anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Recent advancements in next-generation sequencing have revolutionized our understanding of the human microbiome. Despite this progress, challenges persist in comprehending the microbiome's influence on disease, hindered by technical complexities in species classification, abundance estimation, and data compositionality. At the same time, the existence of macroecological laws describing the variation and diversity in microbial communities irrespective of their environment has been recently proposed using 16s data and explained by a simple phenomenological model of population dynamics. We here investigate the relationship between dysbiosis, i.e. in unhealthy individuals there are deviations from the "regular" composition of the gut microbial community, and the existence of macro-ecological emergent law in microbial communities. We first quantitatively reconstruct these patterns at the species level using shotgun data, and addressing the consequences of sampling effects and statistical errors on ecological patterns. We then ask if such patterns can discriminate between healthy and unhealthy cohorts. Concomitantly, we evaluate the efficacy of different statistical generative models, which incorporate sampling and population dynamics, to describe such patterns and distinguish which are expected by chance, versus those that are potentially informative about disease states or other biological drivers. A critical aspect of our analysis is understanding the relationship between model parameters, which have clear ecological interpretations, and the state of the gut microbiome, thereby enabling the generation of synthetic compositional data that distinctively represent healthy and unhealthy individuals. Our approach, grounded in theoretical ecology and statistical physics, allows for a robust comparison of these models with empirical data, enhancing our understanding of the strengths and limitations of simple microbial models of population dynamics.
MEDIPSO is an experimental, randomised, controlled, open-label, single-blinded (evaluator) study. It is a clinical trial in which patients with mild to moderate psoriasis with stable topical treatment are randomly assigned to either the control group or the intervention group. Patients assigned to the intervention group will undergo dietary education for the adoption of the Mediterranean diet, with monthly monitoring - mostly online - by nutritionists with experience in the field. In both groups, blood tests with metabolic parameters will be obtained before and after the study period, and data of anthropometric characteristics and quality of life will be assessed. The effect of the intervention on skin involvement, metabolic parameters and inflammatory cytokines will be assessed, and the emotional and quality of life impact will also be investigated. In addition, a methodological analysis will be carried out in order to improve the design for a larger scale clinical trial in the future.
CYP3A4 inhibitors increase the exposure of lomitapide, with strong inhibitors increasing exposure approximately 27-fold. Concomitant use of moderate or strong CYP3A4 inhibitors with JUXTAPID is contraindicated [see Drug Interactions (7.1)]. In the JUXTAPID clinical trials, one patient with HoFH developed markedly elevated transaminases (ALT 24× ULN, AST 13× ULN) within days of initiating the strong CYP3A4 inhibitor clarithromycin. If treatment with moderate or strong CYP3A4 inhibitors is unavoidable, JUXTAPID should be stopped during the course of treatment.

Grapefruit juice must be omitted from the diet while being treated with JUXTAPID.

Weak CYP3A4 inhibitors can increase the exposure of lomitapide approximately 2-fold; therefore, when JUXTAPID is administered with weak CYP3A4 inhibitors, the dose of JUXTAPID should be decreased by half. Careful titration may then be considered based on LDL-C response and safety/tolerability to a maximum recommended dosage of 30 mg daily except when coadministered with oral contraceptives, in which case the maximum recommended lomitapide dosage is 40 mg daily [see Dosage and Administration (2.3) and Drug Interactions (7.2)].
Sedation will be established by administering Midazolam 1mg, 100mcs of Fentanyl, and 0.5-1mg/kg of body weight of Propofol. Further boluses of Propofol will be given according to the need of the patient and time consumed for oocyte retrieval.
FIELD: biotechnology, molecular biology. SUBSTANCE: tumor factor necrosis (TFN) is prepared by human cells HL-60 or PBLs cultivation followed by isolation and purification of the end product by the successive chromatography on glass beads, mono-Q-resin for rapid liquid chromatography and then by preparative electrophoresis on DS-polyacrylamide gel and PAAT-electrophoresis or liquid chromatography on C 4 -reverse phase. The obtained human TNF shows capability to destroy or inhibit tumor cells and exhibits the following properties: molecular mass - 17000 D (assay by method using SDS-PAGE), isoelectric point - at 5.3, specific activity - 10 ml x U/mg protein. Human TNF is nonglycolized. Human TNF can be used in molecular biology, lymphokinesis, cytotoxic factors. EFFECT: improved method of preparing. 3 cl, 10 dwg, 1 tbl
Triple-blind, randomized trial, parallel group with an allocation ratio 1:1. A total of 60 participants were recruited from the outpatient department and were randomly distributed into two groups (n=30). After informed consent, restorative treatment was accomplished using an etch and rinse adhesive strategy. In group A , titanium dioxide nano-fortified adhesive was used while in group B, adhesive without nanoparticles was utilized for composite restoration. Post-operative sensitivity was evaluated at follow-up period: one day, one week, two weeks and one month. Visual Analogue scale score was used to record the sensitivity status at follow-up intervals.
