anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Over 1 million patients receive mechanical ventilation every year in the United States. In mechanically ventilated patients, despite sedative infusions, sleep is severely disrupted. Sleep disruption, in turn, can lead to activation of sympathetic nervous system and elevated inflammatory cytokines. Both sympathetic hyperactivity and elevated cytokines have been associated with delirium, which, in turn, is associated with increased mortality and higher healthcare costs. Currently, however, there is very little understanding of the inter-relationship between critical illness, sleep, and neuropsychological well-being. The purpose of this study is to collect preliminary data on the short-term effects of sedation with and without sympatholysis on sleep and inflammation in critically ill patients receiving mechanical ventilation. This pilot study will be accomplished by performing sleep studies and circulating cytokine measurements in critically ill patients randomized to receive two different sedation strategies: Dexmedetomidine versus Midazolam and Fentanyl. The ultimate goal of this program of research is to identify sedation practices that are least associated with adverse short- and long-term consequences, and thereby ultimately help improve sleep quality and quality of life in patients surviving critical illness.
Aim: This study was conducted to determine the effect of sacral region-focused therapeutic touch applied during the latent phase of labour on hormone levels, labour comfort, and perception.

Method: This randomised sham controlled experimental trial was conducted with two groups (intervention and control groups) in a state hospital between 08 March 2022 and 01 April 2023. The sample size of the study was calculated using the G\*power 3.1.9.6 programme. As a result of the calculation, twenty-five pregnant women for each group were included in the study. While Therapeutic Touch (TT) focused on sacral region was applied in the intervention group, Sham Therapeutic Touch (STT) was applied in the control group. Data were collected using a Personal Information Form, the Visual Analogue Scale (VAS), a Hormone Values Follow-up Form, the Childbirth Comfort Questionnaire (CCQ) and the Perception of Birth Scale (PBS). IBM SPSS V25 programme was used for statistical analysis of the study. The statistical significance was assessed at the level of p\<0.05.
The development of dementia is a devastating aspect of Parkinson's disease (PD), affecting nearly half of patients within 10 years post-diagnosis. For effective therapies to prevent and slow progression to PD dementia (PDD), the key mechanisms that determine why some people with PD develop early dementia, while others remain cognitively unaffected, need to be understood. Neuroinflammation and tau protein accumulation have been demonstrated in post-mortem PD brains, and in many other neurodegenerative disorders leading to dementia. However, whether these processes mediate dementia risk early on in the PD disease course is not established. To this end, we used PET neuroimaging with 11C-PK11195 to index neuroinflammation and 18F-AV-1451 for misfolded tau in early PD patients, stratified according to dementia risk in our 'Neuroinflammation and Tau Accumulation in Parkinson's Disease Dementia' (NET-PDD) study. The NET-PDD study longitudinally assesses newly-diagnosed PD patients in two subgroups at low and high dementia risk (stratified based on pentagon copying, semantic fluency, MAPT genotype), with comparison to age- and sex-matched controls. Non-displaceable binding potential (BPND) in 43 brain regions (Hammers' parcellation) was compared between groups (pairwise t-tests), and associations between BPND of the tracers tested (linear-mixed-effect models). We hypothesized that people with higher dementia risk have greater inflammation and/or tau accumulation in advance of significant cognitive decline. We found significantly elevated neuroinflammation (11C-PK11195 BPND) in multiple subcortical and restricted cortical regions in the high dementia risk group compared with controls, while in the low-risk group this was limited to two cortical areas. The high dementia risk group also showed significantly greater neuroinflammation than the low-risk group concentrated on subcortical and basal ganglia regions. Neuroinflammation in most of these regions was associated with worse cognitive performance (Addenbrooke's Cognitive Examination-III score). Overall neuroinflammation burden also correlated with serum levels of pro-inflammatory cytokines. In contrast, increases in 18F-AV-1451 (tau) BPND in PD versus controls were restricted to subcortical regions where off-target binding is typically seen, with no relationship to cognition found. Whole-brain 18F-AV-1451 burden correlated with serum phosphorylated tau181 levels. Although there was minimal regional tau accumulation in PD, regional neuroinflammation and tau burden correlated in PD participants, with the strongest association in the high dementia risk group, suggesting possible co-localization of these pathologies. In conclusion, our findings suggest that significant regional neuroinflammation in early PD might underpin higher risk for PDD development, indicating neuroinflammation as a putative early modifiable aetiopathological disease factor to prevent or slow dementia development using immunomodulatory strategies.
