anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Intraventricular hemorrhage (IVH) often affects newborns of low gestational age and low birth weight, requires critical care for neonates, and is linked to long-term neurodevelopmental outcomes. Assessing regional differences in the U.S. in care for neonatal IVH and subsequent outcomes can shed light on ways to mitigate socioeconomic disparities.
METHODS: Using the 2016-2019 National Inpatient Sample (NIS), patients with a primary diagnosis of IVH were identified using ICD-10-CM codes. A retrospective cohort study was conducted with patients stratified by hospital region. Demographics, comorbidities, presentation, intraoperative variables, and inpatient outcomes were assessed. Multivariate logistic regression analyses were used to identify the impact of insurance status on extended LOS (defined as > 75th percentile of LOS), exorbitant cost (defined as > 75th percentile of cost), and mortality.
RESULTS: Included in this study were 1630 newborns with IVH. A larger portion of patients in the South and Midwest were Black, compared to the Northeast and West (Northeast: 12.2% vs Midwest: 30.2% vs South: 22.8% vs West: 5.8%, p < 0.001), while a greater percentage of patients in the West and South were Hispanic (Northeast: 7.3% vs Midwest: 9.5% vs South: 22.8% vs West: 36.2%, p < 0.001). LOS was similar among all regions. Factors associated with prolonged LOS included hydrocephalus and CSF diversions. Median total cost of admission was highest in the West, while the South was associated with decreased odds of exorbitant cost. LOS was associated with exorbitant cost, and large bed-volume hospital, VLBW, and permanent CSF shunt were associated with mortality.
CONCLUSIONS: Demographic variables, but not presenting or intraoperative variables, differed among regions, pointing to possible geographic health disparities. The West had the highest total cost of admission, while the South was associated with reduced odds of exorbitant admission costs.
The treatment of most head and neck cancer patients includes ionizing radiation (IR). Salivary glands in the IR field suffer irreversible damage. There is no conventional treatment available to correct this condition. Our research group has been developing the AdhAQP1 recombinant serotype 5 adenoviral (rAd5) vector based on the hypothesis that a replication deficient rAd5 vector is capable of safely transferring the human aquaporin-1 (hAQP1) cDNA to parotid glands of adult patients with IR-induced salivary hypofunction, resulting in an elevated salivary output, albeit transiently. Salivary glands have proven to be valuable gene transfer targets in numerous pre-clinical animal model studies. hAQP1, the archetypal water channel, is a plasma membrane protein that facilitates water movement across lipid bilayers. Rat and minipig studies have clearly shown that the AdhAQP1 strategy for restoring salivary flow to IR-damaged salivary glands is effective, and studies in rats, non-human primates and minipigs have shown that AdhAQP1 and similar rAd5 vectors are without significant untoward effects after salivary gland delivery. The purpose of this clinical protocol is to test the safety of AdhAQP1, with some measures of efficacy, in adult patients with established IR-induced parotid gland hypofunction. The targeted tissue site for the AdhAQP1 vector in the proposed study is a single parotid gland. In this Phase 1 dose-escalation study, safety will be evaluated using conventional clinical and immunological parameters. The primary outcome measure for biological efficacy will be parotid gland salivary output.
FIELD: medicine. SUBSTANCE: method involves administering plasmapheresis, chemotherapy and endolymphatic injection of preparations. Anti-tumor preparations are injected as patient auto plasma solutions at the first and eighth treatment day into the back part of foot on the opposite side with respect to cancer localization side. The plasma taken from patient is incubated with chemical preparations in volume proportion of 1:1 at 37 C for 30 min and injected in endolymphatic way. Intravenous drooping of chemical preparations incubated with plasma is carried out according to known treatment schedule. EFFECT: enhanced effectiveness of treatment; high survival percentage. 10 dwg
The blood spot validation portion of the study tests the hypothesis that progesterone assays from self-collected daily blood spots are equivalent to serum samples, and that the values obtained can identify women that ovulate. After validating collection methods, enrollment will begin for the feasibility portion of the study looking at thin and heavy women on birth control pills. All women in this portion of the study will take a very-low dose birth control pill that is normally available through a doctor's office. During each month of the study, women will have their blood pressure and weight recorded, and have their blood drawn twice per week or use a finger stick kit daily at home to check for the natural hormones and brain chemicals that tells if an egg develops. During the last week of each menstrual cycle (period week), women will also have their blood drawn to measure the levels of hormone found in the birth control pill. Women will also need to report in a written diary that they have taken their birth control pill for the day.
