anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Patients treated with TRISENOX can develop QTc prolongation, torsade de pointes, and complete atrioventricular block. In the clinical trials of patients with newly-diagnosed low-risk APL treated with TRISENOX in combination with tretinoin, 11% experienced QTc (Framingham formula) prolongation > 450 msec for men and > 460 msec for women throughout the treatment cycles. In the clinical trial of patients with relapsed or refractory APL treated with TRISENOX monotherapy, 40% had at least one ECG tracing with a QTc interval greater than 500 msec. A prolonged QTc was observed between 1 and 5 weeks after start of TRISENOX infusion, and it usually resolved by 8 weeks after TRISENOX infusion. There are no data on the effect of TRISENOX on the QTc interval during the infusion of the drug.

The risk of torsade de pointes is related to the extent of QTc prolongation, concomitant administration of QTc prolonging drugs, a history of torsade de pointes, pre-existing QTc interval prolongation, congestive heart failure, administration of potassium-wasting diuretics, or other conditions that result in hypokalemia or hypomagnesemia. The risk may be increased when TRISENOX is coadministered with medications that can lead to electrolyte abnormalities (such as diuretics or amphotericin B) [see Drug Interactions (7)].

Prior to initiating therapy with TRISENOX, assess the QTc interval by electrocardiogram, correct pre-existing electrolyte abnormalities, and consider discontinuing drugs known to prolong QTc interval. Do not administer TRISENOX to patients with a ventricular arrhythmia or prolonged QTc. If possible, discontinue drugs that are known to prolong the QTc interval. If it is not possible to discontinue the interacting drug, perform cardiac monitoring frequently [see Drug Interactions (7)]. During TRISENOX therapy, maintain potassium concentrations above 4 mEq/L and magnesium concentrations above 1.8 mg/dL. Monitor ECG weekly and more frequently for clinically unstable patients. 

For patients who develop a QTc Framingham greater than 450 msec for men or greater than 460 msec for women, withhold TRISENOX and any medication known to prolong the QTc interval. Correct electrolyte abnormalities. When the QTc normalizes and electrolyte abnormalities are corrected, resume TRISENOX at a reduced dose [see Dosage and Administration (2.3)].
Patients admitted to hospital with COVID-19 symptoms will be approached to undertake a face mask sample and nasopharyngeal swab at two time points 12 hours apart on a single day whilst in hospital. Medical records will be accessed for basic clinical, demographic and microbiological data.
Participants will receive lenvatinib 24 mg, orally once daily until documentation of disease progression (confirmed by investigator's assessment), development of unacceptable toxicity, or withdrawal of consent. Placebo treated participants in the Randomization Phase who have progressive disease confirmed by IIR could request to receive lenvatinib treatment in the OOL Treatment Period.
-261 5 Medical devices may be utilized for local and regional therapeutic agent delivery. These therapeutic agents or compounds may reduce a biological organism's reaction to the introduction of the medical device to the organism. In addition, these therapeutic drugs, agents and/or compounds may be utilized to promote healing, including the prevention of thrombosis. The drugs, agents, and/or 10 compounds may also be utilized to treat specific disorders, including restenosis, vulnerable plaque, and atherosclerosis in type 2 diabetic patients. In regional delivery, liquid formulations may be desirable to increase the efficacy and deliverability of the particular drug. Various materials and coating methodologies may be utilized to maintain the agents or compounds on the medical device until 15 delivered and positioned. 26/03/09,va 17860 speci,261 5014 5040 5054 5028 5014 5040FIG. 4O 7000 5028 FIG. 41 5014 5040 FIG. 43 7000
FIELD: veterinary science. SUBSTANCE: preparation is used for piglet treatment mainly. Preparation has hydrosulfate, polyvinylethynyltrimethylpiperidol, iodine, potassium iodide, polymixin and distilled water. Preparation is given to piglets orally at dose 2.0-2.2 ml/kg body mass, twice per 24 h, for 3-4 days. Preparation is harmless, does not exhibit negative action on physiological, hematological and nonspecific immunity factors of animals. Effectiveness of preparation is 95-98%. EFFECT: high effectiveness of preparation.