Participants will receive placebo at phase 1 (baseline-WK 7) \& treatment response assessed (MADRS score reduced \<50% at WK8). Nonresponders are rerandomized to receive either treatment at phase 2 (WK8-16).The titration schedule is as follows (dosage throughout is BID): at baseline placebo (7 days). At WK 1= placebo (7 days); at WK 2=placebo (14 days) and WK 4=placebo (14 days). Placebo nonresponders rerandomized to placebo: At WK 8=placebo (7 days);WK 9=placebo (7 days);WK 10=placebo (14 days) and WK 12=placebo (14 days). During the participants' final WK (16), they will be instructed to titrate down (done in order to maintain the double blind) the treatment according to the following schedule: placebo (4 days) and placebo (4 days), discontinue.
The present disclosure relates to a new lymphokine molecule termed Monocyte Cytotoxicity Inducing Factor (MCF), to MCF peptides. The disclosure further relates to the development of novel Sezary cell hybridomas which secrete MCF, to the purification of MCF and its constituent polypeptides and to the identification of small peptides with MCF activity. Sezary OKT4+ lymphocytes were fused to CEM.8azar.C, an HGPRTase lacking clone of CEM, to generate hybrid cells, certain of which produced soluble mediators of human monocyte cytotoxicity. A single sezary hybrid clone, FtF3, produced a novel monocyte cytotoxicity inducing factor found to be distinct from IFN gamma  and IFN alpha . MCF, purified by dye ligand and ion-exchange chromatography, comprises two polypeptides of 29 and 14.7kD (P29 and P14.7) which can be further purified by preparative SDS/PAGE and hydrophobic chromatography, respectively. Amino acid composition analyses and immunoblotting of two-dimensional gels indicate that these are distinct but possibly related polypeptides. N-terminal analysis of P29 reveals it to be a previously undescribed cytokine mediator of monocyte function. A peptide having the sequence Gly Ala Ala Val Leu Glu Asp Ser Gln, corresponding to the native N-terminal sequence of P29, also exhibits MCF activity equivalent to that of the intact 29kD protein.
BACKGROUND: Amputees frequently suffer from chronic pain in both their residual limbs (RLP) and phantom limbs (PLP) following their amputation. Targeted muscle reinnervation (TMR) is a nerve transfer technique that has been demonstrated to improve pain secondarily and at time of amputation. The goal of this study is to report on the efficacy of primary TMR at time of above-knee level amputations in the setting of limb-threatening ischemia or infection.
METHODS: This is a retrospective review of a single-surgeon experience with TMR in patients undergoing through- or above-knee level amputations from January 2018 to June 2021. Patient charts were reviewed for the comorbidities in the Charlson Comorbidity Index. Postoperative notes were assayed for presence and absence of RLP and PLP, overall pain severity, chronic narcotic use, ambulatory status, and complications. A control group of patients undergoing lower limb amputation who did not receive TMR from January 2014 to December 2017 was used for comparison.
RESULTS: Forty-one patients with through- or above-knee level amputations and primary TMR were included in this study. The tibial and common peroneal nerves were transferred in all cases to motor branches to the gastrocnemius, semimembranosus, semitendinosus, and biceps femoris. Fifty-eight patients with through- or above-knee level amputations without TMR were included for comparison. The TMR group had significantly less overall pain (41.5 vs. 67.2%, p = 0.01), RLP (26.8 vs. 44.8%, p = 0.04), and PLP (19.5 vs. 43.1%, p = 0.02). There were no significant differences in complication rates.