Abnormal genetic polymorphism of trace amine-associated receptor 1 (TAAR1) rs8192620 site has been confirmed to induce methamphetamine (MA) use and drug craving. However, the genetic susceptibility difference between MA addicts and heroin addicts is unknown. This study evaluated genetic heterogeneity of TAAR1 rs8192620 between MA and heroin addicts and elucidated whether rs8192620 genotypes associated with discrepancy in emotional impulsivity, which would help to instruct individualized treatment in addiction via acting on TAAR1 and evaluate risk of varied drug addiction. Participants consisting of gender-matched 63 MA and 71 heroin abusers were enrolled in the study. Due to mixed drug usage in some MA addicts, MA users were further subdivided into 41 only-MA (only MA taking) and 22 mixed-drug (Magu composed of about 20% MA and 70% caffeine) abusers. Via inter-individual single nucleotide polymorphism (SNP) analysis and two-sample t tests, respectively, the genotypic and Barratt Impulsiveness Scale-11 (BIS-11) scores differences between groups were completed. With following genotypic stratification, the differences in BIS-11 scores between groups were analyzed through two-sample t test. Individual SNP analysis showed significant differences in alleles distribution of rs8192620 between MA and heroin subjects (p = 0.019), even after Bonferroni correction. The TT homozygotes of rs8192620 dominated in MA participants, while C-containing genotypes in heroin (p = 0.026). There was no association of genotypes of TAAR1 rs8192620 with addicts' impulsivity. Our research indicates that the TAAR1 gene polymorphism might mediate the susceptibility discrepancy between MA and heroin abuse.
Participants that are assigned to the control arm will be observed for hand hygiene adherence and duration during the habituation period, intervention period, and 3-12 months post-intervention. They will also be asked to complete study surveys at baseline, post-intervention and 6-months post intervention. They will not receive any of the intervention components.
Patients receive oral erlotinib once daily. After 1 week of erlotinib alone, patients also receive oral temozolomide once daily for 6 weeks and undergo concurrent radiotherapy 5 days a week for 6 weeks. After completion of radiotherapy, patients continue to receive erlotinib once daily alone in the absence of disease progression or unacceptable toxicity. Beginning 4 weeks after the completion of radiotherapy, patients also receive oral temozolomide once daily for 5 days. Temozolomide treatment repeats every 28 days for 6 courses in the absence of disease progression or unacceptable toxicity.
BACKGROUND: Chemotherapy-induced cardiovascular disease is a growing concern in the elderly population who have survived cancer, yet the underlying mechanism remains poorly understood. We investigated the role of ALKBH5 (AlkB homolog 5), a primary N6-methyladenosine (m6A) demethylase, and its involvement in m6A methylation-mediated regulation of targets in aging-associated doxorubicin-induced cardiotoxicity.
METHODS AND RESULTS: To validate the relationship between doxorubicin-induced cardiotoxicity and aging, we established young and old male mouse models. ALKBH5 expression was modulated through adeno-associated virus 9 (in vivo), Lentivirus, and siRNAs (in vitro) to examine its impact on cardiomyocyte m6A modification, doxorubicin-induced cardiac dysfunction, and remodeling. We performed mRNA sequencing, methylated RNA immunoprecipitation sequencing, and molecular assays to unravel the mechanism of ALKBH5-m6A modification in doxorubicin-induced cardiotoxicity. Our data revealed an age-dependent increase in doxorubicin-induced cardiac dysfunction, remodeling, and injury. ALKBH5 expression was elevated in aging mouse hearts, leading to reduced global m6A modification levels. Through mRNA sequencing and methylated RNA immunoprecipitation sequencing analyses, we identified ARID2 (AT-rich interaction domain 2) as the downstream effector of ALKBH5-m6A modulation in cardiomyocytes. Further investigations revealed that ARID2 modulates DNA damage response and enhances doxorubicin-induced cardiomyocyte apoptosis.
CONCLUSIONS: Our findings provide insights into the role of ALKBH5-m6A modification in modulating doxorubicin-induced cardiac dysfunction, remodeling, and cardiomyocyte apoptosis in male mice. These results highlight the potential of ALKBH5-targeted treatments for elderly patients with cancer in clinical settings.
