anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Gastric cancer is the second most common malignant tumor in China, with the highest mortality rate among all types of malignant tumors. Surgical resection is still the most effective treatment for gastric cancer. Minimally invasive surgery breaks the traditional surgical concept that the laparotomy must be performed by laparotomy. It can complete the operation that required a large incision with minimal incision trauma, and has the advantages of less trauma, faster recovery and fewer complications. At present, the application of gastroscopy and laparoscopy for early gastric cancer has reached consensus at home and abroad. Endoscopic mucosal resection of early gastric cancer is suitable for patients with intramucosal cancer and no lymph node metastasis. However, the unclear exposure of the surgical field during the operation causes difficulty in operation or conversion to open surgery is a difficult problem facing this technique. The project designed a magnetic pulling unit that can be connected through an endoscope, including external abdominal magnets, internal abdominal magnets, connecting hooks, and micro surgical tweezers. Using magnetic anchoring technology, the magnetic pulling unit is anchored to the abdominal wall, and micro surgical tweezers are used. The tumor tissue is pulled indirectly, so that the mucosa is lifted up, which is beneficial to the peeling of the submucosa. This method increases the operating space of the main hand of the endoscope, and at the same time, the magnetic clamp is used to connect the clamps so that they can move in all directions, so as to achieve the desired traction of the tumor tissue site, fully expose the surgical field, and facilitate surgical anatomy.
Provided are methods of treating hyperglycemia using a STAT3 inhibitor. Also provided is a STAT3 inhibitor for use in treating hyperglycemia. Further provided are methods of treating impaired spatial vision using a STAT3 inhibitor. Also provided is a STAT3 inhibitor for use in treating impaired spatial vision. In certain embodiments, the STAT3 inhibitor is administered systemically. In certain embodiments, the STAT3 inhibitor is administered orally. In certain embodiments, the STAT3 inhibitor is a small molecule. In certain embodiments, the STAT3 inhibitor is 1-acetyl-5 -hydroxyanthracene- 9,10-dione (CLT-005) or a pharmaceutically acceptable salt thereof. Also provided is a pharmaceutical composition comprising CLT-005, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier, formulated for oral administration.
Temporal Lobe Epilepsy (TLE) is a chronic neurological disorder characterized by recurrent focal seizures originating in the temporal lobe. Despite the variety of antiseizure drugs currently available to treat TLE, about 30% of cases continue to have seizures. The etiology of TLE is complex and multifactorial. Increasing evidence indicates that Alzheimer's disease (AD) and drug-resistant TLE present common pathological features that may induce hyperexcitability, especially aberrant hyperphosphorylation of tau protein. Genetic polymorphic variants located in genes of the microtubule-associated protein tau (MAPT) and glycogen synthase kinase-3β (GSK3B) have been associated with the risk of developing AD. The APOE ε4 allele is a major genetic risk factor for AD. Likewise, a gene-dose-dependent effect of ε4 seems to influence TLE. The present study aimed to investigate whether the APOE ɛ4 allele and genetic variants located in the MAPT and GSK3B genes are associated with the risk of developing AD and drug-resistant TLE in a cohort of the Mexican population. A significant association with the APOE ε4 allele was observed in patients with AD and TLE. Additional genetic interactions were identified between this allele and variants of the MAPT and GSK3B genes.
Fifty one subjects with an excessive COS were included in this study. The subjects will be randomly divided into three groups; Group one (17 patients): leveling of COS using 0.017X0.025-inch stainless steel archwire. Group two (17 patients): leveling of COS using 0.019X0.025-inch stainless steel archwire. Group three (17 patients): leveling of COS using 0.021X0.025-inch Titanium molybdenum archwire.

In the three groups, a 5mm depth reverse COS will be inserted. Records consisted of lateral cephalograms (pre-treatment, at T0 and post-treatment), peri-apical radiographs (at T0 and at T5), study casts (pre-treatment and at each time point during the tudy). Patients will be followed up on monthly visits without removing leveling archwires where alginate impressions were taken for the lower arch. Pain scores during the first week of leveling will be recorded using visual analogue scale (VAS).The amount of COS correction in mm, changes in intercanine in mm, intermolar and arch length in mm, pain scores and lower incisors root resorptions in mm will be measured.
