Enhancement of low frequency sound absorption by placing thin plates on surface or between layers of porous materials.

Rigid thin plates can be used, either on the surface or between layers of materials, to improve the sound absorption properties of porous materials at low frequencies, especially for materials with low sound absorption. Measurement results obtained from a 100 mm impedance tube, for different combinations of porous materials and thin plates, are supplied. Possible physical explanations are discussed.

Endogenous Nampt upregulation is associated with diabetic nephropathy inflammatory-fibrosis through the NF-κB p65 and Sirt1 pathway; NMN alleviates diabetic nephropathy inflammatory-fibrosis by inhibiting endogenous Nampt.

Nicotinamide phosphoribosyltransferase (Nampt) is a key enzyme in the nicotinamide adenine dinucleotide (NAD) biosynthetic pathway. Exogenous extra cellular Nampt has been reported to increase the synthesis of pro-fibrotic molecules in various types of renal cells. However, the role of endogenous Namptenzymatic activity in diabetic renal cells, particularly those associated with inflammation and fibrosis through the nuclear factor (NF)-κB p65 and sirtuin 1 (Sirt1) pathway is still unknown.

Overexpressed eNOS upregulates SIRT1 expression and protects mouse pancreatic β cells from apoptosis.

Loss of sirtuin 1 (SIRT1) activity may be associated with metabolic diseases, including diabetes. The aim of the present study was to investigate the potential effects of overexpressed endothelial nitric oxide synthase (eNOS) on cell proliferation and apoptosis with SIRT1 activation in the Min6 mouse pancreatic β cell line. A pcDNA3.

[Sugar characterization of mini-watermelon and rapid sugar determination by near infrared diffuse reflectance spectroscopy].

In the present paper, the distribution of sugar level within the mini-watermelon was studied, a new sugar characterization method of mini-watermelon using average sugar level, the highest sugar level and the lowest sugar level index is proposed. Feasibility of nondestructive determination of mini-watermenlon sugar level using diffuse reflectance spectroscopy information was investigated by an experiment. PLS models for measuring the 3 sugar levels were established.

Effects of high concentration glucose on the expression of NF-kappaB, Bax and cytochrome C and apoptosis of islet cells in mice.

The roles of NF-kappaB (NF-kappaB) expression, Bax activity and cytochrome C (Cyt C) release, apoptosis of islet cells induced by high concentration glucose were explored in vitro. Pancreatic islet cells, which were isolated from Kunming mice, were cultured with different concentrations of glucose in DMEM, and divided into the following groups: G1, G2, G3, G4, G5, and G6 groups, corresponding to the glucose concentrations of 5.6, 7.

[High glucose lowers insulin receptor substrate 2 expression and induces apoptosis in mouse islet cells in vitro].

Objective: To investigate the role of insulin receptor substrate 2 (IRS2) and Bax on mouse islet cell apoptosis in the presence of high glucose in vitro.

Methods: The pancreatic islet cells were isolated from Kunming mice and divided into 6 groups (G1-G6 groups) for a 72-h culture in the media containing different concentrations of glucose (5.6, 7.

Effects of targeted Bcl-2 expression in mitochondria or endoplasmic reticulum on renal tubular cell apoptosis.

Bcl-2 family proteins are central regulators of apoptosis. As the prototypic member, Bcl-2 protects various types of cells against apoptotic insults. In mammalian cells, Bcl-2 has a dual subcellular localization, in mitochondria and endoplasmic reticulum (ER).

Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins.

Mitochondrial injury, characterized by outer membrane permeabilization and consequent release of apoptogenic factors, is a key to apoptosis of mammalian cells. Bax and Bak, two multidomain Bcl-2 family proteins, provide a requisite gateway to mitochondrial injury. However it is unclear how Bax and Bak cooperate to provoke mitochondrial injury and whether their roles are redundant.