The present invention provides monoclonal antibodies demonstrating specific reactivity with HIV-I p24. One monoclonal antibody designated 31-42-19 recognizes an unique epitope on HIV-I p24 that is not immunogenic in humans. 31-42-19 also reacts with an antigenically cross reactive epitope on HIV-2 p24. Another monoclonal antibody designated 31-90-25 recognizes an epitope within a highly immunogenic region of HIV-I p24. The present invention also provides cell lines capable of producing these monoclonal antibodies. The invention also includes a highly sensitive enzyme immunoassay for the detection of HIV-I p24 in biological fluids, using a monoclonal antibody mixture. The present invention further provides methods for the use of these monoclonal antibodies for the detection of anti-HIV-I p24 antibodies and HIV-2 p24 antigen in biological samples.
It is important for college students to establish healthy habits during college because they are likely to stay with them throughout their lives. The transition to college has been identified as a critical period contributing to the rise in obesity rates. Several studies have shown that the initial transition to college is associated with rapid weight gain and the average weight gain in the first year of college ranges from 3.5 to 8.8 pounds. While decreased dietary fiber, fruits and vegetables and junk food consumption are among the dietary factors that have been linked to increased obesity rates in college students, little is known about the effect of eating patterns on health in this population. Furthermore, lack of sleep, smoking, binge drinking, and infrequent eating are all associated with negative health outcomes. Previous work with college age youth has found that several behaviors cluster together. The goal of the Online Survey portion is to expand on current findings, as well as examine the interrelationships of alcohol use, sleep, smoking, and eating patterns with adiposity and metabolic disease risk in a population of freshmen college students.

Eating frequency research has consistently found a negative association between the number of eating occasions (EOs) per day and adiposity, as well as metabolic disease risk in both youth and adult populations. Our group has shown that infrequent eating is linked to increased obesity measures, blunted insulin action, and deleterious lipid parameters in multiple populations of overweight Hispanic youth (8-18y). However, to date, no group has looked at the effect of eating frequency on adiposity and metabolic disease risk in a sample of overweight Hispanic college freshmen. In 2012, for the first time in history Hispanic high school graduates (69%) were more likely to be enrolled in college than Non-Hispanic Whites (NHW; 67%) and Blacks (63%) and last year Hispanic students represented 24% of freshman enrollment at the University of Texas at Austin (UT), Hispanics also showed the largest increase among all minority groups. Thus, the goal of the In-Person Visit is to examine the relationship between eating frequency and adiposity/metabolic disease risk in this extremely high-risk population of Hispanic freshmen and potentially identify interventions that may reduce this risk within such a crucial period of life.

The human body contains 100 trillion microbes, and microbial genes outnumber human genes 100:110. Over the past decade, interest in the complex ecosystem of gut microbiota has increased immensely and research has uncovered a relationship between gut microbiota, metabolic disease, and obesity. Both diet and obesity have been shown to alter the gut microbiota12,13. However, few studies have investigated how individual dietary components can affect the gut microbiota in humans. The Stool Sample portion of the study is an exploratory investigation of the relationship between dietary components and gut microbiota composition in college-aged Hispanic freshmen.
Microwave ablation（MWA）refers to all electromagnetic methods of inducing tumor destruction by using devices with frequencies greater than or equal to 900MHz. The rotation of dipole molecules accounts for most of the heat generated during MWA. Water molecules as dipoles attempt to continuously reorient at the same rate in microwave's oscillating electric field. As a result of microwave transmission, the water molecules flip back and forth billions of times a second. The vigorous movement of water molecules produce friction and heat, thus inducing cellular death via coagulation necrosis. The microwave unit (KY-2000, Kangyou Medical, Nanjing, China) is capable of producing 100 Watts of power at 2450 MHz.The needle antenna has a diameter of 1.6 mm (16G) and a length of 10 cm. The active tip length is 3mm and 5mm.
The researchers designed a recovery group suited to Taiwanese with mental illness, according to content of the PTR (Ridgway et al., 2002) and recovery-related literature (Davidson et al., 2005; Ridgway, 2001). The group gathered for a one-hour session once a week for 18 weeks.