OBJECTIVES: Primary Coenzyme Q10 Deficiency-7 (OMIM 616276) results from bi-allelic pathogenic variants in the COQ4 gene. Common clinical findings include hypotonia, seizures, respiratory distress, and cardiomyopathy. In this report, we present two patients diagnosed with Primary Coenzyme Q10 Deficiency-7 along with a review of previously published cases, with the aim being to provide a better understanding of the clinical and laboratory manifestations of the disease.
CASE PRESENTATION: A 3-month-and-22-day-old male was admitted to our outpatient clinic due to poor feeding and restlessness. He was born following an uneventful pregnancy to a nonconsanguineous marriage. A physical examination revealed hypotonia, a dolichocephaly, periorbital edema, and long eyelashes. Blood tests revealed metabolic acidosis and elevated serum lactate levels, while the genetic analysis revealed a variant previously reported as pathogenic, c.437T>G (p.Phe146Cys), in the COQ4 gene. Genetic tests were also conducted on both mother and father, and it revealed heterozygous variant, 0.437T>G (p.Phe146Cys), in the COQ4 gene. As a result of these findings, the patient was diagnosed with neonatal encephalomyopathy-cardiomyopathy-respiratory distress syndrome (Primary Coenzyme Q10 Deficiency-7). A 1-year-old male was admitted to our clinic with complaints of hypotonia, seizures, and feeding difficulties. He was born following an uneventful pregnancy to a nonconsanguineous marriage. On his first day of life, he was admitted to the neonatal intensive care unit due to poor feeding and hypotonia. A physical examination revealed microcephaly, a high palate, poor feeding, weak crying, hypotonia, bilateral horizontal nystagmus, and inability to maintain eye contact. Laboratory findings were within normal limits, while a whole exome sequencing analysis revealed a homozygous variant previously reported as pathogenic, c.458C>T (p.A153V), in the COQ4 gene. The patient was diagnosed with Primary Coenzyme Q10 Deficiency-7.
CONCLUSIONS: Primary Coenzyme Q10 Deficiency-7 should be considered in the differential diagnosis of infants presenting with neurological and dysmorphic manifestations.
We will perform a control cycle of daily, first morning voided urine as previously reported by our group, to assess the hormonal features of the menstrual cycle of each of the five participants. Upon completion of the control cycle, the participant will initiate therapy with pioglitazone, 45 mg daily, a dose that has previously been shown to result in a 30% reduction in fasting insulin. She will take the pioglitazone without any monitoring for a second menstrual cycle and then collect urinary hormones for the third menstrual cycle, continuing the pioglitazone until the third menstrual cycle is completed.
The precise and effective isolation of living circulating tumor cells (CTCs) from peripheral blood, followed by their real-time monitoring, is crucial for diagnosing cancer patients. In this study, a cell-imprinted double-network (DN) hydrogel modified with circular multi-DNA (CMD), coined the CMD-imprinted hydrogel with fixed cells as templates (CMD-CIDH), was developed. The hydrogel featured a customized surface for proficient capture of viable CTCs and in situ real-time fluorescent detection without subsequent release. The customized surface, constructed using polyacrylamide/chitosan DN hydrogel as the matrix on the cell template, had a dense network structure, thereby ensuring excellent stability and a low degradation rate. Optimal capture efficiencies, recorded at 93 ± 3% for MCF-7 cells and 90 ± 2% for Hela cells, were achieved by grafting the CMD and adjusting the nodule size on the customized surface. The capture efficiency remained significantly high at 67 ± 11% in simulated breast cancer patient experiments even at a minimal concentration of 5 cells mL-1. Furthermore, CMD grafted onto the surface produced a potent fluorescence signature, enabling in situ real-time fluorescent detection of the target cell's growth state even in complex environments. The customized surface is highly efficient for screening CTCs in peripheral blood and has promising potential for setting up the CTCs culture.
