Green place rather than green space as a health determinant:A 20-year scoping review

Numerous scientific studies, applying different approaches, have provided evidence of the links between the environment and people's health. Green spaces have been the subject of research aimed at exploring their benefits as components of the urban environment. We investigated possible causal relationships between green spaces and health, with the aim of addressing the following question. Does the mere material presence of green spaces contribute to the health of people who live in its vicinity, or are the health-promoting qualities of green spaces attributed to the ability of people to actually see, access, and enjoy them? The latter view highlights the relational dimension of places, and it entails personal relationships with places which are imbued with psychological meaning and significance for those who visit and experience them. We reviewed relevant literature, comprising a total of 189 papers on thi

3-Hydroxyisobutyryl-CoA hydrolase involved in isoleucine catabolism regulates triacylglycerol accumulation in Phaeodactylum tricornutum

Since methylmalonyl-CoA epimerase appears to be absent in the majority of photosynthetic organisms, including diatoms, (S)-methylmalonyl-CoA, the intermediate of isoleucine (Ile) catabolism, cannot be metabolized to (R)methylmalonyl-CoA then to succinyl-CoA. In this study, propionyl-CoA carboxylase (PCC) RNAi silenced strains and 3-hydroxyisobutyryl-CoA hydrolase (HIBCH) overexpression strains were constructed to elucidate the Ile degradation pathway and its influence on lipid accumulation in Phaeodactylum tricornutum based on growth, neutral lipid content and metabolite profile analysis. Knockdown of PCC disturbed the metabolism of Ile through propionyl-CoA to methylmalonyl-CoA, as illustrated by much higher Ile content at day 6. However, Ile decreased to comparable levels to the wild-type at day 10. PCC silencing redirected propionyl-CoA to acetyl-CoA via a modified beta-oxidation pathway, and transcript levels for some branched-chain amino acid (BCAA) degradation-related genes, especially HIBCH, significantly upregulated in the PCC mutant, which enhanced the BCAA degradations and thus resulted in higher triacylglycerol (TAG) content. Overexpression of HIBCH accelerates Ile degradation and results in a lowered Ile content in the overexpression strains, thus enhancing carbon skeletons to the tricarboxylic acid cycle and giving rise to increasing TAG accumulation. Our study provides a good strategy to obtain high-lipid-yield transgenic diatoms by modifying the propionyl-CoA metabolism. This article is part of the themed issue &#39;The peculiar carbon metabolism in diatoms&#39;.</p

CLCA2 Interactor EVA1 Is Required for Mammary Epithelial Cell Differentiation.

CLCA2 is a p53-, p63-inducible transmembrane protein that is frequently downregulated in breast cancer. It is induced during differentiation of human mammary epithelial cells, and its knockdown causes epithelial-to-mesenchymal transition (EMT). To determine how CLCA2 promotes epithelial differentiation, we searched for interactors using membrane dihybrid screening. We discovered a strong interaction with the cell junctional protein EVA1 (Epithelial V-like Antigen 1) and confirmed it by co-immunoprecipitation. Like CLCA2, EVA1 is a type I transmembrane protein that is regulated by p53 and p63. It is thought to mediate homophilic cell-cell adhesion in diverse epithelial tissues. We found that EVA1 is frequently downregulated in breast tumors and breast cancer cell lines, especially those of mesenchymal phenotype. Moreover, knockdown of EVA1 in immortalized human mammary epithelial cells (HMEC) caused EMT, implying that EVA1 is essential for epithelial differentiation. Both EVA1 and CLCA2 co-localized with E-cadherin at cell-cell junctions. The interacting domains were delimited by deletion analysis, revealing the site of interaction to be the transmembrane segment (TMS). The primary sequence of the CLCA2 TMS was found to be conserved in CLCA2 orthologs throughout mammals, suggesting that its interaction with EVA1 co-evolved with the mammary gland. A screen for other junctional interactors revealed that CLCA2 was involved in two different complexes, one with EVA1 and ZO-1, the other with beta catenin. Overexpression of CLCA2 caused downregulation of beta catenin and beta catenin-activated genes. Thus, CLCA2 links a junctional adhesion molecule to cytosolic signaling proteins that modulate proliferation and differentiation. These results may explain how attenuation of CLCA2 causes EMT and why CLCA2 and EVA1 are frequently downregulated in metastatic breast cancer cell lines

Advances in Mechanism of Coexistence and Pharmaceutical Treatment of Chronic Heart Failure and Depression