BACKGROUND: Transient receptor potential (TRP) ankyrin 1 (TRPA1) could mediate ozone-induced lung injury. Optic Atrophy 1 (OPA1) is one of the significant mitochondrial fusion proteins. Impaired mitochondrial fusion, resulting in mitochondrial dysfunction and ferroptosis, may drive the onset and progression of lung injury. In this study, we examined whether TRPA1 mediated ozone-induced bronchial epithelial cell and lung injury by activating PI3K/Akt with the involvement of OPA1, leading to ferroptosis.
METHODS: Wild-type, TRPA1-knockout (KO) mice (C57BL/6 J background) and ferrostatin-1 (Fer-1)-pretreated mice were exposed to 2.5 ppm ozone for 3 h. Human bronchial epithelial (BEAS-2B) cells were treated with 1 ppm ozone for 3 h in the presence of TRPA1 inhibitor A967079 or TRPA1-knockdown (KD) as well as pharmacological modulators of PI3K/Akt-OPA1-ferroptosis. Transcriptome was used to screen and decipher the differential gene expressions and pathways. Oxidative stress, inflammation and ferroptosis were measured together with mitochondrial morphology, function and dynamics.
RESULTS: Acute ozone exposure induced airway inflammation and airway hyperresponsiveness (AHR), reduced mitochondrial fusion, and enhanced ferroptosis in mice. Similarly, acute ozone exposure induced inflammatory responses, altered redox responses, abnormal mitochondrial structure and function, reduced mitochondrial fusion and enhanced ferroptosis in BEAS-2B cells. There were increased mitochondrial fusion, reduced inflammatory responses, decreased redox responses and ferroptosis in ozone-exposed TRPA1-KO mice and Fer-1-pretreated ozone-exposed mice. A967079 and TRPA1-KD enhanced OPA1 and prevented ferroptosis through the PI3K/Akt pathway in BEAS-2B cells. These in vitro results were further confirmed in pharmacological modulator experiments.
CONCLUSION: Exposure to ozone induces mitochondrial dysfunction in human bronchial epithelial cells and mouse lungs by activating TRPA1, which results in ferroptosis mediated via a PI3K/Akt/OPA1 axis. This supports a potential role of TRPA1 blockade in preventing the deleterious effects of ozone.
Observational studies suggest dyslipidemia as an atopic dermatitis (AD) risk factor and posit that lipid-lowering drugs may influence AD risk, but the causal link remains elusive. Mendelian randomization was applied to elucidate the causal role of serum lipids in AD and assess the therapeutic potential of lipid-lowering drug targets. Genetic variants related to serum lipid traits and lipid-lowering drug targets were sourced from the Global Lipid Genetics Consortium GWAS data. Comprehensive AD data were collated from the UK Biobank, FinnGen, and Biobank Japan. Colocalization, Summary-data-based Mendelian Randomization (SMR), and mediation analyses were utilized to validate the results and pinpoint potential mediators. Among assessed targets, only Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) was significantly linked to a reduced AD risk, corroborated across three separate AD cohorts. No association between serum lipid concentrations or other lipid-lowering drug targets and diminished AD risk was observed. Mediation analysis revealed that beta nerve growth factor (b-NGF) might mediate approximately 12.8% of PCSK9's influence on AD susceptibility. Our findings refute dyslipidemia's role in AD pathogenesis. Among explored lipid-lowering drug targets, PCSK9 stands out as a promising therapeutic agent for AD.
Subjects with Non-alcoholic Steatohepatitis (NASH) Cirrhosis and Severe Portal Hypertension will be administered orally with emricasan (5 mg) twice a day. The MBT will be performed at screening, at week 24/week 48/at early termination.
Although kidney transplantation (KT) is the best treatment option for end-stage kidney disease, long-term complications such as chronic kidney allograft dysfunction and cardiovascular disorders are observed. To decrease these complications, preventive measures must be applied in kidney transplant recipients (KTRs). One of these common measures is the increase of water/fluid intake although this is not evidence-based practice. Indeed, surprisingly very limited studies evaluated the impact of increased water/fluid intake on graft function, with small number of KTRs and short term follow-up. We suggest that the water/fluid intake should be personalized based on baseline graft function, time onset after KT (which water homeostasis changes), presence of hyponatremia and hypervolemia, concomitant medications, and patient willingness. Methods for estimating water/fluid intake (direct measurement, 24-h urine volume measurement, urine osmolarity) has both advantages and drawbacks and the best method has not been identified. Increase of water/fluid intake in specific conditions (in hot, and humid weather, before exercise, during Ramadan fasting) or in distinct KTRs (KTRs with de novo nephrolithiasis, frequent urinary tract infections) is not tested. Furthermore, the relationship between water/fluid intake and major cardiovascular adverse events are not known. There is no doubt that minimum amount of water/fluid intake is necessary for graft function (the amount is not known) but there is no evidence for a particular target level of water/fluid intake. In the current review, we summarize the studies assessing fluid/water intake in KTR, explained the pathophysiologic basis of water disorders in early period of KT and late after KT, elucidate conflicts and unknown issues of water intake in KTRs and suggest future research needs.
