Asymmetric response of vegetation GPP to impervious surface expansion: Case studies in the Yellow and Yangtze River Basins.

Terrestrial gross primary production (GPP) changes due to impervious surfaces significantly impact ecosystem services in watersheds. Understanding the asymmetric response of vegetation GPP to impervious surface expansion is essential for regional development planning and ecosystem management. However, the asymmetric response of vegetation GPP to the impacts of impervious surface expansion is unknown in different watersheds. This paper selected the Yellow River and Yangtze River basins as case studies. We characterized the overall change in GPP based on changes in impervious surface ratio (ISR), determined impervious surface expansion's direct and indirect impacts on GPP in the two watersheds, and further analyzed the asymmetric response of the compensatory effects of indirect influences on the impervious surface expansion in different watersheds. The results showed that: (1) The vegetation GPP decreased with increasing ISR in the Yangtze River Basin, while that in the Yellow River Basin first increased and then reduced. (2) The direct impacts of increased ISR reduced vegetation GPP, while the indirect impacts both had a growth-compensating effect. Growth compensation stabilized at approximately 0.40 and 0.30 in the Yellow and Yangtze River Basins. (3) When the ISR was 0.34-0.56, the growth compensation could offset the reduction of GPP due to direct impact and ensure that the background vegetation GPP was not damaged in the Yellow River Basin. In contrast, the background vegetation GPP was inevitably impaired with increased ISR in the Yangtze River Basin. Therefore, this study suggests that the ISR should be ensured to be between 0.34 and 0.56 to maximize the impervious surface of the Yellow River Basin without compromising the background vegetation GPP. While pursuing impervious surface expansion in the Yangtze River Basin, other programs should be sought to compensate for the loss to GPP.

Exploring the comprehensive link between climatic factors and vegetation productivity in China.

Understanding the influence of climatic factors on vegetation dynamics and cumulative effects is critical for global sustainable development. However, the response of vegetation to climate and the underlying mechanisms in different climatic zones remains unclear. In this study, we analyzed the response of vegetation gross primary productivity (GPP) to climatic factors and the cumulative effects across various vegetation types and climatic zones, utilizing data on precipitation (Pr), temperature (Ta), and the standardized precipitation evapotranspiration index (SPEI). The results showed that: (1) GPP showed significant differences among the seven climatic zones, with the highest value observed in zone VII, reaching 1860.07 gC·m- 2, and the lowest in zone I, at 126.03 gC·m- 2. (2) GPP was significantly and positively correlated with temperature in climatic zones I, IV, V, and VI and with precipitation in climatic zones I, II, and IV. Additionally, a significant positive correlated was found between SPEI and GPP in climatic zones I, II, and IV. (3) Drought exerted a cumulative effect on GPP in 45.10% of the regions within China, with an average cumulative duration of 5 months. These effects persisted for 6-8 months in zones I, II, and VII, and for 2-4 months in zones III, IV and VI. Among different vegetation types, forests experienced longest cumulative effect time of 6 months, followed by grasslands (5 months), croplands (4 months), and shrublands (4 months). The cumulative time scale decreased with increasing annual SPEI. The varying responses and accumulation of GPP to drought among different vegetation types in various climatic zones underscore the complexity of vegetation-climate interactions the response and accumulation of GPP to drought.

Increased phagocytosis in the presence of enhanced M2-like macrophage responses correlates with increased primary and latent HSV-1 infection.

After HSV-1 infection, macrophages infiltrate early into the cornea, where they play an important role in HSV-1 infection. Macrophages are divided into M1 or M2 groups based on their activation. M1 macrophages are pro-inflammatory, while M2 macrophages are anti-inflammatory. Macrophage phenotypes can shift between M1 or M2 in vitro and in vivo following treatment with specific cytokines. In this study we looked at the effect of M2 macrophages on HSV-1 infectivity using mice either lacking M2 (M2-/-) or overexpressing M2 (M2-OE) macrophages. While presence or absence of M2 macrophages had no effect on eye disease, we found that over expression of M2 macrophages was associated with increased phagocytosis, increased primary virus replication, increased latency, and increased expression of pro- and anti-inflammatory cytokines. In contrast, in mice lacking M2 macrophages following infection phagocytosis, replication, latency, and cytokine expression were similar to wild type mice. Our results suggest that enhanced M2 responses lead to higher phagocytosis, which affected both primary and latent infection but not reactivation.

