anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
INTRODUCTION: According to current guidelines, pulmonary vein isolation as first-line therapy should be considered for patients with atrial fibrillation (AF), however, optimal timing of the procedure is still unknown in patients with heart failure (HF). We aimed to evaluate the effect of early catheter ablation (CA) in patients with HF and left ventricular ejection fraction (LVEF) below 50%.
METHODS: We analyzed data from a structured registry comprising 227 patients with paroxysmal or persistent AF and HF with LVEF < 50% who underwent radiofrequency CA between 2015 and 2022. Early CA was defined as a procedure performed within 12 months of AF diagnosis. The median follow-up duration was 1748 (1176.3-2353.5) days, with a minimum follow-up of 365 days. Our endpoints were AF recurrence after a 3-months blanking period and all-cause mortality.
RESULTS: Among the 227 patients with a median age of 64.3 years, 97 (42.7%) experienced AF recurrence and 55 (24.2%) died during the follow-up period. The median LVEF was 40% for early CA and 38% for delayed CA (p = .053). Early CA significantly reduced AF recurrence (HR = 0.25 [0.15-0.42], p < .001), however, the timing of procedure did not affect all-cause mortality (p = .16). These findings were consistent regardless of AF subtype or the burden of comorbidities, as assessed by the CHA2DS2-VASc score.
CONCLUSION: The timing of CA of AF appears to be an important factor in patients with HF. Early CA reduced AF recurrence, although it does not impact all-cause mortality. We found similar results regardless of AF subtype or burden of comorbidities.
"Bio-identical" hormones, which are compounded plant-based hormones synthesized into structurally similar to human estradiol and progesterone molecules, became popular in 2004 by celebrity, Suzanne Somers, who let women know there were natural alternatives to the drugs with hormone-like activity. Compounding hormones makes it easy to make dose adjustments in order to manage symptoms. Using this form of hormone delivery, it is possible to try and replicate a normal physiological reproductive pattern of replacement akin to thyroid replacement, etc. Current short-term studies with bio- identical transdermal estradiol and progesterone have not supported increased breast cancer or other issues such as venous thrombosis7. Even the WHI stated that the increase in breast cancer was due to stimulation of cancers already present.

This study of bio-identical physiologic restoration and dosing of estradiol, testosterone and cyclical transdermal progesterone attempts to replicate the reproductive hormone patterns and levels of a premenopausal woman. This dosing schedule has higher doses and levels than current standard estradiol and progesterone hormone therapy for post menopause women. Research shows that the estradiol peak of a menstrual cycle has an impact on cell signaling and receptor response. For example, TP53, the gene major tumor suppressor gene is under estrogen and progesterone control. At the peaks of estradiol and progesterone, TP53 is up regulated conferring cellular protection against mutations8-14.

Physiologic Restoration (PR) with bio-identical rhythmic dosing was originally developed by S.T. Wiley, who developed a template of hormone doses over time and was meant to be adjusted to the individual women depending on their symptoms and, absorption, metabolism, and response to the program. This study will utilize this concept with some improvements to the original proposed template (Sex, Lies, and Menopause, 2004). This regimen has been in national clinical practice since 2004 and has not been formally studied until now. There is unpublished observational data from Dr. Taguchi's high risk population of oncology patients (Santa Barbara Cottage Hospital IRB# 19-71ix) showing that PR is feasible and manages menopause symptoms well without seemingly more adverse effects and better sense of well being and excellent reversal or improvement of osteoporosis.
BACKGROUND: Sepsis is one of the most common clinical diseases, which is characterized by a serious and uncontrollable inflammatory response. LPS-induced inflammation is a critical pathological event in sepsis, but the underlying mechanism has not yet been fully elucidated.
METHODS: The animal model was established for two batches. In the first batch of experiments, Adult C57BL/6J mice were randomly divided into control group and LPS (5 mg/kg, i.p.)group . In the second batch of experiments, mice were randomly divided into control group, LPS group, and LPS+VX765(10 mg/kg, i.p., an inhibitor of NLRP3 inflammasome) group. After 24 hours, mice were anesthetized with isoflurane, blood and intestinal tissue were collected for tissue immunohistochemistry, Western blot analysis and ELISA assays.
