent and an antiinflammatory agent (e.g. allantoin or dipotassium glycyrrhizinate) in combination. The extract of the Hypericum erectum Thunb. is preferably blended in an amount of 0.001-10wt.% based on the hair tonic and growing agent and the antiinflammatory agent is preferably blended on an amount of 0.01-5wt.% based on the hair tonic and growing agent. Furthermore, gaseous carbon dioxide is especially preferably contained in this hair tonic and growing agent.
This study is a prospective, single-center, single-arm, open-label and phase I clinical trial. Subjects with CD4+T cell counts greater than 350/μl and viral loads of \<50 copies/ml over 1 year by antiviral treatment are enrolled. T cells are stimulated with CD3 and CD28, transduced with lentiviral vectors encoding a broadly neutralizing HIV-1 scFv antibody and expanded for approximately 2 weeks. Then, patients are infused with CAR T cells at a dosage of 1×10\^5 CAR-T cells/kg body weight. If this dose is well tolerated, dosing will be increased to 5×10\^5 CAR T cells/kg body weight. After infusion, adverse events, and HIV-1 latent reservoir size and CAR levels in peripheral blood will be monitored to assess the safety of CAR-T-cell treatment, potential therapeutic efficacy and kinetics of CAR T cells.
The present invention relates to the field of pharmaceutical chemistry, and in particular, to a carebastine salt and use thereof. The present invention solves the problems of solid carebastine in the prior art such as poor form, excessive impurities, instability, difficulties in purification, scale-up and synthesis, and low druggability. The carebastine salt of the present invention includes, but is not limited to, an acid addition salt or a base addition salt, and particularly includes a potassium salt, a sodium salt, a methanesulfonate, and a p-toluenesulfonate. The carebastine salt of the present invention possesses use in preparing a medicament as a histamine H1 receptor antagonist. The carebastine salt of the present invention has characteristics such as ease of purification, high stability, simple process, ease of industrial production and the like, and has good hygroscopicity and convenience in storage. Also, the salt of the present invention can quickly enter a body to exert its efficacy, features good oral absorption performance and superior safety and individual difference to ebastine, and is a very promising antiallergic.
The Diagnostic Statistical Manual of Mental Disorders (DSM-5) recommends diagnosing neurocognitive disorders (i.e., cognitive impairment) when a patient scores beyond - 1 SD below neurotypical norms on two tests. I review how this approach will fail due to cognitive tests' power limitations, validity issues, imperfect reliabilities, and biases, before summarizing their resulting negative consequences. As a proof of concept, I use developmental prosopagnosia, a condition characterized by difficulties recognizing faces, to show the DSM-5 only diagnoses 62-70% (n1 = 61, n2 = 165) versus 100% (n1 = 61) through symptoms alone. Pooling the DSM-5 missed cases confirmed the presence of group-level impairments on objective tests, which were further evidenced through meta-analyses, thus validating their highly atypical symptoms. These findings support a paradigm shift towards bespoke diagnostic approaches for distinct cognitive impairments, including a symptom-based method when validated effective. I reject dogmatic adherence to the DSM-5 approach to neurocognitive disorders, and underscore the importance of a data driven, transdiagnostic approach to understanding patients' subjective cognitive impairments. This will ultimately benefit patients, their families, clinicians, and scientific progress.
Participants in the High-Intensity Interval Training (HIIT) group will complete 8 weeks of twice-weekly HIIT of 30 minutes in duration. Heart rate, ratings of perceived exertion, affect and enjoyment will be assessed. This will include a five minute warm-up on a cycle ergometer, followed by 10 x 60 second repetitions on the cycle ergometer interspersed with 60 seconds rest. A five minute cooldown will follow on the cycle ergometer.
