anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND/OBJECTIVES: The purpose of this study is to investigate whether history of silicone oil tamponade may predispose to the development of cystoid macular edema (CMO) following uneventful post-vitrectomy cataract surgery.
SUBJECTS/METHODS: This is a retrospective study that was conducted at a single academic institution. Records of patients who underwent pars plana vitrectomy (PPV) with or without silicone oil tamponade and subsequent cataract surgery between 2017-2020 were reviewed. Macular optical coherence tomography (OCT) findings up to 4 years after surgery were assessed.
RESULTS: A total of 95 eyes were included. Forty-one eyes underwent cataract surgery and had a history of PPV with silicone oil tamponade (Group 1). Fifty-four eyes underwent cataract surgery by phacoemulsification and had a history of PPV with gas tamponade (Group 2). Average follow up time after cataract surgery was 41.1 months. In Group 1, the incidence of OCT-detected CMO was 39.0%, compared to 27.8% in Group 2 (p = 0.247). The incidence of clinically significant CMO in Group 1 was 22.0%, compared to 18.5% in Group 2 (p = 0.679). The duration of CMO was significantly longer in Group 1 (p = 0.041) and cases were less likely to resolve by the last follow up visit (p = 0.040).
CONCLUSIONS: The incidence of OCT-detected or clinically significant pseudophakic CMO is not significantly different between eyes with prior PPV with gas tamponade versus silicone oil tamponade. However, CMO after uneventful cataract surgery may have a prolonged course if there is history of silicone oil tamponade, requiring longer treatment.
<P>PROBLEM TO BE SOLVED: To provide a new material for protecting living bodies from oxidation stresses.  <P>SOLUTION: A polyphenol represented by general formula (I) (R1 to R26 are each independently H, a 1 to 4C alkyl or a 1 to 4C acyl) or its salt. The compound is obtained by subjecting the seed kernel of a plant belonging to Juglandaceae, Juglans to extraction with a nonpolar solvent, removing polar ingredients by a solvent extraction, and purifying by column chromatography. The compound is added to a food composition and orally administered. Thereby, a living body can be protected from oxidation stress.  <P>COPYRIGHT: (C)2006,JPO&NCIPI
Receiving a neurodegenerative disease (NDD) diagnosis, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, or amyotrophic lateral sclerosis, is devastating, particularly given the limited options for treatment. Advances in genetic technologies have allowed for efficient modeling of NDDs in animals and brought hope for new disease-modifying medications. The complexity of the mammalian brain and the costs and time needed to identify and develop therapeutic leads limits progress. Modeling NDDs in invertebrates, such as the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans, offers orders of magnitude increases in speed of genetic analysis and manipulation, and can be pursued at substantially reduced cost, providing an important, platform complement and inform research with mammalian NDD models. In this review, we describe how our efforts to exploit C. elegans for the study of neural signaling and health led to the discovery of a paralytic phenotype (swimming-induced paralysis) associated with altered dopamine signaling and, surprisingly, to the discovery of a novel gene and pathway whose dysfunction in glial cells triggers neurodegeneration. Research to date on swip-10 and its putative mammalian ortholog MBLAC1, suggests that a tandem analysis will offer insights into NDD mechanisms and insights into novel, disease-modifying therapeutics.
The present invention relates to a liposome of a nucleoside phosphonic acid compound and a preparation method for a lipid compound preparation. The present invention uses nucleoside phosphonic acid compounds as active components and is composed of the following components by the mol percentage: 0.99 to 50.00% of nucleoside phosphonic acid compound and 50.00 to 99.01% of lipid. The present invention can be obtained by any of the following methods: a pH gradient method, a calcium ion gradient method and an electrical property pack method. The encapsulation efficiency of the present invention is obviously enhanced. Compared with an ordinary film dispersion method, as for the nucleoside phosphonic acid compound liposome or the lipid compound prepared by the pH gradient method and the calcium ion gradient method, the medicinal encapsulation efficiency is 2 to 4 times of the encapsulation efficiency of the product prepared by the ordinary film dispersion method; as for the nucleoside phosphonic acid compound liposome or the lipid compound prepared by the electrical property pack method, the medicinal encapsulation efficiency is 3 to 10 times of the encapsulation efficiency of the product prepared by the ordinary film dispersion method. By the electrical property pack method, the stability of the preparation can also be enhanced, and the storage life of the preparation is greatly prolonged.