Interrelationship between Alzheimer's disease and cardiac dysfunction: the brain-heart continuum?

Dementia, a devastating neurological disorder commonly found in the elderly, is characterized by severe cognitive and memory impairment. Ample clinical and epidemiological evidence has depicted a close association between dementia and heart failure. While cerebral blood under perfusion and neurohormonal activation due to the dampened cardiac pump function contribute to the loss of nutrient supply and neuronal injury, Alzheimer's disease (AD), the most common type of dementia, also provokes cardiovascular function impairment, in particular impairment of diastolic function. Aggregation of amyloid-ß proteins and mutations of Presenilin (PSEN) genes are believed to participate in the pathological changes in the heart although it is still debatable with regards to the pathological cue of cardiac anomalies in AD process. In consequence, reduced cerebral blood flow triggered by cardiac dysfunction further deteriorates vascular dementia and AD pathology. Patients with atrial fibrillation, heart failure, and other cardiac anomalies are at a higher risk for cognitive decline and dementia. Conclusion: Due to the increased incidence of dementia and cardiovascular diseases, the coexistence of the two will cause more threat to public health, warranting much more attention. Here, we will update recent reports on dementia, AD, and cardiovascular diseases and discuss the causal relationship between dementia and heart dysfunction.

Association between lumbar disc herniation and facet joint osteoarthritis.

BACKGROUND: This study was performed to investigate the association between lumbar disc herniation (LDH) and facet joint osteoarthritis (FJOA) using magnetic resonance imaging (MRI). METHODS: Between March 2012 and September 2018, a total of 441 segments from 394 patients with LDH were included in the study. LDH was classified according to the Michigan State University (MSU) classification, in which the degree of LDH is divided into 3 levels (expressed as 1, 2, and 3) and the location of LDH is divided into 4 zones (described as A, AB, B, and C). Bilateral FJOA was graded from 0 to 3 using the criteria introduced by Weishaupt et al., and bilateral facet orientations were measured on axial MRI slices. A mixed-effects ordinal logistic regression model was utilized to determine the potential factors that may be associated with FJOA, including sex, age, body mass index (BMI), segment, facet orientation and tropism, and the degree and location of LDH. RESULTS: In general, the prevalence of FJOA (grade ≥ 2) was 66.2% in LDH segments. For both the left and right sides, the degree of LDH was associated with the severity of FJOA (p < 0.01). Age and BMI were also associated with the severity of left and right FJOA (p = 0.002 and p < 0.001 for age, p < 0.001 and p = 0.003 for BMI, respectively), while segment, facet orientation, and facet tropism were not (p > 0.05 for all). Notably, MSU-B LDH was associated with greater odds of having more severe FJOA on the herniation side (left: p < 0.001, odds ratio (OR) = 2.714, 95% confidence interval (CI) = 1.583~4.650; right: p = 0.003, OR = 2.615, 95% CI = 1.405~4.870). However, other locations of LDH were not associated with the severity of FJOA (p > 0.05 for all). CONCLUSIONS: Both the degree of LDH and MSU-B LDH are associated with the severity of FJOA. The association between LDH and FJOA highlights the complexity of the etiology of FJOA.

Oxidative damage induces apoptosis and promotes calcification in disc cartilage endplate cell through ROS/MAPK/NF-κB pathway: Implications for disc degeneration.

Cartilage endplate (CEP) cell calcification and apoptosis play a vital role in the intervertebral disc degeneration (IVDD). Oxidative stress is a key factor in inducing programmed cell death and cartilage calcification. However, the cell death and calcification of cartilage endplate cells under oxidative stress have never been described. The present study investigated the apoptosis and calcification in the cartilage endplate cell under oxidative stress induced by H2O2 to understand the underlying mechanism of IVDD. The cartilage endplate cells isolated from human lumbar discs were subjected to different concentrations of H2O2 for various time periods. The cell viability was determined by CCK-8 assay, whereas Western blot, immunofluorescence, and Alcian blue, Alizarin red, and Von Kossa staining evaluated the apoptosis and calcification. The level of mitochondria-specific reactive oxygen species (ROS) was quantified with an oxygen radical-sensitive probe-MitoSOX. The potential signaling pathways were investigated by Western blot after the addition of N-acetyl-l-cysteine (NAC). We found that the oxidative stress induced by H2O2 increased the apoptosis and subsequently the calcification in the cartilage endplate cells through the ROS/p38/ERK/p65 pathway. The apoptosis and the calcification of the cartilage endplate cells induced by H2O2 can be abolished by NAC. These results suggested that regulating the apoptosis and the calcification in the cartilage endplate cells under oxidative stress should be advantageous for the survival of cells and might delay the process of disc degeneration.

