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At present, China’s food inspection and testing mainly concentrate in food processing, packaging and sale, so that supervision over the food production process is lacking, and the regulation of the large number of production and operation entities and of the intertwining of various risks is ineffective. The cost of controlling food quality and safety by means of inspection and testing is high, and a large amount of data has not been fully utilized, causing lack of effective support for quality control in food processing. This article summarizes the current status of research on food inspection and quality control in China, analyzes the existing problems and puts forward some suggestions such as strengthening the ability to analyze and mine data, finding the law of food safety risks, targeted detection of high-risk indicators according to the law, improving the detection efficiency and the risk control ability, and guiding the monitoring and management of food safety risks. Research on quality control in food processing by comprehensive application of test data can promote the development of quality control in food processing, which can in turn improve the level of risk control and ensure food safety.

Pancreatic β-cell dysfunction caused by obesity can be associated with alterations in the levels of miRNAs. However, the role of miRNAs in such processes remains elusive. Here, we show that pancreatic islet miR-27a-5p, which is markedly increased in obese mice and impairs insulin secretion, is mainly delivered by visceral adipocyte–derived extracellular vesicles (EVs). Depleting miR-27a-5p significantly improved insulin secretion and glucose intolerance in db / db mice. Supporting the function of EV miR-27a-5p as a key pathogenic factor, intravenous injection of miR-27a-5p–containing EVs showed their distribution in mouse pancreatic islets. Tracing the injected adeno-associated virus (AAV)-miR-27a-5p (AAV-miR-27a) or AAV-FABP4-miR-27a-5p (AAV-FABP4-miR-27a) in visceral fat resulted in upregulating miR-27a-5p in EVs and serum and elicited mouse pancreatic β-cell dysfunction. Mechanistically, miR-27a-5p directly targeted L-type Ca2+ channel subtype CaV1.2 (Cacna1c) and reduced insulin secretion in β-cells. Overexpressing mouse CaV1.2 largely abolished the insulin secretion injury induced by miR-27a-5p. These findings reveal a causative role of EV miR-27a-5p in visceral adipocyte–mediated pancreatic β-cell dysfunction in obesity-associated type 2 diabetes mellitus. Article Highlights: miR-27a-5p expression in the islets is increased in obesity-associated diabetes mouse models. miR-27a-5p overexpression in β-cells impairs β-cell function in vitro and in vivo. Visceral adipocyte–derived extracellular vesicles and their cargo miR-27a-5p lead to β-cell insulin secretion injury and glucose intolerance by targeting L-type Ca2+ channel subtype CaV1.2. Blockage of visceral adipocyte extracellular vesicle miR-27a-5p expression improves β-cell insulin secretion and glucose tolerance in db / db mice. [ABSTRACT FROM AUTHOR]

The Shadongnan structural zone in the western Bohai Sea area is located in the transitional position from the Shaleitian uplift to the Sha'nan sag. Due to the influence of various factors such as inherited uplift, syn-depositional faults and ancient valleys in different periods, the development of sedimentary facies is relatively complex, restricting the further oil and gas exploration and development. We restored the ancient landform of each three-level sequence in the Dongying formation in the sedimentary period using the strata thickness method, identifying uplifts, slopes, ancient valleys, fault troughs, and shallow and deep sub-sags in the study area. Meanwhile, there are two kinds of ancient landform in the Shadongnan structural zone bounded by the NNE-trending transform fault, with the valley-paleoslope-fault slope-break in the west and the valley-multistage fault slope-break in the east. The former is composed of eroded valleys, buried hill slopes and early syn-depositional faults, while the latter eroded valleys and two or three syn-depositional faults with the same direction and different periods. Our study showed that the valleys located at the edge of the uplifts were the source channels in the early stage and filled with sediments in the late stage. The distribution and filling of the sedimentary system of the valley-paleoslope-fault slope-break were mainly controlled by the ancient slope-fault slopes, and the syn-depositional faults controlling the fault slopes were relatively active in the Shahejie formation and controlled the deposition and filling of the lowstand fans and turbidite fans. By the SQ-Ed3 period, the fault activities gradually weakened, and the fault slope-break distinct the fan delta plain and front in SQ-Ed3 from the deposition of the braided river delta front and shallow lake in SQ-Ed2d and SQ-Ed2u. The Shadongnan No.1 syn-depositional fault with the valley-multistage fault slope-break, which was developed and activated in SQ-Ed3, controlled the formation of the deep sub-sags and the development of the small fan deltas under the first slope break. The Sha'nan syn-depositional fault both formed and activated in SQ-Ed2d was acted as the second slope break separating the bulges and slopes, and controlled the depositional filling of the small fan delta in SQ-Ed2d.

PKA signaling is important for the post-translational modification of proteins, especially those in cardiomyocytes involved in cardiac excitation-contraction coupling. PKA activity is spatially and temporally regulated through compartmentalization by protein kinase A anchoring proteins. Cypher/ZASP, a member of PDZ-LIM domain protein family, is a cytoskeletal protein that forms multiprotein complexes at sarcomeric Z-lines. It has been demonstrated that Cypher/ZASP plays a pivotal structural role in the structural integrity of sarcomeres, and several of its mutations are associated with myopathies including dilated cardiomyopathy. Here we show that Cypher/ZASP, interacting specifically with the type II regulatory subunit RIIα of PKA, acted as a typical protein kinase A anchoring protein in cardiomyocytes. In addition, we show that Cypher/ZASP itself was phosphorylated at Ser(265) and Ser(296) by PKA. Furthermore, the PDZ domain of Cypher/ZASP interacted with the L-type calcium channel through its C-terminal PDZ binding motif. Expression of Cypher/ZASP facilitated PKA-mediated phosphorylation of the L-type calcium channel in vitro. Additionally, the phosphorylation of the L-type calcium channel at Ser(1928) induced by isoproterenol was impaired in neonatal Cypher/ZASP-null cardiomyocytes. Moreover, Cypher/ZASP interacted with the Ser/Thr phosphatase calcineurin, which is a phosphatase for the L-type calcium channel. Taken together, our data strongly suggest that Cypher/ZASP not only plays a structural role for the sarcomeric integrity, but is also an important sarcomeric signaling scaffold in regulating the phosphorylation of channels or contractile proteins.