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Background: Although selective serotonin reuptake inhibitors (SSRIs) are usually considered safe to use in patients with Parkinson’s disease (PD), there are mixed data about their effectiveness, and only a few investigations have led to a total improvement of depressive symptoms in patients with PD.We aimed to conduct a comprehensive systematic review and meta-analysis of all studies that investigated the effectiveness of SSRIs in treating depression in the context of PD.From its commencement to June 2024, the databases of MEDLINE via PubMed, Scopus, Embase, and Google Scholar were electronically searched for the relevant papers. All full-text journal articles assessing the effectiveness of SSRIs in treating depression in patients with PD were included. The tool developed by the Cochrane Collaboration was utilized to evaluate the bias risk. Data were analyzed utilizing a pair-wise comparison meta-analysis using the standardized mean difference.A total of 19 articles and 22 separate interventions were included. We found that SSRI treatment attenuated depression in patients with PD (1.242 standardized mean difference, 95% confidence interval 0.956, 1.529, p < 0.001). The general heterogeneity of the studies was medium (ϰ2 = 72.818, T2 = 0.317, df = 21, I2 = 71.15%, p < 0.001). The funnel plot was reasonably symmetrical. However, three studies were trimmed to the left of the mean. Begg’s test (p = 0.080), Egger’s test (p = 0.121), and funnel plot showed no significant risk of publication bias. The meta-regression showed that the treatment effect increased as a function of paroxetine treatment duration (slope p = 0.001) but decreased as a function of sertraline treatment duration (slope p = 0.019).There are few controlled antidepressant trials on the PD population, even though patients with PD frequently experience depression and use antidepressants. Clinical studies that are larger and better structured are needed in the future to determine if antidepressants are useful for treating patients with PD with depression.Objectives: Although selective serotonin reuptake inhibitors (SSRIs) are usually considered safe to use in patients with Parkinson’s disease (PD), there are mixed data about their effectiveness, and only a few investigations have led to a total improvement of depressive symptoms in patients with PD.We aimed to conduct a comprehensive systematic review and meta-analysis of all studies that investigated the effectiveness of SSRIs in treating depression in the context of PD.From its commencement to June 2024, the databases of MEDLINE via PubMed, Scopus, Embase, and Google Scholar were electronically searched for the relevant papers. All full-text journal articles assessing the effectiveness of SSRIs in treating depression in patients with PD were included. The tool developed by the Cochrane Collaboration was utilized to evaluate the bias risk. Data were analyzed utilizing a pair-wise comparison meta-analysis using the standardized mean difference.A total of 19 articles and 22 separate interventions were included. We found that SSRI treatment attenuated depression in patients with PD (1.242 standardized mean difference, 95% confidence interval 0.956, 1.529, p < 0.001). The general heterogeneity of the studies was medium (ϰ2 = 72.818, T2 = 0.317, df = 21, I2 = 71.15%, p < 0.001). The funnel plot was reasonably symmetrical. However, three studies were trimmed to the left of the mean. Begg’s test (p = 0.080), Egger’s test (p = 0.121), and funnel plot showed no significant risk of publication bias. The meta-regression showed that the treatment effect increased as a function of paroxetine treatment duration (slope p = 0.001) but decreased as a function of sertraline treatment duration (slope p = 0.019).There are few controlled antidepressant trials on the PD population, even though patients with PD frequently experience depression and use antidepressants. Clinical studies that are larger and better structured are needed in the future to determine if antidepressants are useful for treating patients with PD with depression.Methods: Although selective serotonin reuptake inhibitors (SSRIs) are usually considered safe to use in patients with Parkinson’s disease (PD), there are mixed data about their effectiveness, and only a few investigations have led to a total improvement of depressive symptoms in patients with PD.We aimed to conduct a comprehensive systematic review and meta-analysis of all studies that investigated the effectiveness of SSRIs in treating depression in the context of PD.From its commencement to June 2024, the databases of MEDLINE via PubMed, Scopus, Embase, and Google Scholar were electronically searched for the relevant papers. All full-text journal articles assessing the