anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present invention concerns application of camptothecine derivation NSC606985 in preparing drug for acute leukemia. NSC606985 of nano-molar concentration can induce cell line NB4 and cell U937 of leukemia to apoptosis. On the aspect of inducing apoptosis, NSC606985 can induce quickly transmembrane potential of mitochondrion (deltaWm) to falling and activation of caspase-3. Hydrolysis and activation of protein kinase induced C delta (PKC delta) by NSC606985 plays key role and starting effect during these processes. Specific inhibitor rottlerin for PKC delta can restrain entirely the falling of mitochondrion deltaWm and activation of caspase-3 and the Specific inhibitor Z-DEVD-fmk for caspase-3 just weaken partly activation of PKC delta and cell apoptosis. NSC606985 restrains marked clone forming ability of hemopoietic progenitor cell in fresh marrow of patient of acute medullary leukemia. So NSC606985 is potential active drug for treating leukemia.
This prospective cross-sectional study will be conducted in the Surgical Department of the Services Institute of Medical Sciences. A total of 50 patients will beincluded in the study after screening through the inclusion criteria. A control group of 50 inpatients with no personal or family history of gallstones will be also recruited for comparison. Results will be expressed as mean with standard deviation. Students t- test will be used to compare the data between the patients and the control groups (p\<0.05 will be considered statistically significant). SPSS software, version 20 will be used for statistical analysis.
The initial dose is 2 mg once a day. At week 2, the dose can be increased to 4 mg once a day according to the titration. At week 4 and 12, the dose can be increased from 2 mg to 4 mg or from 4 mg to 6 mg according to the titration.
BACKGROUND: It is well established that traumatic brain injury (TBI) causes acute and chronic alterations in systemic immune function and that systemic immune changes contribute to posttraumatic neuroinflammation and neurodegeneration. However, how TBI affects bone marrow (BM) hematopoietic stem/progenitor cells chronically and to what extent such changes may negatively impact innate immunity and neurological function has not been examined.
METHODS: To further understand the role of BM cell derivatives on TBI outcome, we generated BM chimeric mice by transplanting BM from chronically injured or sham (i.e., 90 days post-surgery) congenic donor mice into otherwise healthy, age-matched, irradiated CD45.2 C57BL/6 (WT) hosts. Immune changes were evaluated by flow cytometry, multiplex ELISA, and NanoString technology. Moderate-to-severe TBI was induced by controlled cortical impact injury and neurological function was measured using a battery of behavioral tests.
RESULTS: TBI induced chronic alterations in the transcriptome of BM lineage-c-Kit+Sca1+ (LSK+) cells in C57BL/6 mice, including modified epigenetic and senescence pathways. After 8 weeks of reconstitution, peripheral myeloid cells from TBI→WT mice showed significantly higher oxidative stress levels and reduced phagocytic activity. At eight months after reconstitution, TBI→WT chimeric mice were leukopenic, with continued alterations in phagocytosis and oxidative stress responses, as well as persistent neurological deficits. Gene expression analysis revealed BM-driven changes in neuroinflammation and neuropathology after 8 weeks and 8 months of reconstitution, respectively. Chimeric mice subjected to TBI at 8 weeks and 8 months post-reconstitution showed that longer reconstitution periods (i.e., time post-injury) were associated with increased microgliosis and leukocyte infiltration. Pre-treatment with a senolytic agent, ABT-263, significantly improved behavioral performance of aged C57BL/6 mice at baseline, although it did not attenuate neuroinflammation in the acutely injured brain.
CONCLUSIONS: TBI causes chronic activation and progressive dysfunction of the BM stem/progenitor cell pool, which drives long-term deficits in hematopoiesis, innate immunity, and neurological function, as well as altered sensitivity to subsequent brain injury.
