anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
This study is an open-label, multi-cohort, multi-center clinical trial evaluating the efficacy, safety, and tolerability of LM-108 monoclonal antibody combined with sintilimab in treatment-naïve or previously treated subjects with locally advanced or metastatic non-small cell lung cancer (NSCLC). There are two cohorts in the study:(1)Cohort 1: NSCLC patients who developed secondary resistance after being sensitive to prior treatment with PD-1 inhibitors (monotherapy or in combination with another systemic therapy) for 6 months or more are eligible for this study.(2)Cohort 2: Patients with locally advanced or metastatic NSCLC who have not received prior systemic treatment are eligible for this study.

Subjects in Cohort 1 will receive LM-108 monoclonal antibody combined with sintilimab. Subjects in Cohort 2 will receive LM-108 monoclonal antibody combined with sintilimab and chemotherapy for 4-6 cycles. LM-108 monoclonal antibody combined with sintilimab will be maintained, and the choice of chemotherapy regimen and the duration of use will be determined by the investigator. Treatment will continue until disease progression, unacceptable toxicity, initiation of a new anti-tumor therapy, withdrawal of informed consent, loss to follow-up, death, or other investigator-determined reasons for discontinuation, whichever occurs first, with a maximum treatment duration of 24 months. The primary study endpoint is the objective response rate (ORR) assessed by the investigator based on the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1.
Days 5-50: Participants will receive cigarette packs as per the study randomization schema (e.g. three15-day periods of red, gold, and plain packs; order counterbalanced within subject) with FDA-approved graphic warning labels.
Intervention: Subjects with heart failure will receive a single oral dose of potassium nitrate (10 or 20 mmol KNO3) in 2 gelatin capsules during dose visit 1 and the other dose (10 or 20 mmol KNO3) during dose visit 2. The dose order will be randomized.
1,194,902. Hair preparations. YARDLEY & CO. Ltd. 23 Feb., 1967 [23 Feb., 1966], No. 53913/69. Divided out of 1,194,901. Heading A5B. [Also in Division C3] Polyarmide resins derived from a polycarboxylic acid and an alkylene polyamine are modified by reaction with a substantially equal quantity by weight of a cosmetically acceptable organic acid, ester or amide at 300 Œ .11‹C for 1 to 2.5 hours in an inert atmosphere are used in hair grooming compositions which may also contain a cosmetically acceptable oil, scent and/or colouring matter. Preferred polyamides have molecular weights of 2000 to 15000. Preferred modifying agents are castor oil, liquid lanolin, fatty acids and alkanoamides. In examples proprietary polyamides derived from polymeric fat acids are reacted with liquid lanolin or castor oil and the products are blended at lower temperatures with further liquid lanolin or castor oil (8:92 or 25:75 by weight) to form hair grooming gels.
Exacerbation of pre-existing autoimmune disease or initial presentation of autoimmune and inflammatory disorders has been reported following treatment with Proleukin. Immune-mediated adverse reactions, which may be severe or fatal, can occur in any organ system or tissue. These have included exacerbation of Crohn's disease, colitis, scleroderma, thyroiditis, inflammatory arthritis, diabetes mellitus, oculo-bulbar myasthenia gravis, crescentic IgA glomerulonephritis, cholecystitis, cerebral vasculitis, Stevens-Johnson syndrome, bullous pemphigoid, myocarditis, myositis, and neuritis including optic neuritis resulting in blindness [see Adverse Reactions (6.2)].

Proleukin may increase the risk of allograft rejection in transplant patients [see Contraindications (4)].

Hypothyroidism, sometimes preceded by hyperthyroidism, has been reported following Proleukin treatment. Evaluate thyroid function at baseline and periodically during treatment and initiate thyroid replacement therapy as clinically indicated.

