anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
FIELD: medicinal biology, medicine, hematology. SUBSTANCE: method involves subcutaneous administration of swine or human fetal adrenal cortex extracts to experimental animals at the dose 0.5 ml (two injections). Method enhances the effectiveness of regeneration of hepatic tissue and recovery of parenchyma of pathologically damaged liver at simultaneous decrease of adverse effects of synthetic drug used. Method can be used in clinic for regeneration therapy of liver pathology. EFFECT: improved method of stimulation, enhanced effectiveness of liver regeneration. 1 tbl
Nucleotide-binding Oligomerization Domain 1 (NOD1) is a cytosolic pattern recognition receptor that senses specific bacterial peptidoglycan moieties, leading to the induction of inflammatory response. Besides, sensing peptidoglycan, NOD1 has been reported to sense metabolic disturbances including the ER stress-induced unfolded protein response (UPR). However, the underpinning crosstalk between the NOD1 activating microbial ligands and the metabolic cues to alter metabolic response is not yet comprehensively defined. Here, we show that underlying ER stress aggravated peptidoglycan-induced NOD1-mediated inflammatory response in hepatoma cells. The HepG2 cells, undergoing ER stress induced by thapsigargin exhibited an amplified inflammatory response induced by peptidoglycan ligand of NOD1 (i.e. iE-DAP). This aggravated inflammatory response disrupted lipid and glucose metabolism, characterized by de novo lipogenic response, and increased gluconeogenesis in HepG2 cells. Further, we characterized that the aggravation of NOD1-induced inflammatory response was dependent on inositol-requiring enzyme 1-α (IRE1-α) and protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) activation, in conjunction with calcium flux. Altogether, our findings suggest that differential UPR activation makes liver cells more sensitive towards bacterial-derived ligands to pronounce inflammatory response in a NOD1-dependent manner that impairs hepatic nutrient metabolism.
OBJECTIVE: To investigate whether Buthus martensii karsch (Scorpiones), Scolopendra subspinipes mutilans L. Koch (Scolopendra) and Gekko gecko Linnaeus (Gekko) could ameliorate the hypoxic tumor microenvironment and inhibit lung cancer growth and metastasis by regulating phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin/hypoxia-inducible factor-1α (PI3K/AKT/mTOR/HIF-1α) signaling pathway.
METHODS: Male C57BL/6J mice were inoculated with luciferase labeled LL/2-luc-M38 cell suspension to develop lung cancer models, with rapamycin and cyclophosphamide as positive controls. Carboxy methyl cellulose solutions of Scorpiones, Scolopendra and Gekko were administered intragastrically as 0.33, 0.33, and 0.83 g/kg, respectively once daily for 21 days. Fluorescent expression were detected every 7 days after inoculation, and tumor growth curves were plotted. Immunohistochemistry was performed to determine CD31 and HIF-1α expressions in tumor tissue and microvessel density (MVD) was analyzed. Western blot was performed to detect the expression of PI3K/AKT/mTOR/HIF-1α signaling pathway-related proteins. Enzyme-linked immunosorbent assay was performed to detect serum basic fibroblast growth factor (bFGF), transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor (VEGF) in mice.
RESULTS: Scorpiones, Scolopendra and Gekko prolonged the survival time and inhibited lung cancer metastasis and expression of HIF-1α (all P<0.01). Moreover, Scorpiones, Scolopendra and Gekko inhibited the phosphorylation of AKT and ribosomal protein S6 kinase (p70S6K) (P<0.05 or P<0.01). In addition, they also decreased the expression of CD31, MVD, bFGF, TGF-β1 and VEGF compared with the model group (P<0.05 or P<0.01).
CONCLUSION: Scorpiones, Scolopendra and Gekko all showed beneficial effects on lung cancer by ameliorating the hypoxic tumor microenvironment via PI3K/AKT/mTOR/HIF-1α signaling pathway.
Oxidative stress is the major factor that plays a role in the pathogenesis of age-related macular degeneration (AMD), which is a leading cause of blind registration in the developed world. The term oxidative stress refers to reversible damage to molecules, such as for example DNA, by reactive forms of oxygen (eg. free oxygen radicals). This damage is repaired is normally repaired in our body.

