anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Bone and skeletal muscle are in a single unit that interacts with each other structurally and functionally. While myokines synthesized and released in skeletal muscle modulate the bone formation and destruction process, osteokines synthesized and released by bone cells have positive or negative effects on muscle (4,5,6,7,8,9). In addition to humoral crosstalk mechanisms between muscle and bone, there is also a neuronal crosstalk mechanism defined as bone myoregulation reflex. The aim of this study is to determine the contribution of bone myoregulation reflex as a neuronal crosstalk mechanism on the development of sarcopenia in postmenopausal and senile osteoporosis (10,11,12,13,14). Osteoporotic cases would be determined by standard DXA measurements.

The vibration will be applied with the PowerPlate® Pro5 whole-body vibration (London UK) device. The vibration amplitude will be 2 mm. The vibration frequency will be 30, 33, and 36 Hz. Each vibration frequency will be applied for 45 seconds. A 5-second rest period will be applied between vibrations of 45 seconds.

Surface EMG recordings will be taken from the right soleus muscle using the bipolar technique. A pair of self-adhesive Ag/AgCl (Redline®) electrodes will be adhered to the skin according to the SENIAM protocol(2). Recordings will be taken in the 1-500 Hz frequency band. Surface electromyography (EMG) recordings will be taken with a PowerLab ® (ADInstruments, Oxford, UK) data recorder with a sample rate of 20 KHz. EMG recordings will be analyzed offline with LabChart7 Pro® version 7.3.8 (ADInstruments, Oxford, UK). The acceleration measurement data will be recorded with the PowerLab (ADInstrument London) data acquisition simultaneously with the EMG recording. Acceleration recording will be made with a sample rate of 20 KHz.
Provided are an anti-PD-L1 and 4-1BB bifunctional antibody and medical use thereof. The selected 4-1BB antibody requires the support of a cross-linking effect in terms of immunoreactivity stimulation. Without the cross-linking effect, the 4-1BB antibody has no activity and thus does not produce toxic and side effects in the liver. In a tumor environment, tumor cells have relatively high levels of PD-L1 expression. The PD-L1/4-1BB bifunctional antibody binds by means of a PD-L1 antibody portion thereof to PD-L1 on the surface of a tumor cell, providing a relatively strong cross-linking effect for the 4-1BB antibody. Therefore, the immunostimulatory activity of the PD-L1/4-1BB bifunctional antibody can be significantly improved specifically in the tumor microenvironment, thereby avoiding or reducing the toxic and side effects produced by the 4-1BB antibody in the liver.
Serious and occasionally fatal hypersensitivity (anaphylactic) reactions have been reported in patients receiving therapy with beta-lactams. These reactions are more likely to occur in individuals with a history of sensitivity to multiple allergens. There have been reports of individuals with a history of penicillin hypersensitivity who have experienced severe hypersensitivity reactions when treated with another beta-lactam. Before initiating therapy with INVANZ, careful inquiry should be made concerning previous hypersensitivity reactions to penicillins, cephalosporins, other beta-lactams and other allergens. If an allergic reaction to INVANZ occurs, discontinue the drug immediately. Serious anaphylactic reactions require immediate emergency treatment as clinically indicated.
Sustained delivery compositions that modulate the release of incorporated prophylactic, therapeutic, and/or diagnostic agents, and methods of preparation and use thereof, are disclosed. In particular embodiments, the compositions include a polymeric matrix; a prophylactic, therapeutic, and/or diagnostic agent dispersed and/or dissolved within the polymeric matrix; and a carbohydrate component that is separately dispersed within the polymeric matrix. The carbohydrate component modulates the release of the incorporated agent from the polymeric matrix. The compositions can be prepared by dissolving a biocompatible polymer in a solvent to form a polymer solution, and separately dispersing a carbohydrate and a prophylactic, therapeutic, and/or diagnostic agent within the polymer solution. The polymer solution is then solidified to form a polymeric matrix, wherein a significant amount of the carbohydrates is dispersed in the polymeric matrix separately from the incorporated agent. In particular embodiments, the compositions include a polymeric matrix and a B1 peptide antagonist dispersed within the polymeric matrix.
