anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The present invention relates to immunogenic compositions against influenza. The present invention discloses an immunogenic composition wherein the composition is a multivalent composition comprising recombinant viruses from at least two influenza strains. Also disclosed is a method of stimulating an immune response against influenza a and influenza B comprising administering to a subject in need thereof a multivalent immunogenic composition comprising: a) At least one engineered attenuated influenza A M2-deficient recombinant virus, wherein the engineered influenza a virus comprises a mutant M2 gene comprising SEQ ID No. 1, SEQ ID No. 2, or SEQ ID No. 3; and B) at least one engineered attenuated influenza BM2 deficient recombinant virus, wherein the engineered influenza B virus comprises a mutant BM2 gene comprising SEQ ID NO. 6, SEQ ID NO. 7, SEQ ID NO. 8, SEQ ID NO. 9, SEQ ID NO. 10 or SEQ ID NO. 11.
BACKGROUND: Population screening for risk of type 1 diabetes (T1D) has been proposed to identify those with islet autoimmunity (presence of islet autoantibodies). As islet autoantibodies can be transient, screening with a genetic risk score has been proposed as an entry into autoantibody testing.
METHODS: Children were recruited from eight general pediatric and specialty clinics across Virginia with diverse community settings. Recruiters in each clinic obtained informed consent/assent, a medical history, and a saliva sample for DNA extraction in children with and without a history of T1D. A custom genotyping panel was used to define T1D genetic risk based upon associated SNPs in European- and African-genetic ancestry. Subjects at "high genetic risk" were offered a separate blood collection for screening four islet autoantibodies. A follow-up contact (email, mail, and telephone) in one half of the participants determined interest and occurrence of subsequent T1D.
RESULTS: A total of 3818 children aged 2-16 years were recruited, with 14.2% (n = 542) having a "high genetic risk." Of children with "high genetic risk" and without pre-existing T1D (n = 494), 7.0% (34/494) consented for autoantibody screening; 82.4% (28/34) who consented also completed the blood collection, and 7.1% (2/28) of them tested positive for multiple autoantibodies. Among children with pre-existing T1D (n = 91), 52% (n = 48) had a "high genetic risk." In the sample of children with existing T1D, there was no relationship between genetic risk and age at T1D onset. A major factor in obtaining islet autoantibody testing was concern over SARS-CoV-2 exposure.
CONCLUSIONS: Minimally invasive saliva sampling implemented using a genetic risk score can identify children at genetic risk of T1D. Consent for autoantibody screening, however, was limited largely due to the SARS-CoV-2 pandemic and need for blood collection.
Oral administration of lumateperone caused systemic intracytoplasmic accumulation of pigmented material in dogs, rats, and mice at clinically relevant exposures (AUC). Intracytoplasmic pigmentation appeared to be localized in lysosomes. Accumulation of pigmented material persisted without reversal at the end of 1- to 2-month drug-free periods. Pigmented material was observed in the brain and spinal cord of all three species, and in the heart and eye of rats. Although the composition of the pigmented material was not established, the material is likely polymers or protein adducts formed from aniline metabolites of lumateperone. 

In the dog, accumulation of pigmented material in the brain and spinal cord was associated with neuronal degeneration and necrosis, followed by axonal degeneration and histiocytic inflammation after oral administration of lumateperone for up to 9 months. In the rat, accumulation of pigmented material was associated with degenerative changes and signs of an inflammatory response in the spinal cord, peripheral nervous system, eye, and heart after oral administration of lumateperone for up to 2 years. Although overt degenerative changes were not observed in the rat brain, the presence of pigment-containing infiltrating macrophages is consistent with an inflammatory response. 

The role of intracytoplasmic pigmented material in causing these lesions was not definitively established; however, the colocalization of pigmented material in tissues with degenerative changes and signs of inflammation is supportive. Alternatively, the aniline metabolites of lumateperone may undergo metabolic activation forming reactive metabolites that contribute to the observed toxicities. The role of intracellular accumulation of lumateperone or its non-aniline metabolites in these toxicities could not be ruled out. 

The aniline metabolites thought to be responsible for these toxicities were detected in dogs and rats but were not present in humans at quantifiable levels. Based on all the available evidence, these toxicities do not appear to be relevant to humans.