CONCLUSION: TMR can safely and effectively be performed at time of a through- and above-knee level amputation and improves pain outcomes.
Part 1: Participants will receive FDA-licensed pembrolizumab followed by pemetrexed administered with platinum-based chemotherapy (cisplatin or carboplatin). Part 2: Participants will receive FDA-licensed pembrolizumab followed by pemetrexed.
A valve for use with an aerosol container including a valve body, a valve stem having a dispensing passage, and a sealing ring contacting the valve stem. The sealing ring includes a sealing portion. The valve stem is slidably moveable relative to the sealing ring from a valve-closed position to a valve-open position. The interior of the valve body is in communication with the dispensing passage when the valve stem is in the valve-open position. The sealing ring also includes a wiper component to wipe the valve stem. The valve is preferably a metering valve.
OBJECTIVE: We aimed to evaluate the genotype-phenotype relationship in two Chinese family members with enlarged vestibular aqueduct (EVA).
METHODS: We collected blood samples and clinical data from each pedigree family member. Genomic DNA was isolated from peripheral leukocytes using standard methods. Targeted next-generation sequencing and Sanger sequencing were performed to find the pathogenic mutation in this family. Minigene assays were used to verify whether the novel intronic mutation SLC26A4c.765+4A>G influenced mRNA splicing.
RESULTS: Hearing loss in the patients with EVA was diagnosed using auditory tests and imaging examinations. Two pathogenic mutations, c.765+4A>G and c.919-2A>G were detected in SLC26A4. In vitro minigene analysis confirmed that c.765+4A>G variant could cause aberrant splicing, resulting in skipping over exon 6.
CONCLUSIONS: The SLC26A4c.765+4A>G mutation is the causative variant in the Chinese family with EVA. Particular attention should be paid to intronic variants.
OBJECTIVES: Conventional clipping and endovascular treatment are difficult to apply for some giant intracranial aneurysms (GIAs), and sometimes extracranial-to-intracranial (EC-IC) bypass becomes the optional choice. However, not all GIA patients can benefit from it. This study aims to recognize the underlying problems.
METHODS: We included eligible patients in our care. Then, we researched from three levels: a retrospective review of clinical data, fluid-structural analysis from two representative patient-specific models, and fluid-structural interaction analysis for idealized models to investigate the hemodynamic and biomechanical mechanisms.
RESULTS: In this article, we report nine patients with GIA who underwent EC-IC surgery. Of them, three experienced dangerous postoperative hemorrhage, and one patient died. Among these three patients, two lacked the A1 segment of the anterior cerebral artery (ACA). The numerical simulation showed that after surgery, for the patient with an unruptured aneurysm and existence of ACA, the wall deformation, wall stress, pressure, and area of the oscillatory shear index (OSI) > 0.2 were decreased by 43%, 39%, 33%, and 13%, while the patient without A1 segment having postoperative hemorrhage showed 36%, 45%, 13%, and 55% increased, respectively. Thus, we postulated a dangerous "stump phenomenon" in such conditions and further demonstrated it from idealized models with different sizes of ACA. Finally, we found a larger anastomosis angle and smaller diameter of the graft can alleviate this effect.
CONCLUSIONS: Neurosurgeon should cautiously evaluate the opportunity and risk for such patients who have aplasia of the A1 segment of ACA when making clinical decisions.
We will outfit ½ of the ambulance crews with the King Video Laryngoscope (KVL) for 6 months while the other ½ of the ambulances will use traditional direct laryngoscopy (DL). After 6 months, the groups will switch devices. We will randomly assign those ambulances that first use the KVL. After one year (12 months) we will compare the outcomes between the two methods.
OBJECTIVES: Implementation of alternate erythrocyte sedimentation rate (ESR) measurement method is increasing worldwide due to its various advantages. In this study, we aim to evaluate the analytical performance of the BC-780 automated hematology analyzer in measurement of ESR value.