A packaging cell line capable of complementing recombinant adenoviruses based on serotypes from subgroup B, preferably adenovirus type 35. The cell line is preferably derived from primary, diploid human cells (e.g., primary human retinoblasts, primary human embryonic kidney cells and primary human amniocytes) which are transformed by adenovirus E1 sequences. Also disclosed is a cell line derived from PER.C6 (ECACC deposit number 96022940), which cell expresses functional Ad35 E1B sequences. The new cell lines are useful for producing recombinant adenoviruses designed for gene therapy and vaccination.  The cell lines can also be used for producing human recombinant therapeutic proteins. In addition, the cell lines are useful for producing human viruses other than adenovirus such as influenza virus, herpes simplex virus, rotavirus, measles virus.
BACKGROUND: The concept of schizotypal personality disorder (SPD) emerged from observations of personality characteristics common in relatives of schizophrenic patients. While often studied in family designs, few studies and none with genetic measures, have examined SPD in epidemiological samples.
METHODS: We studied individuals born in Sweden 1940-2000 with an ICD-10 diagnosis of SPD with no prior schizophrenia (SZ) diagnosis (n = 2292). Demographic features, patterns of comorbidity, and Family Genetic Risk Scores (FGRS) were assessed from multiple Swedish registries. Prediction of progression to SZ was assessed by Cox models.
RESULTS: SPD was rare, with a prevalence of 0.044%, and had high levels of comorbidity with autism spectrum disorder (ASD), OCD, ADHD, and major depression (MD), and increased rates of being single, unemployed and in receipt of welfare. Affected individuals had elevated levels of FGRS for SZ (+0.42), ASD (+0.30), MD (+0.29), and ADHD (+0.20). Compared to cases of schizophrenia, they had significantly lower rates of FGRSSZ, but significantly elevated rates of genetic risk for ASD, MD, and ADHD. Over a mean follow-up of 8.7 years, 14.6% of SPD cases received a first diagnosis of SZ, the risk for which was significantly increased by levels of FGRSSZ, male sex, young age at SPD diagnosis and an in-patient SPD diagnosis and significantly decreased by comorbidity with MD, ASD, and ADHD.
CONCLUSIONS: Our results not only support the designation of SPD as a schizophrenia spectrum disorder but also suggest potentially important etiologic links between SPD and ASD and, to a lesser extent, ADHD, OCD, and MD.
The devastating developmental and epileptic encephalopathy of infantile epileptic spasms syndrome (IESS) has numerous causes, including, but not limited to, brain injury, metabolic, and genetic conditions. Given the stereotyped electrophysiologic, age-dependent, and clinical findings, there likely exists one or more final common pathways in the development of IESS. The identity of this final common pathway is unknown, but it may represent a novel therapeutic target for infantile spasms. Previous research on IESS has focused largely on identifying the neuroanatomic substrate using specialized neuroimaging techniques and cerebrospinal fluid analysis in human patients. Over the past three decades, several animal models of IESS were created with an aim to interrogate the underlying pathogenesis of IESS, to identify novel therapeutic targets, and to test various treatments. Each of these models have been successful at recapitulating multiple aspects of the human IESS condition. These animal models have implicated several different molecular pathways in the development of infantile spasms. In this review we outline the progress that has been made thus far using these animal models and discuss future directions to help researchers identify novel treatments for drug-resistant IESS.
