anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
OBJECTIVES: Edaravone dexborneol is neuroprotective against ischemic stroke, with free radical-scavenging and anti-inflammatory effects, but its effects in hemorrhagic stroke remain unclear. We evaluated whether edaravone dexborneol has a neuroprotective effect in intracerebral hemorrhage, and its underlying mechanisms.
MATERIALS AND METHODS: Bioinformatics were used to predict the pathway of action of edaravone dexborneol. An intracerebral hemorrhage model was established using type IV collagenase in edaravone dexborneol, intracerebral hemorrhage, Sham, adeno-associated virus + edaravone dexborneol, and adeno-associated virus + intracerebral hemorrhage groups. The modified Neurological Severity Score was used to evaluate neurological function in rats. Brain water content was measured using the dry-wet weight method. Tumor necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, and γ-aminobutyric acid levels were determined by enzyme-linked immunosorbent assay. The expression levels of neurofilament light chain and γ-aminobutyric acid transaminase were determined by western blot. Nissl staining was used to examine neuronal morphology. Cognitive behavior was evaluated using a small-animal treadmill.
RESULTS: Edaravone dexborneol alleviated neurological defects, improved cognitive function, and reduced cerebral edema, neuronal degeneration, and necrosis in rats with cerebral hemorrhage. The expression levels of neurofilament light chain, tumor necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, and γ-aminobutyric acid were decreased, while γ-aminobutyric acid transaminase expression was up-regulated.
CONCLUSIONS: Edaravone dexborneol regulates γ-aminobutyric acid content by acting on the γ-aminobutyric acid transaminase signaling pathway, thus alleviating oxidative stress, neuroinflammation, neuronal degeneration, and death caused by excitatory toxic injury of neurons after intracerebral hemorrhage.
Hypoxic preconditioning (HPC) has been reported to alleviate neuronal damage and microglial activation in hippocampal CA1 after transient global cerebral ischemia (tGCI). However, the molecular mechanism is unclear. Recent studies identified that nuclear factor-kappa-B (NF-κB)/oligomerization domain-like receptors protein (NLRP) 3 inflammasome pathway is mainly involved in the activation of microglia and that phosphorylated (p)-mixed lineage kinase domain-like (MLKL) is related to the regulation of NF-κB/NLRP3 axis. Hence, in this study, we set out to investigate whether HPC attenuates neuronal damage and microglial activation through inhibiting NF-κB/NLRP3 axis mediated by p-MLKL after tGCI in CA1 of male rats. We found that HPC decreased NLRP3 inflammasome in microglia and inhibited M1 polarization of microglia in CA1 after tGCI. Mechanistically, HPC inhibited the activation of NF-κB signaling pathway and reduced the mRNA and protein levels of NLRP3 inflammasome after tGCI. Additionally, the knockdown of p-MLKL by short hairpin RNA (shRNA) administration inhibited the activation of the NF-κB signaling pathway and reduced the formation of NLRP3 inflammasome, thus attenuating M1 polarization of microglia and decreasing the release of interleukin 1 beta (IL-1β) and necrosis factor alpha (TNF-α) in CA1 post ischemia. We consider that p-MLKL in microglia may be derived from necroptotic neurons after tGCI. In conclusion, the new finding in this study is that HPC-induced neuroprotection against tGCI through inhibiting NF-κB/NLRP3 pathway mediated by p-MLKL.
Methods using in vitro processes are disclosed for inducing or enhancing expression of enteric bacterial antigens or virulence factors. The methods, therefore, produce antigencially enhanced enteric bacteria. Also methods for using the antigenically enhanced bacteria are also disclosed, as well as vaccines containing the enteric bacteria. Specifically, a whole enteric bacteria or components thereof are provided by Helicobacter species. Also there are other enteric bacteria which are useful for the disclosed invention. One type, Campylobacter jejuni is graphically depicted wherein the results of high-performance liquid chromatography of monosaccharides from surface extract hydrolysates of C.jejuni are shown.
Intravenous administration of a liver-directed AAV vector could lead to liver enzyme elevations (transaminitis), especially ALT elevation. Transaminitis is presumed to occur due to immune-mediated injury of transduced hepatocytes and may reduce the therapeutic efficacy of AAV-vector based gene therapy.

