bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of SARS-CoV-2 infection on asthma patients
Authors: Li Xin-yu , Wang Jing-bing , An Hong-bang , Wen Ming-zhe , You Jian-xiong , Yang Xi-tao 
Published: August 2022

BackgroundSARS-CoV-2 causes coronavirus disease 2019 (COVID-19), a new coronavirus pneumonia, and containing such an international pandemic catastrophe remains exceedingly difficult. Asthma is a severe chronic inflammatory airway disease that is becoming more common around the world. However, the link between asthma and COVID-19 remains unknown. Through bioinformatics analysis, this study attempted to understand the molecular pathways and discover potential medicines for treating COVID-19 and asthma.MethodsTo investigate the relationship between SARS-CoV-2 and asthma patients, a transcriptome analysis was used to discover shared pathways and molecular signatures in asthma and COVID-19. Here, two RNA-seq data (GSE147507 and GSE74986) from the Gene Expression Omnibus were used to detect differentially expressed genes (DEGs) in asthma and COVID-19 patients to find the shared pathways and the potential drug candidates.ResultsThere were 66 DEGs in all that were classified as common DEGs. Using a protein-protein interaction (PPI) network created using various bioinformatics techniques, five hub genes were found. We found that asthma has some shared links with the progression of COVID-19. Additionally, protein-drug interactions with common DEGs were also identified in the datasets.ConclusionWe investigated possible links between COVID-19 and asthma using bioinformatics databases, which might be useful in treating COVID-19 patients. More studies on populations affected by these diseases are needed to elucidate the molecular mechanism behind their association.
Non-linear association between serum spermidine and mild cognitive impairment: Results from a cross-sectional and longitudinal study
Authors: Xu Jiahui , Sun Zhaoqing , Zhang Rui , Li Ruixue , Yu Zhecong , Zhang Qianlong , Ma Yanan , Xing Fuguo , Zheng Liqiang 
Published: August 2022

BackgroundAlthough animal studies show that spermidine (SPD) affects cognitive function, the relevant evidence among humans is limited. We aim to examine the association between serum SPD levels and cognitive performance.Materials and MethodsWe conducted a cross-sectional and longitudinal study including a baseline and one follow-up survey. The baseline survey was conducted from June 2019 to August 2019, while the follow-up survey was conducted from June 2021 to August 2021. We analyzed 3,774 adult participants aged &gt;35 years, who had no history of dementia.ResultsThe mean (SD) age of the participants was 57.4 (9.8) years. Relative to the first tertile, the multivariate-adjusted ORs (95% CIs) of mild cognitive impairment (MCI) for the second and third tertile groups were 0.78 (0.65, 0.93) and 0.80 (0.67, 0.96), respectively. Restricted cubic spline models show that there is a non-linear association between SPD and MCI. In line with cross-sectional findings, the longitudinal study showed that a high SPD concentration may indicate a lower risk of MCI [ORs (95% CIs) for the third tertile of 0.62 (0.39, 0.99)].ConclusionOur findings suggest that SPD is favorable for cognitive function. Monitoring the SPD levels may help reduce the incidence of MCI, hence decreasing the burden of MCI.
Spikes and High Frequency Oscillations in Lateral Neocortical Temporal Lobe Epilepsy: Can They Predict the Success Chance of Hippocampus-Sparing Resections?
Authors: Maccabeo Alessandra , van 't Klooster Maryse A. , Schaft Eline , Demuru Matteo , Zweiphenning Willemiek , Gosselaar Peter , Gebbink Tineke , Otte Wim M. , Zijlmans Maeike 
Published: August 2022

PurposeWe investigated the distribution of spikes and HFOs recorded during intraoperative electrocorticography (ioECoG) and tried to elaborate a predictive model for postsurgical outcomes of patients with lateral neocortical temporal lobe epilepsy (TLE) whose mesiotemporal structures are left in situ.MethodsWe selected patients with temporal lateral neocortical epilepsy focus who underwent ioECoG-tailored resections without amygdalo–hippocampectomies. We visually marked spikes, ripples (80–250 Hz), and fast ripples (FRs; 250–500 Hz) on neocortical and mesiotemporal channels before and after resections. We looked for differences in event rates and resection ratios between good (Engel 1A) and poor outcome groups and performed logistic regression analysis to identify outcome predictors.ResultsFourteen out of 24 included patients had a good outcome. The poor-outcome patients showed higher rates of ripples on neocortical channels distant from the resection in pre- and post-ioECoG than people with good outcomes (ppre = 0.04, ppost = 0.05). Post-ioECoG FRs were found only in poor-outcome patients (N = 3). A prediction model based on regression analysis showed low rates of mesiotemporal post-ioECoG ripples (ORmesio = 0.13, pmesio = 0.04) and older age at epilepsy onset (OR = 1.76, p = 0.04) to be predictors of good seizure outcome.ConclusionHFOs in ioECoG may help to inform the neurosurgeon of the hippocampus-sparing resection success chance in patients with lateral neocortical TLE.
Brainstem activation of GABAB receptors in the nucleus tractus solitarius increases gastric motility
Authors: Bellusci Lorenza , Kim Elizabeth , Garcia DuBar Selena , Gillis Richard A. , Vicini Stefano , Sahibzada Niaz 
Published: August 2022