BACKGROUND: Intracerebral hemorrhage (ICH) is a critical neurological condition with few treatment options, where secondary immune responses and specific cell death forms, like pyroptosis, worsen brain damage. Pyroptosis involves gasdermin-mediated membrane pores, increasing inflammation and neural harm, with the NLRP3/Caspase-1/GSDMD pathway being central to this process. Peroxiredoxin II (Prx II), recognized for its mitochondrial protection and reactive oxygen species (ROS) scavenging abilities, appears as a promising neuronal pyroptosis modulator. However, its exact role and action mechanisms need clearer definition. This research aims to explore Prx II impact on neuronal pyroptosis and elucidate its mechanisms, especially regarding endoplasmic reticulum (ER) stress and oxidative stress-induced neuronal damage modulation.
METHODS AND RESULTS: Utilizing MTT assays, Microscopy, Hoechst/PI staining, Western blotting, and immunofluorescence, we found Prx II effectively reduces LPS/ATP-induced pyroptosis and neuroinflammation in HT22 hippocampal neuronal cells. Our results indicate Prx II's neuroprotective actions are mediated through PI3K/AKT activation and ER stress pathway inhibition, diminishing mitochondrial dysfunction and decreasing neuronal pyroptosis through the ROS/MAPK/NF-κB pathway. These findings highlight Prx II potential therapeutic value in improving intracerebral hemorrhage outcomes by lessening secondary brain injury via critical signaling pathway modulation involved in neuronal pyroptosis.
CONCLUSIONS: Our study not only underlines Prx II importance in neuroprotection but also opens new therapeutic intervention avenues in intracerebral hemorrhage, stressing the complex interplay between redox regulation, ER stress, and mitochondrial dynamics in neuroinflammation and cell death management.
Cognitive decline in Parkinson's Disease (PD) is a prevalent and undertreated aspect of disease. Currently, no therapeutics adequately improve this aspect of disease. It has been previously shown that MAS receptor agonism via the glycosylated Angiotensin (1-7) peptide, PNA5, effectively reduces cognitive decline in models of vascular contributions to cognitive impairment and dementia (VCID). PNA5 has a brain/plasma ratio of 0.255 indicating good brain penetration. The goal of the present study was to determine if (1) systemic administration of PNA5 rescued cognitive decline in a mouse model of PD, and (2) if improvements in cognitive status could be correlated with changes to histopathological or blood plasma-based changes. Mice over-expressing human, wild-type α-synuclein (αSyn) under the Thy1 promoter (Thy1-αSyn mice, "line 61") were used as a model of PD with cognitive decline. Thy1-αSyn mice were treated with a systemic dose of PNA5, or saline (1 mg/kg/day) beginning at 4 months of age and underwent behavioral testing at 6 months, compared to WT. Subsequently, mice brains were analyzed for changes to brain pathology, and blood plasma was examined with a Multiplex Immunoassay for peripheral cytokine changes. Treatment with PNA5 reversed cognitive dysfunction measured by Novel Object Recognition and spontaneous alteration in a Y-maze in Thy1-αSyn mice. PNA5 treatment was specific to cognitive deficits, as fine-motor disturbances were unchanged. Enhanced cognition was associated with decreases in hippocampal inflammation and reductions in circulating levels of Macrophage Induced Protein (MIP-1β). Additionally, neuronal loss was blunted within the CA3 hippocampal region of PNA5-treated αsyn mice. These data reveal that PNA5 treatment reduces cognitive dysfunction in a mouse model of PD. These changes are associated with decreased MIP-1β levels in plasma identifying a candidate biomarker for target engagement. Thus, PNA5 treatment could potentially fill the therapeutic gap for cognitive decline in PD.
Group B: Test- Received hyperoxygenation more than or equal to 50% throughout the surgery and received oxygen at 6l/min. upto 2 hrs postoperatively.