Women develop chronic pain during their reproductive years more often than men, and estrogen and progesterone regulate this susceptibility. We tested whether brain progesterone receptor (PR) signaling regulates pain susceptibility. During the estrous cycle, animals were more sensitive to mechanical stimulus during the estrus stage than in the diestrus stage, suggesting a role for reproductive hormones, estrogen, and progesterone. Progesterone treatment of ovariectomized and estrogen-primed mice caused a delayed reduction in the mechanical threshold. Segesterone, a specific agonist of PRs replicated this effect, whereas, the segesterone-induced reduction in mechanical threshold was blocked in the mice lacking PRs in the nervous system. Segesterone treatment also did not alter mechanical threshold in adult male and juvenile female mice. PR activation increased the cold sensitivity but did not affect the heat and light sensitivity. We evaluated whether PR activation altered experimental migraine. Segesterone and nitroglycerin when administered sequentially, reduced the pain threshold but not when given separately. PRs were expressed in several components of the migraine ascending pain pathway, and their deletion blocked the painful effects of nitroglycerin. PR activation also increased the number of active neurons in the components of the migraine ascending pain pathway. These studies have uncovered a pain-regulating function of PRs. Targeting PRs may provide a novel therapeutic avenue to treat chronic pain and migraine in women. PERSPECTIVE: This article provides evidence for the role of progesterone receptors in regulating pain sensitivity and migraine susceptibility in females. Progesterone receptors may be a therapeutic target to treat chronic pain conditions more prevalent in women than men.
<P>PROBLEM TO BE SOLVED: To obtain a hyaluronidase activity inhibitor comprising an extract of Hizikia fusiforme or Corcharus oltorius and provide food and beverage and cosmetic containing the same.  <P>SOLUTION: The hyaluronidase activity inhibitor comprises the extract of Hizikia fusiforme or Corcharus oltorius. The food and beverage and the cosmetic contain the inhibitor. The extracts of Hizikia fusiforme and Corcharus oltorius have high hyaluronidase activity-inhibiting action. Hizikia fusiforme was eaten from old times and Corcharus oltorius is a species of introduced vegetables and is served as a food. The both are highly safe materials, so the extracts are remarkably effective hyaluronidase activity inhibitors and practically useful. The food and beverage for inhibiting hyaluronidase activity having high safety and a good quality in taste are simply obtained by adding the extract or mixing the extract in a powdery state with the food and beverage. The cosmetic has effects such as stabilization of hyaluronic acid widely used in the cosmetic, prevention of dry skin, anti-inflammation and antiallergic activities.  <P>COPYRIGHT: (C)2003,JPO
Pain and asthenia were the most frequently reported miscellaneous adverse effects; their relationship to the tumor and to anemia was likely. Alopecia was reported (3%). Cardiovascular, respiratory, genitourinary, and mucosal side effects have occurred in 6% or less of the patients. Cardiovascular events (cardiac failure, embolism, cerebrovascular accidents) were fatal in less than 1% of the patients and did not appear to be related to chemotherapy. Cancer-associated hemolytic uremic syndrome has been reported rarely. 

Malaise, anorexia, hypertension, dehydration, and stomatitis have been reported as part of 

postmarketing surveillance. 

To report SUSPECTED ADVERSE REACTIONS, contact Meitheal Pharmaceuticals Inc. at 1-844-824-8426 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
Coaching Into Care plus VA-CRAFT consists of four 45-min. telephone coaching calls over 8-12 weeks, delivered by a coach following a manual, while participants are completing the VA-CRAFT for PTSD web-based course.
Exercise has been shown to play an important role in reducing many of the side effects associated with chemotherapy treatment. Exercise can help to improve symptoms of fatigue, nausea, muscle weakness, and pain, which in turn can help to improve patients overall quality of life and wellbeing. In addition to this, exercising during chemotherapy can also help to maintain physical fitness and preserve muscle mass, which has been shown to significantly reduce treatment toxicities. Despite these benefits of exercise, performing regular physical activity during chemotherapy poses significant challenges. Patients are faced with a number of physical and logistical barriers during chemotherapy which makes it difficult to engage in regular exercise. In addition to this, exercise programs that are being designed lack flexibility and individualization, and don't account for the unpredictable nature of chemotherapy treatment. It is, therefore, no surprise that patients struggle to meet the exercise recommendations during chemotherapy, and highlights the need for careful consideration when prescribing exercise during this time. In preparation for this study, the research team held a number of workshops which included a mixture of patients and healthcare professionals with the aim of co-designing an exercise intervention for patients during chemotherapy. Including public and patient involvement (PPI) in the design process will help to ensure that the exercise program that is developed is pragmatic and, most importantly, patient-centred.