Active surveillance (AS) is a conservative management option recommended for patients diagnosed with low-risk prostate cancer (PCa) and selected cases with intermediate-risk PCa. The adoption of prostate MRI in the primary diagnostic setting has sparked interest in its application during AS. This review aims to examine the role and performance of multiparametric MRI (mpMRI) across the entire AS pathway, from initial stratification to follow-up, also relative to the utilization of the Prostate Cancer Radiological Estimation of Change in Sequential Evaluation (PRECISE) criteria. Given the high negative predictive value of mpMRI in detecting clinically significant PCa (csPCa), robust evidence supports its use in patient selection and risk stratification at the time of diagnosis or confirmatory biopsy. However, conflicting results have been observed when using MRI in evaluating disease progression during follow-up. Key areas requiring clarification include addressing the clinical significance of MRI-negative csPCa, optimizing MRI quality, determining the role of biparametric MRI (bpMRI) or mpMRI protocols, and integrating artificial intelligence (AI) for improved performance. CLINICAL RELEVANCE STATEMENT: MRI plays an essential role in the selection, stratification, and follow up of patients in active surveillance (AS) for prostate cancer. However, owing to existing limitations, it cannot fully replace biopsies in the context of AS. KEY POINTS: Multiparametric MRI (mpMRI) has become a crucial tool in active surveillance (AS) for prostate cancer (PCa). Conflicting results have been observed regarding multiparametric MRI efficacy in assessing disease progression. Standardizing MRI-guided protocols will be critical in addressing current limitations in active surveillance for prostate cancer.
OBJECTIVES: Our goal was to quantify the independent association of brain microbleeds with future intracranial hemorrhage (ICrH). Microbleed findings on brain magnetic resonance imaging (MRI) may identify distinctive risk factors for ICrH which could inform the anticoagulant therapy decision for atrial fibrillation (AF) patients. Our study design includes patients with MRIs for numerous reasons, not limited to evaluation of stroke.
MATERIALS AND METHODS: The source population was all patients with AF from a nationwide Swedish health care register. Case patients had an ICrH between 2006 and 2013 and ≥1 brain MRI for an unrelated condition before the ICrH. Each case was matched to four controls who had a brain MRI without a subsequent ICrH. The MRIs were re-reviewed by neuroradiologists. Associations between MRI findings and subsequent ICrH were assessed using logistic regression, adjusting for comorbidities and antithrombotic medications.
RESULTS: A total of 78 cases and 312 matched controls were identified; 29 cases and 79 controls had MRI sequences suitable for analysis of microbleeds. Patients with ≥10 microbleeds had a markedly increased risk of ICrH (adjusted odds ratio 14.56; 95 % confidence interval: 2.86-74.16, p < 0.001). All patients with ≥10 microbleeds had microbleeds in the lobar region and ≥10 lobar microbleeds was associated with intracerebral hemorrhages, univariable OR 8.54 (2.01-36.33), p = 0.004.
CONCLUSIONS: Leveraging a nationwide database with brain imaging obtained prior to ICrH, we identified a strong association between ≥10 microbleeds on brain MRI and subsequent ICrH among AF patients. Lobar brain regions were involved whenever there were ≥10 microbleeds. Brain MRIs may help optimize the anticoagulation decision in selected AF patients.
A local and site-specific drug delivery apparatus for delivering a drug to a specific site is characterized by the combination of a carrier material which reflects or absorbs or emits electromagnetic or mechanical (e.g. ultrasonic) vibrations enabling the monitoring of the material, a drug associated with the carrier material, and a local-delivery mechanism for delivering the carrier material and the drug to a specific site. The local-delivery mechanism may comprise a local-delivery catheter, such as a balloon-type catheter, and the drug delivery apparatus may additionally include a monitor for monitoring the delivery of the drug to the specific site, such as an ultrasonic imaging system. The drug delivery apparatus may also include a vibration generator for inducing release of the drug from the carrier material when the carrier material is at the specific site, such as a generator of ultrasonic energy. Alternatively, the local-delivery mechanism may comprise a targeting agent associated with the carrier material, the targeting agent capable of binding to the specific site within the individual. The targeting agent may be a protein or an antibody, such as a glycogen IIa/IIB receptor antibody, Von Willebrand's factor antibody, an antitumor antibody, hepatic cellular antibody, a white blood cell antibody, or antifibrin.