PURPOSE:To obtain an allergic agent for oral administration, having excellent stability with the elapse of time, capable of improving elution and bioavailability not attainable by the production of conventional procedure and simultaneously reducing toxicity. CONSTITUTION:A composition for oral administration comprises a pyrido[1, pyrimidine derivative of the formula (R is n-propyl or allyl; A is tetrazolyl or carboxyl; (n) is 0-2) such as 9-[(4-acetyl-3-hydroxy-2-n-propylphenoxy) methyl]-3-(1H-tetrazol-5-yl)-4H-pyrido[1,2-a]pyrimidin-4-one and a mixed carrier subjected to surface treatment by mechanical procedure such as impact, compression, friction or shear. 1 pt.wt. of the compound of the formula is blended with 0.005-50 pts.wt., preferably 0.5-10 pts.wt. of the mixed carrier and subjected to surface treatment or the compound of the formula is subjected to surface treatment and blended with the mixed carrier to prepare the objective composition. A ball medium mill, a compression grinding type pulverizer or a high-speed rotary type impact grinder may be cited as a device to be used.
An increasing body of research suggests that promoting microglial autophagy hinders the neuroinflammation initiated though the NLRP3 inflammasome activation in Alzheimer's disease (AD). The function of FoxG1, a crucial transcription factor involved in cell survival by regulating mitochondrial function, remains unknown during the AD process and neuroinflammation occurs. In the present study, we firstly found that Aβ peptides induced AD-like neuroinflammation upregulation and downregulated the level of autophagy. Following low-dose Aβ25-35 stimulation, FoxG1 expression and autophagy exhibited a gradual increase. Nevertheless, with high-concentration Aβ25-35 treatment, progressive decrease in FoxG1 expression and autophagy levels as the concentration of Aβ25-35 escalated. In addition, FoxG1 has a positive effect on cell viability and autophagy in the nervous system. In parallel with the Aβ25-35 stimulation, we employed siRNA to decrease the expression of FoxG1 in N2A cells. A substantial reduction in autophagy level (Beclin1, LC3II, SQSTM1/P62) and a notable growth in inflammatory response (NLRP3, TNF-α, and IL-6) were observed. In addition, we found FoxG1 overexpression owned the effect on the activation of AMPK/mTOR autophagy pathway and siRNA-FoxG1 successfully abolished this effect. Lastly, FoxG1 suppressed the NLRP3 inflammasome and enhanced the cognitive function in AD-like mouse model induced by Aβ25-35. Confirmed by cellular and animal experiments, FoxG1 suppressed NLRP3-mediated neuroinflammation, which was strongly linked to autophagy regulated by AMPK/mTOR. Taken together, FoxG1 may be a critical node in the pathologic progression of AD and has the potential to serve as therapeutic target.
Dapiprazole hydrochloride ophthalmic solution acts through blocking the alpha-adrenergic receptors in smooth muscle. Dapiprazole hydrochloride ophthalmic solution produces miosis through an effect on the dilator muscle of the iris.

Dapiprazole hydrochloride ophthalmic solution does not have any significant activity on ciliary muscle contraction and, therefore does not induce a significant change in the anterior chamber depth or the thickness of the lens.

Dapiprazole hydrochloride ophthalmic solution has demonstrated safe and rapid reversal of mydriasis produced by phenylephrine and to a lesser degree tropicamide. In patients with decreased accommodative amplitude due to treatment with tropicamide, dapiprazole hydrochloride ophthalmic solution partially restores the accommodative amplitude. This activity is not only due to its miotic effect but also to a direct effect on accommodation.

Eye color affects the rate of pupillary constriction. In individuals with brown irides, the rate of pupillary constriction may be slightly slower than in individuals with blue or green irides. Eye color does not appear to affect the final pupil size.

Dapiprazole hydrochloride ophthalmic solution does not significantly alter intraocular pressure in normotensive eyes or in eyes with elevated intraocular pressure.
24 patients with type 2 diabetes from the German Diabetes Study (GDS) with less than 4 years disease duration and not receiving insulin were included in this study. Before the start of the intervention, participants documented their dietary intake by recording a food diary. During the 12-week intervention participants were asked to adhere to a real food-based low-calorie diet supported by an app-guided digital education program as well as a low-calorie recipe book and received weekly coaching calls by nutritionists. Patients were instructed to adhere to a balanced low calorie diet during the intervention. Nutritionists provided structured behavior change focusing on dietary advice, adherence to logging dietary intake and tracking weight. At first visit, patients installed the Changing Health App (Changing Health, Newcastle, UK) and completed an app-based digital education program. This program focused on type 2 diabetes education and behavioral change in combination with weight tracking and dietary monitoring. Patients used the app throughout the study and adherence was monitored via logins. Comprehensive testing before and after the intervention comprised a mixed-meal tolerance test and liver fat.