RESULTS: The C57BL/6J mice injected with LPS for twenty-four hours could exhibit severe inflammatory reaction including an increased IL-1β, IL-18 in serum and activation of NLRP3 inflammasome in intestine. The injection of VX765 could reverse these effects induced by LPS. These results indicated that the increased level of IL-1β and IL-18 in serum induced by LPS is related to the increased intestinal permeability and activation of NLRP3 inflammasome. In the second batch of experiments, results of western blot and immunohistochemistry showed that Slit2 and Robo4 were significant decreased in intestine of LPS group, while the expression of VEGF was significant increased. Meanwhile, the protein level of tight junction protein ZO-1, occludin, and claudin-5 were significantly lower than in control group, which could also be reversed by VX765 injection.
CONCLUSIONS: In this study, we revealed that Slit2-Robo4 signaling pathway and tight junction in intestine may be involved in LPS-induced inflammation in mice, which may account for the molecular mechanism of sepsis.
The diagnosis of sinusoidal obstruction syndrome also know as veno-occlusive disease is often difficult. This is a potentially life-threatening complication that can develop after allogeneic hematopoietic stem cell transplantation. Clinically, sinusoidal obstruction syndrome is charaterized by hepatomegaly, right upper quadrant pain, jaundice and ascites. The diagnosis is based on biological parameters (bilirubin increase ≥ 2mg/dL or 34.2µmol/L) and clinical evaluation (sodium fluid retention with weight gain \> 5%, ascites, painful hepatomegaly) (reference : M. Mohty and al. Revised criteria for sinusoidal obstruction syndrome, Bone Marrow Transplantation (2016) 906-912).

Early therapeutic intervention is pivotal for survival in sinusoidal obstruction syndrome, thus a rapid and reliable diagnosis has to be made. To rule out major differential diagnosis, a reliable imaging method is needed. In practice, doppler ultrasonography, is helpful to detect hepatomegaly and ascites but also is an help to explore well defined criteria of sinusoidal obstruction syndrome already published. For sonography criteria: hepatomegaly (3 measures) with an increase of 2cm versus baseline, gallbladder wall thickening, ascites or 3 criteria of a native VOD; splenomegaly, increase of the portal vein diameter, decrease of the hepatic vein diameter, visualisation of the para umbilical vein and for the doppler : increase of the hepatic artery RI (\>0.75), monophasic flow in the hepatic veins (venous retraction is very typical but very late), flow demodulation on portal vein, decrease in portal flow, portal flow congestion, reversed flow, flow recorded in the para-umbilical vein ; all five last signs are late (reference : Lassau N. et al Prognostic value of doppler ultrasonography in hepatic veno occlusive disease. Transplantation 2002 jul 15 ;74(1) :60-6). These criteria can confirm the diagnosis : 6 signs of wich the first 3 can affirm the diagnosis with certainty in combination with clinical and biological parameters. There is currently a few data in the literature about early detection of this complication with systematic ultrasound. In this study, we want to evaluate in a retrospective study the interest of this technique in the early and systematic detection of sinusoidal obstruction syndrome.
Patients undergoing conventional open posterior lumbar interbody fusion (PLIF) surgery. A long midline skin incision (10-15 cm) is made, after which the paravertebral muscles are detached from the midline and retracted laterally in order to expose the facet joints and pedicle entry point. After the pedicle screws are positioned, the disc will be removed bilaterally and packed with autogenous bone chips, followed by bilateral placement of polyetheretherketone (PEEK) PLIF cages.
Type 2 diabetic people will be screened by clinical symptoms of neuropathy and DN4 questionnaire. Among those who did not have neuropathic symptoms or who have DN4 score below 4 will be considered for the study.Then aerobic capacity will be measured by a cycle ergometer and VO2max will be obtained. Weight, body mass index and muscle mass will be measured by bioimpedance analysis. Physical activity status will be determined by International Physical Activity Score (IPAQ). Cognitive function will be evaluated by Mini Mental test. HbA1c and fasting blood glucose will be measured in venous blood after overnight fasting. Blood pressure will be measured in the sitting position after resting from the left arm. Speed of gait will be measured by an accelerometer.Then, the effect of above mentioned factors on speed of gait will be studied.
