anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PURPOSE:To effectively suppress colonization of intraoral bacteria and prevent periodontosis or carious teeth by using a specific fractionated water-soluble egg yolk as a raw material. CONSTITUTION:The whole bacterial cells of intraoral bacteria (e.g., Bacteroides.gingivalis) are crushed to provide cell walls, which are then treated with trypsin to remove proteins mixed in the cell walls. After washing with water, freeze-drying is carried out to provide bacterial cell ingredients, which are subsequently inoculated into a EHI dialytic culture medium and cultured under anaerobic conditions to afford an antigen. The resultant antigen is then administered to immunize a domestic fowl, such as chicken or duck. Carrageenan, etc., are subsequently added to egg yolk obtained from the domestic fowl to form precipitates, which are then removed. The resultant supernatant is fractionated and precipitated to afford a fractionated water-soluble egg yolk, which is added to a food, such as ice cream or custard pudding, so as to provide 0.0001-50g/kg/day intake of the aforementioned egg, egg yolk or fractionated water-soluble egg yolk.
The increasing interruptions of nocturnal sleep with aging must be distinguished from actual sleep disorders. Morbidity and medication have an impact on sleep. The relationship between sleep and morbidity is mutual. Disturbed sleep modifies many clinical symptoms and diseases affect sleep and the ability to sleep. Geriatric syndromes such as falls, depression and dementia are modified by sleep disorders. Geriatric syndromes can be favorably influenced by the treatment of sleep disorders. Adequate diagnostics are important prerequisites. Coincidences of different sleep disorders are frequent. The medical history of patients and a sleep diary form the basis of the diagnostics. Sleep medicine provides further technical examination procedures. Older people should be examined in a sleep laboratory if the results have consequences that are accepted by the patient. This should be clarified in advance.
Participants complete a total of six training sessions, twice a week for three consecutive weeks. In each session, they spend 40 minutes completing computer-based inhibitory regulation training utilizing four strategies.
Long term carcinogenicity studies have been carried out in mice (oral doses 30 to 150 mg/kg) and rats (oral doses 5 to 75 mg/kg). Results are pending.

Theophylline has been studied in Ames salmonella, in vivo and in vitro cytogenetics, micronucleus and Chinese hamster ovary test systems and has not been shown to be genotoxic.

In a 14 week continuous breeding study, theophylline, administered to mating pairs of B6C3F1mice at oral doses of 120, 270 and 500 mg/kg (approximately 1 to 3 times the human dose on a mg/m2basis) impaired fertility, as evidenced by decreases in the number of live pups per litter, decreases in the mean number of litters per fertile pair, and increases in the gestation period at the high dose as well as decreases in the proportion of pups born alive at the mid and high dose. In 13 week toxicity studies, theophylline was administered to F344 rats and B6C3F1mice at oral doses of 40 to 300 mg/kg (approximately 2 times the human dose on a mg/m2basis). At the high dose, systemic toxicity was observed in both species including decreases in testicular weight.
NEW MATERIAL:A compound shown by the formula I or formula II (R1 is alkyl, pyridyl, thienyl, lower alkoxy, or phenyl which is monosubstituted or disubstituted with lower alkylthio; R2 is H or alkyl; with the proviso that R1 and R2 are not lower alkyl simultaneously). EXAMPLE:A compound shown by the formula III. USE:A cardiac, antiasthmatic agent, or preventive against arteriosclerosis having improved positive inotropic action on the heart, increasing action on coronary blood stream volume, increasing action on heart rate, low toxicity, bronchodilatory action and inhibitory action on blood platelet aggregation. PREPARATION:A compound shown by the formula IV is reacted with a compound (e.g., compound shown by the formula V, etc.) shown by the formula R1COCl usually in an organic solvent such as benzene, etc. in the presence of an acid binder (e.g., dimethylaniline, et.) and a catalyst [e.g., 4-(N,N-dimethyl) aminopyridine, etc.] at room temperature - the boiling point of the solvent for 1-10hr. Then, if necessary, the prepared compound shown by the formula I is reduced to give a compound shown by the formula II.
INTRODUCTION: Our retrospective study aimed at assessing safety of vascular closure devices (VCDs) used in a large single-centre Interventional Radiology (IR) department. Complication and deployment failure rates using collagen-based (Angio-seal) and suture-based (ProGlide) devices for common femoral artery haemostasis were compared.