Cervical cancer is one of the leading causes of cancer death among females, worldwide. The contributory role of different cellular pathways in the process of carcinogenesis is still poorly understood. Our study was focused here to understand the functional evaluation of key regulatory genes of FA-BRCA pathway in the development of CACX and their role in chemo-tolerance of the disease by analyzing the molecular profile of the genes both in normal and tumour tissue of our sample pool, also validated in in silico datasets. Later on, prognostic importance of the genes was further evaluated in plasma DNA and cisplatin-treated in vitro system. We found that expression profile of FA-BRCA pathway genes was gradually reduced from undifferentiated basal-parabasal layers of normal tissue towards the progression of the disease. Further analysis revealed that frequent promoter methylation [32-55%] and deletion [34-52%] events were the plausible reasons for their reduced expression in CACX. Noticeably, invasion of promoter methylation of the genes [11-17%] in plasma CTCs of CACX patients was positively correlated [p < 0.001] with poor prognosis among patients. On the other hand, functional upregulation of these genes at higher concentrations [IC50-70] of cisplatin was a predictor for the development of drug tolerance, as evaluated in our in vitro study. This finding was supported further by low prevalence of γ-H2X foci formation and reduced expression of DNMT1 at higher concentrations of cisplatin. In totality, we discovered that the FA-BRCA pathway must be inactivated for cancer formation. In contrast, elevated gene expression played a substantial role in building of chemo-tolerance and might be associated with developing increased risk of disease recurrence among patients.
Schizophrenia is a devastating brain disorder. Most people with schizophrenia have difficulty filtering out unimportant auditory information. They have an inability to appropriately inhibit, or gate, sensory information that enters the ear. Standard treatments do not address this problem. When the drug ondansetron is taken in addition to typical antipsychotic drugs, P50 auditory gating improves. However, ondansetron has not been used with some of the newer, atypical antipsychotic drugs. This study will evaluate the effect of combining ondansetron with newer, atypical antipsychotic drugs on P50 auditory gating.

Participants in this double-blind study will be randomly assigned to receive either ondansetron or placebo for 3 months. Upon completion of the first 3 months, participants will be crossed over to receive the other treatment for an additional 3 months. All participants will also take an atypical antipsychotic drug, including olanzapine, quetiapine, or aripiprazole. Auditory gating will be assessed using computerized cognitive testing and functional magnetic resonance imaging (fMRI) at baseline and Months 3 and 6. Vital signs and evoked potentials will be assessed at Weeks 1, 3, and 6. Clinical symptoms and cognitive abilities will also be evaluated to determine the effectiveness of ondansetron.
BACKGROUND: Sepsis is a life-threatening condition arising from an aberrant host response to infection. Recent single-cell RNA sequencing investigations identified an immature bone-marrow-derived CD14+ monocyte phenotype with immune suppressive properties termed "monocyte state 1" (MS1) in patients with sepsis. Our objective was to determine the association of MS1 cell profiles with disease presentation, outcomes, and host response characteristics.
METHODS: We used the transcriptome deconvolution method (CIBERSORTx) to estimate the percentage of MS1 cells from blood RNA profiles of patients with sepsis admitted to the intensive care unit (ICU). We compared these profiles to ICU patients without infection and to healthy controls. Host response dysregulation was further studied by gene co-expression network and gene set enrichment analyses of blood leukocytes, and measurement of 15 plasma biomarkers indicative of pathways implicated in sepsis pathogenesis.
RESULTS: Sepsis patients (n = 332) were divided into three equally-sized groups based on their MS1 cell levels (low, intermediate, and high). MS1 groups did not differ in demographics or comorbidities. The intermediate and high MS1 groups presented with higher disease severity and more often had shock. MS1 cell abundance did not differ between survivors and non-survivors, or between patients who did or did not acquire a secondary infection. Higher MS1 cell percentages were associated with downregulation of lymphocyte-related and interferon response genes in blood leukocytes, with concurrent upregulation of inflammatory response pathways, including tumor necrosis factor signaling via nuclear factor-κB. Previously described sepsis host response transcriptomic subtypes showed different MS1 cell abundances, and MS1 cell percentages positively correlated with the "quantitative sepsis response signature" and "molecular degree of perturbation" scores. Plasma biomarker levels, indicative of inflammation, endothelial cell activation, and coagulation activation, were largely similar between MS1 groups. In ICU patients without infection (n = 215), MS1 cell percentages and their relation with disease severity, shock, and host response dysregulation were highly similar to those in sepsis patients.