Nalmefene reverses the effects of natural and synthetic opioids, including respiratory depression, sedation, and hypotension. Pharmacodynamic studies have shown that nalmefene injection has a longer duration of action than naloxone injection at fully reversing doses. Nalmefene has no opioid agonist activity.

The effect of 2.7 mg OPVEE on remifentanil-induced respiratory depression in an experimental ventilatory-response to hypercapnia model, assessed by changes in minute ventilation (MV), was evaluated in sixty-one opioid-experienced, non-dependent subjects. In this study subjects started receiving a hypercapnic gas mixture (50% O2, 43% N2, 7% CO2) at -25 minutes. Just prior to initiation of remifentanil infusion at -15 minutes is the baseline MV (marked as 100% in Figure 1 and marked as observed data as liters/minute in Figure 2). Fifteen minutes after initiating remifentanil infusion, nadir in minute ventilation is observed at time zero, at which point OPVEE was administered. The subjects were then monitored for changes in MV over 120 minutes. Following OPVEE administration the time to onset of effect, that is onset of reversal of respiratory depression, was observed between 2.5 to 5 minutes (Figure 1 and Figure 2). At 5 minutes the estimated mean increase in minute ventilation was 5.745 L/min (Figure 2). Full recovery of respiratory drive was noted between 5 and 15 minutes after OPVEE administration (Figure 1 and Figure 2).

Figure 1: Percentage recovery of respiratory drive after infusion of remifentanil in CO2 stimulated minute ventilation (mean +/- standard deviation) in adult healthy volunteers treated with OPVEE (nalmefene) nasal spray

Figure 2: Reversal of Remifentanil-Induced Respiratory Depression (Mean Minute Ventilation +/- Standard Deviation) by OPVEE (nalmefene) nasal spray

Based on population pharmacokinetic/pharmacodynamic model simulations, the EC50 (drug concentration at which pharmacological effect is half maximum change in response) was 1.50 ng/mL for OPVEE following a single 2.7 mg administration. The time to reach EC50 was 4 minutes for OPVEE. The plasma concentrations remained above the EC50 for 5.94 hours for OPVEE.

Nalmefene is not known to produce respiratory depression, psychotomimetic effects, or pupillary constriction. No pharmacological activity was observed when nalmefene was administered in the absence of opioid agonists.

Nalmefene has not been shown to produce tolerance, physical dependence, or abuse potential.

Nalmefene can produce acute withdrawal symptoms in individuals who are opioid dependent.
OBJECTIVE: This study aimed to determine the effect of 5Hz neuronavigated repetitive transcranial magnetic stimulation (rTMS) to the affected primary motor cortex (M1) on pain, the effect of pain on activities of daily living, disability, mood, neurophysiological parameters and passive shoulder joint range of motion in patients with post-stroke shoulder pain.
DESIGN: Twenty two patients were randomized into an experimental group (rTMS, n=7) who received daily rTMS 5Hz 1000 pulses, five times/week for three weeks (15 sessions) to the affected M1 and a control group (n=11) who received sham stimulation. Outcome measures were Numeric Rating Scale (NRS), Brief Pain Inventory (BPI), Disabilities of the arm, shoulder, and hand questionnaire (Quick DASH), Hospital Depression Anxiety Scale (HADS), joint range of motion (ROM) measurements, neurophysiological parameters. Selected outcome measures were performed before treatment (T0), after the 5th session (T1) of rTMS treatment, after the 10th session (T2), after the 15th session (T3), and four weeks after the end of the treatment (T4). In the analysis of the outcomes, within-group comparisons were performed by using the Wilcoxon or Friedman test and between-group comparisons were performed by using the Mann-Whitney U test.
RESULTS: There was no statistically significant difference between and within groups in terms of change- and followup scores in the NRS measurements (p>0.05). BPI scale was found to be lower in rTMS group at T0 and T3 (p= 0.010). Quick-DASH scores at T4 were found to be significantly lower in rTMS group (p= 0.032). However, no difference was found within each group over time (p>0.05) and there was no statistical difference between the groups in terms of change scores (T3-T0 and T4-T0) (p>0.05) for BPI and Quick-DASH. In rTMS group, there was a statistically significant difference in shoulder external rotation at T3 compared to the baseline (T0) (p=0.039). However, the magnitude of external rotation change (T3-T0) with the treatment was comparable in the groups. No statistically significant change occurred in both treatment groups in other range of motion measurements.