MATERIALS AND METHODS: Data from VCDs deployed over a 6-year period were retrospectively analysed for patient age, procedure indication, puncture mode (antegrade/retrograde), sheath size, deployment failure and complications (haematoma, pseudoaneurysm formation, limb occlusion). Numerical and statistical analysis was undertaken.
RESULTS: Overall, 1321 common femoral artery punctures in 1217 patients were closed using VCDs. Failure rate using ProGlide was significantly higher when compared with Angio-seal (P=<0.001) in sheath sizes ≤8 Fr. Heparin was not administered in embolisation procedures compared with angioplasty with or without stenting. Therefore, haematoma tended to occur more frequently following angioplasty without stenting (P = 0.003) and angioplasty with stenting (P = 0.001), when compared with embolisation. Deployment failure occurred more frequently when heparin was used during the procedure (P = 0.005).
CONCLUSION: Although complications relating to sheath size are well established in the literature, there remains a paucity of data assessing the impact of procedure specific factors when comparing VCDs. Our study challenges that size is the sole determinant of VCD success and invites a more holistic view of VCD deployment strategies. This study advocates continued research into the nuances of other potential confounding variables to optimise patient outcomes.
Psychopathology plays an important role in the emergence of aggression. Having a diagnosis of psychotic disorder or schizophrenia is an important psychopathology that leads to aggression. For these reasons, aggression and how to manage it is an ongoing problem in psychiatric clinics. The prevalence of aggressive behavior in psychiatric wards varies between 8-76%. The prevalence of aggression in schizophrenia patients is stated as 33.3%. This aggression can be verbal, directed towards objects/spaces, towards oneself or physical aggression towards others. Healthcare professionals in psychiatric wards are exposed to these aggressive events carried out by patients. It is reported that 25-85% of healthcare professionals working in psychiatric wards are exposed to aggressive events; the prevalence of aggression towards nurses varies between 11.4-97.6%. Over the years, some methods have been developed and used to manage aggression in psychiatric wards. Chemical and mechanical restraint and seclusion methods are still the leading methods used. There is a need for alternative and evidence-based interventions based on therapeutic nursing approaches to manage aggression in psychiatric wards, which can be easily adopted and implemented in the clinic. Therefore, it was aimed to develop and use the "care bundle" approach, which has been shown to improve patient outcomes in the literature, for aggression management in psychiatric wards. Care bundles are care tools that target a specific patient population, consist of 3-5 evidence-based approaches, and improve patient outcomes when used together. In this study, it was planned to develop the aggression management care package in phase 1, and evaluate the clinical use of the aggression management care bundle in phase 2. The aggression management care bundle was developed following the guidelines of The Institute for Healthcare Improvement.
About 27,000 new cases of renal cell carcinoma (RCC) are diagnosed every year in the United States. 11,000 of these cases will die from the disease. More than half of patients present with advanced or metastatic disease for which chemotherapy plays a very limited role. Therefore, development of another therapeutic approach is needed. Cancers in humans are commonly associated with mutations in dominant and recessive oncogenes. These genes produce mutated proteins that are unique to cancer cells. Von Hipple-Lindau gene, which is associated with the development of the VHL disease, has been recently mapped and cloned; it is found to be mutated in 57% of sporadic renal cell carcinomas.

Data in mice have shown the generation of MHC restricted CTL that are capable of detecting endogenous cytoplasmic peptide derived from mutated oncogenes. In addition, we have recently demonstrated, by conducting different phase I clinical trials in which we vaccinate cancer patients with mutated Ras or p53 peptides corresponding to the abnormality patients harbor in their tumors, that in some patients we can generate immunological responses represented by the generation of lymphocytes (CD4+ and/or CD8+). In the current study, we would like to extend our observations to test whether VHL tumor suppressor protein can be immunologically targeted by vaccination. We have identified specific epitopes along the amino acid sequence of the VHL protein which represent known specific HLA class-I binding motifs. These amino acids stretches in the VHL protein correspond to the area of the point mutation hot spots. Therefore, this protocol treats patients with sporadic RCC who carry VHL mutations in their tumors with corresponding mutant VHL peptide vaccination.