Up to 12 patients will receive three weekly CAR.B7-H3 T cell product infusions at the same dose. To determine the recommended phase 2 dose (RP2D), a modified 3+3 dose escalation design will be used to evaluate two dose levels: Dose Level 1 (7.5x10\^7 cells/infusion), Dose Level 2 (2x10\^8 cells/infusion). If this dose is not tolerated, then a lower dose of 3.75 × 10\^6 cells/infusion will be explored. Up to 3 dose levels of CAR.B7-H3 cells will be tested with at least 3 patients enrolled at each dose cohort before dose escalation is considered based on the incidence of dose limiting toxicity (DLT). An expansion cohort will enroll up to 9 patients at the recommended phase 2 dose. Prior to receiving the infusions, patients will undergo lymphodepletion with fludarabine and cyclophosphamide.
The study will be conducted in Conservative Dentistry Department, Faculty of Dentistry, Cairo University, The operator in charge will be: Mohamed Tarek Heiba. The researcher will bear ultimate responsibility for all activities associated with the conduct of a research project including recruitment of patients, explaining and performing the procedures to them,A total of 40 volunteer patients with at least 2 non-cavitated molar teeth will be assigned in this study. Patients will be randomly divided into two groups according to type of sealant (S) where in group S1, pits and fissures will be sealed with bioactive pits-and-fissure sealant; while group S2, pits and fissures will be sealed with fluoride releasing resin based pits and fissures sealant. Each restoration will be assessed after three, six months,The tooth will be illuminated with a violet light approximately 405 nm thus stimulating both prophyrins to emit red light that contains less energy. the denser the bacteria colonization on tooth's surface, the more intense the red fluorescent signal; in contrast sound enamel sent out a green fluorescent signal. These light signals are recorded by the highly developed optics and analyzed by the device's software. The software filters and quantifies the fluorescence emitted by the dental tissue and converts the relationship between green and red.
The present invention discloses techniques for operation of neurostimulation or drug delivery devices to stop treatment therapy during times when the patient does not need to be treated. Advantageously, the present invention reduces battery usage and/or drug dosage during periods when treatment therapy need not be provided. Further, the present invention slows or reduces the tolerance the patient may develop from the electrical stimulation or treatment therapy. In one embodiment, the present invention includes a timer or a real time clock for shutting off the device during periods when the patient is sleeping in accordance with a preset schedule. The present invention preferably turns off after the patient has fallen asleep and right before the patient has awakened. Alternatively, the invention may include a sensor for sensing conditions indicative of whether the patient is awake or asleep. This sensed information may also be used to determine whether the treatment therapy should be delivered or stopped.
Mass vaccination of children aged 6 weeks to 14 years old with pneumococcal conjugate vaccine. Children 6 weeks to 11 months old receive two doses, spaced 4 weeks apart. All other children receive a single dose. Vaccination is simultaneous, as per a campaign delivery strategy.
For those randomly assigned to the 3-year HFD group, services begin during the third trimester of pregnancy. These families are assigned a Family Support Worker, who begins to initiate contact with the family at approximately 6 months gestation, when possible, so that the family can be engaged and services begun at seven months gestation. The Family Support Worker will provide home visiting services according the existing HFD model, which combines the empirically supported Parents as Teachers Curriculum (see attached description of the Parents as Teachers curriculum) provided in accordance with Healthy Families America standards of service delivery. The 3-year HFD group will receive services to the child's third birthday.
An ultrasound-guided injection of Subsartorial saphenous nerve using Exparel 266 mg (20 cc vial) via a 21-gauge 4-inch Stimuplex A needle (B. Braun Medical Inc., Melsungen, Germany) was performed at mid-thigh level with a high-frequency linear ultrasound transducer. All regional anesthesia was performed by a trained anesthesiologist. Ultrasound pictures (pre-injection and post-injection) was obtained to verify proper local anesthetic placement.
AIMS: Vascular smooth muscle cell (VSMC) plasticity is a state in which VSMCs undergo phenotypic switching from a quiescent contractile phenotype into other functionally distinct phenotypes. Although emerging evidence suggests that VSMC plasticity plays critical roles in the development of vascular diseases, little is known about the key determinant for controlling VSMC plasticity and fate.