Background and aimLocal GABAergic signaling in the dorsal vagal complex (DVC) is essential to control gastric function. While the inhibitory GABAA receptor action on motility in the DVC is well-documented, the role of the GABAB receptor on gastric function is less well-established. Microinjection of baclofen, a selective GABAB receptor agonist, in the dorsal motor nucleus of the vagus (DMV) increases gastric tone and motility, while the effect on motility in the nucleus tractus solitarius (NTS) needs to be investigated. Previous in vitro studies showed that GABAB receptors exert a local inhibitory effect in unidentified NTS neurons. Since the NTS and DMV nuclei have differential control of gastric motility, we compared GABAB receptor activation in the NTS to that reported in the DMV. We microinjected baclofen unilaterally in the NTS while monitoring intragastric pressure and compared its action to optogenetic activation of somatostatin (SST) neurons in transgenic sst-Cre::channelrhodopsin-2 (ChR2) mice. We also performed patch-clamp recordings from SST and DMV neurons in brainstem slices from these mice.MethodsIn vivo drug injections and optogenetic stimulation were performed in fasted urethane/α-chloralose anesthetized male mice. Gastric tone and motility were monitored by an intragastric balloon inserted in the antrum and inflated with warm water to provide a baseline intragastric pressure (IGP). Coronal brainstem slices were obtained from the sst-Cre::ChR2 mice for interrogation with optogenetics and pharmacology using electrophysiology.ResultsThe unilateral microinjection of baclofen into the NTS caused a robust increase in gastric tone and motility that was not affected by ipsilateral vagotomy. Optogenetic activation of SST neurons that followed baclofen effectively suppresses the gastric motility in vivo. In brain slices, baclofen suppressed spontaneous and light-activated inhibitory postsynaptic currents in SST and gastrointestinal-projection DMV neurons and produced outward currents.ConclusionOur results show that GABAB receptors in the NTS strongly increase gastric tone and motility. Optogenetic stimulation in vivo and in vitro suggests that these receptors activated by baclofen suppress the glutamatergic sensory vagal afferents in the NTS and also inhibit the interneurons and the inhibitory neurons that project to the DMV, which, in turn, increase motility via a cholinergic excitatory pathway to the stomach.
A putative causality of vitamin D in common diseases: A mendelian randomization study
Authors: Liu Hui , Shen Xudan , Yu Tunan , Wang Yifan , Cai Sheng , Jiang Xia , Cai Xiujun 
Published: August 2022

BackgroundsVitamin D is considered as a nutrient protecting individuals against an array of diseases based on observational studies. Such a protective effect, however, has not been demonstrated by randomized controlled trials. This study aims to explore a putative causal role of vitamin D in common diseases through a two-sample Mendelian randomization (MR) framework.MethodsCirculating vitamin D was predicted by 41 genetic variants discovered in European populations. Common diseases were verified through two ways, using information from Japanese patients of Biobank Japan and using information from European patients of FinnGen project. We additionally validated the results by replacing vitamin D-associated instrumental variables (IVs) of European population with that of an independent Japanese population and of an independent Indian population. Inverse-variance weighted method was used as the primary analytical approach while a series of MR methods including MR-Egger regression, weighted median, maximum likelihood, MR-PRESSO and multivariate MR were adopted to guarantee MR model assumptions and to detect horizontal pleiotropy.ResultsGenetically predicted vitamin D was significantly associated with an increased risk of Graves' disease (OR = 1.71, 95%CI: 1.25–2.33, P = 0.001) and cataract (OR = 1.14, 95%CI: 1.03–1.28, P = 0.016); while with a decreased risk of esophageal cancer (OR = 0.66, 95%CI: 0.46–0.93, P = 0.019). This significant causal link between vitamin D and cataract was validated replacing IVs identified in the European population with those from Japanese population. No notable associations of vitamin D with other diseases were observed.ConclusionsOur findings indicate a potential causal role of vitamin D in common diseases, which needs further validation.
Hot flushes and sweating, sleep problems, joint and muscular discomfort, and physical and mental exhaustion in breast cancer survivors during the first 24 months of tamoxifen therapy: a prospective observational study
Authors: Sung Sumi , Min Yul Ha , Park Seul Ki , Lee Sae Byul 
Published: August 2022