The invention relates to a Chinese medicinal composition for treating chromatosis and a preparation thereof. The Chromatosis occurs in various kinds of dermatosis, and is caused by forming pigmentation of black skin pigments after skin is often irritated by sunshine, ultraviolet radiation or cosmetics, medicaments and other substance. One part of the black skin pigments sheds with corneum, while one part is precipitated at the bottom layer and discharged from the body through blood circulation. If the functions are disordered, chromatosis forms. According to the formula, the Chinese medicinal composition comprises Chinese patent medicmaments such as campanumaea pilosula, astragalus, largehead atractylodes rhizome, glabrous greenbrier rhizome and the like which have the effects of supplementing the center and boosting qi, and strengthening spleen and benefiting lung as primary materials, and is supplemented with Chinese angelica for enriching blood and activating blood, dioscorea batatas decene for strengthening spleen, reinforcing kidney and moisturizing lung, benefiting brain, replenishing essence and beautifying, white paeony root for nourishing blood and softening liver, red paeony root for clearing heat and cooling blood, and activating blood and dissolving stasis, motherwort herb for eliminating stasis and engendering the new, and activating blood and regulating menstruation, and fresh liquoric root for tonifying spleen and benefiting qi, clearing heat and detoxicating. The medicaments are processed into an oral preparation which has the effects of supplementing center and boosting qi, strengthening spleen and benefiting lung, and activating blood and dissolving stasis. Decades of clinical application proves that the Chinese medicinal composition has good effects of treating the chromatosis.
The invention comprises tetrahydrodibenzazocines of the general formula: <FORM:0969027/C1/1> and their non-toxic acid addition salts, wherein A represents an alkylene group of 2 to 6 carbon atoms, and B represents an alkylamino or dialkylamino group or a saturated mononuclear 5- or 6-membered heterocyclic group linked to A through a nitrogen atom, which group may carry alkyl substituents and when so substituted contains at most 12 carbon atoms ("alkyl" being defined as an alkyl group of not more than 6 C atoms), and the preparation thereof by reacting a compound of the formula: <FORM:0969027/C1/2> with a compound Q-B, wherein one of X and Q represents H and the other -AHalogen. When X is -AHalogen, this compound may be prepared by reacting tetrahydrodibenz(b, f)-ozocine with the compound Hal -AHal. Alternatively the compounds of the invention are prepared by reducing the carbonyl group in compounds of formula: <FORM:0969027/C1/3> (wherein A1 represents a C1- 5 alkylene group) to a methylene group.  Pharmaceutical preparations comprise the compounds of the invention in association with a pharmacologically acceptable carrier. They have antiallergic, anticholinergic, psychotropic and analgesic activity, and may take the form of tablets, pills, capsules, solutions, suspensions, emulsions, syrups or elixirs.  Specification 969,028 is referred to.
BACKGROUND: Cognitive symptoms after coronavirus disease 2019 (Covid-19), the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are well-recognized. Whether objectively measurable cognitive deficits exist and how long they persist are unclear.
METHODS: We invited 800,000 adults in a study in England to complete an online assessment of cognitive function. We estimated a global cognitive score across eight tasks. We hypothesized that participants with persistent symptoms (lasting ≥12 weeks) after infection onset would have objectively measurable global cognitive deficits and that impairments in executive functioning and memory would be observed in such participants, especially in those who reported recent poor memory or difficulty thinking or concentrating ("brain fog").