Following the visualization of the anatomical structures, the nerve block needle was advanced via the in-plane technique beneath the serratus anterior muscles until the fourth rib area. After hydrodissection with 2 ml normal saline, 20 ml 0.25% bupivacaine was injected into the area. A catheter will be placed in this area. Then, 5 ml/hour 0.125% bupivacaine will be infused via serratus anterior plane block catheter.
A method for detecting cancer in a patient. The method comprises the steps of introducing labeled antibodies or labeled AFP to a biological sample of the patient so the labeled antibodies or labeled AFP will react with the AFP receptor binding sites in the biological sample. Next there is the step of identifying AFP receptor binding sites in the biological material which are reacted with the labeled antibodies or labeled AFP to determine the presence of cancer. Preferably, before the introducing step, there is the step of obtaining a biological sample from a body of a patient. A method for treating cancer cells in a patient. The method comprises the steps of introducing AFP receptor antibodies to cancer cells in the patient. Then there is the step of reacting the AFP receptor antibodies with the AFP receptor of the cancer cells to inhibit growth of the cancer cells or kill the cancer cells.  A method for monitoring a patient. The method comprises the steps of treating the patient for cancer. Then there is the step of testing the patient at predetermined intervals after the treatment for AFP receptor site levels. A method for treating a patient. The method comprises the steps of testing the patient for AFP receptor. Then there is the step of introducing AFP receptor antibodies or AFP into the patient to react with cancer cells in the patient if the testing indicates AFP receptors are in the patient. A method for treating cancer cells in a patient. The method comprises the steps of introducing modified AFP to cancer cells in the patient. Then there is the step of reacting the modified AFP with the AFP receptor of the cancer cells to inhibit growth of the cancer cells or kill the cancer cells.
Evidence-based knowledge about the effects of intensive training programs for children with severe early brain damage is limited since research on this topic has methodological weaknesses and shows conflicting results. As intensive training programs require extensive efforts from the child, parents and professionals and represent major costs, the importance of scientifically proven effects is considerable. This research project aims to measure the effects of an intensive habilitation program for young children with severe early brain damage on the child's adaptive, motor, language and social functioning and on parental empowerment, family functioning and stress. In this randomized controlled trial (RCT) 90 children will be divided into an intervention group participating in a Norwegian developed program of intensified habilitation of 12 months duration and a control group, who will receive "services as usual" during the same time period. Between-group analyses will then be performed. Due to a stepped wedge design, the control participants will then be offered training in year two of participation. Within-group analysis of results before and after training will then be performed for all participants. Standardized measures with high responsiveness in documenting intervention effectiveness will be used as primary outcome measures. Intensive training groups will be offered in all Health Regions in Norway and if successful be implemented as standard clinical practice.
PURPOSE:To improve the efficiency of production by culturing a transformed colon bacillus, etc., transformed using a specified vector in a culture medium. CONSTITUTION:A prescribed length of a gene fragment produced using the amidite solid phase synthesis method, etc., is annealed to obtain a human TNF-alpha gene (A) containing a base sequence, etc., of formula I. The resultant component (A) is then integrated to a plasmid capable of propagation in a colon bacillus to obtain a mutagenic plasmid (B) as a plasmid for peptide manifestation. The resultant component (B) is then introduced into a colon bacillus strain (e.g. colon bacillus JM 101) to obtain a transformant (C). The obtained component (C) is subsequently cultured in L-medium, M9 medium, etc., to obtain a cultured material (D). Colon bacillus cell bodys are then separated from the component (D) and the resultant cell bodys are subjected to ultrasonic crushing to obtain a supernatant (E) as a water soluble fraction. The obtained component (E) is then purified by the ammonium sulfate precipitation method, dialysis, the anion-exchange chromatography method, etc., to produce the objective antitumor peptide of formula II (A1 is Asp or Arg; A2 is His or nothing; A3 is Gln or nothing; A4 is Glu or His).