CONCLUSION: High frequency neuronavigated rTMS to the affected M1 did not show any significant beneficial effect on pain, activities of daily living, disability, anxiety and depression, neurophysiological measurements and passive ROM over sham stimulation.
Examples herein may include a computer-implemented method for synchronizing data from multiple link coordinated sensing systems. The method may include receiving a measurement at a first time. The measurement may be associated with a sensing system. The measurement may be associated with a communications interface. The method may include obtaining a latency value. The latency value may be associated with the surgical sensing system. The latency value may be associated with the communications interface. The method may include applying a time code to the received measurement. The time code may be applied based on the first time and the obtained latency value. The method may include ordering an output based on the received measurement and time code.
Methods and compositions are provided for controlling cell distribution within an implantable bioartificial organ by exposing the cells to a treatment that inhibits cell proliferation, promotes cell differentiation, or affects cell attachment to a growth surface within the bioartificial organ. Such treatments include (1) genetically manipulating cells, (2) exposing the cells to a proliferation-inhibiting compound or a differentiation-inducing compound or removing the cells from exposure to a proliferation-stimulating compound or a differentiation-inhibiting compound; exposing the cells to irradiation, and (3) modifying a growth surface of the bioartificial organ with extracellular matrix molecules, molecules affecting cell proliferation or adhesion, or an inert scaffold, or a combination thereof. These treatments may be used in combination. Cells can be transformed with a proliferation-promoting gene such as the oncogene, SV40, linked to a regulatable promoter such as the Mx1 promoter, the promotor is activated in vitro to express the gene to result in cell proliferation, and the promotor is inactivated before or after insertion of the cells in the bioartificial organ to inhibit expression of the gene to reduce or stop cell proliferation in vivo. The promoter can be reactivated in vivo to again express the gene to result in further cell proliferation. The gene may be a proliferation-suppressing gene such as p53 gene or RB gene, or a differentiation-inducing gene such as high mobility group chromosomal protein 14. Inhibiting gene expression in vitro causes cell proliferation, and inducing gene expression reduces or stops cell proliferation in vivo.
DDX3X is a multifunctional ATP-dependent RNA helicase involved in several processes of RNA metabolism and in other biological pathways such as cell cycle control, innate immunity, apoptosis and tumorigenesis. Variants in DDX3X have been associated with a developmental disorder named intellectual developmental disorder, X-linked syndromic, Snijders Blok type (MRXSSB, MIM #300958) or DDX3X neurodevelopmental disorder (DDX3X-NDD). DDX3X-NDD is mainly characterized by intellectual disability, brain abnormalities, hypotonia and behavioral problems. Other common findings include gastrointestinal abnormalities, abnormal gait, speech delay and microcephaly. DDX3X-NDD is predominantly found in females who carry de novo variants in DDX3X. However, hemizygous pathogenic DDX3X variants have been also found in males who inherited their variants from unaffected mothers. To date, more than 200 patients have been reported in the literature. Here, we describe 34 new patients with a variant in DDX3X and reviewed 200 additional patients previously reported in the literature. This article describes 34 additional patients to those already reported, contributing with 25 novel variants and a deep phenotypic characterization. A clinical review of our cohort of DDX3X-NDD patients is performed comparing them to those previously published.
Patients receive pembrolizumab IV over 30 minutes on day 1. Cycles repeat every 3 weeks for up to 2 years (or up to 32 cycles) in the absence of disease progression or unacceptable toxicity. Patients also receive ferumoxytol IV and undergo MRI at baseline, 12 weeks after radiation, at suspected radiographic progression, and 6 weeks after suspected radiographic progression.