effectiveness of SSRIs in treating depression in patients with PD were included. The tool developed by the Cochrane Collaboration was utilized to evaluate the bias risk. Data were analyzed utilizing a pair-wise comparison meta-analysis using the standardized mean difference.A total of 19 articles and 22 separate interventions were included. We found that SSRI treatment attenuated depression in patients with PD (1.242 standardized mean difference, 95% confidence interval 0.956, 1.529, p < 0.001). The general heterogeneity of the studies was medium (ϰ2 = 72.818, T2 = 0.317, df = 21, I2 = 71.15%, p < 0.001). The funnel plot was reasonably symmetrical. However, three studies were trimmed to the left of the mean. Begg’s test (p = 0.080), Egger’s test (p = 0.121), and funnel plot showed no significant risk of publication bias. The meta-regression showed that the treatment effect increased as a function of paroxetine treatment duration (slope p = 0.001) but decreased as a function of sertraline treatment duration (slope p = 0.019).There are few controlled antidepressant trials on the PD population, even though patients with PD frequently experience depression and use antidepressants. Clinical studies that are larger and better structured are needed in the future to determine if antidepressants are useful for treating patients with PD with depression.Results: Although selective serotonin reuptake inhibitors (SSRIs) are usually considered safe to use in patients with Parkinson’s disease (PD), there are mixed data about their effectiveness, and only a few investigations have led to a total improvement of depressive symptoms in patients with PD.We aimed to conduct a comprehensive systematic review and meta-analysis of all studies that investigated the effectiveness of SSRIs in treating depression in the context of PD.From its commencement to June 2024, the databases of MEDLINE via PubMed, Scopus, Embase, and Google Scholar were electronically searched for the relevant papers. All full-text journal articles assessing the effectiveness of SSRIs in treating depression in patients with PD were included. The tool developed by the Cochrane Collaboration was utilized to evaluate the bias risk. Data were analyzed utilizing a pair-wise comparison meta-analysis using the standardized mean difference.A total of 19 articles and 22 separate interventions were included. We found that SSRI treatment attenuated depression in patients with PD (1.242 standardized mean difference, 95% confidence interval 0.956, 1.529, p < 0.001). The general heterogeneity of the studies was medium (ϰ2 = 72.818, T2 = 0.317, df = 21, I2 = 71.15%, p < 0.001). The funnel plot was reasonably symmetrical. However, three studies were trimmed to the left of the mean. Begg’s test (p = 0.080), Egger’s test (p = 0.121), and funnel plot showed no significant risk of publication bias. The meta-regression showed that the treatment effect increased as a function of paroxetine treatment duration (slope p = 0.001) but decreased as a function of sertraline treatment duration (slope p = 0.019).There are few controlled antidepressant trials on the PD population, even though patients with PD frequently experience depression and use antidepressants. Clinical studies that are larger and better structured are needed in the future to determine if antidepressants are useful for treating patients with PD with depression.Conclusions: Although selective serotonin reuptake inhibitors (SSRIs) are usually considered safe to use in patients with Parkinson’s disease (PD), there are mixed data about their effectiveness, and only a few investigations have led to a total improvement of depressive symptoms in patients with PD.We aimed to conduct a comprehensive systematic review and meta-analysis of all studies that investigated the effectiveness of SSRIs in treating depression in the context of PD.From its commencement to June 2024, the databases of MEDLINE via PubMed, Scopus, Embase, and Google Scholar were electronically searched for the relevant papers. All full-text journal articles assessing the effectiveness of SSRIs in treating depression in patients with PD were included. The tool developed by the Cochrane Collaboration was utilized to evaluate the bias risk. Data were analyzed utilizing a pair-wise comparison meta-analysis using the standardized mean difference.A total of 19 articles and 22 separate interventions were included. We found that SSRI treatment attenuated depression in patients with PD (1.242 standardized mean difference, 95% confidence interval 0.956, 1.529, p < 0.001). The general heterogeneity of the studies was medium (ϰ2 = 72.818, T2 = 0.317, df = 21, I2 = 71.15%, p < 0.001). The funnel plot was reasonably symmetrical. However, three studies were trimmed to the left of the mean. Begg’s test (p = 0.080), Egger’s test (p = 0.121), and funnel plot showed no significant risk of publication bias. The meta-regression showed that the treatment effect increased as a function of paroxetine treatment duration (slope p = 0.001) but decreased as a function of sertraline treatment duration (slope p = 0.019).There are few controlled antidepressant trials on the PD population, even though patients with PD frequently experience depression and use antidepressants. Clinical studies that are larger and better structured are needed in the future to determine if antidepressants are useful for treating patients with PD with depression. [ABSTRACT FROM AUTHOR]

