Droplet Morphology-Based Wettability Tuning and Design of Fog Harvesting Mesh to Minimize Mesh-Clogging.

Fog harvesting relies on intercepting atmospheric or industrial fog by placing a porous obstacle, for example, a mesh and collecting the deposited water. In the face of global water scarcity, such fog harvesting has emerged as a viable alternative source of potable water. Typical fog harvesting meshes suffer from poor collection efficiency due to aerodynamic bypassing of the oncoming fog stream and poor collection of the deposited water from the mesh. One pestering challenge in this context is the frequent clogging up of mesh pores by the deposited fog water, which not only yields low drainage efficiency but also generates high aerodynamic resistance to the oncoming fog stream, thereby negatively impacting the fog collection efficiency. Minimizing the clogging is possible by rendering the mesh fibers superhydrophobic, but that entails other detrimental effects like premature dripping and flow-induced re-entrainment of water droplets into the fog stream from the mesh fiber. Herein, we improvise on traditional interweaved metal mesh designs by defining critical parameters, viz., mesh pitch, shade coefficient, and fiber wettability, and deducing their optimal values from numerically and experimentally observed morphology of collected fog water droplets under various operating scenarios. We extend our investigations over a varying range of mesh-wettability, including superhydrophilic and hydrophobic fibers, and go on to find optimal shade coefficients which would theoretically render clog-proof fog harvesting meshes. The aerodynamic, deposition, and overall collection efficiencies are characterized. Hydrophobic meshes with square pores, having fiber diameters smaller than the capillary length scale of water, and an optimal shade coefficient are found to be the most effective design of such clog-proof meshes.

A Review on Ethnobotany, Phytochemistry and Pharmacological Activities of Euphorbia antiquorum L.

Euphorbia antiquorum L. is a small plant in the Euphorbiaceae family that is found primarily in tropical and subtropical Asia. It has a long tradition of being utilized in Chinese, Ayurvedic, and other traditional systems for a variety of ailments. To date, More than 116 bioactive constituents were isolated from Euphorbia antiquorum, with diterpenoids being the most abundant. Extracts and isolated chemicals from various portions of the plant have demonstrated significant pharmacological activities such as anti-inflammatory, analgesic, antidiabetic, anticancer etc. It is necessary to conduct an in-depth investigation of the phytochemicals along with the pharmacological properties of E. antiquorum. This review summarised the knowledge of ethnobotany, phytochemistry and pharmacological activities of the plant which will provide a better understanding to clarify the traditional uses of the species and its relation to modern pharmacology which will ultimately pave the way for its clinical application.

Haplo-insufficiency of Profilin1 in vascular endothelial cells is beneficial but not sufficient to confer protection against experimentally induced atherosclerosis.

Actin cytoskeleton plays an important role in various aspects of atherosclerosis, a key driver of ischemic heart disease. Actin-binding protein Profilin1 (Pfn1) is overexpressed in atherosclerotic plaques in human disease, and Pfn1, when partially depleted globally in all cell types, confers atheroprotection in vivo. This study investigates the impact of endothelial cell (EC)-specific partial loss of Pfn1 expression in atherosclerosis development. We utilized mice engineered for conditional heterozygous knockout of the Pfn1 gene in ECs, with atherosclerosis induced by depletion of hepatic LDL receptor by gene delivery of PCSK9 combined with high-cholesterol diet. Our studies show that partial depletion of EC Pfn1 has certain beneficial effects marked by dampening of select pro-atherogenic cytokines (CXCL10 and IL7) with concomitant reduction in cytotoxic T cell abundance but is not sufficient to reduce hyperlipidemia and confer atheroprotection in vivo. In light of these findings, we conclude that atheroprotective phenotype conferred by global Pfn1 haplo-insufficiency requires contributions of additional cell types that are relevant for atherosclerosis progression.

Haplo-insufficiency of Profilin1 in vascular endothelial cells is beneficial but not sufficient to confer protection against experimentally induced atherosclerosis.