CONCLUSIONS: High MS1 cell percentages are associated with increased disease severity and shock in critically ill patients with sepsis or a non-infectious condition. High MS1 cell abundance likely indicates broad immune dysregulation, entailing not only immunosuppression but also anomalies reflecting exaggerated inflammatory responses.
The present invention provides several embodiments that ultimately result in the in vivo loading of endogenous antigenic peptides from a target cell. The invention also presents a method for inducing an immune response to an endogenous antigen in a subject by delivering an effective amount of an agent that stimulates in vivo loading of the endogenous antigen into an Antigenic Peptide Binding Protein (“APBP”). The APBP presents the endogenous antigen to a T cell in vivo. A polynucleotide encoding an APBP is delivered to a target cell under conditions such that the APBP is expressed in the target cell. Endogenous antigenic peptides bind the APBP forming an APBP:peptide complex. A cytotoxic agent also is administered to the subject and delivered to the target cell in an amount effective to lyse the target cell which releases the complexes. The complexes present the antigenic peptide to a T cell or an antigen presenting cell (APC) which mounts the immune response. An effective amount of an antigen presenting cell (APC) recruitment factor can be administered to the subject to recruit APC to the locus of the target cell. APCs take up the APBP:peptide complexes and the peptides are processed and presented by MHC molecules to T cells in vivo.
Prior to pancreatoduodenectomy, patients undergo thoracic epidural placement and receive bupivacaine and hydromorphone continuous infusion via epidural for up to 72 hours postoperatively. Patients also receive iopamidol via epidural and undergo x-ray imaging on study.
Hypoxia-inducible factors (HIFs) are highly conserved transcription factors that are crucial for adaptation of metazoans to limited oxygen availability. Recently, HIF activation and inhibition have emerged as therapeutic targets in various human diseases. Pharmacologically desirable effects of HIF activation include erythropoiesis stimulation, cellular metabolism optimization during hypoxia and adaptive responses during ischaemia and inflammation. By contrast, HIF inhibition has been explored as a therapy for various cancers, retinal neovascularization and pulmonary hypertension. This Review discusses the biochemical mechanisms that control HIF stabilization and the molecular strategies that can be exploited pharmacologically to activate or inhibit HIFs. In addition, we examine medical conditions that benefit from targeting HIFs, the potential side effects of HIF activation or inhibition and future challenges in this field.
PROBLEM TO BE SOLVED: To prepare the subject therapeutic agent, comprising a trypsin inhibitor as an active ingredient and useful for treating Crohn diseases, idiopathic ulcerative colitis and intestinal type Behcet diseases. SOLUTION: This therapeutic agent for autoimmune enteropathies comprises a trypsin inhibitor as an active ingredient. For example, a human urine-derived trypsin inhibitor which is a glycoprotein, having 65,000-70,000 molecular weight and separated and purified from a human urine, aprotinin, etc., that are the glycoprotein extracted from the bovine lungs or parotid glands are cited as the inhibitor. A steroid is preferably used together with the trypsin inhibitor to enhance therapeutic effects on autoimmune enteropathies. For example, prednisolone and paramethasone are cited as the steroid. The objective therapeutic agent is preferably intraarterially or intravenously administered. For example, the dose thereof is 10,000-1,000,000 units expressed in terms of the trypsin inhibitor and the daily dose thereof is 0.1-100mg expressed in terms of the steroid.
BACKGROUND: Electrocardiographic (ECG) findings of T-wave inversions in V1-V3, with or without accompanying epsilon waves, often raise concerns for the rare, but potentially lethal, arrhythmogenic right ventricular cardiomyopathy (ARVC). However, this pattern may be found in pericardial agenesis, an even rarer pathology. Concomitant myocarditis can confuse this presentation further.
CASE REPORT: We report a case of a previously healthy man who presented with left-sided chest pain, ECG findings suggestive of ARVC, and a final diagnosis of myocarditis with underlying partial pericardial agenesis. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: A growing number of cases have reported pericardial agenesis demonstrating ECG changes similar to ARVC. We discuss an approach to a diagnostically challenging patient. This case emphasizes the importance of a broad differential and the danger of premature closure.