Majority of patients treated with ROCTAVIAN experienced ALT elevations. Most ALT elevations occurred within the first year following ROCTAVIAN administration, especially within the first 26 weeks, were low-grade, and resolved. The median time (range) to the first ALT elevation (defined as ALT ≥ 1.5 × baseline or above ULN) was 7 weeks (0.4, 159 weeks) and the median duration (range) was 4 weeks (0.1, 135 weeks). Some ALT elevations were associated with a decline in factor VIII activity.

The majority of the 112 patients in the clinical trial of ROCTAVIAN required corticosteroids for ALT elevation [see Adverse Reactions (6.1) and Clinical Studies (14)]. The median duration (range) of corticosteroid use was 35 weeks (3, 120 weeks). The median duration (range) of alternate immunosuppressive medications use was 26 weeks (6, 118 weeks). In 20 (18%) patients the duration of immunosuppression was > 1 year.

Monitor ALT and institute corticosteroid treatment in response to ALT elevations, as required. Monitor ALT and factor VIII activity levels weekly and, as clinically indicated, during corticosteroid therapy [see Dosage and Administration (2.3)]. Monitor for and manage adverse reactions secondary to corticosteroid therapy.

Since some ALT elevations have been attributed to alcohol consumption in clinical studies, patients should abstain from alcohol consumption for at least a year following ROCTAVIAN infusion and limit alcohol use thereafter. Concomitant medications may cause hepatotoxicity, or decrease factor VIII activity, or change plasma corticosteroid levels which may impact liver enzyme elevation and/or factor VIII activity [see Drug Interactions (7.0, 7.1, 7.2)]. Closely monitor concomitant medication use including herbal products and nutritional supplements and consider alternative medications in case of potential drug interactions.
The nutritional therapy of group II patients will start post-surgery. It will be based on early enteral nutrition with elementary diet (Peptisorb) with simultaneous parenteral nutrition with two-chamber bag with 480 kcal energetic value and 5.7g of N contained in standard amino acids administered via peripheral veins. Additionally, glutamine (100 ml of Dipeptiven) will be added to the two-chamber bag. The parenteral nutrition will be administered for five days.
Genitourinary syndrome of menopause is a comprehensive term that groups genital, urinary and sexual signs and symptoms mainly due sex hormone deficiency and aging, with a crucial impact on quality of life of midlife women. While this broad definition captures the common underlying physiopathology and the frequent overlap of symptomatology, improving knowledge about different components of genitourinary syndrome of menopause may be relevant for individualized treatment, with possible implications for efficacy, compliance and satisfaction. This narrative review focuses on the vulvar component of genitourinary syndrome of menopause, highlighting anatomical and functional peculiarities of the vulva that are responsible for some of the self-reported symptoms, as well as specific signs at physical examination. Increasing evidence points towards a pivotal role of vulvar vestibular health in the occurrence of sexual pain, one of the most common and distressing symptoms of genitourinary syndrome of menopause, which should be evaluated with validated scales taking a biopsychosocial perspective. This is an essential step in the recognition of different phenotypes of genitourinary syndrome of menopause and in the assessment of the most effective diagnostic and therapeutic algorithm. Menopausal vulvar health deserves more research into tailored non-hormonal and hormonal treatment options.
Group A will consist of 50 participants with a diagnosis of one of the following cancers: breast, colorectal, or prostate cancers who received myelosuppressive cytotoxic chemotherapy at the time of COVID vaccination, or who received chemotherapy within 30 days prior to the initial or booster vaccination, or who started on chemotherapy within 30 days after the initial or booster COVID vaccination. Cytotoxic chemotherapy can be given either in the neoadjuvant/adjuvant setting or metastatic setting.
The efficacy of WAKIX for the treatment of cataplexy in adult patients with narcolepsy was evaluated in two multicenter, randomized, double-blind, placebo-controlled studies (Study 3; NCT01800045 and Study 1; NCT01067222). Patients ≥18 years of age who met the International Classification of Sleep Disorders (ICSD-2) criteria for narcolepsy with cataplexy with at least 3 cataplexy attacks per week and an ESS score of ≥12 were eligible to enroll in Study 3; patients meeting the ICSD-2 criteria for narcolepsy (with or without cataplexy) and an ESS score of ≥14 were eligible to enroll in Study 1.

