anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Although immunotherapy is expanding treatment options for cancer patients, the prognosis of advanced cancer remains poor, and these patients must contend with both cancers and cancer-related thrombotic events. In particular, immune checkpoint inhibitors are associated with an increased risk of atherosclerotic thrombotic events. Given the fundamental role of platelets in atherothrombosis, co-administration of antiplatelet agents is always indicated. Platelets are also involved in all steps of cancer progression. Classical antithrombotic drugs can cause inevitable hemorrhagic side effects due to blocking integrin β3 bidirectional signaling, which regulates simultaneously thrombosis and hemostasis. Meanwhile, many promising new targets are emerging with minimal bleeding risk and desirable anti-tumor effects. This review will focus on the issue of thrombosis during immune checkpoint inhibitor treatment and the role of platelet activation in cancer progression as well as explore the mechanisms by which novel antiplatelet therapies may exert both antithrombotic and antitumor effects without excessive bleeding risk.
Recently-diagnosed (i.e. \< 6 months) primary ITP adult patients (≥ 18 years) characterized by platelet counts less than 100x109/L as defined by the International Working Group.
Early facial nerve reconstruction should be offered in every patient with oncological resections of the facial nerve due to the debilitating functional and psychosocial consequences of facial nerve palsy. Oncologic pathology or oncologic resection accounts for the second most common cause of facial nerve palsy. In the case of these acute injuries, selecting an adequate method for reconstruction to optimize functional and psychosocial well-being is paramount. Authors advocate consideration of the level of injury as a framework for approaching the viable options of reconstruction systematically. Authors breakdown oncologic injuries to the facial nerve in three levels in relation to their nerve reconstruction methods and strategies: Level I (intracranial to intratemporal), Level II (intratemporal to extratemporal and intraparotid), and Level III (extratemporal and extraparotid). Clinical features, common clinical scenarios, donor nerves available, recipient nerve, and reconstruction priorities will be present at each level. Additionally, examples of clinical cases will be shared to illustrate the utility of framing acute facial nerve injuries within injury levels. Selecting donor nerves is critical in successful facial nerve reconstruction in oncological patients. Usually, a combination of facial and nonfacial donor nerves (hybrid) is necessary to achieve maximal reinnervation of the mimetic muscles. Our proposed classification of three levels of facial nerve injuries provides a selection guide, which prioritizes methods for function nerve reconstruction in relation of the injury level in oncologic patients while prioritizing functional outcomes.
<P>PROBLEM TO BE SOLVED: To provide an IκB kinase inhibitor.  <P>SOLUTION: This invention relates to the treatment of cancer. In particular, this invention relates to the use of inhibitors of IκB kinase in order to disturb cancer cell proliferation and to treat cancer including multiple myeloma. This invention relates to a method for disturbing cancer cell proliferation. In particular, this invention provides a method for disturbing cancer cell proliferation by administering inhibitors of IκB kinase described in this specification. This invention further provides a method for treating cancer by administering the inhibitors of IκB kinase to a patient having cancer cells.  <P>COPYRIGHT: (C)2010,JPO&INPIT
Glucagon-like peptide 1 (GLP-1) regulates food intake, insulin production, and metabolism. Our recent study demonstrated that pancreatic α-cells-secreted (intraislet) GLP-1 effectively promotes maternal insulin secretion and metabolic adaptation during pregnancy. However, the role of circulating GLP-1 in maternal energy metabolism remains largely unknown. Our study aims to investigate systemic GLP-1 response to pregnancy and its regulatory effect on fetal growth. Using C57BL/6 mice, we observed a gradual decline in maternal blood GLP-1 concentrations. Subsequent administration of the GLP-1 receptor agonist semaglutide (Sem) to dams in late pregnancy revealed a modest decrease in maternal food intake during initial treatment. At the same time, no significant alterations were observed in maternal body weight or fat mass. Notably, Sem-treated dams exhibited a significant decrease in fetal body weight, which persisted even following the restoration of maternal blood glucose levels. Despite no observable change in placental weight, a marked reduction in the placenta labyrinth area from Sem-treated dams was evident. Our investigation further demonstrated a substantial decrease in the expression levels of various pivotal nutrient transporters within the placenta, including glucose transporter one and sodium-neutral amino acid transporter one, after Sem treatment. In addition, Sem injection led to a notable reduction in the capillary area, number, and surface densities within the labyrinth. These findings underscore the crucial role of modulating circulating GLP-1 levels in maternal adaptation, emphasizing the inhibitory effects of excessive GLP-1 receptor activation on both placental development and fetal growth.NEW & NOTEWORTHY Our study reveals a progressive decline in maternal blood glucagon-like peptide 1 (GLP-1) concentration. GLP-1 receptor agonist injection in late pregnancy significantly reduced fetal body weight, even after restoration of maternal blood glucose concentration. GLP-1 receptor activation significantly reduced the placental labyrinth area, expression of some nutrient transporters, and capillary development. Our study indicates that reducing maternal blood GLP-1 levels is a physiological adaptation process that benefits placental development and fetal growth.