Embedding Pinhole Vertical Gold Nanowire Electronic Skins for Braille Recognition.

Electronic skins (e-skins) have the potential to be conformally integrated with human body to revolutionize wearable electronics for a myriad of technical applications including healthcare, soft robotics, and the internet of things, to name a few. One of the challenges preventing the current proof of concept translating to real-world applications is the device durability, in which the strong adhesion between active materials and elastomeric substrate or human skin is required. Here, a new strategy is reported to embed vertically aligned standing gold nanowires (v-AuNWs) into polydimethylsiloxane, leading to a robust e-skin sensor. It is found that v-AuNWs with pinholes can have an adhesion energy 18-fold greater than that for pinhole-free v-AuNWs. Finite element modeling results show that this is due to friction force from interfacial embedment. Furthermore, it is demonstrated that the robust e-skin sensor can be used for braille recognition.

Percutaneous Pedicle Screw Fixation Alone Versus Debridement and Fusion Surgery for the Treatment of Early Spinal Tuberculosis: A Retrospective Cohort Study.

BACKGROUND Advances in diagnostic imaging techniques make it possible to detect tuberculosis (TB) lesions earlier, when only bone destruction or inflammatory infiltration is demonstrated. These techniques provide doctors with more opportunities to treat TB in the early stages of the disease. Traditional aggressive debridement surgery increases the risk of surgical complications. Therefore, we aimed to determine whether using percutaneous pedicle screw (PPS) fixation alone for the treatment of early spinal TB was a valid and less invasive surgical technique. MATERIAL AND METHODS We retrospectively reviewed the clinical and radiographic outcomes in cases with thoracic or lumbar TB treated with PPS surgery or hybrid surgery between January 2010 and January 2017. The operative time, blood loss, length of hospital stay, and hospitalization costs in the 2 groups were recorded and compared. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) before and at 18 months after surgery were tested to evaluate TB progress. Back pain was measured using the visual analog scale (VAS) before the operation and at the final follow-up. Radiological outcomes were evaluated at 1, 6, 12, and 18 months after surgery. A paired t-test was used to evaluate preoperative and postoperative clinical outcomes using SPSS 19.0 software. P values less than 0.05 were considered to be significant. RESULTS A total of 42 patients were involved in this retrospective study. In both groups, the average preoperative ESR, CRP level, and VAS score for back pain significantly decreased after surgery. In the PPS group, the operative time, blood loss, hospital stay, and hospitalization costs were all significantly lower than those in the hybrid group. X-ray and CT images showed satisfactory bone fusion and good maintenance of spinal alignment in both groups at the final follow-up. CONCLUSIONS PPS fixation alone was a valid and less invasive surgery for the treatment of early spinal TB. Furthermore, the recovery process of spinal TB can be facilitated using a "simple" internal fixation procedure, and bone fusion can be achieved without aggressive debridement and bone graft surgery.

Hydroxysteroid sulfotransferase 2B1 affects gastric epithelial function and carcinogenesis induced by a carcinogenic agent.

