Enhancing Mechanical Properties and Microstructures of Mass-Manufactured Sand Concrete by Incorporating Granite Powder.

The production of manufactured sand and stone processing can cause dust pollution due to the generation of a significant amount of stone powder. This dust (mainly granite powder) was collected and incorporated as a cement replacement into mass-manufactured sand concrete in order to enhance the mechanical properties and microstructures. The heat of the hydration was measured by adding the granite powder into the cementitious material system.

[Analysis on the Current Situation of Phytoplankton in the Typical River-Lake Ecotone of Lake Poyang].

The typical river-lake ecotone (tail end area) of Poyang Lake, which is a sensitive area and prone to outbreaks of cyanobacteria bloom, is vulnerable to frequent human activities. To explore the diversity of phytoplankton community structure and the relevant driving mechanism in the typical river lake junction area of Poyang Lake, the water quality and phytoplankton at seven sampling points in the typical river lake junction area of Poyang Lake, at six sampling points in the middle section of Poyang Lake River, and at one sampling point in the main lake area were investigated in the field from 2019 to 2020 (dry season), April (flood season), July (wet season), and October (recession period). The results showed that there were seven phyla and 64 genera of phytoplankton in the typical river-lake ecotone of Poyang Lake, and the biomass and relative abundance of phytoplankton were dominated by diatoms and cyanobacteria.

Clinical course and treatment efficacy of COVID-19 near Hubei Province, China: A multicentre, retrospective study.

Currently, COVID-19 has been reported in nearly all countries globally. To date, little is known about the viral shedding duration, clinical course and treatment efficacy of COVID-19 near Hubei Province, China. This multicentre, retrospective study was performed in 12 hospitals in Henan and Shaanxi Provinces from 20 January to 8 February 2020.

Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes.

Obesity is a global public health concern and may lead to a variety of complications. Previous studies have indicated that adipokines and energy‑source materials contribute to obesity and obesity‑associated insulin resistance. MicroRNAs (miRs) are endogenous 20‑ to 25‑nucleotide non‑coding RNAs associated with fat metabolism.

Obesity-associated microRNA-26b regulates the proliferation of human preadipocytes via arrest of the G1/S transition.

MicroRNAs (miRNAs) are short, 20‑24 nucleotide non‑coding RNAs, which are involved in multiple biological processes, including obesity. Our previous investigation revealed that miRNA (miR)‑26b is differentially expressed in preadipocytes and mature adipocytes in humans. However, its role in the proliferation of human preadipocytes remains to be fully elucidated.

miR-148a is Associated with Obesity and Modulates Adipocyte Differentiation of Mesenchymal Stem Cells through Wnt Signaling.

Obesity results from numerous, interacting genetic, behavioral, and physiological factors. Adipogenesis is partially regulated by several adipocyte-selective microRNAs (miRNAs) and transcription factors that regulate proliferation and differentiation of human adipose-derived mesenchymal stem cells (hMSCs-Ad). In this study, we examined the roles of adipocyte-selective miRNAs in the differentiation of hMSCs-Ad to adipocytes.

The biological effects of hsa-miR-1908 in human adipocytes.

MicroRNAs (miRNAs) are small non-coding RNAs involved in the regulation of gene expression. MiR-1908 is a recently identified miRNA that is highly expressed in human adipocytes. However, it is not known what role of miR-1908 is involved in the regulation of human adipocytes.

MiR-146b is a regulator of human visceral preadipocyte proliferation and differentiation and its expression is altered in human obesity.

Visceral obesity is an independent risk factor for metabolic syndrome, and abnormal fat accumulation is linked to increases in the number and size of adipocytes. MiR-146b was a miRNA highly expressed in mature adipocytes while very lowly expressed in human mesenchymal stem cells (hMSCs) and human visceral preadipocytes (vHPA). In this paper, we mainly focused on the roles of miR-146b in adipogenesis.

Expression of microRNA-26b, an obesity-related microRNA, is regulated by free fatty acids, glucose, dexamethasone and growth hormone in human adipocytes.

MicroRNAs (miRNAs) are short non-coding RNAs that are involved in numerous biological processes, including obesity and insulin resistance. miR-26b is an obesity-related intronic miRNA located in the intron of the carboxy‑terminal domain, RNA polymerase II, polypeptide A, small phosphatase 1 gene. miR-26b is abundantly expressed in mice and mature human adipocytes, and is associated with the expression of adipokines.