PurposeThis study aimed to explore symptom trajectories over 24 months for hot flushes and sweating, sleep problems, joint and muscular discomfort, and physical and mental exhaustion experienced by premenopausal women diagnosed with tamoxifen-treated breast cancer.MethodsA total of 104 patients participated in the study. The menopausal symptoms were examined using the Menopausal Rating Scale at baseline, 3–6, 12, and 18–24 months after initiating tamoxifen. The changes over four time points were analyzed using repeated measures analysis of variance. The chi-square test was used to examine the differences between “no symptom-to-mild” and “moderate-to-extremely severe” 3–6 months after initiating tamoxifen according to the patients’ chemotherapy treatment experiences.ResultsAll menopausal symptoms occurred in &gt; 70% of patients with breast cancer and persisted until 24 months. More than 50% of patients experienced four menopausal symptoms, with at least two at a serious severity level after initiating tamoxifen. Hot flushes and sweating occurred in the highest number of patients, recording high scores. Sleep problems and physical and mental exhaustion exhibited relatively high scores, even before tamoxifen initiation. There were significant changes over four time points in all symptoms. Young patients aged &lt; 40 years experienced more severe sleep problems, and patients who had previously received chemotherapy experienced more severe joint and muscular discomfort.ConclusionsThis study’s findings may assist in alerting healthcare providers to menopausal symptoms that develop during tamoxifen therapy and the need for early and active intervention to minimize symptom occurrence and distress.
Construction of an immune-related gene signature for the prognosis and diagnosis of glioblastoma multiforme
Authors: Yu Ziye , Yang Huan , Song Kun , Fu Pengfei , Shen Jingjing , Xu Ming , Xu Hongzhi 
Published: August 2022

BackgroundIncreasing evidence has suggested that inflammation is related to tumorigenesis and tumor progression. However, the roles of immune-related genes in the occurrence, development, and prognosis of glioblastoma multiforme (GBM) remain to be studied.MethodsThe GBM-related RNA sequencing (RNA-seq), survival, and clinical data were acquired from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), Chinese Glioma Genome Atlas (CGGA), and Gene Expression Omnibus (GEO) databases. Immune-related genes were obtained from the Molecular Signatures Database (MSigDB). Differently expressed immune-related genes (DE-IRGs) between GBM and normal samples were identified. Prognostic genes associated with GBM were selected by Kaplan–Meier survival analysis, Least Absolute Shrinkage and Selection Operator (LASSO)-penalized Cox regression analysis, and multivariate Cox analysis. An immune-related gene signature was developed and validated in TCGA and CGGA databases separately. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to explore biological functions of the signature. The correlation between immune cell infiltration and the signature was analyzed by single-sample gene set enrichment analysis (ssGSEA), and the diagnostic value was investigated. The gene set enrichment analysis (GSEA) was performed to explore the potential function of the signature genes in GBM, and the protein–protein interaction (PPI) network was constructed.ResultsThree DE-IRGs [Pentraxin 3 (PTX3),TNFSF9, and bone morphogenetic protein 2 (BMP2)] were used to construct an immune-related gene signature. Receiver operating characteristic (ROC) curves and Cox analyses confirmed that the 3-gene-based prognostic signature was a good independent prognostic factor for GBM patients. We found that the signature was mainly involved in immune-related biological processes and pathways, and multiple immune cells were disordered between the high- and low-risk groups. GSEA suggested thatPTX3andTNFSF9were mainly correlated with interleukin (IL)-17 signaling pathway, nuclear factor kappa B (NF-κB) signaling pathway, tumor necrosis factor (TNF) signaling pathway, and Toll-like receptor signaling pathway, and the PPI network indicated that they could interact directly or indirectly with inflammatory pathway proteins. Quantitative real-time PCR (qRT-PCR) indicated that the three genes were significantly different between target tissues.ConclusionThe signature with three immune-related genes might be an independent prognostic factor for GBM patients and could be associated with the immune cell infiltration of GBM patients.
Impact of maternal gestational weight gain in twin pregnancies on early childhood obesity risk: A longitudinal birth cohort study
Authors: Li Sisi , Qiu Yuhan , Yuan Xi , Zhang Qin , Kilby Mark D. , Saffery Richard , Baker Philip N. , Wen Li , Tong Chao , Qi Hongbo 
Published: August 2022