Adverse Childhood Experiences (ACEs) are defined as traumatic events occurring before age 18, such as maltreatment, life-threatening accident, harsh migration experiences or exposure to violence. ACEs are pervasive, with 45% experiencing at least one ACE and 10% experiencing three or more ACEs, placing them at high risk for negative life outcomes. ACEs are more prevalent among minority and immigrant communities due to exposure to poverty, discrimination, community violence, national disasters, and refugee experiences. ACEs screenings have potential value in identifying children experiencing toxic stress and the physical and mental health conditions associated with it such as asthma, Attention Deficit Hyperactive Disorder (ADHD) and anxiety. Yet, they are seldom used in primary care during well-child visits. The Surgeon General of the state of California have addressed this care gap by issuing an ACEs screening policy. Starting January 2020, MediCal, California's Medicaid health care program, will reimburse primary care settings ($29) for using the Pediatric ACEs and Related Life-events Screener (PEARLS) tool to screen children for ACEs during wellness visits. Despite significant investment in California and nationwide, evidence of the public health value of universal child screening policies is unclear. Increased screening efforts often do not translate into higher access to care for children and may even exacerbate disparities by increasing stigma and reinforcing a deficit view of marginalized groups. These results have been attributed to a lack of rigorous studies testing implementation strategies suited for pediatric screening policies. This mixed-method study will fill this gap by refining and testing an implementation strategy using a multi-site controlled trial within a Federally Qualified Health Center in Southern California. Using the EPIS framework, we will employ a hybrid (type 2), randomized controlled trial using a stepped-wedge design (n=5 clinics) to test to test THE central hypothesis that clinics employing a multifaceted implementation strategy will have higher fidelity and reach of the ACEs screening policy. A secondary hypothesis will examine the public health impact of the ACEs policy on child patient-level mental health service and symptom outcomes. Specific aims are: Aim 1. Refine a multifaceted implementation strategy to support the implementation of the ACEs screening policy in community-based clinics, and Aim 2. Pilot test the feasibility, acceptability, fidelity and reach of the implementation strategy and the impact of the ACEs policy on child patient-level outcomes. This project capitalizes on a rare opportunity to pilot test an implementation strategy to maximize the impact of a state-wide policy intended to improve child health in under-resourced settings.
Patients receive 68Ga-FAPi-46 intravenously (IV), and then undergo PET/computed tomography (CT) over 20-90 minutes. On another day, patients receive 18F-FDG and then undergo PET/computed tomography (CT) according to standard of care procedures (if applicable).
BACKGROUND: There is clear evidence that prevalence of primary antibody deficiency (PAD) is higher in children with chronic rhinosinusitis (CRS) than in the general population. The purpose of this multi-institutional and multidisciplinary evidence-based review with recommendations (EBRR) is to thoroughly review the literature on rhinosinusitis with PAD, summarize the existing evidence, and provide recommendations on the evaluation and management of rhinosinusitis in children with PAD.
METHODS: The PubMed, Embase, and Cochrane databases were systematically reviewed from inception through December 2023. Studies on the evaluation and management of rhinosinusitis in PAD patients were included. An iterative review process was utilized in accordance with EBRR guidelines. Levels of evidence and recommendations on the evaluation and management principles for PAD were generated.
RESULTS: A total of 50 studies were included in this evidence-based review. These studies were evaluated on the incidence of PAD in rhinosinusitis patients, the incidence of rhinosinusitis in PAD patients, and on the different treatment modalities used and their outcome. The aggregate quality of evidence varied across the reviewed domains.
