Exposure to urban green spaces and mental health during the COVID-19 pandemic: evidence from two low and lower-middle-income countries.

Introduction: The COVID-19 pandemic has had a significant impact on mental health globally, with limited access to mental health care affecting low- and middle-income countries (LMICs) the most. In response, alternative strategies to support mental health have been necessary, with access to green spaces being a potential solution. While studies have highlighted the role of green spaces in promoting mental health during pandemic lockdowns, few studies have focused on the role of green spaces in mental health recovery after lockdowns. This study investigated changes in green space access and associations with mental health recovery in Bangladesh and Egypt across the pandemic. Methods: An online survey was conducted between January and April 2021 after the first lockdown was lifted in Bangladesh (n = 556) and Egypt (n = 660). We evaluated indoor and outdoor greenery, including the number of household plants, window views, and duration of outdoor visits. The quantity of greenness was estimated using the normalized difference vegetation index (NDVI). This index was estimated using satellite images with a resolution of 10x10m during the survey period (January-April 2021) with Sentinel-2 satellite in the Google Earth Engine platform. We calculated averages within 250m, 300m, 500m and 1000m buffers of the survey check-in locations using ArcGIS 10.3. Multiple linear regression models were used to evaluate relationships between changes in natural exposure and changes in mental health. Results: The results showed that mental health improved in both countries after the lockdown period. People in both countries increased their time spent outdoors in green spaces after the lockdown period, and these increases in time outdoors were associated with improved mental health. Unexpectedly, changes in the number of indoor plants after the lockdown period were associated with contrasting mental health outcomes; more plants translated to increased anxiety and decreased depression. Refocusing lives after the pandemic on areas other than maintaining indoor plants may assist with worrying and feeling panicked. Still, indoor plants may assist with depressive symptoms for people remaining isolated. Conclusion: These findings have important implications for policymakers and urban planners in LMICs, highlighting the need to increase access to natural environments in urban areas to improve mental health and well-being in public health emergencies.

Impact of green space and built environment on metabolic syndrome: A systematic review with meta-analysis.

Metabolic Syndrome presents a significant public health challenge associated with an increased risk of noncommunicable diseases such as cardiovascular conditions. Evidence shows that green spaces and the built environment may influence metabolic syndrome. We conducted a systematic review and meta-analysis of observational studies published through August 30, 2023, examining the association of green space and built environment with metabolic syndrome. A quality assessment of the included studies was conducted using the Office of Health Assessment and Translation (OHAT) tool. The Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) assessment was used to evaluate the overall quality of evidence. Our search retrieved 18 studies that met the inclusion criteria and were included in our review. Most were from China (n = 5) and the USA (n = 5), and most used a cross-sectional study design (n = 8). Nine studies (50 %) reported only green space exposures, seven (39 %) reported only built environment exposures, and two (11 %) reported both built environment and green space exposures. Studies reported diverse definitions of green space and the built environment, such as availability, accessibility, and quality, particularly around participants' homes. The outcomes focused on metabolic syndrome; however, studies applied different definitions of metabolic syndrome. Meta-analysis results showed that an increase in normalized difference vegetation index (NDVI) within a 500-m buffer was associated with a lower risk of metabolic syndrome (odds ratio [OR] = 0.90, 95%CI = 0.87-0.93, I2 = 22.3 %, n = 4). A substantial number of studies detected bias for exposure classification and residual confounding. Overall, the extant literature shows a 'limited' strength of evidence for green space protecting against metabolic syndrome and an 'inadequate' strength of evidence for the built environment associated with metabolic syndrome. Studies with more robust study designs, better controlled confounding factors, and stronger exposure measures are needed to understand better what types of green spaces and built environment features influence metabolic syndrome.

Climate match is key to predict range expansion of the world's worst invasive terrestrial vertebrates.