Hyperglycemia and/or diabetes mellitus has been reported during Proleukin therapy. Monitor patients for hyperglycemia and initiate treatment with insulin as clinically indicated.
CHS-1420 40mg 2 doses at Week 0/Day 0 then 1 dose every 2 weeks starting at Week 1 for 23 weeks. At Week 24 subjects will continue on to CHS-1420 open label until study end.
This is a multi-institution, open-label, non-randomized, Phase II evaluation of oral afatinib daily and intravenous paclitaxel (weekly, 3 weeks on, 1 week off) in patients with trastuzumab refractory HER2-positive metastatic or recurrent esophagogastric adenocarcinoma. An initial biopsy prior to the start of therapy is required for the correlative studies evaluating the biologic effects of afatinib. It will be obtained for all patients whose tumors are feasible to biopsy. At the site investigator's discretion, a second biopsy will also be obtained. At the discretion of the MSK Principal Investigator, select participants who show response on this study and then progress may be asked to have an optional third biopsy.
Octreotide acetate injection exerts pharmacologic actions similar to the natural hormone, somatostatin. It is an even more potent inhibitor of growth hormone, glucagon, and insulin than somatostatin. Like somatostatin, it also suppresses LH response to GnRH, decreases splanchnic blood flow, and inhibits release of serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide.

By virtue of these pharmacological actions, octreotide acetate has been used to treat the symptoms associated with metastatic carcinoid tumors (flushing and diarrhea), and Vasoactive Intestinal Peptide (VIP) secreting adenomas (watery diarrhea).

Octreotide acetate substantially reduces growth hormone and/or IGF-I (somatomedin C) levels in patients with acromegaly.

Single doses of octreotide acetate have been shown to inhibit gallbladder contractility and to decrease bile secretion in normal volunteers. In controlled clinical trials the incidence of gallstone or biliary sludge formation was markedly increased (see WARNINGS).