PURPOSE: An oil-in-water foundation composition and a method for manufacturing the same are provided to lift the skin and to improve anti-wrinkling effect. CONSTITUTION: An oil-in-water foundation composition with shape-memory phenomenon contains 1-3 wt% of PEG-240/HDI copolymer bis-decyltetradeceth-20 ether as a water soluble thickening agent. The composition further contains an aqueous component and an oil component. The aqueous component includes glycerin, butylenes glycol, or purified water. The oil component includes dimethicone, cyclomethicone, cyclomethicone/dimethicone cross polymers or PEG/PPG-19/19 dimethicone. A method for manufacturing the composition comprises: a step of mixing the aqueous component and water soluble thickening agent at 70-85°C and stirring at 4,000-6,000 rpm for 2-10 minutes to prepare a first mixture; a step of adding the oil component to the first mixture at 70-85°C and stirring at 4,000-6,000 rpm for 2-10 minutes to prepare a second mixture; a step of adding a perfume ingredient to the second mixture at 45-55°C and stirring at 2,500-3,000 rpm for 1-5 minutes; and a step of cooling a final product for 1-5 minutes.
Gastric, biliary and pancreatic secretions are decreased by opioids such as hydromorphone. Hydromorphone causes a reduction in motility associated with an increase in tone in the gastric antrum and duodenum. Digestion of food in the small intestine is delayed and propulsive contractions are decreased. Propulsive peristaltic waves in the colon are decreased, and tone may be increased to the point of spasm. The end result is constipation. Hydromorphone can cause a marked increase in biliary tract pressure as a result of spasm of the sphincter of Oddi.
The precise mechanism(s) by which zonisamide exerts its antiseizure effect is unknown. Zonisamide demonstrated anticonvulsant activity in several experimental models. In animals, zonisamide was effective against tonic extension seizures induced by maximal electroshock but ineffective against clonic seizures induced by subcutaneous pentylenetetrazol. Zonisamide raised the threshold for generalized seizures in the kindled rat model and reduced the duration of cortical focal seizures induced by electrical stimulation of the visual cortex in cats. Furthermore, zonisamide suppressed both interictal spikes and the secondarily generalized seizures produced by cortical application of tungstic acid gel in rats or by cortical freezing in cats. The relevance of these models to human epilepsy is unknown.

Zonisamide may produce these effects through action at sodium and calcium channels. In vitro pharmacological studies suggest that zonisamide blocks sodium channels and reduces voltage-dependent, transient inward currents (T-type Ca2+ currents), consequently stabilizing neuronal membranes and suppressing neuronal hypersynchronization. In vitro binding studies have demonstrated that zonisamide binds to the GABA/benzodiazepine receptor ionophore complex in an allosteric fashion which does not produce changes in chloride flux. Other in vitro studies have demonstrated that zonisamide (10 to 30 mcg/mL) suppresses synaptically-driven electrical activity without affecting postsynaptic GABA or glutamate responses (cultured mouse spinal cord neurons) or neuronal or glial uptake of [3H]-GABA (rat hippocampal slices). Thus, zonisamide does not appear to potentiate the synaptic activity of GABA. In vivo microdialysis studies demonstrated that zonisamide facilitates both dopaminergic and serotonergic neurotransmission. 

Zonisamide is a carbonic anhydrase inhibitor. The contribution of this pharmacological action to the therapeutic effects of zonisamide is unknown. However, as a carbonic anhydrase inhibitor, zonisamide may cause metabolic acidosis (see WARNINGS, Metabolic Acidosis subsection).
Patients will be invited to participate in this study prior to the TAAA repair procedure. Prior to the surgery, baseline blood and saliva samples will be collected. Following the surgery, blood and saliva samples will be collected for 48 hours. In addition, hemodynamic data (i.e. vital signs) will be collected for the first 48 hours. The patient data will be reviewed for the first 30 days for morbidity and mortality assessment.
BACKGROUND: This study aimed to investigate the effects of electroacupuncture (EA) on cognitive recovery and synaptic remodeling in a rat model of middle cerebral artery occlusion (MCAO) followed by reperfusion and explore the possible mechanism.