Participants received oral dose of DEN 2.5 mg capsule once daily in the morning, 30 min prior to breakfast during the main phase/extension phase 12-weeks treatment period. Participants were dispensed 3 bottles (bottle A, B and C) and were instructed to take 1 capsule daily from each bottle such that taking 1 capsule from each bottle daily provided the appropriate dose of DEN 2.5 mg to the participants.
Patients can be helped to break free of addictive or habitforming narcotics and antidepressants, by treatment using two drugs. One drug is dextromethorphan (DM), which has been used for decades as an antitussive (coughsuppressing) drug in cough syrups. The other drug is an oxidase inhibitor which suppresses activity of a liver enzyme called cytochrome P4502D6 (also called debrisoquin hydroxylase, sparteine monooxygenase, cytochrome P450DB, and CYP2D6). In most patients, this oxidase enzyme rapidly degrades DM and converts it into a metabolite called dextrorphan. An oxidase inhibitor (such as quinidine) which suppresses cytochrome P4502D6 activity increases the halflife and concentration of DM in the circulating blood. When this combined treatment was administered orally to patients who had become dependent on morphine and antidepressant drugs because of chronic intractable pain, it initially helped the patients reduce their dosages of morphine and other drugs, including antidepressants. When additional testing was done, the combined treatment allowed patients to entirely terminate all use of morphine and antidepressants, with minimal withdrawal or other adverse effects. Importantly, these same patients received no substantial benefit from taking dm by itself, without an oxidase inhibitor. Accordingly, the combination of dextromethorphan plus an antioxidase drug can allow at least some patients to break entirely free of narcotics andor antidepressants, even after years of use for chronic pain and other medical problems, even when they are not substantially helped by dextromethorphan alone.
Emerging evidence suggests that low-grade systemic inflammation plays a key role in altering brain activity, behaviour and affect. Modulation of the gut microbiota using prebiotic fibre offers a potential therapeutic tool to regulate inflammation, mediated via the production of short-chain fatty acids (SCFA). However, the impact of prebiotic consumption on affective symptoms and the possible contribution from inflammation, gut symptoms and the gut microbiome are currently underexamined. In this 12-week study, the effects of a diverse prebiotic blend on inflammation, gut microbiota profiles and affective symptoms in a population with metabolic syndrome (MetS) were examined. Sixty males and females with MetS meeting the criteria for MetS were randomised into a treatment group (n 40), receiving 10 g per day of a diverse prebiotic blend and healthy eating advice, and a control group (n 20), receiving healthy eating advice only. Our results showed a significant reduction in high sensitivity C-reactive protein (hs-CRP) in the treatment (-0·58 [-9·96 to-2·63]) compared with control (0·37 [-3·64 to-3·32]), alongside significant improvements in self-reported affective scores in the treatment compared with the control group. While there were no differences in relative abundance between groups at week 12, there was a significant increase from baseline to week 12 in fecal Bifidobacterium and Parabacteroides in the treatment group, both of which are recognised as SCFA producers. Multivariate regression analyses further revealed an association between gastrointestinal symptoms and hs-CRP with affective scores. Together, this study provides preliminary support for a diverse prebiotic blend for mood, stress and anxiety.