Octreotide acetate suppresses secretion of thyroid stimulating hormone (TSH).
Group supplemented with omega-3 (4g/day) and maltodextrin (40g/day). All groups will undergo a training program with strength exercises for 12 weeks.
BACKGROUND: Prolonged exposure to hyperoxia can lead to hyperoxic acute lung injury (HALI) in preterm neonates. Vitamin D (VitD) stimulates lung maturation and acts as an anti-inflammatory agent. Our objective was to determine if VitD provides a dose-dependent protective effect against HALI by reducing inflammatory cytokine expression and improving alveolarization and lung function in neonatal mice.
METHODS: C57BL/6 mouse neonates were randomized and placed in room air or hyperoxic (85% O2) conditions for 6 days. Control, low (5 ng/neonate) and high (25 ng/neonate) doses of VitD were administered daily beginning at day 2 via oral gavage. Lung tissue was analyzed for edema, changes in pulmonary structure and function, and inflammatory cytokine expression.
RESULTS: Neonatal mice treated with VitD in hyperoxic conditions had improved weight gain, reduced pulmonary edema and increased alveolar surface area compared to untreated pups in hyperoxia. No significant changes in cytokine expression were observed between untreated and VitD neonates. While changes in surfactant protein mRNA expression were impacted by hyperoxia and VitD administration, no significant changes in alveolar type II cell percentages were observed. At 3 weeks, mice in hyperoxia treated with VitD had greater lung compliance, diminished airway reactivity and improved weight gain.
CONCLUSIONS: High dose VitD significantly limited harmful effects of HALI. These results suggest that supplementation of VitD to neonatal mice during hyperoxia exposure provides both short-term and long-term protective benefits against HALI.
BACKGROUND: Systemic lupus erythematosus (SLE) is linked to host gut dysbiosis. Here we performed faecal gut microbiome sequencing to investigate SLE-pathogenic gut microbes and their potential mechanisms.
METHODS: There were 134 healthy controls (HCs) and 114 SLE cases for 16 S ribosomal RNA (rRNA) sequencing and 97 HCs and 124 SLE cases for shotgun metagenomics. Faecal microbial changes and associations with clinical phenotypes were evaluated, and SLE-associated microbial genera were identified in amplicon analysis. Next, metagenomic sequencing was applied for accurate identification of microbial species and discovery of their metabolic pathways and immunogenic peptides both relevant to SLE. Finally, contribution of specific taxa to disease development was confirmed by oral gavage into lupus-prone MRL/lpr mice.
RESULTS: SLE patients had gut microbiota richness reduction and composition alteration, particularly lupus nephritis and active patients. Proteobacteria/Bacteroidetes (P/B) ratio was remarkably up-regulated, and Escherichia was identified as the dominantly expanded genus in SLE, followed by metagenomics accurately located Escherichia coli and Escherichia unclassified species. Significant associations primarily appeared among Escherichia coli, metabolic pathways of purine nucleotide salvage or peptidoglycan maturation and SLE disease activity index (SLEDAI), and between multiple epitopes from Escherichia coli and disease activity or renal involvement phenotype. Finally, gavage with faecal Escherichia revealed that it upregulated lupus-associated serum traits and aggravated glomerular lesions in MRL/lpr mice.
CONCLUSION: We characterize a novel SLE exacerbating Escherichia outgrowth and suggest its contribution to SLE procession may be partially associated with metabolite changes and cross-reactivity of gut microbiota-associated epitopes and host autoantigens. The findings could provide a deeper insight into gut Escherichia in the procession of SLE.
Trauma currently accounts for 10% of the total global burden of disease and over 5 million deaths per year, making it a leading cause of morbidity and mortality worldwide. Although recent advances in early resuscitation have improved early survival from critical injury, the mortality rate in patients with major hemorrhage approaches 50% even in mature trauma systems. A major determinant of clinical outcomes from a major injury is a complex, dynamic hemostatic landscape. Critically injured patients frequently present to the emergency department with an acute traumatic coagulopathy that increases mortality from bleeding, yet, within 48 to 72 hours after injury will switch from a hypocoagulable to a hypercoagulable state with increased risk of venous thromboembolism and multiple organ dysfunction. This review will focus on the role of platelets in these processes. As effectors of hemostasis and thrombosis, they are central to each phase of recovery from injury, and our understanding of postinjury platelet biology has dramatically advanced over the past decade. This review describes our current knowledge of the changes in platelet behavior that occur following major trauma, the mechanisms by which these changes develop, and the implications for clinical outcomes. Importantly, supported by research in other disease settings, this review also reflects the emerging role of thromboinflammation in trauma including cross talk between platelets, innate immune cells, and coagulation. We also address the unresolved questions and significant knowledge gaps that remain, and finally highlight areas that with the further study will help deliver further improvements in trauma care.
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.

In a total of 1836 patients in controlled and uncontrolled clinical trials, 14% of patients received intravenous amiodarone for at least one week, 5% received it for at least 2 weeks, 2% received it for at least 3 weeks, and 1% received it for more than 3 weeks, without an increased incidence of severe adverse reactions. The mean duration of therapy in these studies was 5.6 days; median exposure was 3.7 days.

The most important adverse reactions were hypotension, asystole/cardiac arrest/pulseless electrical activity (PEA), cardiogenic shock, congestive heart failure, bradycardia, liver function test abnormalities, VT, and AV block. Overall, treatment was discontinued for about 9% of the patients because of adverse reactions. The most common adverse reactions leading to discontinuation of intravenous amiodarone therapy were hypotension (1.6%), asystole/cardiac arrest/PEA (1.2%), VT (1.1%), and cardiogenic shock (1%).

Table 5 lists the most common (incidence ≥ 2%) adverse reactions during intravenous amiodarone therapy considered at least possibly drug-related. These data were collected in clinical trials involving 1836 patients with life-threatening VT/VF. Data from all assigned treatment groups are pooled because none of the adverse reactions appeared to be dose-related.