BACKGROUND: A healthy gastric mucosal epithelium exhibits tumor-suppressive properties. Gastric epithelial cell dysfunction contributes to gastric cancer development. Oxysterols provided from food or cholesterol oxidation in the gastric epithelium may be further sulfated by hydroxysteroid sulfotransferase 2B1 (SULT2B1), which is highly abundant in the gastric epithelium. However, the effects of SULT2B1 on gastric epithelial function and gastric carcinogenesis are unclear. METHODS: A mouse gastric tumor model was established using carcinogenic agent 3-methylcholanthrene (3-MCA). A SULT2B1 deletion (SULT2B1-/-) human gastric epithelial line GES-1 was constructed by CRISPR/CAS9 genome editing system. RESULTS: The gastric tumor incidence was higher in the SULT2B1-/- mice than in the wild-type (WT) mice. In gastric epithelial cells, adenovirus-mediated SULT2B1b overexpression reduced the levels of oxysterols, such as 24(R/S),25-epoxycholesterol (24(R/S),25-EC) and 27-hydroxycholesterol (27HC). This condition also increased PI3K/AKT signaling to promote gastric epithelial cell proliferation, epithelization, and epithelial development. However, SULT2B1 deletion or SULT2B1 knockdown suppressed PI3K/AKT signaling, epithelial cell epithelization, and wound healing and induced gastric epithelial cell malignant transition upon 3-MCA induction. CONCLUSIONS: The abundant SULT2B1 expression in normal gastric epithelium might maintain epithelial function via the PI3K/AKT signaling pathway and suppress gastric carcinogenesis induced by a carcinogenic agent.

ALDH2 Polymorphism and Ethanol Consumption: A Genetic-Environmental Interaction in Carcinogenesis.

Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme in the detoxification of toxic aldehydes, especially acetaldehyde, which is commonly considered as a carcinogen. ALDH2 mutation and impaired enzymatic activity will cause acetaldehyde accumulation and thus participate in the development of cancers. It deserves more attention since around 40% of East Asian population carry the inactive ALDH2 allele. Moreover, the risk for cancers will be even higher when ALDH2 mutation combined with heavy alcohol consumption, suggesting a genetic-environmental interaction in carcinogenesis. This may provide us with a potential target for cancer prevention and treatment.

Leptin regulates disc cartilage endplate degeneration and ossification through activation of the MAPK-ERK signalling pathway in vivo and in vitro.

Recent findings demonstrate that leptin plays a significant role in chondrocyte and osteoblast differentiation. However, the mechanisms by which leptin acts on cartilage endplate (CEP) cells to give rise to calcification are still unclear. The aim of this study was to evaluate the effects of leptin that induced mineralization of CEP cells in vitro and in vivo. We constructed a rat model of lumbar disc degeneration and determined that leptin was highly expressed in the presence of CEP calcification. Rat CEP cells treated with or without leptin were used for in vitro analysis using RT-PCR and Western blotting to examine the expression of osteocalcin (OCN) and runt-related transcription factor 2 (Runx2). Both OCN and Runx2 expression levels were significantly increased in a dose- and time-dependent manner. Leptin activated ERK1/2 and STAT3 phosphorylation in a time-dependent manner. Inhibition of phosphorylated ERK1/2 using targeted siRNA suppressed leptin-induced OCN and Runx2 expression and blocked the formation of mineralized nodules in CEP cells. We further demonstrated that exogenous leptin induced matrix mineralization of CEP cells in vivo. We suggest that leptin promotes the osteoblastic differentiation of CEP cells via the MAPK/ERK signal transduction pathway and may be used to investigate the mechanisms of disc degeneration.

Upregulation of 24(R/S),25-epoxycholesterol and 27-hydroxycholesterol suppresses the proliferation and migration of gastric cancer cells.

Gastric cancer (GC) is one of the most common cancers and is the second-leading cause of cancer-associated morbidity worldwide. Oxysterols are oxidized derivatives of cholesterol that may be important in many biological processes, but the levels and roles of oxysterols in gastric tumours remain to be elucidated. The levels of cholesterol, oxysterols and sulfated oxysterols in human gastric tumour tissues, adjacent normal mucosal tissues, cancerous gastric juice and gastric juice obtained from healthy subjects were detected by LC-MS. It was found that the levels of 24(R/S),25-EC and 27HC in human gastric tumour tissues and cancerous gastric juice were significantly increased compared with those of adjacent normal mucosal tissues and gastric juice from healthy subjects. Compared with normal gastric mucosal tissue, the levels of sulfated 25-hydroxycholesterol (25HC3S) and the ratio of 25HC3S/25HC were decreased in human gastric tumour tissues, which might be related to the dramatically decreased SULT2A1 expression in gastric tumour tissue. Both 24(R/S),25-EC and 27HC suppressed gastric cancer proliferation, which was not altered by LXRα-siRNA treatment. The suppression of cell proliferation induced by 27HC was attenuated by LXRß-siRNA, but the suppression of cell proliferation induced by 24(R/S),25-EC was intensified by LXRß-siRNA. Both 24(R/S),25-EC and 27HC dramatically inhibited HGC-27 cell migration, which was attenuated by the co-transfection of cells with LXRα-siRNA and LXRß-siRNA, but not LXRα-siRNA or LXRß-siRNA alone. In conclusion, the accumulated 24(R/S),25-EC and 27HC in human gastric tumour tissues might play important roles in gastric cancer development.