BACKGROUND: Clinical guidelines reserve endoscopic surveillance after a gastric intestinal metaplasia (GIM) diagnosis for high-risk patients. However, it is unclear how closely guidelines are followed in clinical practice. We examined the effectiveness of a standardized protocol for the management of GIM among gastroenterologists at a US hospital.
METHODS: This was a preintervention and postintervention study, which included developing a protocol and education of gastroenterologists on GIM management. For the preintervention study, 50 patients with GIM were randomly selected from a histopathology database at the Houston VA Hospital between January 2016 and December 2019. For the postintervention study, we assessed change in GIM management in a cohort of 50 patients with GIM between April 2020 and January 2021 and surveyed 10 gastroenterologists. The durability of the intervention was assessed in a cohort of 50 GIM patients diagnosed between April 2021 and July 2021.
RESULTS: In the preintervention cohort, GIM location was specified (antrum and corpus separated) in 11 patients (22%), and Helicobacter pylori testing was recommended in 11 of 26 patients (42%) without previous testing. Gastric mapping biopsies were recommended in 14% and surveillance endoscopy in 2%. In the postintervention cohort, gastric biopsy location was specified in 45 patients (90%, P <0.001) and H. pylori testing was recommended in 26 of 27 patients without prior testing (96%, P <0.001). Because gastric biopsy location was known in 90% of patients ( P <0.001), gastric mapping was not necessary, and surveillance endoscopy was recommended in 42% ( P <0.001). One year after the intervention, all metrics remained elevated compared with the preintervention cohort.
CONCLUSIONS: GIM management guidelines are not consistently followed. A protocol for GIM management and education of gastroenterologists increased adherence to H. pylori testing and GIM surveillance recommendations.
Experimental and clinical studies have indicated a potential role of the protein S100β in the pathogenesis and phenotype of neurodegenerative diseases. However, its impact on spinocerebellar ataxia type 2 (SCA2) remains to be elucidated. The objective of the study is to determine the serum levels of S100β in SCA2 and its relationship with molecular, clinical, cognitive, and peripheral inflammatory markers of the disease. Serum concentrations of S100β were measured by enzyme-linked immunosorbent assay in 39 SCA2 subjects and 36 age- and gender-matched controls. Clinical scores of ataxia, non-ataxia symptoms, cognitive dysfunction, and some blood cell count-derived inflammatory indices were assessed. The SCA2 individuals manifested S100β levels similar to the control group, at low nanomolar concentrations. However, the S100β levels were directly associated with a better performance of cognitive evaluation within the SCA2 cohort. Moreover, the S100β levels were inversely correlated with most peripheral inflammatory indices. Indeed, the neutrophil-to-lymphocyte ratio significantly mediated the effect of serum S100β on cognitive performance, even after controlling for the ataxia severity in the causal mediation analysis. Our findings suggested that, within physiologic concentrations, the protein S100β exerts a neuroprotective role against cognitive dysfunction in SCA2, likely via the suppression of pro-inflammatory mechanisms.
Anorectal malformations (ARMs) represent a wide spectrum of congenital anomalies of the anus and rectum, of which more than half are syndromic. Their etiology is highly heterogeneous and still poorly understood. We report a 4-year-old girl who initially presented with an isolated ARM, and subsequently developed a global developmental delay as part of an ARID1B-related Coffin-Siris syndrome (CSS). A co-occurrence of ARMs and CSS in an individual by chance is unexpected since both diseases are very rare. A review of the literature enabled us to identify 10 other individuals with both CSS and ARMs. Among the ten individuals reported in this study, 8 had a variant in ARID1A, 2 in ARID1B, and 1 in SMARCA4. This more frequent than expected association between CSS and ARM indicates that some ARMs are most likely part of the CSS spectrum, especially for ARID1A-related CSS.
Participants recieving passive / sham trancranial direct current stimulation (tDCS) Two times a week, for three weeks. Anode placed at F3, cathode placed at right cerebellum.
Non-operative treatment starts with casting the ankle in equinus position. The rest of the treatment from there on will be identical to the two other arms: Minimal invasive and open surgery. Casting lasts for 2 weeks for all three arms.