AMD is classified in two forms: the dry (non-exudative) and wet (exudative) form. The exudative form of AMD occurs when new blood vessels form to improve the blood supply to retinal tissue. However, the new blood vessels are very delicate and break easily, causing bleeding and serious vision loss. The standardized method used to treat exudative AMD is photodynamic therapy (PDT). This treatment is based upon the infusion of a drug that can be activated by light and produces free radicals that destroy these newly formed vessels. In other words, these new vessels are destroyed by an iatrogenic source of oxidative stress. This means that the factor that originally caused the disease AMD, namely oxidative stress, is finally used as a form of treatment- to destroy these newly formed blood vessels.

In the present study we would like to quantify in a first step the level of systemic oxidative stress in patients with non-exudative and exudative AMD and compare to healthy controls. In a second step we would like to test whether the treatment (PDT) for patients with exudative AMD additionally increases systemic oxidative stress. Oxidative stress is quantified in our laboratory by means of single cell gel electrophoresis or comet assay.
BACKGROUND: The differences in the characteristics of ischemic stroke associated with a mobile versus nonmobile residual left atrial thrombus (LAT) are unclear. We investigated whether the mobility of an LAT detected by transthoracic echocardiography is associated with the clinical features of stroke.
METHODS: This study included 20 consecutive patients with nonvalvular atrial fibrillation who were admitted to our hospital for treatment of acute ischemic stroke and then found to have an LAT on transthoracic echocardiography. The patients were divided into two groups: those with a mobile LAT (Group M) and those with a nonmobile LAT (Group N). The clinical, neuroradiological, and echocardiographic variables were assessed.
RESULTS: The LAT was mobile in 11 patients (Group M) and nonmobile in nine patients (Group N). The median National Institutes of Health Stroke Scale score on admission was higher in Group M than N (17 vs. 7, respectively; p=0.196). Four patients in Group M and one in Group N developed in-hospital stroke recurrence (36% vs. 11%, respectively; p=0.319). The prevalence of large vessel occlusion (15 events in Group M and 10 events in Group N, including in-hospital recurrent events) was significantly higher in Group M than N (73% vs. 30%, respectively; p=0.049), which seemed to lead to poorer functional outcomes in Group M than N (ratio of modified Rankin scale score of 0-2 at discharge: 18% vs. 44%, respectively; p=0.336).
CONCLUSIONS: The mobility of LAT may affect stroke severity in patients with nonvalvular atrial fibrillation.
According to the Global Burden of Disease (GBD) study, chronic kidney disease (CKD) was prevalent in 697.5 million individuals worldwide in 2017. By 2040, it is anticipated that CKD will rank as the fifth most common cause of death. This study aims to examine the epidemiology of CKD in Kazakhstan and to project future trends in CKD prevalence and mortality by 2030. The retrospective analysis was performed on a database acquired from the Unified National Electronic Health System for 703,122 patients with CKD between 2014 and 2020. During the observation period, 444,404 women and 258,718 men were registered with CKD, 459,900 (66%) were Kazakhs and 47% were older than 50. The incidence rate notably decreased: 6365 people per million population (PMP) in 2014 and 4040 people PMP in 2020. The prevalence changed from 10,346 to 38,287 people PMP, and the mortality rate increased dramatically from 279 PMP to 916 PMP. Kazakhstan's central regions, Turkestan and Kyzylorda were identified as the most burdensome ones. The ARIMA model projected 1,504,694 expected prevalent cases in 2030. The predicted mortality climbed from 17,068 cases in 2020 to 37,305 deaths in 2030. By 2030, the prevalence and mortality of CKD will significantly increase, according to the predicted model. A thorough action plan with effective risk factor management, enhanced screening among risk populations, and prompt treatment are required to lessen the burden of disease in Kazakhstan.
BACKGROUND: Many parents of children with advanced cancer report curative goals and continue intensive therapies that can compound symptoms and suffering. Factors that influence parents to choose palliation as the primary treatment goal are not well understood. The objective of this study was to examine experiences impacting parents' report of palliative goals adjusted for time. The authors hypothesized that awareness of poor prognosis, recall of oncologists' prognostic disclosure, intensive treatments, and burdensome symptoms and suffering would influence palliative goal-setting.
METHODS: The authors collected prospective, longitudinal surveys from parents of children with relapsed/refractory neuroblastoma at nine pediatric cancer centers across the United States, beginning at relapse and continuing every 3 months for 18 months or until death. Hypothesized covariates were examined for possible associations with parental report of palliative goals. Generalized linear mixed models were used to evaluate factors associated with parents' report of palliative goals at different time points.
RESULTS: A total of 96 parents completed surveys. Parents were more likely to report a primary goal of palliation when they recalled communication about prognosis by their child's oncologist (odds ratio [OR], 52.48; p = .010). Treatment intensity and previous ineffective therapeutic regimens were not associated with parents' report of palliative goals adjusted for time. A parent who reported new suffering for their child was less likely to report palliative goals (OR, 0.13; p = .008).
CONCLUSIONS: Parents of children with poor prognosis cancer may not report palliative goals spontaneously in the setting of treatment-related suffering. Prognostic communication, however, does influence palliative goal-setting. Evidence-based interventions are needed to encourage timely, person-centered prognostic disclosure in the setting of advanced pediatric cancer.
PLAIN LANGUAGE SUMMARY: Many parents of children with poor-prognosis cancer continue to pursue curative treatments that may worsen symptoms and suffering. Little is known about which factors influence parents to choose palliative care as their child's main treatment goal. To explore this question, we asked parents of children with advanced neuroblastoma across the United States to complete multiple surveys over time. We found that the intensity of treatment, number of treatments, and suffering from treatment did not influence parents to choose palliative goals. However, when parents remembered their child's oncologist talking about prognosis, they were more likely to choose palliative goals of care.
Patients who had received pre-operative bowel preparation(PBP) were identified using electronic medical records. Patients prescribed an enema solution (EVAC enema 118 mL/bot, Purzer Pharmaceutical Co., Ltd) before surgery were allocated to the PBP group. Patients who received no PBP were allocated to none PBP group.
Aldesleukin is an interleukin-2 lymphocyte growth factor. The antitumor activity of aldesleukin has not been fully characterized. In vitro studies performed on human cell lines show enhancement of lymphocyte mitogenesis and cytotoxicity, induction of killer cell activity [lymphokine-activated killer (LAK) and natural killer (NK) cells] and interferon gamma production, and proliferation of human interleukin-2-dependent cell lines.