ObjectivesTo investigate the impact of gestational weight gain (GWG) on the body mass index-for-age z score (BAZ) and obesity risk among twin offspring.MethodsThis study included 263 women who were pregnant with twins and their offspring. Maternal GWG was measured in each trimester, and infant weight and length were measured at 6, 12, and 24 months.ResultsTotal GWG was positively correlated with offspring birthweight and BAZ at 6, 12 and 24 months [adjusted β 0.013 (95% CI: 0.008–0.019), 0.028 (95% CI: 0.005–0.050), 0.033 (95% CI: 0.010–0.056) and 0.025 (95% CI: 0.004–0.047), respectively]. Excessive total GWG was related to an increased relative risk (RR) of large for gestational age (LGA) and overweight at 6 and 12 months. Only the second trimester gestational weight gain rate (GWGR) was positively correlated with birthweight (adjusted β 0.380, 95% CI: 0.256–0.504), and RRs of 6.818 (95% CI: 1.568–29.642) and 2.852 (95% CI: 1.466–5.548) were found for LGA and overweight at 12 months, respectively.ConclusionsTotal GWG and the second trimester GWGR were correlated with BAZ and overweight/obesity risk in twin offspring; the impact was obvious in the first year of life and gradually disappeared over time.Clinical trial registrationChiCTR-OOC-16008203, Registered on 1 April 2016 at the Chinese Clinical Trial Registry.
Protective effect of Astragaloside IV on chronic intermittent hypoxia-induced vascular endothelial dysfunction through the calpain-1/SIRT1/AMPK signaling pathway
Authors: Zhao Fang , Meng Yan , Wang Yue , Fan Siqi , Liu Yu , Zhang Xiangfeng , Ran Chenyang , Wang Hongxin , Lu Meili 
Published: August 2022

Vascular endothelial dysfunction (VED) is linked with the pathogenesis of obstructive sleep apnea (OSA) comorbidities, such as cardiovascular disease. Astragaloside IV (As-IV) has exhibited significant improvement for endothelial dysfunction. Nonetheless, the protective mechanism is not clear. Therefore, the present study investigated the potential mechanism of As-IV on VED. Calpain-1 knockout and wild-type C57BL/6 mice exposed to chronic intermittent hypoxia (CIH) were established and treated with As-IV (40, 80 mg/kg) for 4 weeks. Human coronary artery endothelial cells (HCAECs) subjected to CIH exposure were pretreated with As-IV, MDL-28170 (calpain-1 inhibitor) and SRT1720 (SIRT1 activator) for 48 h in vitro. The endothelial function, inflammation, oxidative stress and mitochondrial function were measured to evaluate VED. Our data revealed that As-IV treatment ameliorated CIH-induced endothelial-dependent vasomotion and augmented nitric oxide (NO) production. As-IV administration suppressed the secretion of inflammation, oxidative stress and mitochondrial dysfunction. As-IV treatment reduced the expression of calpain-1 and restored the downregulated expression of SIRT1 and Thr172 AMPK and Ser1177 eNOS phosphorylation. The effects of calpain-1 knockout and SRT1720 were similar to the effect of As-IV on VED. These findings demonstrated that As-IV ameliorated VED induced by chronic intermittent hypoxia via the calpain-1/SIRT1/AMPK signaling pathway.
Osteocalcin levels decrease during the treatment of an acute depressive episode
Authors: Bartečků Elis , Hořínková Jana , Křenek Pavel , Damborská Alena , Tomandl Josef , Tomandlová Marie , Kučera Jan , Fialová Kučerová Jana , Bienertová-Vašků Julie 
Published: August 2022