This will be a single-blinded randomized-controlled study of GAE versus placebo in a small population with knee pain secondary to arthritis to determine safety and efficacy. After Institutional Review Board (IRB) approval of a written informed consent and over, approximately a 24 month duration, N=21 subjects will be recruited. Only subjects ≥ 40 years will be screened for study recruitment. Subjects will be randomized in a 2:1 ratio of GAE:Placebo and will be blinded from study treatment (see flow chart below). The placebo procedure will be a diagnostic angiogram of the knee, without embolization. Appropriate measures will be taken to ensure patients and nursing staff caring for the patient are blinded to assignment. Each patient will be told at the time of recruitment that they may be randomly assigned to sham, but if after 1 month they have not had symptom improvement, their assigned procedure would be revealed and, if they had undergone a sham procedure, they will be allowed to proceed with embolization. This second procedure should be shorter than a complete angiogram and embolization, as the detailed angiogram will not need to be repeated, and therefore both arms will have similar total radiation dose.

Clinical procedures and evaluations will consist of a preoperative screening assessment to determine if the potential study subject meets the inclusion and exclusion criteria, enrollment, surgical procedure for geniculate artery embolization, and follow-up visits at 24 hours, 2 weeks, 1, 3, 6, \& 12 months. An MRI may be performed after the 1-month visit.
No dose adjustment of KISQALI is necessary in patients with breast cancer who have mild hepatic impairment (Child-Pugh class A) [see Clinical Pharmacology (12.3)]. A reduced starting dose of 400 mg KISQALI is recommended in patients with advanced or metastatic breast cancer who have moderate (Child-Pugh class B) and severe hepatic impairment (Child-Pugh class C) [see Dosage and Administration (2.2)]. 

No dose adjustment of FEMARA is necessary in patients with breast cancer who have mild (Child-Pugh class A) to moderate (Child-Pugh class B) hepatic impairment. The dose of FEMARA in patients with cirrhosis and severe hepatic dysfunction should be reduced by 50% [see Clinical Pharmacology (12.3)]. The recommended dose of FEMARA for such patients is 2.5 mg administered every other day. The effect of hepatic impairment on FEMARA exposure in noncirrhotic cancer patients with elevated bilirubin levels has not been determined [see Clinical Pharmacology (12.3)].
<P>PROBLEM TO BE SOLVED: To provide a functional substance which acts excellently as a foaming promoter, a skin detergent, a hair wash and/or a body odor adsorbent; a detergent composition containing the functional substance; and a body odor adsorption composition.  <P>SOLUTION: Micronized allophane having an average particle size of 0.01 to 100 μm increases a foaming promotion effect, promotes foaming and foam cutting in a short period of time, and strengthens durability of foam. Further, adsorption power to oily soil due to free fatty acid (particularly, unsaturated fatty acid), and secreted sebum and keratotic plug is increased; and the function as the skin detergent and the hair wash is significantly strengthened. Furthermore, the function as the body odor adsorbent is remarkably strengthened, and the body odor of old personss and a foot smell are powerfully adsorbed. Still furthermore, conformability to a human skin is significantly improved.  <P>COPYRIGHT: (C)2011,JPO&INPIT
MiRNAs are related to neuronal proliferation and apoptosis following cerebral ischemia-reperfusion injury (CIRI). This study focused on miR-30c-5p in the disease. An oxygen-glucose deprivation/re-oxygenation (OGD/R) model was prepared in HT22 cells and transfected to overexpress miR-30c-5p and G Protein Subunit Alpha I2 (GNAI2) respectively or co-transfected to silence miR-30c-5p and GNAI2. Meanwhile, a middle cerebral artery occlusion (MCAO) model was constructed in mice, and miR-30c-5p and GNAI2 were silenced in vivo simultaneously. The mice were evaluated for neurological damage, apoptosis, and inflammation. HT22 cells were tested for cytotoxicity, proliferation, apoptosis, and inflammatory factors. The interaction between miR-30c-5p and GNAI2 was predicted, analyzed, and confirmed. MiR-30c-5p was found to be downregulated in both experimental models. miR-30c-5p reduced lactate dehydrogenase production, inflammatory response, inhibit apoptosis, and enhanced neuronal proliferation, while GNAI2 overexpression showed the opposite results. Downregulated miR-30c-5p worsened neurological function, apoptosis, and inflammation of MCAO mice while silencing GNAI2 attenuated the influence of downregulated miR-30c-5p. MiR-30c-5p can improve neuronal apoptosis and inflammatory response caused by CIRI and is neuroprotective by targeting GNAI2, providing a new target for treating CIRI.