Regulation of Catalytic DNA Activities with Thermosensitive Gold Nanoparticle Surfaces.

The regulation of the activities of catalytic DNA is of great importance in many applications, especially in biosensing, controllable drug carriers, and gene therapy. In this work, the surfaces of gold nanoparticles (AuNPs) are simultaneously modified with a thermoresponsive polymer, poly( N-isopropylacrylamide) (pNIPAM), and catalytic DNA to form thermosensitive catalytic DNA/pNIPAM/AuNP systems. The thermosensitive pNIPAM on the surfaces of AuNPs enables the temperature-controlled catalytic activities of the system in a narrow temperature range. The catalytic DNA/pNIPAM/AuNP system exhibits almost no catalytic activity at temperatures below the lower critical solution temperature (LCST) of pNIPAM and become highly catalytic when the temperature is higher than the LCST. Two kinds of catalytic DNA, the entropy-driven DNA catalytic network and the Mg2+-dependent DNAzyme, were chosen as model catalytic systems, and the results showed that the regulation of catalytic activities for both systems was achieved efficiently. These systems may have important potentials in future biosensing and biomedical applications.

Gene Set-Based Integrative Analysis Revealing Two Distinct Functional Regulation Patterns in Four Common Subtypes of Epithelial Ovarian Cancer.

Clear cell (CCC), endometrioid (EC), mucinous (MC) and high-grade serous carcinoma (SC) are the four most common subtypes of epithelial ovarian carcinoma (EOC). The widely accepted dualistic model of ovarian carcinogenesis divided EOCs into type I and II categories based on the molecular features. However, this hypothesis has not been experimentally demonstrated. We carried out a gene set-based analysis by integrating the microarray gene expression profiles downloaded from the publicly available databases. These quantified biological functions of EOCs were defined by 1454 Gene Ontology (GO) term and 674 Reactome pathway gene sets. The pathogenesis of the four EOC subtypes was investigated by hierarchical clustering and exploratory factor analysis. The patterns of functional regulation among the four subtypes containing 1316 cases could be accurately classified by machine learning. The results revealed that the ERBB and PI3K-related pathways played important roles in the carcinogenesis of CCC, EC and MC; while deregulation of cell cycle was more predominant in SC. The study revealed that two different functional regulation patterns exist among the four EOC subtypes, which were compatible with the type I and II classifications proposed by the dualistic model of ovarian carcinogenesis.

Gene Set-Based Functionome Analysis of Pathogenesis in Epithelial Ovarian Serous Carcinoma and the Molecular Features in Different FIGO Stages.

Serous carcinoma (SC) is the most common subtype of epithelial ovarian carcinoma and is divided into four stages by the Federation of Gynecologists and Obstetrics (FIGO) staging system. Currently, the molecular functions and biological processes of SC at different FIGO stages have not been quantified. Here, we conducted a whole-genome integrative analysis to investigate the functions of SC at different stages. The function, as defined by the GO term or canonical pathway gene set, was quantified by measuring the changes in the gene expressional order between cancerous and normal control states. The quantified function, i.e., the gene set regularity (GSR) index, was utilized to investigate the pathogenesis and functional regulation of SC at different FIGO stages. We showed that the informativeness of the GSR indices was sufficient for accurate pattern recognition and classification for machine learning. The function regularity presented by the GSR indices showed stepwise deterioration during SC progression from FIGO stage I to stage IV. The pathogenesis of SC was centered on cell cycle deregulation and accompanied with multiple functional aberrations as well as their interactions.