• Fungal β-diversity significantly differed between the DW and NW treatments. • No significant bacterial β-diversity difference between the DW and NW treatments. • Compared to the CK, the NW treatment significantly increased bacterial ACE, Chao1 and Shannon diversity indices. • Compared to the CK, the NW treatment significantly increased fungal ACE diversity. • AP and TN are the main factors affecting bacterial Shannon diversity after DW and NW. The global temperature is continuously rising, and the impacts of nighttime warming (NW) and daytime warming (DW) on ecosystems have drawn widespread attention. However, most studies on the effects of daytime and nighttime warming on ecosystems have focused primarily on aboveground processes, but little is known about how they affect underground processes, particularly soil microorganisms. Therefore, we examined the effects of daytime and nighttime experimental warming (CK: control, DW: daytime warming, NW: nighttime warming, DW + NW: daily warming) on soil bacterial and fungal diversities at the Experimental Station of Zengcheng Forestry Science Research Institute in Guangdong, China. The results showed that, compared with the CK treatment, the NW rather than DW treatment significantly increased the abundance-based coverage estimator (ACE) diversity index of bacteria and fungi. Fungal beta diversity significantly differed between the DW and NW treatments, while there was no significant difference in bacterial beta diversity. Our research indicated that the NW treatment creates a more favourable microenvironment than the DW treatment, accelerating the mineralization of soil carbon, nitrogen, and phosphorus nutrients, which may be the reason for changes in microbial diversity. Our study provides important theoretical support and practical guidance for predicting the impact of global climate change on the diversity of microbial ecosystems. [ABSTRACT FROM AUTHOR]

Anshen Dingzhi prescription (ADP), which was first published in the masterpiece of traditional Chinese Medicine in the Qing Dynasty, " Yi Xue Xin Wu " (1732 CE), is documented to interrupt panic-related disorders. However, the mechanism of its action is still not clear. This study aims to investigate the effects of ADP on post-traumatic stress disorder (PTSD)-like behaviors and explore the mechanism from perspective of sirtuin1 (SIRT1)-peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α)-dependent mitochondrial function. The changes of SIRT1-PGC-1α signal and mitochondrial function were evaluated in the hippocampus of mice receiving single prolonged stress (SPS). Later, the roles of this signaling pathway played in fear memory generalization and anxiety-like behavior in SPS mice was investigated using two agonists of this signaling pathway. On this basis, the effects of ADP (36.8 mg/kg) with definite therapeutic effects, on mitochondrial function were investigated and further confirmed by a SIRT1 inhibitor. Finally, the possible components of ADP targeting PGC-1α were monitored through bioinformatics. Compared with control mice, SIRT1-PGC-1α signal in the hippocampus was impaired in SPS mice, accompanied with dysfunction of mitochondria and abnormal expression of synaptic proteins. The agonists of SIRT1-PGC-1α signal, ZLN005, as well as resveratrol improved the behavioral changes of mice caused by SPS, reversed the decline of proteins in SIRT1-PGC-1α signal, mitochondrial dysfunction, and the abnormal expression of synaptic proteins. The fingerprint was established for the quality control of ADP. At a dose of 36.8 mg/kg, ADP could prevent fear memory generalization and anxiety-like behavior in SPS mice. Mechanically, ADP promoted SIRT1-PGC-1α signal and repaired mitochondrial function. Importantly, SIRT1 inhibitor, selisistat eliminated the ameliorative effects of ADP on behavioral and mitochondrial function. Through molecular docking simulation, the brain-entering components of ADP, including malkangunin, Rg5, fumarine, frutinone A, celabenzine, and inermin had high binding energy with PGC-1α. Dysfunction of SIRT1-PGC-1α-dependent mitochondrial function is attributed to SPS-triggered fear generalization and anxiety-like behavior, and ADP could improve PTSD-like behaviors likely through activating this signaling pathway. [Display omitted] • SIRT1-PGC-1α signal was inactivated in the hippocampus of SPS mice. • Activation of SIRT1-PGC-1α signal prevented fear generalization. • ADP prevented fear generalization and anxiety-like behaviors of SPS mice. • ADP repairs hippocampal SIRT1-PGC-1α signal. [ABSTRACT FROM AUTHOR]