PURPOSE:To produce a polypeptide having HCV antigenic activity by culturing Eschericha coli transformed with a recombinant vector prepared by integrating a structural protein gene of hepatitis C virus in a culture medium. CONSTITUTION:Escherichia coli is transformed with a recombinant vector prepared by integrating a structural protein gene of hepatitis C virus expressed by formula I. The resultant transformed Escherichia coli is then cultured in a culture medium to produce a polypeptide having HCV antigenic activity. The produced polypeptide is subsequently collected from the resultant culture. The structural protein gene of the hepatitis C virus can be inserted into the downstream side of a promoter of a vector utilizing a restriction enzyme site derived from a linker added in preparing the cDNA library, a restriction enzyme site derived from a plasmid in which the structural protein gene is inserted or a restriction enzyme site in the interior of the structural protein gene, etc. The obtained recombinant vector is capable of expressing the structural protein gene of the hepatitis C virus in the bacterial cell of Escherichia coli.
Abnormal shifts in global climate, leading to extreme weather, significantly threaten the safety of individuals involved in outdoor activities. Hypothermia-induced coma or death frequently occurs in clinical and forensic settings. Despite this, the precise mechanism of central nervous system injury due to hypothermia remains unclear, hindering the development of targeted clinical treatments and specific forensic diagnostic indicators. The GEO database was searched to identify datasets related to hypothermia. Post-bioinformatics analyses, DEGs, and ferroptosis-related DEGs (FerrDEGs) were intersected. GSEA was then conducted to elucidate the functions of the Ferr-related genes. Animal experiments conducted in this study demonstrated that hypothermia, compared to the control treatment, can induce significant alterations in iron death-related genes such as PPARG, SCD, ADIPOQ, SAT1, EGR1, and HMOX1 in cerebral cortex nerve cells. These changes lead to iron ion accumulation, lipid peroxidation, and marked expression of iron death-related proteins. The application of the iron death inhibitor Ferrostatin-1 (Fer-1) effectively modulates the expression of these genes, reduces lipid peroxidation, and improves the expression of iron death-related proteins. Severe hypothermia disrupts the metabolism of cerebral cortex nerve cells, causing significant alterations in ferroptosis-related genes. These genetic changes promote ferroptosis through multiple pathways.
Epilepsy is a highly prevalent chronic neurological disorder with great negative impact on patients' daily lives. Despite this there is still no adequate technological support to enable epilepsy detection and continuous outpatient monitoring in everyday life. Hyperdimensional (HD) computing is a promising method for epilepsy detection via wearable devices, characterized by a simpler learning process and lower memory requirements compared to other methods. In this work, we demonstrate additional avenues in which HD computing and the manner in which its models are built and stored can be used to better understand, compare and create more advanced machine learning models for epilepsy detection. These possibilities are not feasible with other state-of-the-art models, such as random forests or neural networks. We compare inter-subject model similarity of different classes (seizure and non-seizure), study the process of creating general models from personal ones, and finally posit a method of combining personal and general models to create hybrid models. This results in an improved epilepsy detection performance. We also tested knowledge transfer between models trained on two different datasets. The attained insights are highly interesting not only from an engineering perspective, to create better models for wearables, but also from a neurological perspective, to better understand individual epilepsy patterns.
Odd Courses 1, 3, 5, 7: Rituximab 375 mg/m2 IV Day 1 \& 8 Courses 1 \& 3; Imatinib oral 600 mg days 1-14 Course 1 then continuously; Cyclophosphamide 300 mg/m2 IV every; 12 hours for 6 doses; Mesna 600 mg/m2/day IV Days 1-3; Doxorubicin 50 mg/m2 IV CVC Day 4; VSLI 2.25 mg/M2 IV Day 1 \& 8; Pegfilgrastim 6 mg/kg after chemotherapy + G-CSF 10 µg/kg/day; Dexamethasone 40 mg IV or P.O. daily days 1-4 and days 11-14 +/- 3 days.