[Process in the role of vasoactive intestinal peptide in the treatment of ulcerative colitis by regulating the balance of T follicular helper cells/T follicular regulatory cells].

Ulcerative colitis (UC) is an autoimmune disease based on the persistent damage of colonic mucosal barrier. It has been found that the abnormal expression of follicular helper T (Tfh) cells and follicular regulatory T (Tfr) cells is closely related to the occurrence and development of UC. Tfh cells can secrete pro-inflammatory factors and assist B cells to produce antibodies, which can promote the development of UC, while Tfr cells can inhibit the activity of Tfh cells and secrete anti-inflammatory factors. How to regulate the balance between them has become one of the potential therapeutic targets of UC. Vasoactive intestinal peptide (VIP) has preventive and therapeutic effect on UC, and its mechanism is closely related to the regulation of Tfh/Tfr cell balance, which can provide help for the treatment of UC.

Dynamic process of ecosystem water use efficiency and response to drought in the Yellow River Basin, China.

Ecosystem water use efficiency (WUE) is a crucial indicator of the impact of climate change on terrestrial ecosystems, reflecting the balance between biological processes (photosynthesis and transpiration) and physical processes (evapotranspiration). However, the response mechanisms and driving processes of WUE to drought remain to be further understood. In this study, we analyzed the spatial and temporal dynamics and response mechanisms of WUE in the Yellow River Basin (YRB) using data on Gross Primary Productivity (GPP), Evapotranspiration (ET) and Standardized Precipitation Evapotranspiration Index (SPEI), which revealed the cumulative effect of drought on WUE and assessed the ecosystem's resilience. The study results showed that (1) GPP, ET and WUE in the YRB exhibited a significant increasing trend, with 63.04 % of the area showing a marked increase in WUE. (2) GPP was the dominant factor influencing WUE in 65.36 % of the area, particularly in cropland and grassland, while ET was more influential in forested areas. Vapor pressure deficit (VPD) was identified as the principal driver affecting vegetation GPP in semi-arid and semi-humid regions of the YRB. In contrast, soil moisture (SM) was the limiting factor in arid areas. (3) 71.00 % of the WUE in the basin was affected by drought cumulative effects, with an average cumulative duration of 4.5 months. Arid regions experienced the most extended duration of 7.29 months, compared to 3.05 months in semi-humid regions. (4) 74.85 % of the regional ecosystems exhibited ecological resilience to drought, particularly in the source areas of the western basin of the YRB. Shrublands have the highest drought resilience among vegetation types, while grasslands have the lowest. The resilience of each climatic zone was in the order of semi-humid, semi-arid, and arid order. This study comprehensively analyzed of the spatial and temporal dynamics and response mechanisms of WUE in the YRB, offering a new perspective and scientific basis for understanding and predicting the ecosystem response to climate change.

PHB2 ameliorates Doxorubicin-induced cardiomyopathy through interaction with NDUFV2 and restoration of mitochondrial complex I function.

BACKGROUND: Doxorubicin (DOX) is among the most widely employed antitumor agents, although its clinical applications have been largely hindered by severe cardiotoxicity. Earlier studies described an essential role of mitochondrial injury in the pathogenesis of DOX cardiomyopathy. PHB2 (Prohibitin 2) is perceived as an essential regulator for mitochondrial dynamics and oxidative phosphorylation (OXPHOS) although its involvement in DOX cardiomyopathy remains elusive. METHODS: To decipher the possible role of PHB2 in DOX cardiomyopathy, tamoxifen-induced cardiac-specific PHB2 conditional knockout mice were generated and subjected to DOX challenge. Cardiac function and mitochondrial profiles were examined. Screening of downstream mediators of PHB2 was performed using proteomic profiling and bioinformatic analysis, and was further verified using co-immunoprecipitation and pulldown assays. RESULTS: Our data revealed significantly downregulated PHB2 expression in DOX-challenged mouse hearts. PHB2CKO mice were more susceptible to DOX cardiotoxicity compared with PHB2flox/flox mice, as evidenced by more pronounced cardiac atrophy, interstitial fibrosis and decrease in left ventricular ejection fraction and fractional shortening. Mechanistically, PHB2 deficiency resulted in the impairment of mitochondrial bioenergetics and oxidative phosphorylation in DOX cardiotoxicity. Proteomic profiling and interactome analyses revealed that PHB2 interacted with NDUFV2 (NADH-ubiquinone oxidoreductase core subunit V2), a key subunit of mitochondrial respiratory Complex I to mediate regulatory property of PHB2 on mitochondrial metabolism. PHB2 governed the expression of NDUFV2 by promoting its stabilization, while PHB2 deficiency significantly downregulated NDUFV2 in DOX-challenged hearts. Cardiac overexpression of PHB2 alleviated mitochondrial defects in DOX cardiomyopathy both in vivo and in vitro. CONCLUSIONS: Our study defined a novel role for PHB2 in mitochondrial dynamics and energetic metabolism through interacting with NDUFV2 in DOX-challenged hearts. Forced overexpression of PHB2 may be considered a promising therapeutic approach for patients with DOX cardiomyopathy.