This study is a non-interventional, observational study in which Zemplar® Injection is prescribed in the usual manner in accordance with the terms of the local Summary of Product Characteristics (SmPC) with regards to dose, population and indication. The study population consists of participants receiving hemodialysis in whom the diagnosis of secondary hyperparathyroidism has been established, and who are not adequately controlled with the oral VDR activator (calcitriol or alfacalcidol). Participants will be included via consecutive sampling. To be included, participants should have a clinical indication to initiate treatment with Zemplar® Injection due to: (1) a diagnosis of secondary hyperparathyroidism and (2) because they require a change in treatment for secondary hyperparathyroidism (e.g. due to a lack of effectiveness of the previous treatment). Each participant will be observed during his/her Zemplar® Injection treatment regimen for a maximum period of 12 months.
Patients will meet once per week with dietitian for the first 6 weeks in 60 minute sessions. Dietitian will telephone each patient weekly for the final 6 weeks of counseling and support.
The estimation of the postmortem interval (PMI) is a significant challenge in legal medicine and forensic sciences due to the dynamic and continuous decomposition of organisms after death. Thanatochemistry has emerged as a promising area to estimate PMI by measuring the concentrations of postmortem biochemical markers. This systematic review and meta-analysis aimed to summarize evidence on postmortem biochemical alterations in vitreous humor (VH) and synovial fluid (SF) to estimate early PMI. Comprehensive searches of electronic databases identified studies measuring postmortem biomarker concentrations in both matrices. Our analysis included three meta-analytical approaches: calculating standardized mean differences to assess variations in biochemical parameters, executing correlation meta-analysis (ρ) to explore relationships between these parameters and PMI, and conducting meta-regression to derive a predictive model. Results from five eligible studies indicated no correlation between sodium levels and PMI in both matrices. However, a strong correlation was found between potassium levels and PMI in VH (ρ = 0.69; 95 % CI 0.52 to 0.86) and SF (ρ = 0.81; 95 % CI 0.75 to 0.87), with the meta-regression yielding the optimal predictive equation for SF: [K+] = 6.15 + 0.21 × PMI. These findings support the use of potassium as a reliable biomarker for PMI estimation, particularly in SF.
Participants will receive 2 or 3 21-day cycles of second-line chemotherapy regimen; R-ICE: rituximab 375 mg/m\^2 before chemotherapy,ifosfamide 5 g/m\^2 24hour(hr) infusion on Day 2+mesna,carboplatin area under the curve (AUC) 5 on Day 2, maximum dose 800 mg,etoposide 100 mg/ m\^2/day on Days 1-3; R-ESHAP: rituximab 375 mg/m\^2 Day 1,etoposide 40 mg/m\^2/day IV on Days 1-4,methylprednisolone 500 mg/day IV on Days 1-4 or 5,cisplatin at 25 mg/m\^2/day Days 1-4,cytarabine 2 g/m\^2 on Day 5; R-GDP: rituximab 375 mg/m\^2 Day 1(or Day 8),gemcitabine 1g/m\^2 on Days 1 and 8,dexamethasone 40 mg on Days 1-4,cisplatin 75mg/m\^2 on Day 1 or carboplatin AUC=5; or R-DHAP: Rituximab 375 mg/ m\^2 before chemotherapy,dexamethasone 40 mg/day on Days 1-4,highdose cytarabine 2 g/m\^2 every 12 hours for 2 doses on Day 2 following/platinum,cisplatin 100 mg/m\^2 24hr infusion on Day 1 or oxaliplatin 100 mg/m\^2. Participants who will respond will get high dose therapy and autologous stem cell transplant.