CONCLUSION: Based on the currently available evidence, the incidence of PAD in children with recalcitrant CRS can be significantly elevated. Despite the presence of multiple studies addressing rhinosinusitis and PAD, the level of evidence supporting different treatment options continues to be lacking. Optimal management requires a multidisciplinary approach through collaboration with clinical immunology. There is need for higher level studies that compare different treatments in children with PAD and rhinosinusitis.
Children with chronic kidney disease (CKD) can have an inherent vulnerability to dehydration. Younger children are unable to freely access water, and CKD aetiology and stage can associate with reduced kidney concentrating capacity, which can also impact risk. This article aims to review the risk factors and consequences of mild dehydration and underhydration in CKD, with a particular focus on evidence for risk of CKD progression. We discuss that assessment of dehydration in the CKD population is more challenging than in the healthy population, thus complicating the definition of adequate hydration and clinical research in this field. We review pathophysiologic studies that suggest mild dehydration and underhydration may cause hyperfiltration injury and impact renal function, with arginine vasopressin as a key mediator. Randomised controlled trials in adults have not shown an impact of improved hydration in CKD outcomes, but more vulnerable populations with baseline low fluid intake or poor kidney concentrating capacity need to be studied. There is little published data on the frequency of dehydration, and risk of complications, acute or chronic, in children with CKD. Despite conflicting evidence and the need for more research, we propose that paediatric CKD management should routinely include an assessment of individual dehydration risk along with a treatment plan, and we provide a framework that could be used in outpatient settings.
Although ranitidine has been reported to bind weakly to cytochrome P-450 in vitro, recommended doses of the drug do not inhibit the action of the cytochrome P-450-linked oxygenase enzymes in the liver. However, there have been isolated reports of drug interactions that suggest that ranitidine may affect the bioavailability of certain drugs by some mechanism as yet unidentified (e.g., a pH-dependent effect on absorption or a change in volume of distribution).

Increased or decreased prothrombin times have been reported during concurrent use of ranitidine and warfarin. However, in human pharmacokinetic studies with dosages of ranitidine up to 400 mg per day, no interaction occurred; ranitidine had no effect on warfarin clearance or prothrombin time. The possibility of an interaction with warfarin at dosages of ranitidine higher than 400 mg per day has not been investigated.

In a ranitidine-triazolam drug-drug interaction study, triazolam plasma concentrations were higher during b.i.d. dosing of ranitidine than triazolam given alone. The mean area under the triazolam concentration-time curve (AUC) values in 18 to 60 year old subjects were 10% and 28% higher following administration of 75 mg and 150 mg ranitidine tablets, respectively, than triazolam given alone. In subjects older than 60 years of age, the mean AUC values were approximately 30% higher following administration of 75 mg and 150 mg ranitidine tablets. It appears that there were no changes in pharmacokinetics of triazolam and α-hydroxytriazolam, a major metabolite, and in their elimination. Reduced gastric acidity due to ranitidine may have resulted in an increase in the availability of triazolam. The clinical significance of this triazolam and ranitidine pharmacokinetic interaction is unknown.
The standard diet consists on an energy goal based on weight formula (20-25 kcal/kg/die). According to the ICU nutritional protocol, EN is started at an initial rate of 10ml/h, and increased by 20ml/h every 12 hours in the absence of significant gastric residuals (\<250ml), with the aim of reaching the energy goal within 72 hours from admission. The EN formulae used are standard (1-1,5 kcal/ml, 40g/l protein). If enteral nutrition is not tolerated or is not indicated, supplemental PN is used to make up the energy shortfall. The PN formula used is standard (1000 kcal/l, 37 g/l protein).
