anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Bronchopulmonary dysplasia (BPD) is characterized by alveolar dysplasia, and evidence indicates that interferon regulatory factor 4 (IRF4) is involved in the pathogenesis of various inflammatory lung diseases. Nonetheless, the significance and mechanism of IRF4 in BPD remain unelucidated. Consequently, we established a mouse model of BPD through hyperoxia exposure, and ELISA was employed to measure interleukin-17 A (IL-17 A) and interleukin-6 (IL-6) expression levels in lung tissues. Western blotting was adopted to determine the expression of IRF4, surfactant protein C (SP-C), and podoplanin (T1α) in lung tissues. Flow cytometry was utilized for analyzing the percentages of FOXP3+ regulatory T cells (Tregs) and FOXP3+RORγt+ Tregs in CD4+ T cells in lung tissues to clarify the underlying mechanism. Our findings revealed that BPD mice exhibited disordered lung tissue structure, elevated IRF4 expression, decreased SP-C and T1α expression, increased IL-17 A and IL-6 levels, reduced proportion of FOXP3+ Tregs, and increased proportion of FOXP3+RORγt+ Tregs. For the purpose of further elucidating the effect of IRF4 on Treg phenotype switching induced by hyperoxia in lung tissues, we exposed neonatal mice with IRF4 knockout to hyperoxia. These mice exhibited regular lung tissue structure, increased proportion of FOXP3+ Tregs, reduced proportion of FOXP3+RORγt+ Tregs, elevated SP-C and T1α expression, and decreased IL-17 A and IL-6 levels. In conclusion, our findings demonstrate that IRF4-mediated Treg phenotype switching in lung tissues exacerbates alveolar epithelial cell injury under hyperoxia exposure.
PURPOSE: An MRI(magnetic resonance imaging) contrast media containing hollow nanoparticle is provided to use in MRI having emphasized T1 and T2 effects. CONSTITUTION: An MRI(magnetic resonance imaging) contrast media comprises a hollow nanoparticle containing paramagnetic material. The paramagnetic material is manganese, gadolinium, erbium, chrome, iron, cobalt, nickel lanthan element or actinium element. The inner diameter of nanoparticle is 2~20 nm. The nanoparticle is coated with biocompatible material, polyethyleneglycol. A nanoparticle for drug delivery in a cell is coated in a hollow nanoparticle. The drug is doxorubicin(DOX).
Following the submission of tumor tissue for the FoundationOne® companion diagnostic (F1CDx) test, participants with tumors that have a ≥16%genomic loss of heterozygosity (LOH) will be assigned to this cohort. Twenty participants will be enrolled. Once twenty participants are enrolled, the cohort will be closed to further enrollment. Participants in this study cohort will commence treatment as specified on Day 1 of each cycle.
A cosmetic composition containing schizandrin which is isolated from Schizandra chinensis Baillon. is provided to ensure the effects of anti-oxidation, anti-wrinkle, skin whitening, and irritation relief. A cosmetic composition comprises schizandrin and its extract as active ingredient. The schizandrin extract is contained in 10ppm~10000ppm based on the total amount. The schizandrin and its extract is obtained by extracting dried Schizandra chinensis Baillon. with 10-95%(V/V) of ethanol solution at room temperature, filtering suspension, decompress-concentrating under 50°C, and mixing the concentrate in a solvent such as butyleneglycol. The solvent is purified water, methanol, ethanol, glycerin, ethylacetate, butyleneglycol, propyleneglycol, dichloromethane, hexane or its mixture. The cosmetic composition is used in the form of gel, aqueous liquid, cream, essence, oil in water or water in oil emulsion.