Chronic pain and alcohol use disorder (AUD) are highly comorbid, and patients with chronic pain are more likely to meet the criteria for AUD. Evidence suggests that both conditions alter similar brain pathways, yet this relationship remains poorly understood. Prior work shows that the anterior insular cortex (AIC) is involved in both chronic pain and AUD. However, circuit-specific changes elicited by the combination of pain and alcohol use remain understudied. The goal of this work was to elucidate the converging effects of binge alcohol consumption and chronic pain on AIC neurons that send projections to the dorsolateral striatum (DLS). Here, we used the Drinking-in-the-Dark (DID) paradigm to model binge-like alcohol drinking in mice that underwent spared nerve injury (SNI), after which whole-cell patch-clamp electrophysiological recordings were performed in acute brain slices to measure intrinsic and synaptic properties of AIC→DLS neurons. In male, but not female, mice, we found that SNI mice with no prior alcohol exposure consumed less alcohol compared with sham mice. Electrophysiological analyses showed that AIC→DLS neurons from SNI-alcohol male mice displayed increased neuronal excitability and increased frequency of miniature excitatory postsynaptic currents. However, mice exposed to alcohol prior to SNI consumed similar amounts of alcohol compared with sham mice following SNI. Together, our data suggest that the interaction of chronic pain and alcohol drinking have a direct effect on both intrinsic excitability and synaptic transmission onto AIC→DLS neurons in mice, which may be critical in understanding how chronic pain alters motivated behaviors associated with alcohol.
<P>PROBLEM TO BE SOLVED: To develop an advantageous normal medicine free from defects of grave side actions, giving little influence on normal cells, acting against tumor cells, etc., and usable as a substitute for glucocorticoid widely used as an antiinflammatory agent, antiallergic agent and immunosuppressive agent and as an immunosuppressive agent such as FK-506.  <P>SOLUTION: Galectin-9, especially a stabilized galectin-9 is active to suppress the binding of CD44 to a ligand (hyaluronic acid) and inhibits the adhesion (cell adhesion) of an active CD44-expression cell to hyaluronic acid. A substance selected from galectin-9 and its modified material (stabilized galectin-9) is used as a CD44 function suppressing factor to provide an antiallergic agent, an immunosuppressive agent and an antitumor agent and obtain e.g. a treating/prevention agent and a treating/prevention method for suppressing the promotion of bronchial hypersensitivity in bronchial asthma, etc., and suppressing airway inflammation. The invention further provides a carcinostatic technique.  <P>COPYRIGHT: (C)2007,JPO&INPIT
BACKGROUND: The association between physical frailty and performance in different cognitive domains in the absence of cognitive disorders is poorly understood. Hence, we aimed to explore the associations between frailty levels based on the Fried Physical Frailty Phenotype and performance of different cognitive domains. We also aimed to examine the associations between cognitive function and each criterion in the Fried Frailty Scale using the same cognitive domains in a non-dementia population aged 60-96 years.
METHODS: This cross-sectional study included 4,329 participants aged 60-96 years, drawn from the "Good Aging in Skåne" population study. Frailty indices included handgrip strength, physical endurance, body mass index (BMI), physical activity, and walking speed. Cognitive function was assessed across eight domains: episodic memory, processing speed, semantic memory, verbal fluency, working memory, attention, executive function, and visual perception. We constructed adjusted multiple linear regression models for each cognitive domain, with the frailty levels as the independent variable. Likewise, we constructed linear regression models with each cognitive domain as the dependent variable and frailty criteria as independent variables.