Berberine alleviates myocardial diastolic dysfunction by modulating Drp1-mediated mitochondrial fission and Ca2+ homeostasis in a murine model of HFpEF.

Heart failure with preserved ejection fraction (HFpEF) displays normal or near-normal left ventricular ejection fraction, diastolic dysfunction, cardiac hypertrophy, and poor exercise capacity. Berberine, an isoquinoline alkaloid, possesses cardiovascular benefits. Adult male mice were assigned to chow or high-fat diet with L-NAME ("two-hit" model) for 15 weeks. Diastolic function was assessed using echocardiography and noninvasive Doppler technique. Myocardial morphology, mitochondrial ultrastructure, and cardiomyocyte mechanical properties were evaluated. Proteomics analysis, autophagic flux, and intracellular Ca2+ were also assessed in chow and HFpEF mice. The results show exercise intolerance and cardiac diastolic dysfunction in "two-hit"-induced HFpEF model, in which unfavorable geometric changes such as increased cell size, interstitial fibrosis, and mitochondrial swelling occurred in the myocardium. Diastolic dysfunction was indicated by the elevated E value, mitral E/A ratio, and E/e' ratio, decreased e' value and maximal velocity of re-lengthening (-dL/dt), and prolonged re-lengthening in HFpEF mice. The effects of these processes were alleviated by berberine. Moreover, berberine ameliorated autophagic flux, alleviated Drp1 mitochondrial localization, mitochondrial Ca2+ overload and fragmentation, and promoted intracellular Ca2+ reuptake into sarcoplasmic reticulum by regulating phospholamban and SERCA2a. Finally, berberine alleviated diastolic dysfunction in "two-hit" diet-induced HFpEF model possibly because of the promotion of autophagic flux, inhibition of mitochondrial fragmentation, and cytosolic Ca2+ overload.

Water Quality Degradation Due to Heavy Metal Contamination: Health Impacts and Eco-Friendly Approaches for Heavy Metal Remediation.

Water quality depends on its physicochemical and biological parameters. Changes in parameters such as pH, temperature, and essential and non-essential trace metals in water can render it unfit for human use. Moreover, the characteristics of the local environment, geological processes, geochemistry, and hydrological properties of water sources also affect water quality. Generally, groundwater is utilized for drinking purposes all over the globe. The surface is also utilized for human use and industrial purposes. There are several natural and anthropogenic activities responsible for the heavy metal contamination of water. Industrial sources, including coal washery, steel industry, food processing industry, plastic processing, metallic work, leather tanning, etc., are responsible for heavy metal contamination in water. Domestic and agricultural waste is also responsible for hazardous metallic contamination in water. Contaminated water with heavy metal ions like Cr (VI), Cd (II), Pb (II), As (V and III), Hg (II), Ni (II), and Cu (II) is responsible for several health issues in humans, like liver failure, kidney damage, gastric and skin cancer, mental disorders and harmful effects on the reproductive system. Hence, the evaluation of heavy metal contamination in water and its removal is needed. There are several physicochemical methods that are available for the removal of heavy metals from water, but these methods are expensive and generate large amounts of secondary pollutants. Biological methods are considered cost-effective and eco-friendly methods for the remediation of metallic contaminants from water. In this review, we focused on water contamination with toxic heavy metals and their toxicity and eco-friendly bioremediation approaches.