METHODS: Analyzer performance including precision study, carryover, sample stability and potential interferences are examined. Samples with ESR values spanning the whole analytical ESR range are included for method comparison study. Samples with different hematocrit (Hct) and mean corpuscular volume (MCV) values are also analyzed and compared with the results obtained from the Westergren reference method.
RESULTS: Precisions and carryover results are consistent with the manufacturers' claim. ESR values do not change significantly in the samples stored at 2-8 °C for 24 h (h) or at room temperature (RT) for 8 h, but significantly decreased (p<0.001) when stored at RT for 24 h. Significant increase in ESR value is documented in samples that are hemolyzed (hemoglobin concentration ranged from 1.28-6.01 g/L) (p=0.010) or lipemic (triglyceride above 4.75 mmol/L) (p=0.001). Method comparison study yields a proportional difference with a regression equation=3.08+ 0.98x. Bland-Altman analysis shows a mean absolute bias of 3.12 mm. The obtained absolute mean biases are below 5 mm in all analytical categories except for the group where MCV>100 fL.
CONCLUSIONS: Most tested parameters met the manufacturer's specifications and were comparable to the reference method. Despite the presence of positive bias, it falls within acceptable criteria. Extensive validation against potential interferences such as hemolysis/lipemia is still necessary in future.
This open-label, multi-institution, phase II study evaluated the activity of gefitinib at individually escalated doses up to 750mg to achieve the skin toxicity grade greater than or equal to 2. Patients were started on gefitinib 250mg orally daily for 2 weeks. At 2 weeks, patients were reevaluated and given skin toxicity grade according to the National Cancer Institute Common Toxicity Criteria version 3.0 (CTC 3.0). Patients with grade 2 or greater skin toxicity remained on 250 mg daily; in patients with grade 0-1 skin toxicity the dose was escalated to 500 mg daily and again to 750 mg daily on next evaluation until grade 2 or greater skin toxicity was developed.

The protocol was later amended because of the reported lower efficacy of the 250 mg dose and patients were then started at 500 mg per day. There was no further dose escalation beyond 750 mg per day irrespective of the response or grade of skin toxicity. Therapy was discontinued upon disease progression, unacceptable toxicity, death or patient's withdrawal of consent. Dose interruptions were used as the first approach to managing the toxicity of the patients who experienced grade 3-4 non-hematological toxicities. Gefitinib was interrupted for up to a maximum of 14 days until the toxicities dropped to grade 1 or less. Adherence to therapy was monitored using drug diaries that were collected at each physician visit and assessed against pill counts.
A double-blind controlled trial with two arms will be conducted at Brigham and Women's Hospital (BWH). We will screen subjects with stable atherosclerosis to complete enrollment of 40 subjects in the study (see inclusion and exclusion criteria section below). A central pharmacist at BWH will randomize the patients to 40mg of atorvastatin (n=20) or 10mg of rosuvastatin (n=20) for 28 days. If the patient is already on a statin a two-week washout period will be required prior to trial initiation. Our subjects, clinicians, data collectors, outcomes assessors and statisticians will be blind with regards to the patient allocation. There are a total of 3 visits for each patient: a short screening visit, an initial visit for baseline data (90 min.) and a final visit after 28 days. Our participants will be asked to take the medication every day at the same time between 9pm and 10pm. Each visit will take place between 7am and 9am. Patients will be instructed to fast overnight for a minimum of 8hrs. They will also be advised not to make any other changes to their current medications and lifestyle for 28 days while in the study and to record in a diary any side effects, missed doses, or changes in concomitant medication.
In this proposed project, we will focus on the identification of potential biomarkers in EBC with ability to predict development of multi-organ failure. Currently, no tools could be used to evaluate the effect of mitochondrial dysfunction in sepsis. All the human studies discussing mitochondrial dysfunction in sepsis use tissue biopsies as study materials. Repeated tissue biopsy is invasive and not applicable. EBC could be collected non-invasively and conveniently. A study has demonstrated the use of metabolomic technologies in mitochondrial diseases. We believe that the metabolomic biomarkers of EBC could be used to demonstrate mitochondrial dysfunction in lungs and respiratory tracts of septic patients. Such metabolomic biomarkers may also reflect similar on-going mitochondrial dysfunction in other organ systems, and could potentially become a novel diagnostic tool and a therapeutic target in future sepsis therapy.