RESULTS: Physical frailty was associated with poor performance in episodic memory, processing speed, semantic memory, verbal fluency, working memory, attention, and executive functions (p<0.001 for all associations). Weaker hand grip strength was independently associated with poorer performance in all cognitive domains (p < 0.015).
CONCLUSION: Higher levels of frailty were associated with poorer performance in all cognitive domains except visual perception. Describing frailty by considering cognitive functioning may provide a better understanding of frailty.
Lung carcinoma is a malignant disease characterized by uncontrolled alveolar type II epithelial cell growth in lung tissues. Worldwide in 2012, lung cancer occurred in 1.8 million people and resulted in 1.6 million deaths, making it the most common cause of cancer-related death in men and second most common in women after breast cancer. The most common age at diagnosis is 70 years, and less than 20% of people diagnosed with lung cancer can survive five years post diagnosis. The two main types of lung carcinomas are small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC). NSCLC represents the most common type of lung cancers, and approximately 85% of lung cancers are NSCLC. Squamous cell carcinoma, adenocarcinoma, and large cell carcinoma are all subtypes of NSCLC, the latter associated with high mortality in overall cancer populations with limited treatment options.

In this study, the investigators performed a Phase I, open label, agent-combination exploration, multicenter clinical trial to establish the treatment efficacy of several chemotherapeutic agents in patients with recurrent NSCLC who have undergone prior surgery for the primary disease. Up to four cohorts have been enrolled to determine the effectiveness and safety of single or combinational therapeutic strategy. Besides the five-year disease-free survival, overall survival and five-year metastasis-free survival post treatment, the investigators also take into account the anticancer agent-induced tumor stroma damage extent, which may provide further evidence to support the treatment efficacy and assess the potential influence of a damaged tumor microenvironment on disease progression or regression in clinical settings.
In the copolymerization in bulk of more than 50 mol. per cent of acrylonitrile and one or more esters of methacrylic acid with a lower alcohol, using non-peroxidic catalysts, e.g. azodiisobutyric acid dinitrile, 0.5 to 5 per cent of maleic acid or its anhydride is added before, during or after polymerization.  Cross-linking monomers, e.g. divinyl benzene, vinyl and allyl acrylates and methacrylates, glycol diacrylate, butane diol divinyl ether and lead methacrylate may also be present in quantities of 0.5 to 5 per cent.  The maleic acid or anhydride may be added to a solution of the copolymer in dimethyl formamide.  In an example, acrylonitrile, methyl methacrylate and azodiisobutyric acid dinitrile are boiled for 100 minutes, maleic anhydride is dissolved in the viscous liquid and the polymerization completed at 35 DEG  C. in a glass mould with exclusion of oxygen. The products, which are practically colourless and of reduced brittleness, may be used as glass substitutes and for shoe inlays or arch supports.
With confirmation that the target vessel is completely occluded by the target CTO lesion, the operator shall initially attempt crossing the proximal end of the target CTO lesion by advancing ShockWireTM device ≥ 1cm. The SoundBite Crossing device can be activated as needed to perform the procedure and may be used for the entire length of the lesion(s).
Primary immune thrombocytopenia (ITP) is an acquired autoimmune disorder characterized by the destruction of platelets. Although it was long believed that the critical role of autoantibodies in platelet destruction, primarily through the Fc-dependent platelet clearance pathway, recent findings indicate that the significance of the Fc-independent platelet clearance pathway mediated by hepatocytes, thus shedding light on a previously obscure aspect of ITP pathogenesis. Within this context, the desialylation of platelets has emerged as a pivotal biochemical marker. Consequently, targeting platelet desialylation emerges as a novel therapeutic strategy in the pathogenesis of ITP. Notably, prevailing research has largely focused on antiplatelet antibodies and the glycosylation-associated mechanisms of platelet clearance, while comprehensive analysis of platelet desialylation remains scant. In response, we retrospectively discuss the historical progression, inducing factors, generation process, and molecular regulatory mechanisms underlying platelet desialylation in ITP pathogenesis. By systematically evaluating the most recent research findings, we contribute to a comprehensive understanding of the intricate processes involved. Moreover, our manuscript delves into the potential application of desialylation regulatory strategies in ITP therapy, heralding novel therapeutic avenues. In conclusion, this manuscript not only fills a critical void in existing literature but also paves the way for future research by establishing a systematic theoretical framework. By inspiring new research ideas and offering insights into the development of new therapeutic strategies and targeted drugs, our study is poised to significantly advance the clinical management of ITP.