Study 3 included a 7-week treatment period: a 3-week dose titration phase followed by a 4-week stable dose phase. 105 patients were randomized to receive WAKIX or placebo. The dose of WAKIX was initiated at 4.45 mg once daily for the first week, increased to 8.9 mg for the second week, and could remain the same or be decreased or increased at the next two weekly intervals to a maximum of 35.6 mg, based on clinical response and tolerability. No dose adjustments were permitted during the 4-week stable dose phase. 65% of patients reached a stable dose of 35.6 mg. Median age in the study was 37 years and 51% of the patients were male. Race was not collected in this study.

WAKIX demonstrated statistically significantly greater improvement on the primary endpoint, the change in geometric mean number of cataplexy attacks per week from baseline to the average of the 4 week stable dosing period for WAKIX compared to placebo (Table 4).

Study 1 was described in Section 14.1. In the subset of patients with a history of cataplexy (n=49), WAKIX demonstrated statistically significantly greater improvement on the secondary endpoint, the change from baseline in geometric mean daily rate of cataplexy at Week 8 for WAKIX compared to placebo (Table 4).

In both Study 3 and Study 1, examination of demographic subgroups by sex did not suggest differences in response.
Long noncoding (Lnc) RNAs are novel regulators in melanoma. Lnc nuclear enriched autosomal transcript 1 (NEAT1) was reportedly upregulated in melanoma; however, the functional roles and mechanisms of Lnc NEAT1 need further investigation. Therefore, we used quantitative real-time PCR to determine the mRNA levels of Lnc NEAT1, miR-152-3p, and cyclin-dependent protein kinase 6 (CDK6). The protein level of CDK6 was determined by Western blot. Cell counting kit 8 and colony formation assays were used to assess cell proliferation. Cell migration was measured by wound healing and Transwell assays. Direct binding of the indicated molecules was verified by an RNA-binding protein immunoprecipitation assay and a dual luciferase reporter assay. The results revealed that Lnc NEAT1 and CDK6 were elevated, while miR-152-3p was downregulated in melanoma. Furthermore, Lnc NEAT1 was positively correlated with CDK6 expression and negatively correlated with miR-152-3p level. Furthermore, Lnc NEAT1 facilitated proliferation, migration, and invasion of melanoma cells. The underlying mechanism is that Lnc NEAT1 serves as a sponge for miR-152-3p to suppress the inhibitory effect of miR-152-3p on CDK6. Furthermore, the miR-152-3p/ CDK6 axis was implicated in the progression of melanoma accelerated by Lnc NEAT1. Taken together, Lnc NEAT1 may promote melanoma development by serving as an endogenous sponge of miR-152-3p, increasing CDK6 expression, and identifying a new target for the treatment of melanoma.
A novel feline fibroblastic cell line infected with Snyder-Theilen feline leukemia virus is provided. The cell line produces large amounts of FeLV when cultured in a medium free from serum supplement. The latter aspect is a substantial advantage since it reduces the expense of culturing and eliminates the need to separate serum from culture medium prior to preparing a vaccine. Feline fibroblastic cell line FF64/280 was deposited at the American Type Culture Collection on Apr. 17, 1984, and granted accession no. VR 2085.
The study was planned as a parallel, single-blind, randomized, controlled experimental study with a pretest-posttest design. The sample group of the research was the nursing department of a Faculty of Health Sciences in Pamukkale University. Eligibility was determined by the Premenstrual Syndrome Scale and personal information form. The sample size was calculated in the PS Power and Sample Size Calculations 3.1.6 program by using data from a previous study with a large effect size (α =0.05, d=0.86). Accordingly, it was found that at least 32 participants should be taken for each group to sampling for 80% power. To avoid possible data loss, all participants (n=74) determined to be eligible were included in the study. A simple randomization method was used in this study. Outcomes were measured at baseline, 4 weeks, and 12 weeks after the intervention began. Data were collected using the Premenstrual Syndrome Scale, Premenstrual Symptoms Impact Scale, System Usability Scale, and personal information form.
The XIENCE 28 USA Study will evaluate the safety of 1-month DAPT following XIENCE implantation in HBR patients. A minimum of 640 to a maximum of 800 subjects will be registered from approximately 50 sites in the United States and Canada. Subject registration is capped at 75 per site. Eligibility of P2Y12 receptor inhibitor discontinuation will be assessed at 1-month follow-up. Subjects who are free from myocardial infarction (MI), repeat coronary revascularization, stroke, or stent thrombosis (ARC definite/probable) within 1 month (prior to 1-month visit but at least 28 days) after stenting AND have been compliant with 1-month DAPT without interruption of either aspirin and/or P2Y12 receptor inhibitor for \> 7 consecutive days are considered as "1-month clear", and will discontinue P2Y12 receptor inhibitor as early as 28 days and continued with aspirin monotherapy through 12-month follow-up.