Actin cytoskeleton plays an important role in various aspects of atherosclerosis, a key driver of ischemic heart disease. Actin-binding protein Profilin1 (Pfn1) is overexpressed in atherosclerotic plaques in human disease, and Pfn1, when partially depleted globally in all cell types, confers atheroprotection in vivo . This study investigates the impact of endothelial cell (EC)-specific partial loss of Pfn1 expression in atherosclerosis development. We utilized mice engineered for conditional heterozygous knockout of the Pfn1 gene in ECs, with atherosclerosis induced by depletion of hepatic LDL receptor by gene delivery of PCSK9 combined with high-cholesterol diet. Our studies show that partial depletion of EC Pfn1 has certain beneficial effects marked by dampening of select pro-atherogenic cytokines (CXCL10 and IL7) with concomitant reduction in cytotoxic T cell abundance but is not sufficient to reduce hyperlipidemia and confer atheroprotection in vivo . In light of these findings, we conclude that atheroprotective phenotype conferred by global Pfn1 haplo-insufficiency requires contributions of additional cell types that are relevant for atherosclerosis progression.

The recent update and advancements of natural products in targeting the Wnt/ß-Catenin pathway for cancer prevention and therapeutics.

The Wnt/ß-Catenin pathway (Wnt/ß-CatP) is implicated in accelerating carcinogenesis and cancer progression, contributing to increased morbidity and treatment resistance. Even though it holds promise as a focus for cancer treatment, its intricate nature and diverse physiological effects pose significant challenges. Recent years have witnessed significant advancements in this domain, with numerous natural products demonstrating promising preclinical anti-tumor effects and identified as inhibitors of the Wnt/ß-CatP through various upstream and downstream mechanisms. This study provides a comprehensive overview of the current landscape of Wnt/ß-Cat-targeted cancer therapy, examining the impact of natural products on Wnt/ß-Cat signaling in both cancer prevention and therapeutic contexts. A comprehensive search was conducted on scientific databases like SciFinder, PubMed, and Google Scholar to retrieve relevant literature on Wnt-signaling, natural products, ß-Catenin (ß-Cat), and cancer from 2020 to January 2024. As per the analysis of the relevant reference within the specified period, it has been noted that a total of 58 phytoconstituents, predominantly phenolics, followed by triterpenoids and several other classes, along with a limited number of plant extracts, have exhibited activity targeting the Wnt/ß-CatP. Most ß-Cat regulating modulators restrict cancer cell development by suppressing ß-Cat expression, facilitating proteasomal degradation, and inhibiting nuclear translocation. Multiple approaches have been devised to block the activity of ß-Cat in cancer therapy, a key factor in cancer progression, leading to the discovery of various Wnt/ß-CatP regulators. However, their exploration remains limited, necessitating further research using clinical models for potential clinical use in cancer prevention and therapeutics.

Optimal sampling of spatial patterns improves deep learning-based early warning signals of critical transitions.

Complex spatio-temporal systems like lakes, forests and climate systems exhibit alternative stable states. In such systems, as the threshold value of the driver is crossed, the system may experience a sudden (discontinuous) transition or smooth (continuous) transition to an undesired steady state. Theories predict that changes in the structure of the underlying spatial patterns precede such transitions. While there has been a large body of research on identifying early warning signals of critical transitions, the problem of forecasting the type of transitions (sudden versus smooth) remains an open challenge. We address this gap by developing an advanced machine learning (ML) toolkit that serves as an early warning indicator of spatio-temporal critical transitions, Spatial Early Warning Signal Network (S-EWSNet). ML models typically resemble a black box and do not allow envisioning what the model learns in discerning the labels. Here, instead of naively relying upon the deep learning model, we let the deep neural network learn the latent features characteristic of transitions via an optimal sampling strategy (OSS) of spatial patterns. The S-EWSNet is trained on data from a stochastic cellular automata model deploying the OSS, providing an early warning indicator of transitions while detecting its type in simulated and empirical samples.

Fusobacterium nucleatum: An Overview of Evidence, Demi-Decadal Trends, and Its Role in Adverse Pregnancy Outcomes and Various Gynecological Diseases, including Cancers.