Administration of aldesleukin in animals and humans produces multiple immunological effects in a dose-dependent manner. These effects include activation of cellular immunity and the production of cytokines including tumor necrosis factor, IL-1, and interferon gamma. In vivo experiments in murine melanoma and sarcoma tumor models have shown inhibition of tumor growth.
In published studies, clinically significant hypokalemia has been consistently less common in patients who received 12.5 mg of hydrochlorothiazide than in patients who received higher doses. Nevertheless, periodic determination of serum electrolytes should be performed in patients who may be at risk for the development of hypokalemia. Patients should be observed for signs of fluid or electrolyte disturbances, i.e., hyponatremia, hypochloremic alkalosis, and hypokalemia and hypomagnesemia.

Warning signs or symptoms of fluid and electrolyte imbalance include dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, and gastrointestinal disturbances such as nausea and vomiting.

Hypokalemia may develop, especially with brisk diuresis when severe cirrhosis is present, during concomitant use of corticosteroid or adrenocorticotropic hormone (ACTH) or after prolonged therapy. Interference with adequate oral electrolyte intake will also contribute to hypokalemia. Hypokalemia and hypomagnesemia can provoke ventricular arrhythmias or sensitize or exaggerate the response of the heart to the toxic effects of digitalis. Hypokalemia may be avoided or treated by potassium supplementation or increased intake of potassium rich foods.