We will enroll 300 pulmonary nodules penplein this study. After bronchoscopy, surgical examination or clinical follow-up, pulmonary nodules were finally diagnosed as malignant or benign.
Because the psychosocial health of Chinese cancer patients and their caregivers are linked, there is a need to improve health outcomes for not just the patients, but also for the caregivers. While many caregiving interventions have focused on the caregiver-patient dyad as the "the unit of care", interventions that solely target caregivers are crucial given the emotional, social, financial, and physical toll of caregiving. To address this need, investigators are testing a writing intervention, Expressive Helping (EH), with Chinese family members who are providing care for their family members diagnosed with cancer. Over four brief structured writing sessions, participants write about their cancer caregiving experiences, disclosing their emotions and providing encouragement and guidance, with the knowledge that their narratives will be shared with and used as a resource for other Chinese cancer caregivers. Participants will be adult cancer caregivers of Chinese descent. After screening and consent, eligible participants will be enrolled in a 1:1 randomized controlled trial. Assessments of psychological symptoms will occur at baseline (prior to randomization), 1-month post-intervention, and 3-month post-intervention. Investigators will also assess potential mediators and moderators of the potential intervention effects. Investigators interacting with the participants will be blind to condition assignment.
Microbial systems have been synthetically engineered to deploy therapeutic payloads in vivo1,2. With emerging evidence that bacteria naturally home in on tumours3,4 and modulate antitumour immunity5,6, one promising application is the development of bacterial vectors as precision cancer vaccines2,7. Here we engineered probiotic Escherichia coli Nissle 1917 as an antitumour vaccination platform optimized for enhanced production and cytosolic delivery of neoepitope-containing peptide arrays, with increased susceptibility to blood clearance and phagocytosis. These features enhance both safety and immunogenicity, achieving a system that drives potent and specific T cell-mediated anticancer immunity that effectively controls or eliminates tumour growth and extends survival in advanced murine primary and metastatic solid tumours. We demonstrate that the elicited antitumour immune response involves recruitment and activation of dendritic cells, extensive priming and activation of neoantigen-specific CD4+ and CD8+ T cells, broader activation of both T and natural killer cells, and a reduction of tumour-infiltrating immunosuppressive myeloid and regulatory T and B cell populations. Taken together, this work leverages the advantages of living medicines to deliver arrays of tumour-specific neoantigen-derived epitopes within the optimal context to induce specific, effective and durable systemic antitumour immunity.
The lidocaine is replaced by identical volumes and rates of 0.9% saline. At the end of the operation, the patient controlled intravenous analgesia without lidocaine is used.
Among 355 patients who received ROZLYTREK across clinical trials, 32 patients (9%) experienced hyperuricemia reported as adverse reactions with symptoms, as well as elevated uric acid levels. Grade 4 hyperuricemia occurred in 1.7% of patients, including one patient who died due to tumor lysis syndrome. Among the 32 patients with hyperuricemic adverse reactions, 34% required urate-lowering medication to reduce uric acid levels, 6% required dose reduction and 6% required dose interruption. Hyperuricemia resolved in 73% of patients following initiation of urate-lowering medication without interruption or dose reduction of ROZLYTREK. No patients discontinued ROZLYTREK due to hyperuricemia.

Assess serum uric acid levels prior to initiation of ROZLYTREK and periodically during treatment. Monitor patients for signs and symptoms of hyperuricemia. Initiate treatment with urate-lowering medications as clinically indicated and withhold ROZLYTREK for signs and symptoms of hyperuricemia. Resume ROZLYTREK at same or reduced dose upon improvement of signs or symptoms based on severity [see Dosage and Administration (2.7)].