PURPOSE:To prepare the titled compound useful as a preventive and remedy for arteriosclerosis, at a low cost, in high yield, by immersing adzuki beans or its powder in water to extract the adzuki saponin component, partitioning the extract with n-butanol, and concentrating and purifying the organic layer. CONSTITUTION:Adzuki beans or its powder is immersed in cold water or boiling water to extract the adzuki saponin component with water, and the extract is separated from the beans without delay. The obtained liquid is so-called astringent solution discharged from the process for the preparation of bean jam. The liquid is filtered, and the filtrate is extracted with ethyl acetate, etc. The water layer is separated, and partitioned with n-butanol. The n-butanol layer is separated and concentrated to obtain crude saponin. The product is dissolved in methanol, etc., the solution is added dropwise to e.g. ethyl ether to effect reprecipitation, and the obtained powder having light red color is decolored and purified with active charcoal, etc. to obtain the objective compound in the form of white powder.
Patients randomised to the REN group will receive a single 45-minutes stimulation from the REN device (modulated frequency of 100-120 Hz and a pulse width of 400 µs) and will also receive two doses of normal saline though an IV. Two doses of saline will be used to match the dosage, route of administration, and duration to ketorolac and metoclopramide, as described above in the standard-of-care IV group.
BACKGROUND: Inflammatory response has been recognized as a pivotal pathophysiological process during cerebral ischemia. ChemR23 signaling is involved in the pathophysiology of various inflammatory diseases. Nevertheless, the role of ChemR23 signaling in ischemic stroke remains largely unknown.
METHODS: Permanent ischemic stroke mouse model was accomplished by middle cerebral artery occlusion (MCAO). Resolvin E1 (RvE1) or chemerin-9 (C-9), the agonists of ChemR23, were administered by intracerebroventricular (i.c.v) injection before MCAO induction. Then, analysis of neurobehavioral deficits and brain sampling were done at Day 1 after MCAO. The brain samples were further analyzed by histological staining, immunofluorescence, RNA sequencing, ELISA, transmission electron microscope, and western blots. Furthermore, oxygen-glucose deprivation (OGD) was employed in SH-SY5Y to mimic MCAO in vitro, and ChemR23 signaling pathway was further studied by overexpression of ChemR23 or administration of related agonists or antagonists. Analysis of cell death and related pathway markers were performed.
RESULTS: ChemR23 expression was upregulated following MCAO. Under in vitro and in vivo ischemic conditions, ChemR23 deficiency or inhibition contributed to excessive NLRP3-mediated maturation and release of IL-1β and IL-18, as well as enhanced cleavage of GSDMD-N and neuronal pyroptosis. These influences ultimately aggravated brain injury and neuronal damage. On the other hand, ChemR23 activation by RvE1 or C-9 mitigated the above pathophysiological abnormalities in vivo and in vitro, and overexpression of ChemR23 in SH-SY5Y cells also rescued OGD-induced neuronal pyroptosis. Blockade of NLRP3 mimics the protective effects of ChemR23 activation in vitro.
CONCLUSION: Our data indicated that ChemR23 modulates NLRP3 inflammasome-mediated neuronal pyroptosis in ischemic stroke. Activation of ChemR23 may serve as a promising potential target for neuroprotection in cerebral ischemia.
Hydroxypropyl cellulose (HPC) is used in the mfr. of film -forming compsns. (I) for topical treatment of trauma of body tissue, bacterial and fungal infections. (I) comprises HPC, an esterification agent (II), which reacts with HPC to form a reaction prod., which is sol. in the solvent used in the compsns. but insol. in body fluids at body temps. and a volatile solvent for HPC and the reaction prod. Also claimed is a compsn. for in situ formation of medicament films on body tissue comprising HPC, a weak organic acid (IIa) which reacts with HPC to form a reaction prod., which is sol. in the solvent used in the compsn. but insol. in body fluids at body temps., a volatile solvent for HPC and the reaction prod. and a separate medicinal component. (II) is (IIa) pref. salicylic acid or aa mixt. of salicylic and tannic acid. The compsn. may also include boric acid.