Other adverse reactions reported in less than 2% of patients receiving intravenous amiodarone in controlled and uncontrolled studies included the following: abnormal kidney function, atrial fibrillation, diarrhea, increased ALT, increased AST, lung edema, nodal arrhythmia, prolonged QT interval, respiratory disorder, shock, sinus bradycardia, Stevens-Johnson syndrome, thrombocytopenia, VF, and vomiting.
The present invention relates to a method of treating alcoholism or alcohol abuse by administering to a subject a pharmaceutically effective amount of an opioid antagonist before imminent drinking. Particularly, the present invention relates to a method of treating alcoholism or alcohol abuse by administering transmucosally to a subject a pharmaceutically effective amount of an opioid antagonist before imminent drinking. Preferably, the opioid antagonist used in the method is nalmefene or a pharmaceutically acceptable salt thereof. The invention also relates to a method of treating alcoholism or alcohol abuse by administering to a subject before imminent drinking a transmucosal preparation comprising a pharmaceutically effective amount of an opioid antagonist, wherein the transmucosal preparation has rapid onset of action. Advantageously, a FAH+ subject is treated. Further, the invention relates to a method of treating alcoholism or alcohol abuse of a FAH+ subject, comprising extinguishing an alcohol-drinking response by administering to the FAH+ subject a pharmaceutically effective amount of nalmefene or a pharmaceutically acceptable salt thereof.
The control is a "wait-list" control, and will have the option to participate in the intervention at the end of the initial 12-week study period. The control group will be asked to not change any of their dietary or exercise habits over the course of the 12 weeks.
There is an exponential rise in the prevalence of type 2 diabetes and obesity in Singapore coincident with rapid nutritional and socioeconomic transition. Differing birth weights, even in the normal ranges, predisposes individuals to the risk of type 2 diabetes and obesity. We aim to examine the causal pathways, developmental contribution and effects of a weight loss intervention to this differential by evaluating the hypothesis that genomic, birth weight, developmental, lifestyle and environmental factors contribute to the variation in phenotype observed in adults with obesity and metabolic syndrome.