METHODS AND RESULTS: We found that smooth muscle cell-specific deletion of Lkb1 in tamoxifen-inducible Lkb1flox/flox;Myh11-Cre/ERT2 mice spontaneously and progressively induced aortic/arterial dilation, aneurysm, rupture, and premature death. Single-cell RNA sequencing and imaging-based lineage tracing showed that Lkb1-deficient VSMCs transdifferentiated gradually from early modulated VSMCs to fibroblast-like and chondrocyte-like cells, leading to ossification and blood vessel rupture. Mechanistically, Lkb1 regulates polypyrimidine tract binding protein 1 (Ptbp1) expression and controls alternative splicing of pyruvate kinase muscle (PKM) isoforms 1 and 2. Lkb1 loss in VSMC results in an increased PKM2/PKM1 ratio and alters the metabolic profile by promoting aerobic glycolysis. Treatment with PKM2 activator TEPP-46 rescues VSMC transformation and aortic dilation in Lkb1flox/flox;Myh11-Cre/ERT2 mice. Furthermore, we found that Lkb1 expression decreased in human aortic aneurysm tissue compared to control tissue, along with changes in markers of VSMC fate.
CONCLUSION: Lkb1, via its regulation of Ptbp1-dependent alterative splicing of PKM, maintains VSMC in contractile states by suppressing VSMC plasticity.
An investigator will deliver a 20-30-minute briefing on intervention delivery to all staff at participating practices, followed by one-on-one audit training (1 hour) with the staff member responsible for conducting the audit. Each practice conducts an audit of their patients with diabetes to identify all people who have not attended retinopathy screening with the national programme. At 6 months, practices conducts a re-audit. Practice staff add electronic alerts to the records of eligible patients, to prompt GPs and nurses to remind patients. Practices are reimbursed at study entry with further payment following intervention cessation based on number of patients audited. Face-to-face verbal reminders are delivered by GPs and practice nurses to eligible patients attending for an appointment during the study period. All eligible patients receive a reminder phone call from a practice nurse and a GP-endorsed reminder letter accompanied by an information leaflet.
Sham acupuncture plus standard care (SSC) will be provided. Subjects in the SSC group will receive 9 sessions of sham acupuncture and standard care for 3 weeks. The Streitberger sham acupuncture will be employed. The selection of acupoints is the same as ASC.
For patients who have never taken risperidone, establish tolerability with oral risperidone prior to initiating UZEDY.

UZEDY must be administered by a healthcare professional as an abdominal or upper arm subcutaneous injection. Do not administer UZEDY by any other route.

For detailed preparation and administration instructions, see Dosage and Administration (2.4).

To start UZEDY, switch from oral daily risperidone. Initiate UZEDY, as either a once monthly injection or a once every 2 month injection, the day after the last dose of oral therapy. See Table 1 to determine how to switch from oral risperidone to UZEDY once monthly (50 mg, 75 mg, 100 mg, or 125 mg) or once every 2 months (100 mg, 150 mg, 200 mg, or 250 mg) given via abdominal or upper arm subcutaneous injection. Neither a loading dose nor supplemental oral risperidone doses are recommended when switching. 

Patients can switch between doses of UZEDY once monthly and once every 2 months by administering the first dose of the new dosing regimen on the next scheduled date of administration in the original dosing regimen. Revise the dose administration schedule to reflect the change.

When a dose of UZEDY is missed, administer the next UZEDY injection as soon as possible. Do not administer more frequently than recommended.
<P>PROBLEM TO BE SOLVED: To provide a memantine medication solving the problem of Alzheimer's disease and Parkinson's disease not being fundamentally cured because of unknown causes, and achieving excellent therapeutic effects though the reasons are uncertain.  <P>SOLUTION: The causative agents of the diseases are homocystein and homocysteic acid. A metabolism promoter of these causative materials, e.g. pyrrolo-quinoline quinone of a green tea component, and an analogous compound thereof, materials inhibiting the cytotoxicities of the causative materials, and materials inhibiting the production of the causative materials can be therapeutic drugs in addition to the therapeutic agent by an antagonist of the homocysteic acid such as the memantine medication. These fundamental therapies become possible by using them.  <P>COPYRIGHT: (C)2005,JPO&NCIPI