Nusinersen is a modified antisense oligonucleotide, where the 2'-hydroxy groups of the ribofuranosyl rings are replaced with 2'-O-2-methoxyethyl groups and the phosphate linkages are replaced with phosphorothioate linkages. Nusinersen binds to a specific sequence in the intron downstream of exon 7 of the SMN2 transcript. The structural formula is: 

SPINRAZA is supplied as a sterile, preservative-free, colorless solution for intrathecal use in a single-dose glass vial. Each 1 mL solution contains 2.4 mg of nusinersen (equivalent to 2.53 mg of nusinersen sodium salt). Each 1 mL also contains calcium chloride dihydrate (0.21 mg) USP, magnesium chloride hexahydrate (0.16 mg) USP, potassium chloride (0.22 mg) USP, sodium chloride (8.77 mg) USP, sodium phosphate dibasic anhydrous (0.10 mg) USP, sodium phosphate monobasic dihydrate (0.05 mg) USP, and Water for Injection USP. The product may contain hydrochloric acid or sodium hydroxide to adjust pH. The pH is ~7.2. 

The molecular formula of SPINRAZA is C234H323N61O128P17S17Na17 and the molecular weight is 7501.0 daltons.
One vaccination with rB/HPIV3 vaccine (at higher dose) given as nose drops to HPIV3-seropositive children 15 to 59 months of age). This arm may enroll after Arm 1 depending on the effect of the vaccine on Arm 1.
Individuals with serious mental illnesses (SMI), as well as those experiencing suicidality or psychiatric crisis encounter police officers frequently in the community. Almost a third of people with SMI have police involved in their pathway to mental health care. Although a variety of strategies to reduce law enforcement involvement in mental health crisis response are emerging, people with SMI and/or those in crisis will continue to encounter police when officers must serve as first responders, and importantly, during officers' routine patrol duties. As such, officers need training to safely and effectively interact in these situations. The Crisis Intervention Team (CIT) model is a collaborative approach that includes a 40-hour training of officers. CIT has been implemented in thousands of U.S. communities, and some agencies are now mandating all of their officers complete CIT training. Despite widespread support and growing research, a randomized, controlled trial (RCT) has never been conducted to assess the effectiveness of CIT training on officers' actual skills and behaviors. Prior research has relied on officers' self-report of their de-escalation skills and has not directly measured actual performance in a rigorous, standardized, controlled fashion. Furthermore, multi-site studies are lacking, and potential officer-level factors that may moderate CIT training outcomes have yet to be systematically assessed.

This study will partner with six sites across the country representing diverse geographic areas and constituency demographics. There are four Specific Aims of the study. First, the investigators will conduct a rigorous, multisite randomized controlled trial (RCT) of CIT mental health training. Each agency will provide 40 officers, for a total of 240. Among the 40 officers from each agency, half will be randomized to CIT training. Data will be collected using Standardized Scenarios, which will be rated centrally in a blinded fashion (blinded by site, study arm, and time). The primary outcome is actual verbal crisis de-escalation skills / non-verbal physical behavior. Second, the investigators will determine the impact of CIT training on two secondary outcomes: use of procedural justice and disposition-related decision-making.
The invention discloses a MACA polysaccharide composition and a preparation method thereof. The MACA polysaccharide composition includes the extracts of traditional Chinese medicines, comprising, by weight, 15-25 parts of MACA, 15-25 parts of astragalus membranaceus, 0.5-1 part of lucid ganoderma and 15-25 parts of lentinula edodes. The preparation method of the traditional Chinese medicine polysaccharide composition, which includes a step of mixing and dissolving the extracts according to the ratio to obtain various required dosage forms. The composition is used for preparing health-caring products for enhancing immunity, improving antivirus capability of human body, especially preventing diseases caused be air pollution and improving resistance of human body against seasonal cold and viral cold. The composition is high in effective component content and can be used for effectively preventing and treating flue and related diseases during serious air pollution and frequent occurrence of flu by applying the composition in the form of an electuary or an oral liquid. With other therapy medicines, the composition can accelerate recovery of human body.
All tachypneic children under 5 yrs age presenting to study centres. No exclusions.