Understanding the determinants of the range expansion of invasive alien species is crucial for developing effective prevention and control strategies. Nevertheless, we still lack a global picture of the potential factors influencing the invaded range expansion across taxonomic groups, especially for the world's worst invaders with high ecological and economic impacts. Here, by extensively collecting data on 363 distributional ranges of 19 of world's worst invasive terrestrial vertebrates across 135 invaded administrative jurisdictions, we observed remarkable variations in the range expansion across species and taxonomic groups. After controlling for taxonomic and geographic pseudoreplicates, model averaging analyses based on generalized additive mixed-effect models showed that species in invaded regions having climates more similar to those of their native ranges tended to undergo a larger range expansion. In addition, as proxies of propagule pressure and human-assisted transportation, the number of introduction events and the road network density were also important predictors facilitating the range expansion. Further variance partitioning analyses validated the predominant role of climate match in explaining the range expansion. Our study demonstrated that regions with similar climates to their native ranges could still be prioritized to prevent the spread of invasive species under the sustained global change.

A Two-Step Transcriptome Analysis of the Human Heart Reveals Broad and Disease-Responsive Expression of Ectopic Olfactory Receptors.

G-protein-coupled receptors (GPCRs) are critical regulators of cardiac physiology and a key therapeutic target for the treatment of heart disease. Ectopic olfactory receptors (ORs) are GPCRs expressed in extra-nasal tissues which have recently emerged as new mediators in the metabolic control of cardiac function. The goals of this study were to profile OR gene expression in the human heart, to identify ORs dysregulated by heart failure caused by ischemic cardiomyopathy, and to provide evidence suggestive of a role for those altered ORs in the pathogenesis of heart failure. Left ventricular tissue from heart failure patients (n = 18) and non-failing heart samples (n = 4) were subjected to a two-step transcriptome analysis consisting of the quantification of 372 distinct OR transcripts on real-time PCR arrays and simultaneous determination of global cardiac gene expression by RNA sequencing. This strategy led to the identification of >160 ORs expressed in the human heart, including 38 receptors differentially regulated with heart failure. Co-expression analyses predicted the involvement of dysregulated ORs in the alteration of mitochondrial function, extracellular matrix remodeling, and inflammation. We provide this dataset as a resource for investigating roles of ORs in the human heart, with the hope that it will assist in the identification of new therapeutic targets for the treatment of heart failure.

Prolonged cardiac NR4A2 activation causes dilated cardiomyopathy in mice.

Transcription factors play a fundamental role in cardiovascular adaptation to stress. Nuclear receptor subfamily 4 group A member 2 (NR4A2; NURR1) is an immediate-early gene and transcription factor with a versatile role throughout many organs. In the adult mammalian heart, and particularly in cardiac myocytes, NR4A2 is strongly up-regulated in response to beta-adrenergic stimulation. The physiologic implications of this increase remain unknown. In this study, we aimed to interrogate the consequences of cardiac NR4A2 up-regulation under normal conditions and in response to pressure overload. In mice, tamoxifen-dependent, cardiomyocyte-restricted overexpression of NR4A2 led to cardiomyocyte hypertrophy, left ventricular dilation, heart failure, and death within 40 days. Chronic NR4A2 induction also precipitated cardiac decompensation during transverse aortic constriction (TAC)-induced pressure overload. Mechanistically, NR4A2 caused adult cardiac myocytes to return to a fetal-like phenotype, with a switch to glycolytic metabolism and disassembly of sarcomeric structures. NR4A2 also re-activated cell cycle progression and stimulated DNA replication and karyokinesis but failed to induce cytokinesis, thereby promoting multinucleation of cardiac myocytes. Activation of cell cycle checkpoints led to induction of an apoptotic response which ultimately resulted in excessive loss of cardiac myocytes and impaired left ventricular contractile function. In summary, myocyte-specific overexpression of NR4A2 in the postnatal mammalian heart results in increased cell cycle re-entry and DNA replication but does not result in cardiac myocyte division. Our findings expose a novel function for the nuclear receptor as a critical regulator in the self-renewal of the cardiac myocyte and heart regeneration.

Quantitative Estimation of Protein in Sprouts of Vigna radiate (Mung Beans), Lens culinaris (Lentils), and Cicer arietinum (Chickpeas) by Kjeldahl and Lowry Methods.