All registered subjects will be followed at 1, 3, 6 and 12 months post index procedure. The data collected from the XIENCE 28 USA Study will be pooled with the data from the XIENCE 28 Global Study (Protocol # ABT-CIP-10235) to compare with the historical control of non-complex HBR subjects treated with standard DAPT duration of up to 12 months from the XIENCE V USA Study.
This study evaluated the effectiveness and cost-effectiveness of two types of outpatient treatment with and without Assertive Continuing Care (ACC) for 320 adolescents with substance use disorders. Study participants were randomly assigned to one of four conditions: (a) Chestnut's Bloomington Outpatient Treatment (CBOP) without ACC; (b) CBOP with ACC; (c) Motivational Enhancement Therapy/Cognitive Behavior Therapy-7 session model (MET/CBT7) without ACC; and (d) MET/CBT7 with ACC. All study conditions attained high rates of participant engagement and retention. Follow-up interviews were completed with over 90% of the adolescents at three, six, nine, and 12 months after treatment admission. There was a significant time by condition effect over 12 months, with CBOP having a slight advantage for average percentage of days abstinent. Unlike previous findings that ACC provided incremental effectiveness following residential treatment, there were no statistically significant findings with regard to the incremental effectiveness of ACC following outpatient treatment. Analysis of the costs of each intervention combined with its outcomes revealed that the most cost-effective condition was MET/CBT7 without ACC.
We are proposing a randomized, parallel-groups 5-week study of relapse prevention in detoxified opioid-dependent individuals. This trial represents an initial test of the feasibility and efficacy of an outpatient opioid detoxification strategy employing induction onto long-acting naltrexone (Vivitrol), in combination with the recently adapted version of Behavioral Naltrexone Therapy for Depot Naltrexone (Depot-BNT). Participants will be randomized into one of two outpatient detoxification strategies: (1) standard 7-day buprenorphine induction and taper from 8 mg to 0 mg (N=33), followed on Day 15 by a naloxone challenge and a dose of long-acting injectable naltrexone (Vivitrol) (consistent with the FDA-approved recommendation of 7 or more days between last opioid dose and Vivitrol induction) vs. (2) a modification of our current inpatient naltrexone induction procedure, consisting of a single day of buprenorphine followed by a washout day and 4 days of ascending oral naltrexone doses, followed by long-acting injectable naltrexone (Vivitrol) 380 mg on Day 8 (N=67). We are seeking to obtain Vivitrol samples from Alkermes; if we are successful in obtaining such samples, we will offer all participants who complete the study a second injection 4 weeks after the first, and a third injection will be offered at Week 12. All participants will receive an intensive behavioral therapy for five weeks and will be followed for up to 24 weeks to assess the long-term outcome of the initial treatment. Study assessments will be collected at baseline and at each study visit (twice weekly in Weeks 2-5; weekly in Weeks 6-9 for participants who receive a second Vivitrol injection and participate in follow-up care). Repeated assessments will also be completed at one and four months following the end of treatment. The primary aim of this study is to test the hypothesis that an outpatient opioid detoxification strategy using naltrexone will increase the likelihood of successful induction onto long-acting injectable naltrexone, compared to a buprenorphine taper in opioid-dependent patients. The primary outcome measure will be percentage in each treatment group (oral naltrexone vs. buprenorphine taper) receiving the Vivitrol injection at Day 8 or 15. Key secondary outcomes will be: two-week opioid abstinence during Weeks 4-5, retention in the 8-day detoxification procedure (time to dropout) and severity of opiate withdrawal during the first 5 weeks of treatment. We anticipate that the outpatient opioid detoxification method developed in this project will be uniquely suited to the needs of the rapidly expanding population of prescription opioid-abusing individuals seeking an alternative to opioid agonist maintenance. The current proposal will also yield important data on how to improve long-term outcomes for the buprenorphine taper method of opioid detoxification, through the addition of long-acting naltrexone.