Through chemoproteomics using potent unique irreversible inhibitors, the inventors found that the major brain Tubulin Carboxypeptidase (TCP) is a complex of angiostatin-1 (VASH1) and small angiostatin binding protein (SVBP). When complexed with SVBP, VASH1 and its homolog angiostatin 2(VASH2) exhibit robust and specific Tyr/Phe carboxypeptidase activity on microtubules. Thus, the inventors have identified for the first time the enzymatic activities of angiostatin and the angiostatin/SVBP complex. Knockdown of angiostatin or SVBP in cultured neurons results in a significant reduction in tyrosinated α -tubulin levels and the appearance of severe differentiation defects. In addition, knockdown of angiostatin disrupts neuronal migration in the developing mouse neocortex. These results identified the angiostatin/SVBP complex as a TCP enzyme. Accordingly, the present invention relates to methods and pharmaceutical compositions for treating Tubulin Carboxypeptidase (TCP) -associated diseases, such as neurological disorders and cardiovascular diseases, using inhibitors of angiostatin or the activity or expression of the angiostatin/SVBP complex.
The overall objective of this pilot study is to assess whether a mild to moderate-intensity strengthening exercise program can be safely implemented in boys with DMD. In Aim 1, the investigators will determine the dose response and safety of mild to moderate-intensity isometric resistance exercise in children with DMD. Twelve ambulatory boys with DMD will participate in an isometric exercise dosing protocol, in which the load is progressively increased. In this early proof of concept pilot study, two large muscle groups will be studied: the knee extensors and the knee flexors. T2 weighted magnetic resonance imaging (MRI) of the thigh muscles will be used to monitor evidence of muscle damage at each intensity level and determine a safe exercise range. Other safety measures will include a verbal pain rating scale, clinical examination, and serum creatine kinase (CK) levels. In Aim 2, the investigators will implement a pilot intervention study to examine the feasibility and safety of a 12 week in-home isometric strengthening program in children with DMD. In this study, 20 boys with DMD will be randomized to either an exercise group or a control group. Ten boys with DMD randomized to the exercise group will complete a progressive exercise program using the parameters and dose identified in Aim 1. Assessment of strength and safety will be performed at regular time intervals throughout the study. Ten boys with DMD randomized to not participate in an exercise intervention will be tested at similar time intervals and serve as controls. The data from this pilot study will serve to perform the power analysis needed to design an appropriately powered clinical intervention study.
A method and a system are provided for processing electronic medical records for predicting a health condition of a patient. The method may determine a first set of datasets of a first patient based on one or more first electronic medical records. The method may extract one or more second sets of datasets of one or more second patients from a database server based on the first set of datasets. The method may generate one or more bipartite graphs based on the first set of datasets and the one or more second sets of datasets. The method may determine a set of edges from the one or more edges based on a matching score in each bipartite graph. The method may further predict the health condition of the first patient based on at least the matching score associated with each of the one or more bipartite graphs.
PURPOSE: To obtain a hard gelatin capsular preparation with high storage stability by dissolving nifedipine in a vehicle compatible with human organs and not rendering the capsule brittle when it is stored at room temperature. CONSTITUTION: This hard gelatin capsular preparation contains nifedipine in such form as to be dissolved in a vehicle compatible with human organs and not rendering the capsule brittle when it is stored at room temperature. In this case, the vehicle is esp. pref. a polyoxyethylene glycol fatty acid ester which is formed, for example, by reaction of about 40 to 60mol ethylene oxide with 1mol hydrogenated castor oil. In this capsular preparation, the weight ratio (nifedipine/vehicle) is advantageously about (1:10) to (1:70).