The present invention is directed to an MRI technique to assess tumor malignancy non-invasively. It is based on the principle that most malignant epithelial tumor cells express mucins that are heavily underglyocsylated. This phenomenon of aberrant expression has been well-documented in the literature. When benign tumor cells having normal mucin glycosylation with CEST MRI are imaged a strong CEST MRI signal effect is seen. When tumor cells lose their glycans and become malignant, the difference in MRI CEST signal is detectable. Thus, the intrinsic properties of tumor cell surface mucin glycosylation can be used as a surrogate marker for predicting tumor malignancy. This can be accomplished without injecting exogenous probes or labels, which have their own problems in terms of clinical approval, cost, and pharmacokinetics of binding to all tumor cells in question. Normal tissue can be used as a reference in determining changes in contrast associated with malignancy.
Stripe rust and powdery mildew are serious diseases that severely decrease the yield of wheat. Planting wheat cultivars with powdery mildew and stripe rust resistance genes is the most effective way to control these two diseases. Introducing disease resistance genes from related species into the wheat genome via chromosome translocation is an important way to improve wheat disease resistance. In this study, nine novel T1RS.1AL translocation lines were developed from the cross of wheat cultivar Chuannong25 (CN25) and a Chinese rye Qinling. The results of non-denaturing fluorescence in situ hybridization and PCR showed that all new lines were homozygous for the T1RS.1AL translocation. These new T1RS.1AL translocation lines exhibited strong resistance to stripe rust and powdery mildew. The cytogenetics results indicated that the resistance of the new lines was conferred by the 1RS chromosome arms, which came from Qinling rye. The genetic analysis indicated that there were new dominant resistance genes on the 1RS chromosome arm resistant to stripe rust and powdery mildew, and their resistance patterns were different from those of Yr9, Pm8, and Pm17 genes. In addition, the T1RS.1AL translocation lines generally exhibited better agronomic traits in the field relative to CN25. These T1RS.1AL translocations have great potential in wheat-breeding programs in the future.
Carrot (Daucus carota) is one of the most popular and nutritious vegetable crops worldwide. However, significant yield losses occur every year due to leaf blight, a disease caused by a fungal pathogen (Alternaria dauci). Past research on resistance to leaf blight disease in carrots has been slow because of the low-quality genome assemblies of both carrot and the pathogen. Here, we report the greatly improved assemblies and annotations of telomere-to-telomere (T2T) reference genomes of carrot DH13M14 (451.04 Mb) and A. dauci A2016 (34.91 Mb). Compared with the previous carrot genome versions, our assembly featured notable improvements in genome size, continuity, and completeness of centromeres and telomeres. In addition, we generated a time course transcriptomic atlas during the infection of carrots by A. dauci and captured their dynamic gene expression reprogramming during the interaction process. During infection, A. dauci genes encoding effectors and enzymes responsible for the degradation of plant cell wall components, e.g., cellulose and pectin, were identified, which appeared to increase pathogenic ability through upregulation. In carrot, the coordinated gene expression of components of pattern- and effector-triggered immunity (PTI and ETI) in response to A. dauci attack was characterized. The biosynthesis or signal transduction of plant hormones, including JA, SA, and ethylene, was also involved in the carrot response to A. dauci. This work provides a foundation for understanding A. dauci pathogenic progression and carrot defense mechanisms to improve carrot resistance to leaf blight disease. The Carrot Database (CDB) developed also provides a useful resource for the carrot community.
lncRNA ZNF593 antisense (ZNF593-AS) transcripts have been implicated in heart failure through the regulation of myocardial contractility. The decreased transcriptional activity of ZNF593-AS has also been detected in cardiac hypertrophy. However, the function of ZNF593-AS in cardiac hypertrophy remains unclear. Herein, we report that the expression of ZNF593-AS reduced in a mouse model of left ventricular hypertrophy and cardiomyocytes in response to treatment with the hypertrophic agonist phenylephrine (PE). In vivo, ZNF593-AS aggravated pressure overload-induced cardiac hypertrophy in knockout mice. By contrast, cardiomyocyte-specific transgenic mice (ZNF593-AS MHC-Tg) exhibited attenuated TAC-induced cardiac hypertrophy. In vitro, vector-based overexpression using murine or human ZNF593-AS alleviated PE-induced myocyte hypertrophy, whereas GapmeR-induced inhibition aggravated hypertrophic phenotypes. By using RNA-seq and gene set enrichment analyses, we identified a link between ZNF593-AS and oxidative phosphorylation and found that mitofusin 2 (Mfn2) is a direct target of ZNF593-AS. ZNF593-AS exerts an antihypertrophic effect by upregulating Mfn2 expression and improving mitochondrial function. Therefore, it represents a promising therapeutic target for combating pathological cardiac remodeling.