BACKGROUND: Osteoarthritis (OA) is a chronic disease that may lead to joint structure degeneration, cartilage destruction, osteophyte formation, subchondral bone disruption, and pain. In this scenario, a higher proportion of the proinflammatory macrophage type 1 (M1) than the anti-inflammatory macrophage type 2 (M2) could be highlighted as a hallmark of OA progression. The balance between these two macrophage types emerges as a new therapeutic target in OA. This study aimed to evaluate the analgesia and macrophage profile in the treatment of experimental osteoarthritis (EOA) with systemic dimethyl fumarate (DMF) or local intra-articular monomethyl fumarate (MMF).
RESULTS: DMF via gavage or MMF via intra-articular in the right knee of EOA rats showed improvements in gait parameters and the nociceptive recovery of the mechanical threshold assessment by adapted electronic von Frey treatment on the twenty-first day (long-lasting phase). DMF treatment decreased proinflammatory TNF-α while increasing anti-inflammatory IL-10 cytokines from the macerated capsule on the fifth day (inflammatory phase). MMF treatment showed joint capsule mRNA extraction downregulating iNOS and TNF-α gene expression while upregulating IL-10 and MCP-1. However, CD206 was not significant but higher than untreated EOA rats' joints on the seventh day (inflammatory phase).
CONCLUSIONS: Our studies with EOA model induced by MIA suggest a new perspective for human treatment committed with OA based on macrophage polarization as a therapeutic target, switching the proinflammatory profile M1 to the anti-inflammatory profile M2 with DMF systematic or by MMF locally treatment according to the OA severity.
Growth factor receptor-bound protein 2 (GRB2) is a negative regulator of insulin signaling and a positive regulator of angiogenesis. Its expression is increased in a mouse model of retinal neovascularization and in patients with type 2 diabetes mellitus (T2DM). This case-control study aimed to investigate the association between the rs9896052 polymorphism (A>C) upstream of GRB2 and proliferative diabetic retinopathy (PDR) in patients with T2DM from Southern Brazil, taking into consideration self-reported skin color (white or non-white) and the known duration of diabetes (<10 years or ≥10 years). Genotypes were determined by real-time PCR in 838 patients with T2DM (284 cases with PDR and 554 controls without DR). In the total study group and in the analysis stratified by skin color, the genotype and allele frequencies were similar between cases and controls. However, among patients with less than 10 years of diabetes, the C allele was more frequent in cases than in controls (63.3% versus 51.8%, p = 0.032), and the CC genotype was independently associated with an increased risk of PDR (adjusted OR = 2.82, 95% CI 1.17-6.75). In conclusion, our findings support the hypothesis that the rs9896052 polymorphism near GRB2 is associated with PDR in Brazilian patients with T2DM.
Patients receive carboplatin IV over 1 hour on day 1 and veliparib PO BID on days 1-7 or 1-14. Courses repeat every 21 days in the absence of disease progression or unacceptable toxicity. Patients may undergo fluorothymidine PET scan and peripheral blood cell and tumor tissue collection periodically for correlative studies.
This is a randomized study (study drug assigned by chance) using a 2:1 randomization. It is an open-label (all people know study drug), active-controlled (comparing to a different drug used for the same condition), parallel-group (different treatment groups continue with separate treatments throughout the study), multicenter study. This study will be divided into 3 phases, screening, treatment, follow-up and optional extension phase (OEP). During screening, potential participants will be assessed for study eligibility after providing signed informed consent. Approximately 570 patients who satisfy all inclusion and exclusion criteria will be randomly assigned in a 2:1 ratio to either the trabectedin (n=380) or dacarbazine (n=190) treatment groups. During the treatment phase, patients will receive study drug once every 3 weeks, until disease progression (defined by Response Evaluation Criteria in Solid Tumors \[RECIST\] Version 1.1 criteria) or signs of toxicity. Assessments will be performed to evaluate the effectiveness of the drug, and patient safety will be monitored. During the follow-up phase, after the last dose of study drug, clinical outcomes for patients will be evaluated. Trabectedin will be administered at a dose of 1.5 milligram per square meters (mg/m\^2) through a catheter into a large vein as a 24-hour intravenous (IV) infusion, once every 3 weeks, until disease progression or signs of toxicity. Dacarbazine will be administered at a dose of 1.0 g/m\^2 as a 20-120 minute infusion, once every 3 weeks, until disease progression or signs of toxicity. In the OEP, participants who were previously randomized to the dacarbazine group will have the option to receive trabectedin at the discretion of the investigator.