<P>PROBLEM TO BE SOLVED: To provide an adoptive immunity gene cell therapy using a cell in which a foreign gene is transduced by a retrovirus.  <P>SOLUTION: An antigen gene is transduced into a precursor cell by using the retrovirus in which a variation is induced into NCR (negative control range) in LTR (terminal repeating sequence) and NRE (negative regulation range) in PBS (primer bound site). The precursor cell is differentiated into a desired cell to provide a cell suitable for adoptive immunotherapy. The cell differentiated and induced from the precursor cell is e.g. a dendritic cell.  <P>COPYRIGHT: (C)2006,JPO&NCIPI
Participants assigned to "nebulised UFH" will receive nebulised UFH in addition to the standard care required as determined by the treating team. Nebulised UFH (25,000 Units in 5 mL) will be administered 6-hourly via an Aerogen Solo vibrating mesh nebuliser while patients receive invasive mechanical ventilation in ICU and for a maximum of 10 days.
After a magnetic resonance imaging (MRI) scan of brain performed, an FLT PET scan using 3'-Deoxy-3'-18f-Fluorothymidine solution performed. After solution is injected into a vein, the PET scanner takes pictures of the radioactive solution as it moves through the body and collects at various sites in the body. The entire procedure should last about 60-70 minutes.
At the screening visit (Visit 1), following written informed consent, subjects will provide a medical, medication and migraine history. A physical and neurological exam and pregnancy test (if appropriate) will be performed. Vital signs will be recorded for all subjects. The Headache Impact Test (HIT-6) and Baseline Patient Perception of Migraine Questionnaire (PPMQ-R) will be completed with the Baseline Completeness of Response Survey (CORS) considering migraine therapy (triptan) utilized during the 3 months prior to enrollment. The Completeness of Response Survey will collect traditional and non-traditional symptoms. Subjects are instructed to treat all migraines that occur in the next 2 months. Subjects will treat with a single tablet of Treximet™ as soon as they have a headache indicative of migraine and are encouraged to treat when the headache is mild. A Headache Diary documenting onset of headache pain and associated symptoms, time of treatment with study medication, symptoms at 2 hours following treatment, time of relief, recurrence of symptoms within 24 hours post-treatment, and adverse events will be dispensed with study medication. Subjects may take a 2nd dose of study medication or medication determined by the investigator for rescue of persistent or recurring headache at 2 or more hours following the 1st dose of study medication. Alternate rescue medication can be provided at the discretion of the investigator but may not include triptan, non-steroidal anti-inflammatory (short-acting NSAID between 6 hours before and 2 hours after study medication or long-acting NSAID between 24 hours before and 24 hours after study medication), or ergotamine-containing or ergot-type medication. Subjects must be headache-free for 24 hours before recording the onset of a "new" migraine attack. The study coordinator will contact subjects at Month 1 to verify treatment and diary compliance.

At Visit 2, following 2 months of treatment with Treximet™, the subject will return to the study site and return completed Headache Diaries. The End of Study CORS, CORS Comparator and End of Study PPMQ-R will be completed considering response with study medication. Adverse events will be documented and Diaries and Questionnaires will be reviewed.
Trimethoprim is rapidly absorbed following oral administration. It exists in the blood as unbound, protein-bound, and metabolized forms. Ten to twenty percent of trimethoprim is metabolized, primarily in the liver; the remainder is excreted unchanged in the urine. The principal metabolites of trimethoprim are the 1- and 3-oxides and the 3'- and 4'-hydroxy derivatives. The free form is considered to be the therapeutically active form. Approximately 44% of trimethoprim is bound to plasma proteins. 

Mean peak serum concentrations of approximately 1.0 mcg/mL occur 1 to 4 hours after oral administration of a single 100 mg dose. A single 200 mg dose will result in serum levels approximately twice as high. The half-life of trimethoprim ranges from 8 to 10 hours. However, patients with severely impaired renal function exhibit an increase in the half-life of trimethoprim, which requires either dosage regimen adjustment or not using the drug in such patients (see DOSAGE AND ADMINISTRATION). During a 13 week study of trimethoprim administered at a daily dosage of 200 mg (50 mg q.i.d.), the mean minimum steady-state concentration of the drug was 1.1 mcg/mL.