Background: Age-related cognitive decline has a significant impact on the health and longevity of older adults. Circulating very long-chain saturated fatty acids (VLSFAs) may actively contribute to the improvement of cognitive function. The objective of this study was to investigate the associations between arachidic acid (20:0), docosanoic acid (22:0), tricosanoic acid (23:0), and lignoceric acid (24:0) with cognitive function in older adults. Methods: This study used a dataset derived from the 2011–2014 National Health and Nutrition Examination Survey (NHANES). A total of 806 adults (≥ 60 years) were included who underwent comprehensive cognitive testing and plasma fatty acid measurements. Multivariable linear regression, restricted cubic spline (RCS), and interaction analyses were used to assess associations between VLSFAs and cognitive function. Partial Spearman' s correlation analysis was used to examine the correlations between VLSFAs and palmitic acid (16:0), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, triglycerides, systemic inflammatory markers, and dietary nutrients. Results: Multivariable linear regression analysis, adjusting for sociodemographic, clinical conditions, and lifestyle factors, showed that 22:0 and 24:0 levels were positively associated with better global cognitive function (β = 0.37, 95% confidence interval [CI] = 0.01, 0.73; β = 0.73, 95% CI = 0.29, 1.2, respectively) as well as better CEARD-DR Z-score (β = 0.82, 95% CI = 0.36, 1.3 and β = 1.2, 95% CI = 0.63, 1.8, respectively). RCS analysis showed linear associations between higher 22:0 and 24:0 levels and better cognitive performance in both global cognitive function and CERAD-DR tests. Conclusions: The study suggests that higher levels of 22:0 and 24:0 are associated with better global cognitive function in older adults. 22:0 and 24:0 may be important biomarkers for recognizing cognitive impairment, and supplementation with specific VLSFAs (22:0 and 24:0) may be an important intervention to improve cognitive function. Further studies are needed to elucidate the underlying biological mechanisms between VLSFAs and cognitive function. [ABSTRACT FROM AUTHOR]

BackgroundMethodsResultsConclusionsThe Prognostic Nutritional Index (PNI) has been described as a useful screening tool for patient prognosis in several diseases. As a potential diagnostic index, it has attracted the interest of many physicians. However, the correlation between the PNI and post-stroke cognitive impairment (PSCI) remains unclear.A total of 285 patients with acute ischemic stroke were included. PNI was assessed as serum albumin (g/L) + 5× lymphocyte count (109/L) and was dichotomized according to the prespecified cut-off points 48.43 for the high and low groups. PSCI was defined as Mini-Mental State Examination (MMSE) < 27 at the 6–10 months follow-up. Multiple logistic regression and linear regression analyses were performed to examine the association between PNI and cognitive outcomes.A low PNI was independently associated with PSCI after adjusting for age, sex, education, National Institutes of Health Stroke Scale (NIHSS), deep white matter hyperintensity (DWMH), and stroke history (odds ratio [OR]: 2.158; 95% confidence interval [CI]: 1.205–3.863). The PNI scores were significantly associated with MMSE and attention domain (β = 0.113, p = 0.006; β = 0.109, p = 0.041, respectively). The PNI improved the model’s discrimination when added to the model with other clinical risk factors.A low PNI was independently associated with the occurrence of PSCI and the PNI scores were specifically associated with the scores of global cognition and attention domain. It can be a promising and straightforward screening indicator to identify the person with impaired immune-nutritional status at higher risk of PSCI. [ABSTRACT FROM AUTHOR]