ObjectivesOsteocalcin is a protein secreted by osteoblasts with a versatile endocrine role. Several domains in which it plays a role—stress response, monoamine synthesis, and cognitive functioning—are implicated also in the pathophysiology of major depressive disorder. In search of possible objective biomarkers of depression, the aim of the study was to assess the relationship between osteocalcin and depressive symptoms during the treatment of depressive episode.MethodsThe study included female inpatients with at least moderate depressive episode. In these patients, depression severity was measured using the Montgomery-Åsberg Depression Rating Scale (MADRS), and osteocalcin levels were assessed before the stabilization of antidepressive treatment and after 6 weeks. Relationships between osteocalcin levels and symptoms were analyzed with mixed-effect and linear models, taking into account age, menopausal status, and body mass index.ResultsIn 11 out of 13 enrolled inpatients, osteocalcin levels decreased during the first 6 weeks of treatment; this decrease was significant according to the mixed-effects model (t = −2.345, p = 0.019). According to the linear model, this decrease was significantly associated with reduction in depressive symptom severity (t = 2.673, p = 0.028). Osteocalcin was not associated with initial depressive symptom severity, and initial osteocalcin levels did not predict response to treatment. Limitations of the study include low sample size and inclusion of both pre- and postmenopausal women of various ages.ConclusionsThis preliminary study suggests that osteocalcin may be a candidate biomarker of antidepressive treatment response and that this topic warrants further investigation.
Reduced glucocorticoid receptor expression in blood mononuclear cells of patients with borderline personality disorder
Authors: López-Villatoro José Manuel , MacDowell Karina S. , Diaz-Marsá Marina , De La Torre-Luque Alejandro , Prittwitz Clara , Galvez-Merlin Alejandra , Leza Juan C. , Carrasco Jose L. 
Published: August 2022

IntroductionAbnormal cortisol suppression in borderline personality disorder has been consistently reported in previous studies, suggesting that a hypersensitivity response of the hypothalamic-pituitary-adrenal (HPA) axis might occur in these patients. In this study, the abnormalities of the cortisol response in borderline personality disorder (BPD) are investigated through the cellular expression of the glucocorticoid receptors (GR) in BPD patients and its relationship with traumatic experiences.MethodologySixty-nine male and female patients diagnosed with BPD and 62 healthy controls were studied. Peripheral blood mononuclear cells were obtained to investigate the expression of glucocorticoid receptors. Western blot was used to measure protein expression. Statistical correlations of GR expression with BPD clinical features and intensity of previous traumatic events were investigated.ResultsA significant decrease in the nuclear expression of glucocorticoid receptors was found in BPD patients compared to healthy controls in a regression analysis controlling for the effect of medication. GR expression decrease correlated significantly with clinical levels of anxiety and depression, but not with previous traumatic experiences in patients.ConclusionsBPD patients had a lower nuclear expression of glucocorticoid receptors than healthy controls, when it was controlled for the effect of medication. The reduced GR expression in BPD patients was not associated with previous traumatic events and might be associated with other aspects of BPD, such as emotional instability; more studies with larger samples of patients are still needed to understand the relevance and the implications of these findings.
Emphasis on heat strain to the ocular surface: A functional and clinical study of a modified goggle
Authors: Shao Yuting , Wu Jingzhong , Wu Peichen , Liu Xin , Shen Jiaqi , Zhang Li , Bi Yanlong 
Published: August 2022

PurposeThe limitations of conventional goggles have caused immense inconvenience, and even damage, to the physical and mental health of healthcare workers. Hence, this study aimed to build a modified goggle (MG) with better physical performance. The temperature-humidity index (THI) was used as an indicator to investigate the impact of goggle-related heat strain on the ocular surface.MethodsThe basic functions of antifog, anti-ultraviolet (UV), and anti-blue-light radiation capabilities were evaluated. Furthermore, the clinical impact on noninvasive keratography tear film break-up time (NIKBUT), intraocular pressure, central corneal thickness, Schirmer test I, and the Dry Eye-related Quality of life Score (DEQS) were assessed in 40 healthcare workers by comparing MG with standard goggles (SG). The relationships between THI and the above parameters were explored.ResultsMG had a significantly longer antifog time than SG (212.75 ± 23.95 vs. 138.35 ± 5.54 min, p &lt; 0.05), stronger antiultraviolet ability at 400 nm (99.99 vs. 45.55%), and optimal anti-blue-light performance at 440 nm (33.32 vs. 13.31%). Tear film stability after wearing the goggle was significantly worse than that before wearing them (p &lt; 0.05). Both goggles achieved moderate to strong heat strain, with a THI of &gt;80 at all timepoints. The MG group showed lower THI and DEQS and higher NIKBUT than the SG group (p &lt; 0.05). THI was significantly correlated with DEQS, NIKBUT, and real fogging time (r = 0.876, −0.532, −0.406; all p &lt; 0.05).ConclusionWearing goggles for a long time may cause heat strain to the eyes, thereby leading to eye discomfort and changes in the microenvironment of the ocular surface. Our MG exhibited better antifog, antiultraviolet, and optimal anti-blue-light performance and lower heat strain than SG, thus making it ideally suited for healthcare workers.