METHOD: Focal cerebral ischemia was modeled in healthy adult Sprague-Dawley rats by MCAO. The MCAO rats were classified into four groups: sham, MCAO, MCAO + GB20 (receiving EA at GB20) and MCAO + NA (receiving EA at a "non-acupoint" location not corresponding to any traditional acupuncture point location about 10 mm above the iliac crest). Neurological deficit scores and behavior were assessed before and during the treatment. After intervention for 7 days, the hippocampus was dissected to analyze growth-associated protein (GAP)-43, synaptophysin (SYN) and postsynaptic density protein (PSD)-95 expression levels by Western blotting. Bioinformatic analysis and primary hippocampal neurons with calcium-voltage gated channel subunit alpha 1B (CACNA1B) gene overexpression were used to screen the target genes for EA against MCAO.
RESULTS: Significant amelioration of neurological deficits and learning/memory were found in MCAO + GB20 rats compared with MCAO or MCAO + NA rats. Protein levels of GAP-43, SYN and PSD-95 were significantly improved in MCAO + GB20-treated rats together with an increase in the number of synapses in the hippocampal CA1 region. CACNA1B appeared to be a target gene of EA in MCAO. There were increased mRNA levels of CACNA1B, calmodulin (CaM), Ca2+/calmodulin-dependent protein kinase type II (CaMKII) and cyclic adenosine monophosphate response element binding (CREB) and increased phosphorylation of CaM, CaMKII and CREB in the hippocampal region in MCAO + GB20 versus MCAO and MCAO + NA groups. CACNA1B overexpression modulated expression of the CaM-CaMKII-CREB axis.
CONCLUSION: EA treatment at GB20 may ameliorate the negative effects of MCAO on cognitive function in rats by enhancing synaptic plasticity. EA treatment at GB20 may exert this neuroprotective effect by regulating the CACNA1B-CaM-CaMKII-CREB axis.
Corneal neovascularization (CoNV) is predominantly initiated by inflammatory processes, resulting in aberrant vascular proliferation and consequent visual impairment. Existing therapeutic interventions for CoNV demonstrate limited efficacy and potential for adverse reactions. Protein arginine methyltransferase 1 (PRMT1) is associated with the regulation of inflammation and M2 macrophage polarization. Nevertheless, the precise mechanism by which PRMT1 operates in CoNV remains uncertain. This study explored the impact of PRMT1 inhibition in a murine model of CoNV induced by alkali burn. Our findings indicated a direct relationship between PRMT1 levels and corneal damage. Moreover, our observations indicated an increase in fibroblast growth factor 2 (FGF2) expression in CoNV, which was reduced after treatment with a PRMT1 inhibitor. The inhibition of PRMT1 alleviated both corneal injury and CoNV, as evidenced by decreased corneal opacity and neovascularization. Immunofluorescence analysis and evaluation of inflammatory factor expression demonstrated that PRMT1 inhibition attenuated M2 macrophage polarization, a phenomenon that was reversed by the administration of recombinant FGF2 protein. These results were confirmed through experimentation on Human Umbilical Vein Endothelial Cells (HUVECs) and Mouse leukemia cells of monocyte macrophage cells (RAW264.7). Furthermore, it was established that FGF2 played a role in PI3K/Akt signal transduction, a critical regulatory pathway for M2 macrophage polarization. Importantly, the activity of this pathway was found to be suppressed by PRMT1 inhibitors. Mechanistically, PRMT1 was shown to promote M2 macrophage polarization, thereby contributing to CoNV, through the FGF2/PI3K/Akt pathway. Therefore, targeting PRMT1 may offer a promising therapeutic approach.
Moderate exercise can induce discomfort in joints when done infrequently or when done too intensely or for too long a period. This discomfort is often realized as either pain or stiffness in the joint that was the focus of the exercise. For example, one's knees will hurt after jogging for several miles, particularly if jogging for the first time. This study is intended to evaluate whether NEM® brand eggshell membrane can alleviate joint pain or stiffness, either directly following exercise or 12 hours post-exercise versus placebo. The study will also evaluate NEM's effect, on cartilage turnover via the cartilage degradation biomarker c-terminal cross-linked telopeptide of type II collagen (CTX-II). Participants will perform a minimum of 40 steps per leg utilizing an aerobics step at the clinical site. They will follow this exercise regimen on alternating days for 2 consecutive weeks. Changes in pain \& stiffness (immediate \& 12-hour) will be compared to both baseline and to the placebo group. Urine samples will also be collected at baseline and at the end of Week 1 \& Week 2. The change in CTX-II from baseline will be compared to the placebo group.