Polyporaceae is an important fungal family that has been a source of natural products with a range of pharmaceutical activities in China. In our previous study, two polysaccharides, PCWPW and PCWPS, with significant antioxidant and antidepressant activity were obtained from Poria cocos. In this study, we evaluated their potential molecular mechanisms in the immunomodulation of macrophages. PCWPW and PCWPS were characterized by GC–MS analysis to contain 1,3-linked Glcp. ELISA assays results demonstrated that the secretion of TNF-α was significantly enhanced by PCWPW/PCWPS. RNA-seq data demonstrated that PCWPS treatment modulated the expression of immune-related genes in macrophages, which was further confirmed by RT-qPCR assays. The activation of TNF-α secretion was found to be mannose receptor (MR) dependent and suppressed by MR inhibitor pretreatment. Moreover, the amount of TNF-α cytokine secretion in PCWPW/PCWPS-induced RAW264.7 cells was decreased when pretreated with NF-κB or MAPK signaling pathway inhibitors. Collectively, our results suggested that PCWPW and PCWPS possessed immunomodulatory activity that regulates TNF-α expression through the NF-κB/MAPK signaling pathway by binding to mannose receptors. Therefore, PCWPW and PCWPS isolated from Poria cocos have potential as drug candidates for immune-related disease treatment. [ABSTRACT FROM AUTHOR]

In recent years, deep learning approaches have shown remarkable advancements in Multivariate Time Series Classification (MTSC) tasks. However, the existing approaches primarily focus on capturing the long-term correlations of time series or identifying local key sequence fragments, inevitably neglecting the synergistic properties between global and local components. Additionally, most representation learning methods for MTSC rely on self-supervised learning, which limits their ability to fully exploit label information. Hence, this paper proposes a novel approach termed Dual-Stream Encoder and Dual-Level Contrastive Learning Network (DSDCLNet), which integrates a Dual-Stream Encoder (DSE) and Dual-level Contrastive Learning (DCL). First, to extract multiscale local-global features from multivariate time series data, we employ a DSE architecture comprising an Attention-Gated Recurrent Unit (AGRU) and a Dual-layer Multiscale Convolutional Neural Network (DMSCNN). Specifically, DMSCNN consists of a series of multi-scale convolutional layers and a max pooling layer. Second, to maximize the utilization of label information, a new loss function is designed, which combines classification loss, instance-level contrastive loss, and temporal-level contrastive loss. Finally, experiments are conducted on the UEA datasets and the results demonstrate that DSDCLNet achieves the highest average accuracy of 0.77, outperforming traditional approaches, deep learning approaches, and self-supervised approaches on 30, 23, and 27 datasets, respectively. [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) in sepsis is a vital and dangerous organ failure caused by an infection-induced dysregulation of the host reaction. Malvidin possesses significant anti-inflammatory and antioxidant bioactivities. This study explored the critical roles of malvidin in sepsis AKI and the crosstalk among mitochondrial function, nucleotide-binding oligomerization-like receptor 3 (NLRP3) inflammasome and nuclear factor erythroid 2 (Nrf2) signaling pathway. First, C57BL/6 mice were administered lipopolysaccharide intraperitoneally for 6 h to create an AKI model of sepsis. Hematoxylin-eosin staining and serum biomarker assays showed that malvidin protected from AKI in sepsis. Real-time fluorescence quantitative polymerase chain reaction analysis revealed that malvidin was able to inhibit inflammatory cytokines and mediators. Western blot assays indicated that malvidin suppressed NLRP3 inflammasome activation and enhanced antioxidant properties. Additionally, human renal tubular epithelial cells were stimulated by lipopolysaccharide/adenosine triphosphate to establish an NLRP3 inflammasome activation model in vitro , and in line with findings in vivo , malvidin significantly inhibited NLRP3 inflammasome activation. Furthermore, our data indicate that malvidin restored mitochondrial quality and function, reduced reactive oxygen species production, increased mitochondrial membrane potential, enhanced mitochondrial DNA copy number, and promoted peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) nuclear translocation. Moreover, inhibitor blockade assays indicated that both PGC-1α and Nrf2 affected the inhibition of the NLRP3 inflammasome by malvidin. Finally, immunoprecipitation assays showed that malvidin promoted PGC-1α and Nrf2 interactions. Overall, malvidin alleviated lipopolysaccharide-induced sepsis AKI, improved mitochondrial function and mitochondrial biogenesis, and inhibited the NLRP3 inflammasome through the PGC-1α/Nrf2 signaling pathway, suggesting that malvidin might translate into clinical applications for sepsis AKI therapy. • Mv inhibited NLRP3 inflammasome and oxidative stress both in vitro and in vivo. • Mv reduced mitochondrial dysfunction and promoted mitochondrial biogenesis. • Mv's inhibitory impact on NLRP3 inflammasome activation was regulated by the PGC-1/Nrf2 signaling pathway. • Mv can facilitate the interaction between PGC-1α and Nrf2. [ABSTRACT FROM AUTHOR]