The moss Physcomitrium patens is a model system for the evolutionary study of land plants, and as such, it may contain as yet unannotated genes with functions related to the adaptation to water deficiency that was required during the water-to-land transition. In this study, we identified a novel gene, Bryophyte Co-retained Gene 1 (BCG1), in P. patens that is responsive to dehydration and rehydration. Under de- and rehydration treatments, BCG1 was significantly co-expressed with DHNA, which encodes a dehydrin (DHN). Examination of previous microarray data revealed that BCG1 is highly expressed in spores, archegonia (female reproductive organ), and mature sporophytes. In addition, the bcg1 mutant showed reduced dehydration tolerance, and this was accompanied by a relatively low level of chlorophyll content during recovery. Comprehensive transcriptomics uncovered a detailed set of regulatory processes that were affected by the disruption to BCG1. Experimental evidence showed that BCG1 might function in antioxidant activity, the abscisic acid pathway, and in intracellular Ca2+ homeostasis to resist desiccation. Overall, our results provide insights into the role of a bryophyte co-retained gene in desiccation tolerance.
At present, the liposomal doxorubicin developed on the basis of doxorubicin has been used for the first-line treatment of advanced breast cancer, and both NCCN and CSCO guidelines have related recommendations. However, the application of liposomal doxorubicin in adjuvant therapy of breast cancer still lacks sufficient evidence-based medicine. The current research shows that doxorubicin under the encapsulation of liposomes prolongs the half-life of the drug, reduces the cardiotoxicity, and the drug is continuously enriched in the tumor tissue to improve the anti-tumor activity. In addition, liposomal doxorubicin has the advantage of less hair loss during chemotherapy, which meets the needs of some clinical patients for hair protection. There is still a lack of clinical studies on the use of AC (liposomal doxorubicin/cyclophosphamide) with other early breast cancer adjuvant chemotherapy regimens. This study aimed to evaluate the efficacy and safety of AC (liposomal doxorubicin + cyclophosphamide) and TC (docetaxel + cyclophosphamide) regimens as adjuvant therapy for HR+ HER2- early breast cancer.
A complete remedy for AIDS is difficult to obtain. As such, a useful process was designed to search for an anti-HIVi agent that has an immuno response modification activity capable of releasing immuno suppression, activating killer cells to destroy persistent infection cells, elevating antibody titer to activate ADCC activity, and vice versa. The process consists of 4 elements: guinea pig or mouse peritoneal derived adherent macrophages/monocytes as effector cells; cyclophosphamide as an immuno suppressor; chicken RBC as target cells; and the anti-HIVi agent candidate to be examined. Immunovir and components were isolated from Pyrus serotina Rehder and other species of Rosaceae by column chromatography. Another useful process is the comparison of fluorescent antibody (FA) titer patterns among one round, two round, and non-medicated infected monkeys. The results of such processes can show that the anti-HIVi agent, such as these immunovirs, are noble candidates for the complete remedy of AIDS.
No evidence of carcinogenicity was observed in a 2-year bioassay in rats at oral doses of leflunomide up to the maximally tolerated dose of 6 mg/kg (approximately 1/40 the maximum human M1 systemic exposure based on AUC). However, male mice in a 2-year bioassay exhibited an increased incidence in lymphoma at an oral dose of 15 mg/kg, the highest dose studied (1.7 times the human M1 exposure based on AUC). Female mice, in the same study, exhibited a dose-related increased incidence of bronchoalveolar adenomas and carcinomas combined beginning at 1.5 mg/kg (approximately 1/10 the human M1 exposure based on AUC). The significance of the findings in mice relative to the clinical use of leflunomide is not known.

Leflunomide was not mutagenic in the Ames Assay, the Unscheduled DNA Synthesis Assay, or in the HGPRT Gene Mutation Assay. In addition, leflunomide was not clastogenic in the in vivo Mouse Micronucleus Assay nor in the in vivo Cytogenetic Test in Chinese Hamster Bone Marrow Cells. However, 4-trifluoromethylaniline (TFMA), a minor metabolite of leflunomide, was mutagenic in the Ames Assay and in the HGPRT Gene Mutation Assay, and was clastogenic in the in vitro Assay for Chromosome Aberrations in the Chinese Hamster Cells. TFMA was not clastogenic in the in vivo Mouse Micronucleus Assay nor in the in vivo Cytogenetic Test in Chinese Hamster Bone Marrow Cells. Leflunomide had no effect on fertility in either male or female rats at oral doses up to 4.0 mg/kg (approximately 1/30 the human M1 exposure based on AUC).