Protein scarcity is the most vital cause of long-lasting diseases and even untimely deaths in some developing nations. The application of protein in food is advantageous from the point of view of non-toxicity, biocompatibility, and dietary benefits. This study aimed to determine the protein contents of the sprouts of Vigna radiates (mung beans), Lens culinaris (lentils), and Cicer arietinum (chickpeas) using the Kjeldahl and Lowry methods. The results obtained from the Kjeldahl method identified protein concentrations of 2.54, 2.63, and 2.19%, whereas the Lowry method results identified protein concentrations of 2.96%, 4.10%, and 1.6% in mung beans, lentils, and chickpeas, respectively. In both the methods, lentils were found to have the highest amount of protein followed by mung beans and chickpeas. Both the Kjeldahl and Lowry methods demonstrated good protein values and low variation in the protein amount in the analyzed samples. Furthermore, the methods had greater sensitivity and comparable experimental variability. The outcomes revealed that assays can be applied for protein analysis in legumes. In the context of a lack of suitable standard procedures for evaluating legumes' compositions, the present study is suitable for food control laboratories. In addition, the studied samples represent a significant source of protein and can be used to fulfil the daily requirements for protein intake and other food applications.

Eminent Industrial and Biotechnological Applications of Laccases from Bacterial Source: a Current Overview.

Laccases are blue multicopper oxidases that oxidize a wide range of phenolic as well as non-phenolic substrates in the presence or absence of mediators. They occur in various species of bacteria, fungi, insects, and plants; bacterial laccases show high substrate specificity. Bacteria produce these enzymes either extracellularly or intracellularly and exhibit stability to a wide range of pH and temperature. Therefore, they are suitable for various industrial processes such as food, textile, and paper and pulp industry. They are also valuable for producing biofuels, pharmaceuticals, biosensors, and degradation of various environmental pollutants and xenobiotics compounds. Since bacterial laccases are more versatile in the sense of nutritional needs and ecological factors, their use can provide a promising solution to various problems related to industry and the field of biotechnology. However, there is a need for a thorough understanding of the chemistry and activity of bacterial laccases to enable their full potential use in bioremediation and biofuel production.

UCP3 (Uncoupling Protein 3) Insufficiency Exacerbates Left Ventricular Diastolic Dysfunction During Angiotensin II-Induced Hypertension.

Background Left ventricular diastolic dysfunction, an early stage in the pathogenesis of heart failure with preserved ejection fraction, is exacerbated by joint exposure to hypertension and obesity; however, the molecular mechanisms involved remain uncertain. The mitochondrial UCP3 (uncoupling protein 3) is downregulated in the heart with obesity. Here, we used a rat model of UCP3 haploinsufficiency (ucp3+/-) to test the hypothesis that decreased UCP3 promotes left ventricular diastolic dysfunction during hypertension. Methods and Results Ucp3+/- rats and ucp3+/+ littermates fed a high-salt diet (HS; 2% NaCl) and treated with angiotensin II (190 ng/kg per min for 28 days) experienced a similar rise in blood pressure (158±4 versus 155±7 mm Hg). However, UCP3 insufficiency worsened diastolic dysfunction according to echocardiographic assessment of left ventricular filling pressures (E/e'; 18.8±1.0 versus 14.9±0.6; P<0.05) and the isovolumic relaxation time (24.7±0.6 versus 21.3±0.5 ms; P<0.05), as well as invasive monitoring of the diastolic time constant (Tau; 15.5±0.8 versus 12.7±0.2 ms; P<0.05). Exercise tolerance on a treadmill also decreased for HS/angiotensin II-treated ucp3+/- rats. Histological and molecular analyses further revealed that UCP3 insufficiency accelerated left ventricular concentric remodeling, detrimental interstitial matrix remodeling, and fetal gene reprogramming during hypertension. Moreover, UCP3 insufficiency increased oxidative stress and led to greater impairment of protein kinase G signaling. Conclusions Our findings identified UCP3 insufficiency as a cause for increased incidence of left ventricular diastolic dysfunction during hypertension. The results add further support to the use of antioxidants targeting mitochondrial reactive oxygen species as an adjuvant therapy for preventing heart failure with preserved ejection fraction in individuals with obesity.