Steady-state concentrations were achieved within 2 to 3 days of chronic administration and were maintained throughout the experimental period.

Excretion of trimethoprim is primarily by the kidneys through glomerular filtration and tubular secretion. Urine concentrations of trimethoprim are considerably higher than are the concentrations in the blood. After a single oral dose of 100 mg, urine concentrations of trimethoprim ranged from 30 to 160 mcg/mL during the 0 to 4 hour period and declined to approximately 18 to 91 mcg/mL during the 8 to 24 hour period. A 200 mg single oral dose will result in trimethoprim urine levels approximately twice as high. After oral administration, 50% to 60% of trimethoprim is excreted in the urine within 24 hours, approximately 80% of this being unmetabolized trimethoprim.

Since normal vaginal and fecal flora are the source of most pathogens causing urinary tract infections, it is relevant to consider the distribution of trimethoprim into these sites. Concentrations of trimethoprim in vaginal secretions are consistently greater than those found simultaneously in the serum, being typically 1.6 times the concentrations of simultaneously obtained serum samples. Sufficient trimethoprim is excreted in the feces to markedly reduce or eliminate trimethoprim-susceptible organisms from the fecal flora.

Trimethoprim also passes the placental barrier and is excreted in human milk.
A device for mineralizing potable water contains the reservoir made of the inorganic glass, which consists of three section in the shape of the truncated cone each. The apex of the central cone is directed downwards, the apex of the upper cone – upwards, and the apex of the lower cone – downwards. The planes of the bases of the upper and lower section coincide with the corresponding bases of the central section. At the top of the upper section, there is an opening for water inlet. At the top of the lower section, there is the outlet opening for the mineralized water. In the central section, there is a perforated partition, with the perforations in the shape of the honeycomb. The cavity of the lower section is intended for the minerals and the rock fragments, which are deposited on the perforated footsteps and washed by the downstream water flow.
In the production of metal sulphydryl compounds of keratin degradation products, the keratin is hydrolyzed with dilute acids and the solution is freed from electrolytes by dialysis and evaporated to dryness or the acid is neutralized and the degradation product precipitated by an organic solvent; and the degradation product is reduced by sodium hydrosulphite in aqueous neutral or nearly neutral solution, a compound of a heavy metal such as gold, silver, copper, bismuth, antimony or arsenic being then added to saturate the sulphydryl groups.  More than one metal may be used.  Instead of sodium hydrosulphite, its derivatives such as formaldehyde sulphoxylate may be used.  Examples describe the production of the silver, copper, gold and antimony compounds.  Among the metal compounds employed to react with the reduced keratin degradation products are potassium auribromide, sodium antimonyl tartrate, phenylglycinamide-p-arsonic acid, 4-hydroxy-3-acetylaminophenyl arsonic acid, 2-hydroxy-4-acetylaminophenyl arsonic acid, and 4-hydroxy-3-aminophenyl arsonic acid.  Specification 412,366 is referred to.
The BIOAIR project focuses on the sub-group of asthma patients that suffer from severe or difficult-to-control asthma, and who have frequent asthma exacerbations ('attacks'). This sub-group of asthma patients consists of around 10% of all asthma patients, but accounts for more than half of the total community costs for asthma. It is as yet unknown why these patients are so much more severely ill compared to the majority of asthma patients that have controlled disease. No adequate treatment has yet been established. The BIOAIR study was initiated in order to find out more about the mechanisms underlying severe asthma. Since some of the changes that occur in severe asthma are similar to patients with chronic obstructive lung disease (COPD), a group of COPD patients was included and will be studied as well. A group with controlled mild-to-moderate asthma was included for comparative reasons.
OBJECTIVE: Disease recurrence, particularly intravesical recurrence (IVR) after radical nephroureterectomy (RNU) for upper tract urothelial carcinoma (UTUC), is common. We investigated whether violations of onco-surgical principles before or during RNU, collectively referred to as surgical violation (SV), were associated with survival outcomes.  Material and methods: Data from a consecutive series of patients who underwent RNU for UTUC 2001-2012 at Skåne University Hospital Lund/Malmö were collected. Preoperative insertion of a nephrostomy tube, opening the urinary tract during surgery or refraining from excising the distal ureter were considered as SVs. Survival outcomes in patients with and without SV (IVR-free [IVRFS], disease-specific [DSS] and overall survival [OS]) were assessed using multivariate Cox regression analyses (adjusted for tumour stage group, prior or concomitant bladder cancer, comorbidity and preoperative urinary cytology).