Although there are many large studies that examined the effect of birth weight on the expression of obesity and the metabolic syndrome phenotype, most of these studies usually lack in-depth physiological and epigenetic/genomic studies due to their large sample sizes. We therefore aim to explore such detailed aspects of physiological and epigenetic/genomic profiles on smaller but statistically powered samples, focusing on evaluating body composition, nutritional and metabolic phenotype in relationship to epigenetic/genetic markers and developmental history. In addition, we examine the effects of a weight loss intervention on these parameters. This will assist in weighing the importance of developmental and genetic pathways in contributing to individual risk and the response and efficacy to an intervention.
PURPOSE:To enable safety use by incorporating trehalose into a peritoneal dialysis liquid as an osmotic agent to allow the obtaining of a neutralized peritoneal dialysis liquid without special pharmaceutical innovation while eliminating a rise in the concentration of glucose in blood during a peritoneal dialysis. CONSTITUTION:This peritoneal dialysis liquid contains trehalose as an osmotic agent. The concentration of the trehalose is preferably 0.13-23% (W/V). The peritoneal dialysis liquid may contain a cation such as sodium ion, calcium ion, potassium ion or magnesium ion or an anion such as chloride ion or sulfate ion as an electrolyte considering electrolytic balance of a patient to be dialyzed. The concentration of the ion is preferably 110-150mEq/l for sodium, 90-120mEq/l for chlorine, 0-6mEq/l for calcium and 0-4mEq/l for magnesium. The osmotic pressure is 280-800mOsm/l and pH in a range of 6.0-7.6.
Participants in this arm will receive services from the NavSTAR Patient Navigation team. The Patient Navigator will work with patients for up to 3 months post-hospital discharge to resolve internal barriers (e.g., ambivalence about treatment; low motivation; competing life demands, etc.) and external barriers (e.g., lack of transportation; lack of ID card, etc.) to appropriate utilization and engagement in addiction treatment and medical care. Interventions include motivational interventions and patient navigation with proactive case management, tailored to participants' specific needs.
Timely and accurate diagnosis of neuropathic pain is critical for optimizing therapeutic outcomes and minimizing treatment delays. According to current standards, the diagnosis of definite neuropathic pain requires objective confirmation of a lesion or disease affecting the somatosensory nervous system. This can be provided by specialized neurophysiological techniques as conventional methods like nerve conduction studies and somatosensory evoked potentials may not be sufficient as they do not assess pain pathways. These specialized techniques apply various stimuli, such as thermal, electrical, or mechanical, alongside assessments of spinal/cortical potential or electromyographic reflex recordings. The selection of techniques is guided by the patient's clinical history and examination. The most common neurophysiological tests used in clinical practice are pain-related evoked potentials (PREPs) providing an objective evaluation of nociceptive pathways. Four types of PREPs are employed: laser evoked potentials, contact-heat evoked potentials, intra-epidermal electrical stimulation evoked potentials, and pinprick evoked potentials, with the two former ones being the most robust and reliable ones. These techniques investigate small-diameter fibers, primarily Aδ-fibers, and spinothalamic tracts allowing the identification of peripheral or central nervous system lesions. Yet, they are limited in capturing neuronal mechanisms underlying neuropathic pain or in providing objective quantification of pain sensation. Two neurophysiological measures which investigate the pain system beyond its integrity are the nociceptive withdrawal reflex and the N13 component of somatosensory evoked potentials. Both of these methods are more commonly used in research than clinical practice, but they pose interesting approaches to quantify central sensitization, a key underlying mechanism of neuropathic pain. Future investigations in neuropathic pain are therefore warranted.
The present disclosure relates to pharmaceutical compositions comprising engineered macrophages and methods of use thereof. In some aspects, the present disclosure relates to engineered macrophages derived from pluripotent stem cells. In some embodiments, the stem cell genome is edited to knock-out (e g., SIRPa) and/or knock-in (e g., CAR) genes of interest prior to differentiation into macrophages. In some embodiments, engineered macrophages lack a SIRPa receptor. In some embodiments, the engineered macrophages express chimeric antigen receptors that induce and/or enhance phagocytosis. Alternatively, or additionally, in some embodiments, macrophages are engineered with combinatorial antigen-sensing circuits to improve tumor recognition and phagocytosis. Other aspects of the disclosure relate to methods of treating cancer in a subject and/or methods of enhancing cancer cell phagocytosis.
Symptoms of OCD is a rather common co-morbid condition in patients with Schizophrenia. Some studies suggest that obsessive-compulsive symptoms may be present in 7.8-46% of schizophrenic patients and who seem to be poorly responsive to drug therapy. The serotonergic medications in combination with cognitive-behavioral therapy stil remain the preferred treatment for OCD symptoms. There are controversial data regarding effect of neuroleptics on symptoms of OCD. It was noted that the use of Risperdone, Quatiapine and Clozapine might aggravate OCD symptoms. Serotonin antagonism of these neuroleptics is believed to exacerbate obsessive-compulsive symptoms in schizophrenia. On the other hand, Pourovsky M. at(2000) reported three cases of Schizophrenia with symptoms of OCD successfully treated with Olanzapine.One of our patients with Schizophrenia and co-morbid symptoms of OCD who was unsuccessfully treated with various neuroleptics in combination with anti-obsessive agents,demonstrated significant improvement in both Schizophrenic and obsessive compulsive symptoms after she was switched to Aripiprazole. This result encouraged us to initiate pilot study of effectiveness of Aripiprazole in the treatment of specific population of schizophrenic patients with symptoms of OCD.
Subjects assigned to sequence ABAB will receive a single 80 mg dose of the test product Telmisartan (1 x 80 mg tablet) marked as A in the sequence in Periods 1 and 3 and a single 80 mg dose of the reference product Micardis (1 x 80 mg tablet) marked as B in the sequence in periods 2 and 4. These treatments will be administered orally with approximately 240 mL of water at ambient temperature, in the morning, following a 10-hour overnight fast. The tablet must be swallowed whole and must not be chewed or broken.