Crosstalk between beta-adrenergic and insulin signaling mediates mechanistic target of rapamycin hyperactivation in liver of high-fat diet-fed male mice.

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. While increased nutrient intake and sympathetic activity have been associated with the disease, the pathogenesis of NAFLD remains incompletely understood. We investigated the impact of the interaction of high dietary fat and sugar intake with increased beta-adrenergic receptor (ß-AR) signaling on the activity of nutrient-sensing pathways and fuel storage in the liver. C57BL/6J mice were fed a standard rodent diet (STD), a high-fat diet (HFD), a high-fat/high-sugar Western diet (WD), a high-sugar diet with mixed carbohydrates (HCD), or a high-sucrose diet (HSD). After 6 week on diets, mice were treated with isoproterenol (ISO) and the activity of liver mTOR complex 1 (mTORC1)-related signaling analyzed by immunoblotting and correlated with tissue triglyceride and glycogen contents. ISO-stimulated AKT- and ERK-mediated activation of mTORC1 in STD-fed mice. Consumption of all four high-calorie diets exacerbated downstream activation of ribosomal protein S6 kinase beta-1 (S6K1) in response to ISO. S6K1 activity was greater with the fat-enriched HFD and WD and correlated with the presence of metabolic syndrome and a stronger activation of AKT and ERK1/2 pathways. Fat-enriched diets also increased triglyceride accumulation and inhibited glycogen mobilization under ß-AR stimulation. In conclusion, crosstalk between ß-AR and insulin signaling may contribute to HFD-induced hepatic steatosis through ERK1/2- and AKT-mediated hyperactivation of the mTORC1/S6K1 axis. The findings provide further rationale for the development of therapies aimed at targeting augmented ß-AR signaling in the pathogenesis of NAFLD.

Restoration of Cardiac Function After Myocardial Infarction by Long-Term Activation of the CNS Leptin-Melanocortin System.

Heart failure has a high mortality rate, and current therapies offer limited benefits. The authors demonstrate that activation of the central nervous system leptin-melanocortin pathway confers remarkable protection against progressive heart failure following severe myocardial infarction. The beneficial cardiac-protective actions of leptin require activation of brain melanocortin-4 receptors and elicit improvements in cardiac substrate oxidation, cardiomyocyte contractility, Ca2+ coupling, and mitochondrial efficiency. These findings highlight a potentially novel therapeutic approach for myocardial infarction and heart failure.

Pre-exposure Prophylaxis With Various Doses of Hydroxychloroquine Among Healthcare Personnel With High-Risk Exposure to COVID-19: A Randomized Controlled Trial.

Objective This trial aimed to evaluate the safety and efficacy of pre-exposure prophylaxis (PrEP) with various hydroxychloroquine (HCQ) doses against a placebo among healthcare personnel (HCP) with high-risk exposure to coronavirus disease 2019 (COVID 19). Methods A phase II, randomized, placebo-controlled trial was conducted including 200 subjects with no active or past severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (antibody testing and reverse transcription-polymerase chain reaction (RT-PCR) were taken at the time of enrollment). Subjects of experimental groups one to three received HCQ in various doses and the control group received a placebo. The study outcomes in terms of safety and efficacy were monitored. Participants exhibiting COVID-19 symptoms were tested for SARS-CoV-2 during the study and by the end of week 12 with RT-PCR or serology testing (COVID-19 IgM/IgG antibody testing). Results Out of the total participants, 146 reported exposure to a confirmed COVID-19 case in the first month, and 192 were exposed by week 12 of the study. Moreover, the precautionary use of personal protective equipment (PPE) significantly varied; initially more than 80% of the exposed HCPs were not ensuring PPE being used by the patients treated by them, which gradually developed over time. Mild treatment-related side effects were observed among the interventional and placebo arm patients. There was no significant clinical benefit of PrEP with HCQ as compared to placebo (p>0.05). Conclusion It is concluded that the PrEP HCQ does not significantly prevent COVID-19 among high-risk HCPs.