The purpose of this pilot study is to test the feasibility and effects of a functional mobility training program on the motor ability and physical activity of young children who are developmentally delayed and at risk for cerebral palsy (CP). The study includes a sample of 10 participants between 12-36 months of age who have at least a 4 month motor delay and are at risk for CP in a single-subject research design with repeated measures during baseline and intervention phases. Participants will have biweekly assessments during the 6 week baseline phase and the subsequent 6 week mobility training phase, followed by a final assessment after 6 weeks of treatment withdraw. Assessments and training will occur in the Functional and Applied Biomechanics (FAB) section. The mobility training program consists of three days per week of 30 minute treatment sessions using dynamic body weight support during a variety of functional motor tasks. Children will be assisted, but not limited, by the dynamic weight support system while they are encouraged to participate in a variety of age-appropriate mobility tasks. It is hypothesized that this system combined with the functional activity practice will facilitate the development of postural control and strength, and thereby improve walking ability. The primary outcome measures are completion rate and gross motor ability as measured by the Gross Motor Function Measure (GMFM). Secondary outcome measures include the amount of gross motor delay as measured by the Bayley Motor Scale (BMS),, the Functional Mobility Scale (FMS), spatiotemporal gait measures, and amount of physical activity in daily life. Results of this pilot study will be used to refine the mobility training program, evaluate the appropriateness of the selected outcome measures, and to provide preliminary data for a larger scale clinical trial.
A method, system and medium are provided for enabling re-creation of a state of a computing system as it existed at a selected time. A plurality of data elements are tracked including functions and reference information employed in calculating one or more of the data elements. Versions of functions and reference information are also tracked. Thereby, a time at which to recreate the state of the system is selectable and the data elements that were available at or before the selected time are identifiable. And the versions of functions and reference information that were available at the selected time are identifiable. The state of the system at the selected time can thus be reviewed or analyzed as desired.
Patients may be randomized to the active comparator arm. Participants randomized to this arm will receive 30, 50, or 70mg Vyvanse daily.
<P>PROBLEM TO BE SOLVED: To provide human antibodies that have MN binding and cell adhesion-neutralizing activities.  <P>SOLUTION: This invention is composed of monoclonal human MN antibodies or MN antibody fragments that target the GEEDLP repeat within the proteoglycan domain. The proteoglycan domain of the MN cell surface protein contains four of these identical GEEDLP repeats. The human MN antibodies or antibody fragments have been used to quantify MN expression in cancer cells and tumors using FACS and immunohistochemical methods, and to diagnose cancers in which MN is upregulated. An example is also provided where a human anti-MN IgG1 mediates tumor cell lysis through antibody-dependent cell-mediated cytotoxicity. Therefore, these antibodies will be useful for the treatment of cancers in which MN is upregulated or can be useful for the diagnosis of cancers in which MN is upregulated.  <P>COPYRIGHT: (C)2011,JPO&INPIT
BACKGROUND: Penile squamous cell carcinoma (PSCC) is a rare disease that is more prevalent in developing countries, such as Brazil, and is linked to poor genital hygiene, which promotes the proliferation of microorganisms. Dysbiosis has an effect on the local immune response, increases the risk of viral infection, and can generate inflammatory processes. Current knowledge of the microbiota found in penile tissues is limited, and the bacterial diversity of the PSCC remains unknown. In this investigation, the microbiota associated with penile cancer and its potential role in tumor development and progression were identified.
METHODS: The 16S rRNA gene was analyzed by next-generation sequencing in 19 tumors and their respective non-tumor adjacent tissues to perform taxonomic classification, analysis of core microbiome, abundance, and diversity of amplicon sequence variants (ASVs) (QIIME2 v.2020.2), and in silico functional prediction (PICRUST2, p < 0.05).
RESULTS: In both tissues, the phyla Proteobacteria and Firmicutes, and genera Alcaligenes and Fusobaterium, were the most prevalent. Tumors presented a greater relative abundance of Fusobacteriota, Campilobacteria, and Fusobacterium (p = 0.04, p = 0.04, and p = 0.039, respectively). In addition, the beta diversity analysis revealed a tendency for the formation of two distinct groups when only advanced tumors (pT2 and pT3) were considered. Further, the functional analysis identified the top 35 pathways, and 79.5% of PSCC samples contained pro-inflammatory microorganisms.