TNF-α, IL-6, and leptin increase the expression of miR-378, an adipogenesis-related microRNA in human adipocytes.

Obesity has become a global public health problem associated with complications including type 2 diabetes, cardiovascular disease, and several cancers. Adipocyte differentiation (adipogenesis) plays an important role in obesity and energy homeostasis. Adipose tissue secretes multiple cytokines and adipokines which can cause the complications of obesity, especially insulin resistance.

The role of microRNA-26b in human adipocyte differentiation and proliferation.

Recent findings indicate that microRNAs (miRNAs) are involved in the regulatory network of adipogenesis and obesity. Thus far, only a few human miRNAs are known to function as adipogenic regulators, fanning interest in studies on the functional role of miRNAs during adipogenesis in humans. In a previous study, we used a microarray to assess miRNA expression during human preadipocyte differentiation.

FFAs and adipokine-mediated regulation of hsa-miR-143 expression in human adipocytes.

Accumulating evidence suggests that microRNAs (miRNAs) play an important role in regulating the pathways in adipose tissue that control processes such as adipogenesis, insulin resistance, and inflammation. MiR-143 is a well-characterized miRNA involved in adipogenesis and may be involved in regulating insulin resistance. Free fatty acids (FFAs) and adipokines, such as tumor necrosis factor-α (TNF-α), leptin, resistin, and interleukin-6 (IL-6), have already been identified as main regulators of obesity and insulin sensitivity.

MiR-335, an adipogenesis-related microRNA, is involved in adipose tissue inflammation.

During the development of obesity, adipose tissue releases a host of different adipokines and inflammatory cytokines, such as leptin, resistin, tumor necrosis factor α (TNF-α), Interleukin-6 (IL-6), and adiponectin, which mediate insulin resistance. Recently, some microRNAs (miRNAs) regulated by adiponectin were identified as novel targets for controlling adipose tissue inflammation. Therefore, the relationship between adipokines and miRNA is worth studying.

Modulation of hsa-miR-26b levels following adipokine stimulation.

MicroRNAs (miRNAs) are short non-coding RNAs that are involved in post-transcriptional regulation of gene expression. Hsa-miR-26b is an intronic miRNA located in the intron of CTDSP1 (carboxy-terminal domain, RNA polymerase II, polypeptide A, small phosphatase 1). In the present study, the expression of hsa-miR-26b was examined during human preadipocyte differentiation.

Overexpression of TFAM protects 3T3-L1 adipocytes from NYGGF4 (PID1) overexpression-induced insulin resistance and mitochondrial dysfunction.

NYGGF4, also known as phosphotyrosine interaction domain containing 1(PID1), is a recently discovered gene which is involved in obesity-related insulin resistance (IR) and mitochondrial dysfunction. We aimed to further elucidate the effects and mechanisms underlying NYGGF4-induced IR by investigating the effect of overexpressing mitochondrial transcription factor A (TFAM), which is essential for mitochondrial DNA transcription and replication, on NYGGF4-induced IR and mitochondrial abnormalities in 3T3-L1 adipocytes. Overexpression of TFAM increased the mitochondrial copy number and ATP content in both control 3T3-L1 adipocytes and NYGGF4-overexpressing adipocytes.

Knockdown of NYGGF4 (PID1) rescues insulin resistance and mitochondrial dysfunction induced by FCCP in 3T3-L1 adipocytes.

NYGGF4 is a recently identified gene that is involved in obesity-associated insulin resistance. Previous data from this laboratory have demonstrated that NYGGF4 overexpression might contribute to the development of insulin resistance (IR) and to mitochondrial dysfunction. Additionally, NYGGF4 knockdown enhanced insulin sensitivity and mitochondrial function in 3T3-L1 adipocytes.

IL-6 induces lipolysis and mitochondrial dysfunction, but does not affect insulin-mediated glucose transport in 3T3-L1 adipocytes.

Interleukin-6 (IL-6) has emerged as an important cytokine involved in the regulation of metabolism. However, the role of IL-6 in the etiology of obesity and insulin resistance is not fully understood. Mitochondria are key organelles of energy metabolism, and there is growing evidence that mitochondrial dysfunction plays a crucial role in the pathogenesis of obesity-associated insulin resistance.