The coprevalence of chronic heart failure (CHF) and depression is 10%-79%, the pathogenesis of these two diseases is related to the activation of immune inflammatory system, insulin resistance and intestinal flora imbalance, and relevant regulation is bidirectional and complex. There is a lack of efficient drugs for both CHF and depression recommended by available diagnosis and treatment guidelines and present clinical practice. But it has recently been reported that some drugs (sacubitril/valsartan, new antidepressants, shensongyangxin and qiliqiangxin capsules, regulators of the intestinal flora) may be partially effective for CHF with depression.We reviewed the mechanism of coexistence and pharmaceutical treatment of CHF and depression, providing new ideas and evidence for clinical diagnosis and treatment of CHF and depression

Predicting Fire Season Severity in South America Using Sea Surface Temperature Anomalies

Fires in South America cause forest degradation and contribute to carbon emissions associated with land use change. Here we investigated the relationship between year-to-year changes in satellite-derived estimates of fire activity in South America and sea surface temperature (SST) anomalies. We found that the Oceanic Ni o Index (ONI) was correlated with interannual fire activity in the eastern Amazon whereas the Atlantic Multidecadal Oscillation (AMO) index was more closely linked with fires in the southern and southwestern Amazon. Combining these two climate indices, we developed an empirical model that predicted regional annual fire season severity (FSS) with 3-5 month lead times. Our approach provides the foundation for an early warning system for forecasting the vulnerability of Amazon forests to fires, thus enabling more effective management with benefits for mitigation of greenhouse gas and air pollutant emissions

Long-Term Protection of CHBP Against Combinational Renal Injury Induced by Both Ischemia-Reperfusion and Cyclosporine A in Mice.

Renal ischemia-reperfusion (IR) injury and cyclosporine A (CsA) nephrotoxicity affect allograft function and survival. The prolonged effects and underlying mechanisms of erythropoietin derived cyclic helix B peptide (CHBP) and/or caspase-3 small interfering RNA (CASP-3siRNA) were investigated in mouse kidneys, as well as kidney epithelial cells (TCMK-1), subjected to transplant-related injuries. Bilateral renal pedicles were clamped for 30 min followed by reperfusion for 2 and 8 weeks, with/without 35 mg/kg CsA gavage daily and/or 24 nmol/kg CHBP intraperitoneal injection every 3 days. The ratio of urinary albumin to creatinine was raised by IR injury, further increased by CsA and lowered by CHBP at 2, 4, 6 and 8 weeks, whereas the level of SCr was not significantly affected. Similar change trends were revealed in tubulointerstitial damage and fibrosis, HMGB1 and active CASP-3 protein. Increased apoptotic cells in IR kidneys were decreased by CsA and CHBP at 2 and/or 8 weeks. p70 S6 kinase and mTOR were reduced by CsA with/without CHBP at 2 weeks, so were S6 ribosomal protein and GSK-3β at 8 weeks, with reduced CASP-3 at both time points. CASP-3 was further decreased by CHBP in IR or IR + CsA kidneys at 2 or 8 weeks. Furthermore, in TCMK-1 cells CsA induced apoptosis was decreased by CHBP and/or CASP-3siRNA treatment. Taken together, CHBP predominantly protects kidneys against IR injury at 2 weeks and/or CsA nephrotoxicity at 8 weeks, with different underlying mechanisms. Urinary albumin/creatinine is a good biomarker in monitoring the progression of transplant-related injuries. CsA divergently affects apoptosis in kidneys and cultured kidney epithelial cells, in which CHBP and/or CASP-3siRNA reduces inflammation and apoptosis

p63 orchestrates serine and one carbon metabolism enzymes expression in head and neck cancer

background: head and neck squamous cell carcinoma (HNSCC) is characterized by high proliferation and limited differentiation. the altered expression of the p53 family members, and specifically of p63, represents a pivotal event in the pathogenesis of HNSCC. physiologically, p63 affects metabolism through the direct transactivation of the enzyme hexokinase 2, and subsequently controls the proliferation of epithelial cells; nonetheless, its role in cancer metabolism is still largely unclear. the high energetic demand of cancer and the consequent needs of a metabolic reshape, also involve the serine and glycine catabolic and anabolic pathways, including the one carbon metabolism (OCM), to produce energetic compounds (purines) and to maintain cellular homeostasis (glutathione and S-adenosylmethionine). results: the involvement in serine/glycine starvation by other p53 family members has been reported, including HNSCC. Here, we show that in HNSCC p63 controls the expression of the enzymes regulating the serine biosynthesis and one carbon metabolism. p63 binds the promoter region of genes involved in the serine biosynthesis as well as in the one carbon metabolism. p63 silencing in a HNSCC cell line affects the mRNA and protein levels of these selected enzymes. moreover, the higher expression of TP63 and its target enzymes, negatively impacts on the overall survival of HNSCC patients. conclusion: these data indicate a direct role of p63 in the metabolic regulation of HNSCC with significant clinical effects

Pretreating poplar cuttings with low nitrogen ameliorates salt stress responses by increasing stored carbohydrates and priming stress signaling pathways