BACKGROUND: Patient-reported outcomes are an important emerging metric increasingly utilised in clinical, research and registry settings. These outcomes, while vital, are underutilised and require refinement for the specific patient population of those undergoing bariatric surgery. This study aimed to investigate and compare how pre-surgical patients, post-surgical patients, and healthcare practitioners evaluate patient-reported outcomes of bariatric surgery to identify outcomes that are considered most important.
METHODS: A modified Delphi survey was distributed to patients pre- and post-surgery, and to a variety of healthcare practitioners involved in bariatric care. Across two rounds, participants were asked to rate a variety of physical and psychosocial outcomes of bariatric surgery from 0 (Not Important) to 10 (Extremely Important). Outcomes rated 8-10 by at least 70% of participants were considered highly important (prioritised). The highest-rated outcomes were compared between the three groups as well as between medical and allied health practitioner subgroups.
RESULTS: 20 pre-surgical patients, 95 post-surgical patients, and 28 healthcare practitioners completed both rounds of the questionnaire. There were 58 outcomes prioritised, with 21 outcomes (out of 90, 23.3%) prioritised by all three groups, 13 (14.4%) by two groups, and 24 (26.7%) prioritised by a single group or subgroup. Unanimously prioritised outcomes included 'Co-morbidities', 'General Physical Health', 'Overall Quality of Life' and 'Overall Mental Health'. Discordant outcomes included 'Fear of Weight Regain', 'Suicidal Thoughts', 'Addictive Behaviours', and 'Experience of Stigma or Discrimination'.
CONCLUSION: While there was considerable agreement between stakeholder groups on many outcomes, there remain several outcomes with discordant importance valuations that must be considered. In particular, healthcare practitioners prioritised 20 outcomes that were not prioritised by patients, emphasising the range of priorities across stakeholder groups. Future work will consider these priorities to ensure resulting measures encompass all important outcomes and are beneficial and valid for end users.
PCT No. PCT/GB96/00942 Sec. 371 Date Feb. 2, 1998 Sec. 102(e) Date Feb. 2, 1998 PCT Filed Apr. 22, 1996 PCT Pub. No. WO96/33211 PCT Pub. Date Oct. 24, 1996Compounds of general formula I wherein: R1 and R70 independently represent a hydrogen atom or an optionally substituted alkyl or acyl group; R2 represents a hydrogen atom or an optionally substituted alkyl or acyl group or is absent when R6 represents a group -CH= as hereinafter described; R73 represents a hydrogen atom or an optional substituent or is absent when R6 represents a methylene group or a group -CH= as hereinafter described; Y represents an optional substituent; n represents 0, 1, 2, 3, or 4; R3 represents a hydrogen atom, or an optionally substituted alkyl group; R74 represents a hydrogen atom, a hydroxy group or an optionally substituted alkyl or acyl group; R7 represents a hydrogen atom or an alkyl group; R75 represents an optionally substituted alkyl group; and i) R6 and R71 independently represent a hydrogen atom or an optionally substituted alkyl or acyl group; and R72 represents a hydrogen atom; or ii) R71 represents a hydrogen atom or an optionally susbtituted alkyl or acyl group and R72 represents a hydrogen atom or R71 and R72 are joined together such that a double bond is formed between the carbon atoms to which they are attached; and R6 represents an optionally substituted methylene group bonded to the indole moiety thereby forming a tricyclic moiety; or R6 represents an optionally substituted group -CH= bonded to the indole moiety thereby to form an aromatic tricyclic moiety; for use in therapy and as antimitotic reagents are described.