RESULTS: Of the 141,583 participants who started the online cognitive assessment, 112,964 completed it. In a multiple regression analysis, participants who had recovered from Covid-19 in whom symptoms had resolved in less than 4 weeks or at least 12 weeks had similar small deficits in global cognition as compared with those in the no-Covid-19 group, who had not been infected with SARS-CoV-2 or had unconfirmed infection (-0.23 SD [95% confidence interval {CI}, -0.33 to -0.13] and -0.24 SD [95% CI, -0.36 to -0.12], respectively); larger deficits as compared with the no-Covid-19 group were seen in participants with unresolved persistent symptoms (-0.42 SD; 95% CI, -0.53 to -0.31). Larger deficits were seen in participants who had SARS-CoV-2 infection during periods in which the original virus or the B.1.1.7 variant was predominant than in those infected with later variants (e.g., -0.17 SD for the B.1.1.7 variant vs. the B.1.1.529 variant; 95% CI, -0.20 to -0.13) and in participants who had been hospitalized than in those who had not been hospitalized (e.g., intensive care unit admission, -0.35 SD; 95% CI, -0.49 to -0.20). Results of the analyses were similar to those of propensity-score-matching analyses. In a comparison of the group that had unresolved persistent symptoms with the no-Covid-19 group, memory, reasoning, and executive function tasks were associated with the largest deficits (-0.33 to -0.20 SD); these tasks correlated weakly with recent symptoms, including poor memory and brain fog. No adverse events were reported.
CONCLUSIONS: Participants with resolved persistent symptoms after Covid-19 had objectively measured cognitive function similar to that in participants with shorter-duration symptoms, although short-duration Covid-19 was still associated with small cognitive deficits after recovery. Longer-term persistence of cognitive deficits and any clinical implications remain uncertain. (Funded by the National Institute for Health and Care Research and others.).
Tumour-specific molecular targets and alternative therapeutic strategies for triple-negative breast cancer (TNBC) are urgently needed. The protease cathepsin D (cath-D) is aberrantly secreted and a marker of poor prognosis in breast cancer. Using degradomic analyses by TAILS, we discovered that the matricellular protein SPARC is a substrate of extracellular cath-D. In vitro, cath-D induced limited proteolysis of SPARC C-terminal extracellular Ca2+ binding domain at acidic pH, leading to the production of SPARC fragments (34-, 27-, 16-, 9-, and 6-kDa). SPARC cleavage also occurred in vivo in TNBC and mouse mammary tumours. Moreover, the C-terminal 9-kDa SPARC fragment inhibited MDA-MB-231 TNBC cell adhesion and spreading on fibronectin, and stimulated their migration, endothelial transmigration and invasion more potently than full-length SPARC. These results highlight a novel crosstalk between proteases and matricellular proteins in the TNBC microenvironment through limited proteolysis of SPARC, and reveal that the 9-kDa C-terminal SPARC fragment is an attractive therapeutic target for TNBC. Thus, the invention relates to an inhibitor of SPARC fragment for use for treating cancer, and in particularly triple cancer negative breast cancer.
Initial MicroScan® (Microvision Medical) SDF measurement are recorded in the obstetric preoperative area within two hours prior to administration of spinal anesthesia. In the operating room participants will receive a standard spinal anesthetic (hyperbaric bupivacaine, fentanyl and preservative free morphine) followed by a second comparative MicroScan® (Microvision Medical) SDF measurement within 10 minutes of initiation of spinal anesthetic. Participants who experience hypotension will receive bolus phenylephrine and/or ephedrine treatment as needed.
BACKGROUND: While melanomas commonly harbor losses of 9p21, on which CDKN2A resides, the presence of additional tumor suppressor elements at this locus is incompletely characterized. Here we assess the expression levels and functional role of microRNA-876-3p (miR-876), whose gene also maps to 9p21.
METHODS: Expression of miR-876 was assessed in human tissues and cell lines using quantitative miRNA reverse transcriptase polymerase chain reaction (qRT-PCR). MIR876 copy number was determined in The Cancer Genome Atlas (TCGA) melanoma cohort. The consequences of regulation of miR-876 expression were assessed on melanoma cell colony formation, migration, invasion, apoptosis, cell cycle progression, and drug sensitivity in culture, and on in vivo tumor growth in a xenograft model. Genome-wide transcriptomic changes induced by miR-876 overexpression were determined using RNA sequencing (RNA-Seq).