Dilutional hyponatremia is life-threatening and may occur in edematous patients in hot weather; appropriate therapy is water restriction rather than salt administration, except in rare instances when the hyponatremia is life-threatening. In actual salt depletion, appropriate replacement is the therapy of choice.
OBJECTIVE: Aim: To clarify the association between different types of uterine contractility dysfunction and the inflammation of the uterus and chorioamniotic membranes.
PATIENTS AND METHODS: Materials and Methods: The association between the inflammation of the uterine layers, chorioamniotic membranes, umbilical cord, and different types of labor activity abnormalities was examined in 382 patients with singleton pregnancies at 28-42 weeks' gestation who underwent Caesarean section (CS) for abnormal uterine contractions and other complications. Statistical analyses included the Mann-Whitney U, Chi-squared test, and logistic regression.
RESULTS: Results: In the control group, slight infiltration with polymorphonuclear leukocytes (PMNs) and macrophages of the myometrium and decidua of the lower uterine segment at term pregnancy was found in 59.7% and 73.6% of cases. The main clinical risk factors for placental and decidual membrane inflammation in patients with excessive uterine activity (EUA) were prematurity, multiparity, group B streptococcus (GBS) colonization, and duration of ruptured fetal membranes before the CS. Moderate or marked myometrial inflammation of both uterine segments in the EUA group was diagnosed only in patients with cervical dilation of >6 cm and duration of labor of >8h. In women with hypotonic uterine activity (HUA), decidual and myometrial inflammation was significantly associated with nulliparity and intrapartum factors, such as protracted active first stage of labor, advanced cervical dilation, and number of vaginal examinations. In all cases, inflammation of the myometrium was accompanied by deciduitis.
CONCLUSION: Conclusions: Mild inflammation of the decidual membrane and myometrium of the lower segment at term pregnancy is a common physiological phenomenon contributing to labor initiation. Uterine hyperfunction comes as the response of the unaffected myometrium to the release of high concentrations of proinflammatory cytokines produced by the inflamed decidual and chorioamniotic membranes into the bloodstream. Marked myometrial inflammation that occurs in prolonged labor is an additional factor aggravating the hypotonic uterine activity.
Hyperphosphatemia or severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) infection can promote cardiovascular adverse events in patients with chronic kidney disease. Hyperphosphatemia is associated with elevated inflammation and sterol regulatory element binding protein 2 (SREBP2) activation, but the underlying mechanisms in SARS‑CoV‑2 that are related to cardiovascular disease remain unclear. The present study aimed to elucidate the role of excess inorganic phosphate (PI) in SARS‑CoV‑2 N protein‑induced NLRP3 inflammasome activation and the underlying mechanisms in vascular smooth muscle cells (VSMCs). The expression levels of SARS‑CoV‑2 N protein, SREBP cleavage‑activating protein (SCAP), mature N‑terminal SREBP2, NLRP3, procaspase‑1, cleaved caspase‑1, IL‑1β and IL‑18 were examined by western blotting. The expression levels of SREBP2, HMG‑CoA reductase, HMGCS1, low density lipoprotein receptor, proprotein convertase subtilisin/kexin type 9 (PCSK9), SREBP1c, fatty acid synthase, stearyl coenzyme A desaturase 1, acetyl‑CoA carboxylase α and ATP‑citrate lyase were determined by reverse transcription‑quantitative PCR. The translocation of SCAP or NLRP3 from the endoplasmic reticulum to the Golgi was detected by confocal microscopy. The results showed that excess PI promoted SCAP‑SREBP and NLRP3 complex translocation to the Golgi, potentially leading to NLRP3 inflammasome activation and lipogenic gene expression. Furthermore, PI amplified SARS‑CoV‑2 N protein‑induced inflammation via the SCAP‑SREBP pathway, which facilitates NLRP3 inflammasome assembly and activation. Inhibition of phosphate uptake with phosphonoformate sodium alleviated NLRP3 inflammasome activation and reduced SREBP‑mediated lipogenic gene expression in VSMCs stimulated with PI and with SARS‑CoV‑2 N protein overexpression. Inhibition of SREBP2 or small interfering RNA‑induced silencing of SREBP2 effectively suppressed the effect of PI and SARS‑CoV‑2 N protein on NLRP3 inflammasome activation and lipogenic gene expression. In conclusion, the present study identified that PI amplified SARS‑CoV‑2 N protein‑induced NLRP3 inflammasome activation and lipogenic gene expression via the SCAP‑SREBP signaling pathway.
PURPOSE: Research has documented that adolescent sleep is impacted by various stressors, including interpersonal experiences and structural disadvantage. This study extends existing knowledge by empirically examining interconnected individual experiences of structural inequity and assessing its association with subjective and objective sleep outcomes.
METHODS: We utilized data from the Adolescent Brain and Cognitive Development Study to identify seven conceptual domains of structural inequity: perceived discrimination, low school inclusivity, neighborhood safety, unmet medical needs, legal problems, material hardship, and housing insecurity. We operationalized experiences of structural inequity as latent classes, a cumulative exposure, and each domain separately. Sleep disturbances were measured using the Sleep Disturbance Scale, and sleep duration was assessed using Fitbits. Mixed effects linear regression estimated the association between our measures of structural inequity, longitudinal sleep disturbances, and cross-sectional sleep duration.
RESULTS: Latent class analysis revealed common exposure profiles (low risk, interpersonal, and systemic) of experiences of structural inequity across our sample. In longitudinal models, structural inequity was associated with higher Sleep Disturbance Scale scores, whether measured as latent classes, a cumulative exposure, or individual domains. Individuals with interpersonal exposures, those with at least one exposure, and those with legal problems, material hardship, and housing insecurity had lower mean sleep duration.
DISCUSSION: Results are consistent with literature that frames structural inequity as a lifelong determinant of sleep disturbance and duration. Adolescence represents a crucial time for interventions aimed at improving sleep and redressing inequities throughout the life course; our work can inform the development of policies and interventions toward this end.
In addition to being given a sleep hygiene handout as a standard of care, participants will be asked to apply pressure on each of following points (bilaterally where indicated). There are 5 acupoints with 4 of the acupoints performed on both the left and the right sides of the body giving a total of 9 points to stimulate. Each of the 9 acupoints will be stimulated for 3 minutes per point giving a total treatment time of 27 minutes done once daily.
Placebo given PO once a day for 12 weeks. Participants begin open label extension (130 mg evacetrapib given PO once a day for 40 weeks) after week 12.
DEMEROL Injection contains meperidine, a Schedule II controlled substance. As an opioid, DEMEROL Injection exposes users to the risks of addiction, abuse, and misuse [see Drug Abuse and Dependence (9)].