Participants start on standard of care dosing. After 2 days blood samples will be analysed and exposure will be determined using MIPD. Wherever necessary dose adjustments will be made.
The present invention is considered to be an alternative for the control of chronic degenerative diseases, since it is a food supplement and a sustainable, affordable product that will have an increased development upon suitably informing population about the advantages thereof, this may facilitate its inclusion into the market of food supplements without any problem and with the advantage over further products as there is no similar composition currently available on the country or the world up to now. The composition is a mixture of an amino acid (glycerin) in a ratio of 15 gr daily with Maguey inulin, which is a soluble and absorbable fiber, in a ratio of 6 gr daily, fructose 3 gr as a sweetener, in different natural flavors of hibiscus, lemon, pineapple, grape, cranberry. The manufacture of the composition is performed under a sterile environment for avoiding pollution, preferably using: a) glycerin powder from 400 gr. to 450 gr., b) inulin powder from 100 gr. to 150 gr., c) fruct ose powder from 10 gr, to 50 gr., d) citric acid from 5 gr. to 10 gr.
###  Bone and Cardiac Imaging

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Note 1:Wear waterproof gloves during the entire preparation procedure and during subsequent patient dose withdrawals from the reaction vial. 

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Note 2:Make all transfers of sodium pertechnetate Tc 99m solution during the preparation procedure with an adequately shielded syringe. 

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Note 3:Keep the Radioactive Preparationin the lead shield described below (with cap in place) during the useful life of the Radioactive Preparation. Make all withdrawals and injections of the Radioactive Preparationwith an adequately shielded syringe. 

  1. A Technescan PYPreaction vial is removed from the refrigerator and approximately five (5) minutes are allowed for the contents to come to room temperature. 
  2. Attach radioassay information label with radiation warning symbol to the reaction vial and place the vial in a lead Dispensing Shield fitted with a lead cap and having a minimum wall thickness of 1/8 inch. Do not remove reaction vial from the Dispensing Shield except, temporarily, for Step 5 below.
  3. Sodium pertechnetate Tc 99m solution (1 to 10 milliliters) is added to the reaction vial. In choosing the amount of technetium Tc 99m radioactivity to be used in the preparation of the Technetium Tc 99m Pyrophosphate Injection, the labeling efficiency, number of patients, administered radioactive dose, and radioactive decay must be taken into account. The recommended maximum amountof technetium Tc 99m to be added to the reaction vial is 3.7 gigabecquerels (100 millicuries). 
  4. With the reaction vial in the Dispensing Shield (with cap in place), shake sufficiently to bring the lyophilized material into solution. Allow to stand for five (5) minutes at room temperature.
  5. Using proper shielding, the reaction vial should be visually inspected. The resulting solution should be clear and free of particulate matter. If not, the reaction vial should not be used.
  6. Assay the product in a suitable calibrator and record the time, date of preparation and the activity of the Technetium Tc 99m Pyrophosphate Injection onto the radioassay information label. Store the reaction vial in the Dispensing Shield at 20° to 25°C (68° to 77°F) when not in use and discard after six (6) hours from the time of preparation.



###  Blood Pool Imaging

  1. A Technescan PYPreaction vial is removed from the refrigerator and approximately five (5) minutes are allowed for the contents to come to room temperature. 
  2. Reconstitute the reaction vial with 3 milliliters of sterile, non-pyrogenic normal saline containing no preservatives.
  3. Shake the reaction vial sufficiently to bring the lyophilized material into solution. Allow to stand for five (5) minutes at room temperature.
  4. The reaction vial should be visually inspected. The resulting solution should be clear and free of particulate matter. If not, the reaction vial should not be used.
  5. Store reconstituted reaction vial at 20° to 25°C (68° to 77°F) when not in use and discard after six (6) hours from time of preparation.