RESULTS: miR-876 expression was significantly decreased in primary melanoma samples when compared with nevi, and in human melanoma cell lines when compared with human melanocytes. Analysis of the TCGA cohort revealed deletions in MIR876 in > 50% of melanomas. miR-876 overexpression resulted in decreased melanoma cell colony formation, migration, and invasion, which was accompanied by cell cycle arrest and increased apoptosis. Intra-tumoral injections of miR-876 significantly suppressed melanoma growth in vivo. RNA-Seq analysis of miR-876-treated tumors revealed downregulation of several growth-promoting genes, along with upregulation of tumor suppressor genes, which was confirmed by qRT-PCR analysis. Computational analyses identified MAPK1 (or ERK2) as a possible target of miR-876 action. Overexpression of miR-876 significantly suppressed luciferase expression driven by the MAPK1/ERK2 3' UTR, and resulted in decreased ERK protein expression in melanoma cells. MAPK1/ERK2 cDNA overexpression rescued the effects of miR-876 on melanoma colony formation. miR-876 overexpression sensitized melanoma cells to treatment with the BRAF inhibitor vemurafenib.
CONCLUSIONS: These studies identify miR-876 as a distinct tumor suppressor on 9p21 that is inactivated in melanoma and suggest miR-876 loss as an additional mechanism to activate ERK and the mitogen activated protein kinase (MAPK) pathway in melanoma. In addition, they suggest the therapeutic potential of combining miR-876 overexpression with BRAF inhibition as a rational therapeutic strategy for melanoma.
The major human spirochetal pathogens (Leptospira, Borrelia, and Treponema) are difficult to diagnose and lack vaccines to prevent infections. Infection by these spirochetes does not generate general protective immunity, allowing reinfection by different strains to occur. These stealth pathogens have uncommon physiology, pathogenesis, and clinical presentations and possess unique immune evasion mechanisms to facilitate their host adaptation and persistence. Collectively, host-spirochete interactions orchestrate systemic infections in a manner distinct from organ- and tissue-specific diseases caused by many bacterial pathogens. Difficulties in growing and genetic manipulation of infectious spirochetes have hindered the full understanding of their virulence factors despite decades to centuries of research. This article highlights the current understanding of the intricacies of spirochetal pathogenesis and diseases. Our comprehensive review of the progress versus gaps in knowledge lays a foundation for researchers to direct their studies toward the development of effective diagnostics and vaccines to protect patients from serious, chronic spirochetal diseases.
PURPOSE: Seizures are characterized by periictal autonomic changes. Wearable devices could help improve our understanding of these phenomena through long-term monitoring. In this study, we used wearable electrocardiogram (ECG) data to evaluate differences between temporal and extratemporal focal impaired awareness (FIA) seizures monitored in the hospital and at home. We assessed periictal heart rate, respiratory rate, heart rate variability (HRV), and respiratory sinus arrhythmia (RSA).
METHODS: We extracted ECG signals across three time points - five minutes baseline and preictal, ten minutes postictal - and the seizure duration. After automatic Rpeak selection, we calculated the heart rate and estimated the respiratory rate using the ECG-derived respiration methodology. HRV was calculated in both time and frequency domains. To evaluate the influence of other modulators on the HRV after removing the respiratory influences, we recalculated the residual power in the high-frequency (HF) and low-frequency (LF) bands using orthogonal subspace projections. Finally, 5-minute and 30-second (ultra-short) ECG segments were used to calculate RSA using three different methods. Seizures from temporal and extratemporal origins were compared using mixed-effects models and estimated marginal means.
RESULTS: The mean preictal heart rate was 69.95 bpm (95 % CI 65.6 - 74.3), and it increased to 82 bpm, 95 % CI (77.51 - 86.47) and 84.11 bpm, 95 % CI (76.9 - 89.5) during the ictal and postictal periods. Preictal, ictal and postictal respiratory rates were 16.1 (95 % CI 15.2 - 17.1), 14.8 (95 % CI 13.4 - 16.2) and 15.1 (95 % CI 14 - 16.2), showing not statistically significant bradypnea. HRV analysis found a higher baseline power in the LF band, which was still significantly higher after removing the respiratory influences. Postictally, we found decreased power in the HF band and the respiratory influences in both frequency bands. The RSA analysis with the new methods confirmed the lower cardiorespiratory interaction during the postictal period. Additionally, using ultra-short ECG segments, we found that RSA decreases before the electroclinical seizure onset. No differences were observed in the studied parameters between temporal and extratemporal seizures.