CONCLUSION: We describe the first microbiome of penile carcinoma, which revealed an abundant and diverse microbiota as well as inflammatory-related taxa (the phyla Proteobacteria and Firmicutes, the genera Fusobacterium and Prevotella, and the species Finegoldia magma and Pseudomonas geniculata) and molecular pathways (chitin derivates degradation, the protocatechuic acid pathway, inositol metabolism, and the sucrose pathway), which have also been linked to inflammation and carcinogenesis. Moreover, we found specific and abundant ASVs in both tumor and non-tumor tissues. Our data encourage further study to better understand the role of these microorganisms in penile carcinogenesis, offering an opportunity for advances in diagnosis, prognosis, and early therapy.
Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare disorder of phosphate homeostasis. We describe a single-center experience of genetically proven HHRH families and perform systematic review phenotype-genotype correlation in reported biallelic probands and their monoallelic relatives. Detailed clinical, biochemical, radiological, and genetic data were retrieved from our center and a systematic review of Pub-Med and Embase databases for patients and relatives who were genetically proven. Total of nine subjects (probands:5) carrying biallelic SLC34A3 mutations (novel:2) from our center had a spectrum from rickets/osteomalacia to normal BMD, with hypophosphatemia and hypercalciuria in all. We describe the first case of genetically proven HHRH with enthesopathy. Elevated FGF23 in another patient with hypophosphatemia, iron deficiency anemia, and noncirrhotic periportal fibrosis led to initial misdiagnosis as tumoral osteomalacia. On systematic review of 58 probands (with biallelic SLC34A3 mutations; 35 males), early-onset HHRH and renal calcification were present in ~ 70% and late-onset HHRH in 10%. c.575C > T p.(Ser192Leu) variant occurred in 53% of probands without skeletal involvement. Among 110 relatives harboring monoallelic SLC34A3 mutation at median age 38 years, renal calcification, hypophosphatemia, high 1,25(OH)2D, and hypercalciuria were observed in ~30%, 22.3%, 40%, and 38.8%, respectively. Renal calcifications correlated with age but were similar across truncating and non-truncating variants. Although most relatives were asymptomatic for bone involvement, 6/12(50%) had low bone mineral density. We describe the first monocentric HHRH case series from India with varied phenotypes. In a systematic review, frequent renal calcifications and low BMD in relatives with monoallelic variants (HHRH trait) merit identification.
The present invention relates to a photochromic material comprising a proteorhodopsin apoprotein and a retinal analog. In one embodiment, the retinal analog is an azulenic retinoid compound. In another embodiment, the retinal analog is a compound that is structurally similarly to all-trans-retinal. The proteorhodopsin apoprotein and the retinal analog form a photochromic material having different spectral properties from those of a corresponding photochromic material formed by the same proteorhodopsin apoprotein and all-trans-retinal. In one embodiment of the application, the retinal analog-containing proteorhodopsin has an absorbance spectrum that does not overlap significantly with that of all-trans-retinal-containing proteorhodopsin. In another embodiment of the application, the retinal analog-containing proteorhodopsin yields a red-shifted visual chromophore compared with the all-trans-retinal-containing proteorhodopsin chromophore. The photochromic material of the present invention is useful as an optical data storage carrier, a fraud-proof optical data carrier, security ink, and in other optical applications.
Lead (Pb) is a widespread toxic endocrine disruptor that could cause liver damage and gut microbiota dysbiosis. However, the causal relationship and underlying mechanisms between the gut microbiota and Pb-induced liver injury are unclear. In this study, we investigated the metabolic toxicity caused by Pb exposure in normal chow (Chow) and high-fat diet (HFD) mice and confirmed the causal relationship by fecal microbial transplantation (FMT) and antibiotic cocktail experiments. The results showed that Pb exposure exacerbated HFD-induced hepatic lipid deposition, fibrosis, and inflammation, but it had no significant effect on Chow mice. Pb increased serum lipopolysaccharide (LPS) levels and induced intestinal inflammation and barrier damage by activating TLR4/NFκB/MLCK in HFD mice. Furthermore, Pb exposure disrupted the gut microbiota, reduced short-chain fatty acid (SCFA) concentrations and the colonic SCFA receptors, G protein-coupled receptor (GPR) 41/43/109A, in HFD mice. Additionally, Pb significantly inhibited the hepatic GPR109A-mediated adenosine 5'-monophosphate-activated protein kinase (AMPK) pathway, resulting in hepatic lipid accumulation. FMT from Pb-exposed HFD mice exacerbated liver damage, disturbed lipid metabolic pathways, impaired intestinal barriers, and altered the gut microbiota and metabolites in recipient mice. However, mice exposed to HFD + Pb and HFD mice had similar levels of these biomarkers in microbiota depleted by antibiotics. In conclusion, our study provides new insights into gut microbiota dysbiosis as a potential novel mechanism for human health related to liver function impairment caused by Pb exposure.