RESULTS: Of 150 patients, 47 (31%) were subjected to at least one SV. Overall, SV was not associated with IVRFS (HR 0.81, 95% CI 0.4-1.6) but with worse DSS (HR 1.9, 95% CI 1.03-3.7) and OS (HR 1.9, 95% CI 1.2-3) in multivariable analysis. Additional analyses with a broader definition of SV including also preoperative instrumentation of the upper urinary tract (ureteroscopy and/or double J stenting) showed similar outcomes for DSS (HR 2.1, 95% CI 1.1-4.3).
CONCLUSION: Worse survival outcomes, despite no difference in IVR, for patients that were subjected to the violation of sound onco-surgical principles before or during RNU for UTUC strengthen the notion that adhering to such principles is a cornerstone in upper tract urothelial cancer surgery.
BACKGROUND: Central nervous system (CNS) disorders, such as stroke, often lead to spasticity, which result in limb deformities and significant reduction in quality of life. Spasticity arises from disruptions in the normal functioning of cortical and descending inhibitory pathways in the brainstem, leading to abnormal muscle contractions. Contralateral seventh cervical nerve cross transfer (CC7) surgery has been proven to effectively reduce spasticity, but the specific mechanism for its effectiveness is unclear.
METHODS: This study aimed to investigate the changes in the dorsal root ganglia (DRG) following CC7 surgery. A comprehensive anatomical analysis was conducted through cadaveric study and magnetic resonance imaging (MRI) study, to accurately measure the regional anatomy of the C7 DRG. DRG perfusion changes were quantitatively assessed by comparing pre- and postoperative dynamic contrast-enhanced (DCE) MRI.
RESULTS: In CC7 surgery, the C7 nerve root on the affected side is cut close to the DRG (3.6 ± 1.0 mm), while the C7 nerve root on the healthy side is cut further away from the DRG (65.0 ± 10.0 mm). MRI studies revealed that after C7 proximal neurotomy on the affected side, there was an increase in DRG volume, vascular permeability, and perfusion; after C7 distal neurotomy on the healthy side, there was a decrease in DRG volume, with no significant changes in vascular permeability and perfusion.
CONCLUSION: This study provides preliminary insights into the mechanisms of spasticity reduction following CC7 surgery, indicating that changes in the DRG, such as increased vascular permeability and perfusion, could disrupt abnormal spinal γ-circuits. The resulting high-perfusion state of DRG, possibly due to heightened neuronal activity and metabolic demands, necessitating further research to verify this hypothesis.
<P>PROBLEM TO BE SOLVED: To obtain a treating agent and to provide a treating device for AIDS.  <P>SOLUTION: The treating agent of AIDS (HIV) is an oral or injectable catechin or tannin tablet or powder obtained by extracting tea and used against bacteria or viruses. The agent not only suppresses propagation but also sterilizes them and is safe even by taking a large amount. Its supply is plenty and it is inexpensive. The treating agent for AIDS (HIV) is a combination drug of IL-2 with INF-γ for reinforcing CTL (a killer T cell). The treating device of AIDS (HIV) is an ex vivo thermally sterilizing device of a blood perfusion type.  <P>COPYRIGHT: (C)2004,JPO&NCIPI
One of the most often used delivery methods is the episiotomy. Severe side effects like infection, dehiscence of the incision, and perineal discomfort are possible. In addition to increased blood loss during birth, mothers who undergo episiotomy have the risk of experiencing delayed wound healing along with increased pain in the early puerperium. After birth, episiotomy treatment begins right away and would involve both pain management and local wound care. The data will be assessed on the baseline 3rd day and 7th day of treatment. A numeric pain rating scale (NPRS) will be used to assess the severity of Pain. REEDA scale will be used for Redness, Edema, Ecchymosis, Discharge, and Approximation (closeness of skin edges). SPSS version 25 will be used for analysis.