Loss of Uncoupling Protein 3 Attenuates Western Diet-Induced Obesity, Systemic Inflammation, and Insulin Resistance in Rats.

OBJECTIVE: Uncoupling protein 3 (UCP3) is a mitochondrial carrier related to fatty acid metabolism. Although gene variants of UCP3 are associated with human obesity, their contribution to increased adiposity remains unclear. This study investigated the impact that loss of UCP3 has on diet-induced obesity in rats. METHODS: Male UCP3 knockout rats (ucp3-/- ) and wild-type littermates (ucp3+/+ ) were fed a high-fat, high-carbohydrate Western diet for 21 weeks. Body composition was analyzed by EchoMRI. Whole-body insulin sensitivity and rates of tissue glucose uptake were determined by using hyperinsulinemic-euglycemic clamp. Changes in tissue physiology were interrogated by microscopy and RNA sequencing. RESULTS: Loss of UCP3 decreased fat mass gain, white adipocytes size, and systemic inflammation. The ucp3-/- rats also exhibited preserved insulin sensitivity and increased glucose uptake in interscapular brown adipose tissue (iBAT). Brown adipocytes from ucp3-/- rats were protected from cellular degeneration caused by lipid accumulation and from reactive oxygen species-induced protein sulfonation. Increased glutathione levels in iBAT from ucp3-/- rats were linked to upregulation of genes encoding enzymes from the transsulfuration pathway in that tissue. CONCLUSIONS: Loss of UCP3 partially protects rats from diet-induced obesity. This phenotype is related to induction of a compensatory antioxidant mechanism and prevention of iBAT whitening.

Dietary Fat and Sugar Differentially Affect ß-Adrenergic Stimulation of Cardiac ERK and AKT Pathways in C57BL/6 Male Mice Subjected to High-Calorie Feeding.

BACKGROUND: High dietary fat and sugar promote cardiac hypertrophy independently from an increase in blood pressure. The respective contribution that each macronutrient exerts on cardiac growth signaling pathways remains unclear. OBJECTIVE: The goal of this study was to investigate the mechanisms by which high amounts of dietary fat and sugar affect cardiac growth regulatory pathways. METHODS: Male C57BL/6 mice (9 wk old; n = 20/group) were fed a standard rodent diet (STD; kcal% protein-fat-carbohydrate, 29-17-54), a high-fat diet (HFD; 20-60-20), a high-fat and high-sugar Western diet (WD; 20-45-35), a high-sugar diet with mixed carbohydrates (HCD; 20-10-70), or a high-sucrose diet (HSD; 20-10-70). Body composition was assessed weekly by EchoMRI. Whole-body glucose utilization was assessed with an intraperitoneal glucose tolerance test. After 6 wk on diets, mice were treated with saline or 20 mg/kg isoproterenol (ISO), and the activity of cardiac growth regulatory pathways was analyzed by immunoblotting. Data were analyzed by ANOVA with data from the STD group included for references only. RESULTS: Compared with HCD and HSD, WD and HFD increased body fat mass 2.7- to 3.8-fold (P < 0.001), induced glucose intolerance (P < 0.001), and increased insulin concentrations >1.5-fold (P < 0.05), thereby enhancing basal and ISO-stimulated AKT phosphorylation at both threonine 308 and serine 473 residues (+25-63%; P < 0.05). Compared with HFD, the high-sugar diets potentiated ISO-mediated stimulation of the glucose-sensitive kinases PYK2 (>47%; P < 0.05 for HCD and HSD) and ERK (>34%; P < 0.05 for WD, HCD, and HSD), thereby leading to increased phosphorylation of protein synthesis regulator S6K1 at threonine 389 residue (>64%; P < 0.05 for WD, HCD, and HSD). CONCLUSIONS: Dietary fat and sugar affect cardiac growth signaling pathways in C57BL/6 mice through distinct and additive mechanisms. The findings may provide new insights into the role of overnutrition in pathological cardiac remodeling.