<P>PROBLEM TO BE SOLVED: To efficiently execute medical service by an electronic medical chart method without using wasteful paper for a temporarily necessary document so as not to increase trash.  <P>SOLUTION: This electronic medical chart system uses electronic paper 10 rewritable plural times, capable of holding contents of electronically displayed information without electric power. In a medical institution, a computer executing management of a patient information database of a patient's case history, a medical treatment record or the like, or a service process of a receipt or the like is connected with a writing device 4 for writing the information into the electronic paper 10, the information about a patient having a medical examination is written into the electronic paper 10, and a medical worker executes the service while looking at the electronic paper 10. The temporarily necessary personal information or medical treatment information is written into the electronic paper 10 for use. Because the electronic paper 10 can be rewritten into the next information and be reused when the information becomes unnecessary, the trash of the wasteful paper is not generated.  <P>COPYRIGHT: (C)2004,JPO
The third group comprised 13 patients who were in the growth and developmental stage. The skeletal age of the individual was determined through the acquisition of hand-wrist X-rays and the application of the Greulich and Pyle atlas at T1.
After a six minute walk test, participant will sit down and rest for up to 1 hour. They will then be given a Fentanyl tablet to put in between upper gum and cheek. Study physician will determine the morphine equivalent daily dose (MEDD) in real time using standardized equianalgesic ratios. Based on clinical practice and similarly to the dose used for breakthrough pain, an FBT dose equivalent to 20-50% of the MEDD used. After 30 minutes, participant asked about any side effects they may be having, and repeat the walking test. During each walk test, participant asked 6 times how hard it is to catch their breath. The total distance walked will also be recorded. Completion of two questionnaires at beginning of study visit. It should take about 10 minutes to complete. At the end of study visit, completion of last questionnaire. It should take about 5 minutes to complete the questionnaire.
Part 1: Bilateral comparison. Patients will have two comparable Treatment Areas: PAT-001, 0.1% (e.g., left side) and Vehicle, 0.0% (e.g., right side). The application of vehicle only lasts from Weeks 0-8.
Azacitidine is an effective and well established therapy in patients with acute myeloid leukemia (AML). In fact, in previous measurable residual disease (MRD) triggered studies, azacitidine allowed for a delay towards an overt hematological relapse in the majority of patients. However, the majority of patients ultimately relapsed even though they received multiple cycles of preemptive therapy. Hypomethylating agents (HMA) can enhance antitumor immune responses by upregulating tumor antigene expression, class 1 major histocompatibility complex, and co-stimulatory molecules, while concurrently dampening this antitumor effect by upregulating expression of checkpoint receptors or ligands, including programmed cell death protein 1 (PD-1), programmed cell death ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). Upregulation of these immune checkpoint molecules might be a mechanism of resistance to hypomethylating drugs. It has been shown that PD-L1 Messenger ribonucleic acid (mRNA) is up-regulated acute myeloid leukemia cluster of differentiation 34 (CD34+) cells and importantly, patients resistant to treatment with hypomethylating agents such as azacitidine have an up-regulated expression compared to responding patients. In addition, it is known that PD-1 promoter demethylation correlates with a higher PD-1 expression and a worse response rate to hypomethylating agents as well as a shorter overall survival. In this context it is of note that PD-1 promoter demethylation can be caused by hypomethylating agents and hence the mode of action of the drug itself could cause resistance to therapy in these patients. This might also explain why hypomethylating agents are not curative and can not eradicate early leukemic progenitor cells. The investigators, therefore, perform a phase II trial evaluating a combination therapy of pembrolizumab and azacitidine in nucleophosmin (NPM1) mutated AML patients with MRD and impending hematological relapse after conventional chemotherapy. This trial aims at improving response rates observed with single agent azacitidine within the studies NCT00422890 and NCT01462578.
Synthesis and characterization of starch based pH-responsive nanoparticles for controlled drug delivery are described. Polymethacrylic acid grafted starch (PMAA-g-St) nanoparticles with various molar ratio of starch to MAA were synthesized by a new one-pot method that enabled simultaneous grafting of PMAA and nanoparticle formation in an aqueous medium. NMR data showed that polysorbate 80 was polymerized into the graft polymer. Nanoparticles were relatively spherical with narrow size distribution and porous surface morphology and exhibited pH-dependent swelling in physiological pH range. The particle size and magnitude of volume phase transition were dependent on PMAA content and formulation parameters such as surfactant levels, cross-linker amount, and total monomer concentration. The results showed that the new pH-responsive nanoparticles possessed useful properties for controlled drug delivery.
Cabozantinib 60 milligrams (mg) tablet, orally, once daily for up to 26 weeks. Participants received interventions as part of routine medical care.