CONCLUSIONS: We found significant increases in the ictal and postictal heart rates and lower respiratory rates. Isolating the respiratory influences on the HRV showed a postictal reduction of respiratory modulations on both LF and HF bands, suggesting a central role of respiratory influences in the periictal HRV, unlike the baseline measurements. We found a reduced cardiorespiratory interaction during the periictal period using other RSA methods, suggesting a blockade in vagal efferences before the electroclinical onset. These findings highlight the importance of respiratory influences in cardiac dynamics during seizures and emphasize the need to longitudinally assess HRV and RSA to gain insights into long-term autonomic dysregulation.
BACKGROUND: Acute lung injury (ALI) is characterized by acute pulmonary inflammatory infiltration. Alveolar epithelial cells (AECs) release numerous pro-inflammatory cytokines, which result in the pathological changes seen in ALI. Ophiopogonin D (OD), extracted from the roots of Ophiopogon japonicus (Thunb.) Ker Gawl. (Liliaceae), reduces inflammation; however, the efficacy of OD in ALI has not been reported and the underlying molecular mechanisms remain unclear.
PURPOSE: This study investigated the anti-inflammatory effects of OD, as well as the underlying mechanisms, in AECs and a mouse ALI model.
METHODS: Lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α) were used to stimulate macrophages and A549 cells, and a mouse ALI model was established by intratracheal LPS administration. The anti-inflammatory effects and mechanisms of OD in the TNF-α-induced in vitro inflammation model was evaluated using real-time quantitative polymerase chain reaction qPCR), enzyme-linked immunosorbent assay (ELISA), western blotting, nuclear and cytoplasmic protein extraction, and immunofluorescence. The in vivo anti-inflammatory activity of OD was evaluated using hematoxylin and eosin staining, qPCR, ELISA, and western blotting.
RESULTS: The bronchoalveolar lavage fluid and lung tissue of LPS-induced ALI mice exhibited increased TNF-α expression. TNF-α induced a significantly greater pro-inflammatory effect in AECs than LPS. OD reduced inflammation and mitogen-activated protein kinase (MAPK) and transcription factor p65 phosphorylation in vivo and in vitro and promoted signal transducer and activator of transcription 3 (STAT3) phosphorylation and A20 expression, thereby inducing apoptosis signal-regulating kinase 1 (ASK1) proteasomal degradation.
CONCLUSION: OD exerts an anti-inflammatory effect by promoting STAT3-dependent A20 expression and ASK1 degradation. OD may therefore have therapeutic value in treating ALI and other TNF-α-related inflammatory diseases.
Participants received GSK3884464 or placebo through oral administration in the treatment sequence: GSK3884464 70 mg/ SD8/ Placebo C3 across 3 treatment periods. There was a minimum of 7 days washout period between dosing in each session.
At enrolment, subjects were stratified into two age strata (18 to 60 years, over 60 years). Total duration of the study is three weeks. Vaccinations were to be administered on day 1. Blood samples were collected at day 1 (baseline, before the vaccination) and at day 22 (three weeks after the vaccination). Sera were tested by Hemagglutination Inhibition (HI) assay. Safety was assessed until 3 weeks after the vaccination.
PURPOSE:To obtain a specific monoclonal antibody suitable for the assay of ribonuclease inhibitor (RNI), by a method wherein ribonuclease inhibitor is sampled from an organ tissue of a rat or the like to be dosed to a different animal to immunize and a fused cell is cultured between the antibody-produced cell obtained from the animal and a specific cell. CONSTITUTION:Ribonuclease inhibitor (RNI) is sampled from a cell of an organ such as liver of a man, an ox, a rat or the like. The RNI is hypodermically injected to another animal to immunize. An antibody-produced cell as spleen cell, lymph node cell or the like is obtained from the animal thus immunized. The cell is fused with a cell stock which is a myeloma cell from a mouse, rabbit or the like that lacks in hypoxanthinephosphoribosyl transferase with a 8-azaguanine resistance to clone high valence RNI-produced cell in the fused cell. The cell thus obtained is cultured or injected into an abdominal cavity to obtain RNI specific monoclonal antibody from a culture or abdominal dropsy. The use of the antibody can produce a monoclonal antibody that enables highly accurate immunological measurement of RNI without being obstructed even in a tissue with a high ribonuclease activity of a kidney, pancreas or the like.