Gynecological and obstetric infectious diseases are crucial to women's health. There is growing evidence that links the presence of Fusobacterium nucleatum (F. nucleatum), an anaerobic oral commensal and potential periodontal pathogen, to the development and progression of various human diseases, including cancers. While the role of this opportunistic oral pathogen has been extensively studied in colorectal cancer in recent years, research on its epidemiological evidence and mechanistic link to gynecological diseases (GDs) is still ongoing. Thus, the present review, which is the first of its kind, aims to undertake a comprehensive and critical reappraisal of F. nucleatum, including the genetics and mechanistic role in promoting adverse pregnancy outcomes (APOs) and various GDs, including cancers. Additionally, this review discusses new conceptual advances that link the immunomodulatory role of F. nucleatum to the development and progression of breast, ovarian, endometrial, and cervical carcinomas through the activation of various direct and indirect signaling pathways. However, further studies are needed to explore and elucidate the highly dynamic process of host-F. nucleatum interactions and discover new pathways, which will pave the way for the development of better preventive and therapeutic strategies against this pathobiont.

Ventricular arrhythmia inducibility in porcine infarct model after stereotactic body radiation therapy.

BACKGROUND: Ventricular arrhythmia (VA) is the primary mechanism of sudden death in patients with structural heart disease. Cardiac stereotactic body radiation therapy (SBRT) delivered to the scar in the left ventricle significantly reduces the burden of VA. OBJECTIVE: The goal of this study was to investigate the impact of SBRT on scar morphology and VA inducibility in a porcine infarct model. METHODS: Myocardial infarction (MI) was created in 10 Yorkshire pigs involving the left anterior descending artery territory. Cardiac positron emission tomography and computed tomography were performed for targeted SBRT. Alternative pigs received SBRT at 25 Gy in a single fraction. The terminal experiment included endocardial mapping, programmed ventricular stimulation, and tissue harvesting. RESULTS: Of the 10 pigs infarcted, 2 died prematurely after MI and 8 (4 MI and 4 MI+SBRT) survived. Mean time from MI to SBRT was 48 ± 12 days, and mean time from SBRT to harvest was 32 ± 12 days. Scar was localized on intracardiac mapping in all pigs, and the scar was denser in the MI+SBRT compared with the MI-only group (33% ± 20% vs 14% ± 11%; P = .07). All 4 MI pigs had inducible VA during programmed stimulation, whereas only 1 of 4 pigs had inducible VA in the MI+SBRT arm (100% vs 25%; P = .07). No myocardial fibrosis was seen in the remote areas in either group. CONCLUSION: SBRT reduced VA inducibility in pigs with scarring after MI. Endocardial mapping revealed denser scar in pigs receiving SBRT compared with those that did not, suggesting that SBRT suppresses VA inducibility through better scar homogenization.

Role of the CCL5 and Its Receptor, CCR5, in the Genesis of Aldosterone-Induced Hypertension, Vascular Dysfunction, and End-Organ Damage.

BACKGROUND: Aldosterone has been described to initiate cardiovascular diseases by triggering exacerbated sterile vascular inflammation. The functions of CCL5 (C-C motif chemokine ligand 5) and its receptor CCR5 (C-C motif chemokine receptor 5) are well known in infectious diseases, their contributions to aldosterone-induced vascular injury and hypertension remain unknown. METHODS: We analyzed the vascular profile, blood pressure, and renal damage in wild-type (CCR5+/+) and CCR5 knockout (CCR5-/-) mice treated with aldosterone (600 µg/kg per day for 14 days) while receiving 1% saline to drink. Vascular function was analyzed in aorta and mesenteric arteries, blood pressure was measured by telemetry and renal injury and inflammation were analyzed via histology and flow cytometry. Endothelial cells were used to study the molecular signaling whereby CCL5 induces endothelial dysfunction. RESULTS: Aldosterone treatment resulted in exaggerated CCL5 circulating levels and vascular CCR5 expression in CCR5+/+ mice accompanied by endothelial dysfunction, hypertension, and renal inflammation and damage. CCR5-/- mice were protected from these aldosterone-induced effects. Mechanistically, we demonstrated that CCL5 increased NOX1 (NADPH oxidase 1) expression, reactive oxygen species formation, NFκB (nuclear factor kappa B) activation, and inflammation and reduced NO production in isolated endothelial cells. These effects were abolished by antagonizing CCR5 with Maraviroc. Finally, aorta incubated with CCL5 displayed severe endothelial dysfunction, which is prevented by blocking NOX1, NFκB, or CCR5. CONCLUSIONS: Our data demonstrate that CCL5/CCR5, through activation of NFκB and NOX1, is critically involved in aldosterone-induced vascular and renal damage and hypertension placing CCL5 and CCR5 as potential therapeutic targets for conditions characterized by aldosterone excess.