BACKGROUND: Smoking is a risk factor for liver cirrhosis; however, the underlying mechanisms remain largely unexplored. The α7 nicotinic acetylcholine receptor (α7nAChR) has recently been detected in nonimmune cells possessing immunoregulatory functions. We aimed to verify whether nicotine promotes liver fibrosis via α7nAChR.
METHODS: We used osmotic pumps to administer nicotine and carbon tetrachloride to induce liver fibrosis in wild-type and α7nAChR-deficient mice. The severity of fibrosis was evaluated using Masson trichrome staining, hydroxyproline assays, and real-time PCR for profibrotic genes. Furthermore, we evaluated the cell proliferative capacity and COL1A1 mRNA expression in human HSCs line LX-2 and primary rat HSCs treated with nicotine and an α7nAChR antagonist, methyllycaconitine citrate.
RESULTS: Nicotine exacerbated carbon tetrachloride-induced liver fibrosis in mice (+42.4% in hydroxyproline assay). This effect of nicotine was abolished in α7nAChR-deficient mice, indicating nicotine promotes liver fibrosis via α7nAChR. To confirm the direct involvement of α7nAChRs in liver fibrosis, we investigated the effects of genetic suppression of α7nAChR expression on carbon tetrachloride-induced liver fibrosis without nicotine treatment. Profibrotic gene expression at 1.5 weeks was significantly suppressed in α7nAChR-deficient mice (-83.8% in Acta2, -80.6% in Col1a1, -66.8% in Tgfb1), and collagen content was decreased at 4 weeks (-22.3% in hydroxyproline assay). The in vitro analysis showed α7nAChR expression in activated but not in quiescent HSCs. Treatment of LX-2 cells with nicotine increased COL1A1 expression (+116%) and cell proliferation (+10.9%). These effects were attenuated by methyllycaconitine citrate, indicating the profibrotic effects of nicotine via α7nAChR.
CONCLUSIONS: Nicotine aggravates liver fibrosis induced by other factors by activating α7nAChR on HSCs, thereby increasing their collagen-producing capacity. We suggest the profibrotic effect of nicotine is mediated through α7nAChRs.
OBJECTIVE: Direct-acting antiviral (DAA) drugs have resulted in high rates of virological cure in chronic hepatitis C (CHC)-infected patients. We used noninvasive tests to assess fibrosis in subjects who had been cured with DAA.
METHODS: Retrospective data collection (2014-2019) from the medical record of CHC patients at the hepatology clinic was performed. Subjects co-infected with HIV and hepatitis B, post-liver transplant, and lost to follow-up were excluded. We evaluated fibrosis at baseline and 1 year after completing therapy using vibration-controlled transient elastography (VCTE), fibrosis-4 (FIB-4), and aspartate aminotransferase-toplatelet ratio index (APRI) scores.
RESULTS: With 210 medical records reviewed, 41 were included. The mean age was 62.8 years; 61% were men. Significant fibrosis regression was observed 1-year post-treatment using 3 noninvasive methods: VCTE, APRI, and FIB-4 score. Prior to treatment, 46% of the patients had advanced fibrosis compared to 25% 1 year after treatment. The VCTE scores of 4 subjects (with body mass indices [BMIs] > 30) indicated a worsening of fibrosis. We did not find a statistically significant association between BMI and VCTE, FIB-4, or APRI score.
CONCLUSION: In most CHC patients, DAA therapy leads to liver fibrosis regression. Obesity may play an important role in the worsening of hepatic fibrosis or the absence of fibrosis regression.