Long non-coding RNAs (lncRNAs) are a group of epigenetic regulators that have been implicated in kidney diseases including acute kidney injury (AKI). However, very little is known about the specific lncRNAs involved in AKI and the mechanisms underlying their pathologic roles. Here, we report a new lncRNA derived from the pseudogene GSTM3P1, which mediates ischemic AKI by interacting with and promoting the degradation of mir-668, a kidney-protective microRNA. GSTM3P1 and its mouse orthologue Gstm2-ps1 were induced by hypoxia in cultured kidney proximal tubular cells. In mouse kidneys, Gstm2-ps1 was significantly upregulated in proximal tubules at an early stage of ischemic AKI. This transient induction of Gstm2-ps1 depends on G3BP1, a key component in stress granules. GSTM3P1 overexpression increased kidney proximal tubular apoptosis after ATP depletion, which was rescued by mir-668. Notably, kidney proximal tubule-specific knockout of Gstm2-ps1 protected mice from ischemic AKI, as evidenced by improved kidney function, diminished tubular damage and apoptosis, and reduced kidney injury biomarker (NGAL) induction. To test the therapeutic potential, Gstm2-ps1 siRNAs were introduced into cultured mouse proximal tubular cells or administered to mice. In cultured cells, Gstm2-ps1 knockdown suppressed ATP depletion-associated apoptosis. In mice, Gstm2-ps1 knockdown ameliorated ischemic AKI. Mechanistically, both GSTM3P1 and Gstm2-ps1 possessed mir-668 binding sites and downregulated the mature form of mir-668. Specifically, GSTM3P1 directly bound to mature mir-668 to induce its decay via target-directed microRNA degradation. Thus, our results identify GSTM3P1 as a novel lncRNA that promotes kidney tubular cell death in AKI by binding mir-668 to inducing its degradation.
Quinazoline compds. of formula (I) are prepd. by reacting compd. of formula (II) with epichlorohydrin or epibromohydrin in the presence of a base, e.g. NaOH, KOH, alkoxide and carbonate. In the formulas, one of R6 and R7 is oxiranylmethyl and the other is methyl or oxiranylphenyl; R2 and R4 are each H, C1-5 alkyl, phenyl, substd. phenyl or phenylalkyl; one of Ra and Rb is H and the other is H or methyl.  (I) are useful as industrial antimicrobial agents, disinfectants and antiseptics.
The invention discloses Gui Lu Erxian Plaster for treating hyperplasia of prostate gland and relates to a new application of Gui Lu Erxian plaster. The Gui Lu Erxian Plaster has the functions of warming kidney and increasing semen and benefiting blood and is originally applied to the treatment of weak kidney due to a long disease, waist and knee sourness, insufficient blood, spermatorrhea and impotence. The clinic treatment of 30 cases of the patients of hyperplasia of prostate gland by the Gui Lu Erxian Plaster in No. 8 Hospital of Wuhan City proves that the Gui Lu Erxian Plaster has remarkable efficacy on the hyperplasia of prostate gland and tiny side effect, safe efficacy and good adaptability to the patient and can be widely applied in the clinic treatment. The clinic test proves that the Gui Lu Erxian Plaster can be used for treating the symptoms of pollakiuria, urinary urgency and high frequency of night urination, etc. caused by the hyperplasia of prostate gland.
Experiencing the death of a family member and providing end-of-life caregiving can be stressful on families - this is well-documented in both the caregiving and bereavement literatures. Adopting a linked-lived theoretical perspective, exposure to the death and dying of one family member could be conceptualized as a significant life stressor that produces short and long-term health consequences for surviving family members. This study uses familial-linked administrative records from the Utah Population Database to assess how variations in family hospice experiences affect mortality risk for surviving spouses and children. A cohort of hospice decedents living in Utah between 1998 and 2016 linked to their spouses and adult children (n = 37,271 pairs) provides an ideal study population because 1) hospice typically involves family members in the planning and delivery of end-of-life care, and 2) hospice admission represents a conscious awareness and acknowledgment that the decedent is entering an end-of-life experience. Thus, hospice duration (measured as the time between admission and death) is a precise measure of the family's exposure to an end-of-life stressor. Linking medical records, vital statistics, and other administrative microdata to describe decedent-kin pairs, event-history models assessed how hospice duration and characteristics of the family, including familial network size and coresidence with the decedent, were associated with long-term mortality risk of surviving daughters, sons, wives (widows), and husbands (widowers). Longer hospice duration increased mortality risk for daughters and husbands, but not sons or wives. Having other family members in the state was protective, and living in the same household as the decedent prior to death was a risk factor for sons. We conclude that relationship type and sex likely modify the how of end-of-life stressors (i.e., potential caregiving demands and bereavement experiences) affect health because of normative gender roles. Furthermore, exposure to dementia deaths may be particularly stressful, especially for women.