Soil salinity is a widespread stress in semi-arid forests worldwide, but how to manage nitrogen (N) nutrition to improve plant saline tolerance remains unclear. Here, the cuttings of a widely distributed poplar from central Asia, Populus russikki Jabl., were exposed to either normal or low nitrogen (LN) concentrations for two weeks in semi-controlled greenhouse, and then they were added with moderate salt solution or not for another two weeks to evaluate their physiological, biochemical, metabolites and transcriptomic profile changes. LN-pretreating alleviated the toxicity caused by the subsequent salt stress in the poplar plants, demonstrated by a significant reduction in the influx of Na+ and Cl- and improvement of the K+/Na+ ratio. The other salt-stressed traits were also ameliarated, indicated by the variations of chlorophyll content, PSII photochemical activity and lipid peroxidation. Stress alleviation resulted from two different processes. First, LN pretreatment caused a significant increase of non-structural carbohydrates (NSC), allowed for an increased production of osmolytes and a higher potential fueling ion transport under subsequent salt condition, along with increased transcript levels of the cation/H+ ATPase. Second, LN pretreatment enhanced the transcript levels of stress signaling components and phytohormones pathway as well as antioxidant enzyme activities. The results indicate that early restrictions of N supply could enhance posterior survival under saline stress in poplar plants, which is important for plantation programs and restoration activities in semi-arid areas.This research was supported by Natural Science Foundation of China ( 31770644 and 31270660 ), Project of Innovation research team in Sichuan Education Administration in China (No. 13TD0023 )

THE ANTIBACTERIAL EFFECT OF URENA LOBATA L. FROMV GUANGXI ON MICE WITH STAPHYLOCOCCUS AUREUS PNEUMONIA

Background: Alcohol extract from the root of Urena lobata L. (ULL) had broad spectrum antimicrobial activity. Studies in vitro have sho that ULL aqueous extract has antibacterial effect on S. aureusis, and the combination therapy of the ULL aqueous extract with cefazolin sodium showed additive effect. Materials and Methods: The mice underwent nasal inhalation with S. aureus, a subset of mice were intra-gastric gavage with ULL and/or intravenous injection cefazolin sodium twice daily. After being exposed to S. aureus for 5 days, 10 days and 14 days respectively, the white blood cells count (WBC), neutrophils absolute value (NEU) and the neutrophil percentage (NEU%) in peripheral blood, as well as the levels of serum immunoglobulin (Ig) G and IgM were determined using commercial kits. The colony count of S. aureus, the levels of interleukin (IL) -6 and IL-10 of mice lung tissue were detected, and the pathological changes of lung tissue were examined using H & E staining. Results: ULL significantly protected against S. aureus pneumonia, as evidenced by the remarkable decrease in the rate of S. aureus colony count/lung weight, WBC, NEU and NEU% in peripheral blood, as well as the attenuation of lung histopathological damage. Additionally, ULL+cefazolin could have markedly reduced the rate of S. aureus colony count/lung weight when compared with cefazolin. Furthermore, ULL and ULL+cefazolin both could significantly decrease the serum levels of IgG and IgM, and the levels of IL-6, IL-10 in mice lung tissue. Conclusion: This study first demonstrated that ULL may have potential use as a therapeutic agent for S. aureus pneumonia, and the roles of IgG, IgM, IL-6 and IL-10 in ULL protection against S. aureus pneumonia remain to be further studied

Pathogenic genes implicated in sleep-related hypermotor epilepsy: a research progress update

Sleep-related hypermotor epilepsy (SHE) is a focal epilepsy syndrome characterized by a variable age of onset and heterogeneous etiology. Current literature suggests a prevalence rate of approximately 1.8 per 100,000 persons. The discovery of additional pathogenic genes associated with SHE in recent years has significantly expanded the knowledge and understanding of its pathophysiological mechanisms. Identified SHE pathogenic genes include those related to neuronal ligand- and ion-gated channels (CHRNA4, CHRNB2, CHRNA2, GABRG2, and KCNT1), genes upstream of the mammalian target of rapamycin complex 1 signal transduction pathway (DEPDC5, NPRL2, NPRL3, TSC1, and TSC2), and other genes (CRH, CaBP4, STX1B, and PRIMA1). These genes encode proteins associated with ion channels, neurotransmitter receptors, cell signal transduction, and synaptic transmission. Mutations in these genes can result in the dysregulation of encoded cellular functional proteins and downstream neuronal dysfunction, ultimately leading to epileptic seizures. However, the associations between most genes and the SHE phenotype remain unclear. This article presents a literature review on the research progress of SHE-related pathogenic genes to contribute evidence to genotype–phenotype correlations in SHE and establish the necessary theoretical basis for future SHE treatments