Assessment of left ventricular function in patients with type 2 diabetes mellitus by non-invasive myocardial work.

Background: Diabetes mellitus (DM) is a chronic disease that poses a serious risk of cardiovascular diseases. Therefore, early detection of impaired cardiac function with non-invasive myocardial imaging is critical for improving the prognosis of patients with DM. Purpose: This study aimed to assess the left ventricular (LV) function in patients with type 2 diabetes mellitus (T2DM) by non-invasive myocardial work technique. Materials and methods: In all, 67 patients with T2DM and 28 healthy controls were included and divided into a DM group and a control group. Two-dimensional dynamic images of apical three-chamber view, apical two-chamber view, and apical four-chamber view were collected from all subjects, consisting of at least three cardiac cycles. LV myocardial strain parameters, including global longitudinal strain (GLS) and peak strain dispersion (PSD), as well as myocardial work parameters, including global constructive work (GCW), global wasted work (GWW), global work index (GWI), and global work efficiency (GWE), were obtained and analyzed. Results: A total of 15 subjects were randomly selected to assess intra-observer and inter-observer consistency of myocardial work parameters and strain parameters, which showed excellent results (intra-class correlation coefficients: 0.856 - 0.983, P<0.001). Compared with the control group, the DM group showed significantly higher PSD (37.59 ± 17.18 ms vs. 27.72 ± 13.52 ms, P<0.05) and GWW (63.98 ± 43.63 mmHg% vs. 39.28 ± 25.67 mmHg%, P<0.05), and lower GWE (96.38 ± 2.02% vs. 97.72 ± 0.98%, P<0.001). Furthermore, the PSD was positively correlated with GWW (r = 0.565, P<0.001) and negatively correlated with GWE (r = -0.569, P<0.001). Conclusion: Uncoordinated LV myocardial strain, higher GWW, and lower GWE in patients with T2DM may serve as indicators for the early assessment of cardiac impairment in T2DM.

The role of regulatory T cells on the activation of astrocytes in the brain of high-fat diet mice following lead exposure.

Lead (Pb) exposure can cause damage to the central nervous system (CNS)*. Pb can accumulate in the hippocampus, leading to learning and memory impairments. Recent studies have shown that high-fat diet (HFD) is also associated with cognitive impairment. However, there are few reports on CNS damage due to HFD and Pb exposure. We aimed to investigate the effect of Pb on cognitive functions of HFD-fed mice, focusing on the role of regulatory T (Treg) cells in astrocyte activation. C57BL/6J mice were randomly divided into control, HFD, Pb, and HFD + Pb groups. TGF-ß and IL-10 secreted by Treg cells and the intracellular transcription factor Foxp3 were evaluated as a measure of Treg cell function; astrocyte activation was assessed by evaluating glial fibrillary acidic protein (GFAP) expression. The learning and memory ability was significantly lower in the HFD + Pb group than in other groups. The brain Treg cell ratio was significantly decreased and the protein levels of TGF-ß, IL-10, and Foxp3 were significantly lower, whereas the protein level of GFAP was higher in the HFD + Pb group. The hippocampus of the HFD + Pb group mice showed significantly higher levels of neurotoxic reactive astrocyte markers and astrogliosis was also much higher compared to HFD and Pb groups. Furthermore, all-trans retinoic acid treatment increased the brain Treg cell ratio, reversed cognitive decline, and suppressed astrocyte activation in the HFD + Pb group mice. We concluded that HFD along with Pb exposure could aggravate the activation of astrocytes in the brain, and the brain Treg cells may be involved in inhibiting astrocyte activation in HFD-fed mice exposed to Pb.

Obtaining of Mesoporous Aluminosilicates with High Hydrothermal Stability by Composite Organic Templates: Utility and Mechanism.

We have reported the synthesis of mesoporous aluminosilicates (MAs) with high hydrothermal stability via assembly of basic characteristic structure units of typical microporous zeolite Y. In spite of this, high consumption of organic template and H2O remains a major obstacle to its industrial application. Herein, a facile and effective strategy called "composite templates" was employed to decrease significantly the amount of P123 and H2O. In this method, composite micelles of P123/poly(vinyl alcohol) (PVA) could be more easily dispersed in the solution due to the lowering of water's surface tension caused by the free hydroxyl groups of PVA. Moreover, the improved assembly ability of composite micelles in high concentration solution leads to the synthesis of hydrothermally stable MAs with 45% decrease of organic template P123 and 81% that of water amount. It was found that by the introduction of composite templates, the textural properties such as the surface area of materials, volume of pore, size of pore, and thickness were enlarged simultaneously. Meanwhile, this article presented an understanding into the assembly of composite micelles in the process of synthesis of MAs.

Effects of lead exposure on the activation of microglia in mice fed with high-fat diets.

Lead (Pb) exposure can cause central nervous system (CNS) damage. The process of Pb neurotoxicity is accompanied by the microglia activation. In addition, microglia activation was observed under the intervention of high-fat diets (HFD). This study was designed to investigate the effect of Pb on the cognitive function of mice with HFD, with focus on the microglia activation in brain. Male C57BL/6J mice, 8 weeks of age, were randomly divided into control, HFD, Pb, and HFD + Pb groups. The results showed that HFD following Pb exposure could exacerbate the learning and memory impairment in mice. Pb exposure could promote microglia activation and increase the expression of M1 microglia marker and decrease the expression of M2 microglia marker in the hippocampus of mice with HFD. Our finding suggested that Pb exposure may aggravate CNS damage by promoting M1 polarization and inhibiting M2 polarization of hippocampal microglia in HFD mice.