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Obesity is a major risk factor for diabetes and cardiovascular diseases such as hypertension, heart failure, and stroke. Impaired endothelial function occurs in the earliest stages of obesity and underlies vascular alterations that give rise to cardiovascular disease. However, the mechanisms that link weight gain to endothelial dysfunction are ill-defined. Increasing evidence suggests that endothelial cells are not a population of uniform cells but are highly heterogeneous and are organized as a communicating multicellular network that controls vascular function.

To investigate the hypothesis that disrupted endothelial heterogeneity and network-level organization contribute to impaired vascular reactivity in obesity.

To study obesity-related vascular function without complications associated with diabetes, a state of prediabetic obesity was induced in rats. Small artery diameter recordings confirmed nitric-oxide mediated vasodilator responses were dependent on increases in endothelial calcium levels andnse. Altered cell heterogeneity and arrangement in obesity decreases endothelial function and provides a novel framework for understanding compromised endothelial function in cardiovascular disease.

The distribution of cells in the endothelial network is critical in determining overall vascular response. Altered cell heterogeneity and arrangement in obesity decreases endothelial function and provides a novel framework for understanding compromised endothelial function in cardiovascular disease.Over the past decade, the study of metabolic abnormalities in cancer cells has risen dramatically. Cancer cells can thrive in challenging environments, be it the hypoxic and nutrient-deplete tumor microenvironment or a distant tissue following metastasis. The ways in which cancer cells utilize lipids are often influenced by the complex interactions within the tumor microenvironment and adjacent stroma. Adipocytes can be activated by cancer cells to lipolyze their triglyceride stores, delivering secreted fatty acids to cancer cells for uptake through numerous fatty acid transporters. Cancer-associated fibroblasts are also implicated in lipid secretion for cancer cell catabolism and lipid signaling leading to activation of mitogenic and migratory pathways. As these cancer-stromal interactions are exacerbated during tumor progression, fatty acids secreted into the microenvironment can impact infiltrating immune cell function and phenotype. Lipid metabolic abnormalities such as increased fatty acid oxidation and de novo lipid synthesis can provide survival advantages for the tumor to resist chemotherapeutic and radiation treatments and alleviate cellular stresses involved in the metastatic cascade. In this review, we highlight recent literature that demonstrates how lipids can shape each part of the cancer lifecycle and show that there is significant potential for therapeutic intervention surrounding lipid metabolic and signaling pathways.In this paper, a basic fractional-order model is proposed to describe the transmission of African swine fever. Two cases are considered constant control and optimal control. In the former case, the existence and uniqueness of positive solution is proved firstly; then the basic reproduction number and the sufficient conditions for the stability of two equilibriums are obtained by using the next generation matrix method and Lyapunov LaSalle’s invariance principle. In the latter case, optimal control is considered. By using the Hamiltonian function and Pontryagin’s maximum principle, the optimal control formula is obtained. MSX In addition, some examples and numerical simulations (based on Adama-Bashforth-Moulton predictor-corrector method) are performed to verify the theoretical results. At last, we present some brief discussion and conclusion.

The underlying mechanism of cognitive impairment in bipolar II depression (BD II) remains unclear. Studies show disturbances of the hypothalamus-pituitary-thyroid (HPT) axis are suspected of correlating to brain neurometabolic alterations and cognitive deficits in psychiatric disorders. While, the nature of their inter-relationships in BD II depression remain enigmatic.

106 patients with unmedicated BD II depression and 100 healthy controls underwent cognitive function assessment using Trail Making Test, Part-A (TMT-A), Digit Symbol Substitution Test (DSST), and Semantic Verbal Fluency testing (SVF). Of those, 69 patients and 53 healthy controls had serum thyroid hormone levels measured including free tri-iodothyronine (FT3), total tri-iodothyronine (TT3), free thyroxin (FT4), total thyroxin (TT4) and thyroid-stimulating hormone (TSH). Additionally, 79 of the patients and 76 of the healthy controls underwent proton magnetic resonance spectroscopy (H-MRS) to obtain ratios of N-acetyl aspartate to creatine ohort.

Our results demonstrate coinciding thyroid hormone abnormalities, cognitive dysfunction, and neurometabolic alterations of the PFC-thalamic circuitry occur in an early course of BD II depression. Further understanding of the interaction between thyroid-stimulating hormone and NAA/Cr of PFC-thalamic circuitry may shed light on the etiology of associated cognitive impairment.

Our results demonstrate coinciding thyroid hormone abnormalities, cognitive dysfunction, and neurometabolic alterations of the PFC-thalamic circuitry occur in an early course of BD II depression. Further understanding of the interaction between thyroid-stimulating hormone and NAA/Cr of PFC-thalamic circuitry may shed light on the etiology of associated cognitive impairment.Substance addiction is a chronic and complicated disease involving genetic and environmental factors. Coregulated by the above factors, perturbations of the gut microbiome have been shown to have an essential role in the development of many neuropsychiatric disorders, including addiction. However, shifts in the gut microbiome during different stages of morphine addiction remain uncharacterized. In the present study, we harvested fecal samples from mice at the acquisition (both the control and morphine groups), extinction and reinstatement stages of morphine-induced conditioned place preference (CPP). Gut microbiome profiles were detected with 16S ribosomal RNA gene sequencing. We observed an increase in community richness following morphine conditioning, and it decreased after 4 weeks of abstinence. The abundance of Verrucomicrobia increased and Bacteroides decreased at the acquisition of morphine-induced CPP, while a recovery trend was found at the extinction stage. Several discriminative genera were identified for the characterization of different stages of morphine CPP.