INTRODUCTION: Neuromuscular scoliosis (NMS) is associated with an abnormal muscle tone. Traditional conservative treatments, with the historical practice of early posterior fusion, have proven ineffective. Recently, growth-sparing techniques have gained traction owing to their ability to maximize trunk height. However, these techniques have a substantial risk of complications, particularly rod breakage, with reported incidence rates ranging from 15 % to 42 %. The objective of this study was to conduct a descriptive analysis of NMS patients who experienced rod breakage following the minimally invasive fusionless surgery (MIFS) technique.
METHODS: This was a single-center, retrospective study that included all NMS patients who underwent surgery between January 2015 and January 2021 and subsequently presented with rod breakage after MIFS. The MIFS technique is based on proximal fixation with double hook claws made of pedicular and -sus laminar hooks and pelvic fixation with iliosacral screws.
RESULTS: The mean follow-up was 5.2 ± 2.2 years. The mean dominant etiology of NMS was cerebral palsy (67 %). Of the 217 patients who underwent surgery, 15 (6.9 %) developed rod breakage. Rod breakage occurred 2.7 ± 1.3 years after the initial surgery. Four cases of rod fracture recurrence were reported in ambulatory patients with dystonia or hyperactivity.
CONCLUSION: Compared with other fusionless techniques, the minimally invasive bipolar technique appears promising for patients with NMS, with a lower rate of rod breakage. We recommend the use of a four-rod construct for ambulatory patients or for those with dystonia or hyperactivity.
Device: endovascular treatment For patients randomized to endovascular treatment arm, EVT has to be initiated within 12 hours of estimated time of basilar artery occlusion. If an appropriate thrombus or residual stenosis is identified, the choice of EVT strategy will be made by the treating neurointerventionalist. The endovascular procedures allowed by the steering committee include mechanical thrombectomy, intra-arterial thrombolysis, balloon angioplasty, stent implantation, or any combination of above procedures. We recommend applying ADAPT as the first choice of treatment. All mechanical thrombectomy devices for EVT, which are approved by CFDA for this purpose, are allowed in the trial.
BACKGROUND: Climate change exacerbates abiotic stresses, which are expected to intensify their impact on crop plants. Drought, the most prevalent abiotic stress, significantly affects agricultural production worldwide. Improving eggplant varieties to withstand abiotic stress is vital due to rising drought from climate change. Despite the diversity of wild eggplant species that thrive under harsh conditions, the understanding of their drought tolerance mechanisms remains limited. In the present study, we used chlorophyll fluorescence (ChlaF) imaging, which reveals a plant's photosynthetic health, to investigate desiccation tolerance in eggplant and its wild relatives. Conventional fluorescence measurements lack spatial heterogeneity, whereas ChlaF imaging offers comprehensive insights into plant responses to environmental stresses. Hence, employing noninvasive imaging techniques is essential for understanding this heterogeneity.
RESULTS: Desiccation significantly reduced the leaf tissue moisture content (TMC) across species. ChlaF and TMC displayed greater photosystem II (PSII) efficiency after 54 h of desiccation in S. macrocarpum, S. torvum, and S. indicum, with S. macrocarpum demonstrating superior efficiency due to sustained fluorescence. PSII functions declined gradually in S. macrocarpum and S. torvum, unlike those in other species, which exhibited abrupt declines after 54 h of desiccation. However, after 54 h, PSII efficiency remained above 50% of its initial quantum yield in S. macrocarpum at 35% leaf RWC (relative water content), while S. torvum and S. indicum displayed 50% decreases at 31% and 33% RWC, respectively. Conversely, the susceptible species S. gilo and S. sisymbriifolium exhibited a 50% reduction in PSII function at an early stage of 50% RWC, whereas in S. melongena, this reduction occurred at 40% RWC.
CONCLUSION: Overall, our study revealed notably greater leaf desiccation tolerance, especially in S. macrocarpum, S. torvum, and S. indicum, attributed to sustained PSII efficiency at low TMC levels, indicating that these species are promising sources of drought tolerance.