Although the risk of addiction in any individual is unknown, it can occur in patients appropriately prescribed DEMEROL Injection. Addiction can occur at recommended dosages and if the drug is misused or abused.

Assess each patient's risk for opioid addiction, abuse, or misuse prior to prescribing DEMEROL Injection, and monitor all patients receiving DEMEROL Injection for the development of these behaviors and conditions. Risks are increased in patients with a personal or family history of substance abuse (including drug or alcohol abuse or addiction) or mental illness (e.g., major depression). The potential for these risks should not, however, prevent the proper management of pain in any given patient. Patients at increased risk may be prescribed opioids such as DEMEROL Injection but use in such patients necessitates intensive counseling about the risks and proper use of DEMEROL Injection along with intensive monitoring for signs of addiction, abuse, and misuse.

Opioids are sought for nonmedical use and are subject to diversion from ‎legitimate prescribed use. Strategies to reduce these risks include prescribing the drug in the smallest appropriate quantity. Contact local state professional licensing board or state-controlled substances authority for information on how to prevent and detect abuse or diversion of this product.
Cognitive dysfunction in Alzheimer's disease (AD) patients are thought to arise in part from underlying losses of cholinergic input to cerebral cortex and hippocampus. Consistent marked decreases of alpha4beta2 nicotinic acetylcholine receptors (nAChRs) are found in postmortem AD brains. However, knowledge of the in vivo status of this receptor system is limited due to the lack of suitable tracers for PET/SPECT imaging. We plan to use a new SPECT tracer, \[123I\]5-I-A-85380, which appears suitable for imaging the alpha4beta2 subtype of nAChRs, in order to delineate abnormalities of this receptor system in a "subgroup" of 20 mild to moderately demented AD patients against 20 age matched healthy controls, the "subgroup" being characterized by carrying the AD susceptibility Apolipoprotein E epsilon4 allele. In addition, we plan to examine the relationship between cognitive dysfunction and alpha4beta2 nAChr deficits in the cerebral cortex and hippocampus of these AD patients. This study represents our initial effort toward our long-term goal of understanding the role this important receptor system plays in the pathophysiological mechanisms and drug manipulation of AD.