PURPOSE: A system of two formulation type for transferring an active ingredient is provided to easily apply to deep wrinkle site and hair and to reform after applying. CONSTITUTION: A system of two formulation type for transferring an active ingredient comprises: a first formulation prepared by supporting cosmetically active ingredient on anhydrous water-soluble film; and a second formulation which contains a component promoting absorption of the active ingredient to the skin and dissolve the first formulation. The first formulation is patch type and the second formulation is liquid or gel phase. The anhydrous water-soluble film is dissolved in water in one second to ten minutes. The film is made of hydrophilic coating polymer. The polymer is pullulan.
Examining kidney fibrosis is crucial for mechanistic understanding and developing targeted strategies against chronic kidney disease (CKD). Persistent fibroblast activation and tubular epithelial cell (TEC) injury are key CKD contributors. However, cellular and transcriptional landscapes of CKD and specific activated kidney fibroblast clusters remain elusive. Here, we analyzed single cell transcriptomic profiles of two clinically relevant kidney fibrosis models which induced robust kidney parenchymal remodeling. We dissected the molecular and cellular landscapes of kidney stroma and newly identified three distinctive fibroblast clusters with "secretory", "contractile" and "vascular" transcriptional enrichments. Also, both injuries generated failed repair TECs (frTECs) characterized by decline of mature epithelial markers and elevation of stromal and injury markers. Notably, frTECs shared transcriptional identity with distal nephron segments of the embryonic kidney. Moreover, we identified that both models exhibited robust and previously unrecognized distal spatial pattern of TEC injury, outlined by persistent elevation of renal TEC injury markers including Krt8 and Vcam1, while the surviving proximal tubules (PTs) showed restored transcriptional signature. We also found that long-term kidney injuries activated a prominent nephrogenic signature, including Sox4 and Hox gene elevation, which prevailed in the distal tubular segments. Our findings might advance understanding of and targeted intervention in fibrotic kidney disease.
Buprenorphine-sufentanil group receives sufentanil 0.03mcg/kg followed by sufentanil 0.01-0.03 mcg/kg q10 min PRN, IV ketorolac 0.5mg/kg up to 30mg max and IV acetaminophen 15mg/kg up to 1000mg for pain control intraoperatively. In the PACU, IV buprenorphine 0.3mg IV q30 minutes would be given as the first line choice for pain control for 3 doses. IV PCA sufentanil is used as a second line therapy if patient comfort is not achieved by IV buprenorphine alone. The patient receives 0.3 mg buprenorphine IV Q6hr PRN, scheduled IV acetaminophen 1 gram for 24 hrs and methocarbamol 750mg QID after discharge from the PACU and transfer to the floor. The patient is converted to buprenorphine2mg q6hr PRN and 975 gram PO APAP scheduled for pain control on postoperative day 1. The patient receives their home dose of Suboxone starting on postoperative day 1 if tolerating PO intake. On postoperative day 2, patients would be transitioned to an increased dose of their Suboxone.
Participants assigned to this arm downloaded both the MyPennMedicine mobile app and Ginger iO mood tracking app. They were also given a lottery incentive if they completed 70% of the daily mood ratings.
Circulating monocytes participate in pain chronification but the molecular events that cause their deployment are unclear. Using a mouse model of hyperalgesic priming (HP), we show that monocytes enable progression to pain chronicity through a mechanism that requires transient activation of the hydrolase, N-acylethanolamine acid amidase (NAAA), and the consequent suppression of NAAA-regulated lipid signaling at peroxisome proliferator-activated receptor-α (PPAR-α). Inhibiting NAAA in the 72 hours following administration of a priming stimulus prevented HP. This effect was phenocopied by NAAA deletion and depended on PPAR-α recruitment. Mice lacking NAAA in CD11b+ cells - monocytes, macrophages, and neutrophils - were resistant to HP induction. Conversely, mice overexpressing NAAA or lacking PPAR-α in the same cells were constitutively primed. Depletion of monocytes, but not resident macrophages, generated mice that were refractory to HP. The results identify NAAA-regulated signaling in monocytes as a control node in the induction of HP and, potentially, the transition to pain chronicity.