The invention mainly relates to application of five shikonin derivatives to preparation of pyruvate kinase inhibitors. The shikonin derivatives are one of deoxyshikonin, isobutyryl shikonin, beta,beta-dimethylacrylshikonin, Isovalerylshikonin and [(2-methyl-n-butyl)shikonin. A currently reported M2 pyruvate kinase (PKM2) inhibitor is Compound 3. According to the invention, natural shikonin derivatives have higher inhibiting effects on the PKM2 compared with the Compound 3. The natural shikonin derivatives serving as pyruvate kinase inhibitors have important application value. The invention has the advantages that: the five new pyruvate kinase inhibitors, namely natural shikonin derivatives, provide bases for screening of new medicines and have important application prospects.
Process for stimulating a lymphocyte proliferative response in humans is claimed comprising treatment with a recombinant HIV portion of an ITLV-III protein selected from R10, PB1, 590 and KH1. Novel recombinant HTLV-III fusion proteins denoted R10, PB1, 590, KH1 and the HIV portion of each of these proteins are useful in the diagnosis, prophylaxis or therapy of AIDS. The proteins are esp. useful for prepg vaccines for the HTLV-III virus. Plasmid pR10 contains 1275 bp of DNA encoding the HTLV-III env gene from the KpnI site to the BglII site. This plasmid can be used to produce the novel recombinant HTLV-III 95kD fusion protein R10. Plasmid pPB1 contains 540 bp of DNA encoding the HTLV-III env gene from the PVuII site to the BglII site. This plasmid can be used to produce the novel recombinant HTLV-III 26 kD fusion protein PB1. Plasmid p590 contains 1055 bp of DNA encoding the HTLV-III env gene from the PVuII site to the Hind III site. This plasmid can be used to produce the novel recombinant HTLV-III 86kD protein 590. Plasmid pKH1 contains 1830 bp of DNA encoding the HTLV-III gene from the KpnI site to the Hind III site. This plasmid can be used to produce the novel recombinant HTLV-III 70kD protein KH1. Oligonucleotide-directed site-specific mutagenesis can be used to eliminate the non-HTLV-III amino acids blanking the env gene fusion proteins.
The Kinesio Taping group (KTG) (n = 31 elderly women) were submitted to the protocol of applying Kinesio Taping for gastrocnemius muscle and the muscles of the median foot. The application of the tapes was bilateral limbs. The subjects were evaluated post-application and 48 hours after application of the tape.
To assess the efficacy of stent grafts (SGs) in managing central venous obstruction disease (CVOD) in hemodialysis (HD) patients with arteriovenous (AV) access, and to identify predictive factors influencing the SG treatment outcomes. HD subjects with CVOD who underwent SGs placement at our center between August 2018 and June 2022 were enrolled. Survival curve analysis using the Kaplan-Meier method and log-rank test was performed. Cox proportional hazards regression analysis was employed to identify predictive factors associated with outcomes. A total of 59 SG implantation procedures for CVOD were analyzed, comprising 30 cases of stenosis and 29 cases of occlusion. The access circuit primary patency (ACPP) at 6, 12, and 24 months post-SG placement were 80.9%, 53.8%, and 31.4%, respectively, while, the target lesion primary patency (TLPP) were 91.3%, 67.6%, and 44.5%, respectively. Subgroup analysis revealed higher TLPP in the stenosis group compared to the occlusion group, although the difference was not statistically significant (P = 0.165). The TLPP was significantly improved by SG placement in those who had antecedent balloon dilations (P < 0.001). Cox proportional hazards regression identified target lesion length ≥ 30 mm and procedure defects as independent predictors of lower TLPP after SG treatment for CVOD in HD patients. SG placement demonstrates safety and efficacy in managing CVOD among HD patients, leading to improved TLPP of endovascular therapy (EVT) for CVOD. Notably, long target lesions (≥ 30 mm) and procedure defects emerged as predictive factors influencing TLPP.
It is intended to provide a method of screening a chemical which requires little labor and is usable as a substitute for vivisection and an apparatus therefor. A plate 4 made of a transparent material is provided with a plural number of wells 5. The wells 5 contain a liquid enabling the development of fish embryos and a test chemical. Fish embryos are soaked in the wells 5. After a definite period of time at a definite temperature, each embryo develops into an individual. In case where the test chemical affects the development of the embryo, the embryo is malformed or dies.