Identification of characteristic aroma compounds in chicken meat and their metabolic mechanisms using gas chromatography-olfactometry, odor activity values, and metabolomics.

Aroma has an important influence on the aroma quality of chicken meat. This study aimed to identify the characteristic aroma substances in chicken meat and elucidate their metabolic mechanisms. Using gas chromatography-olfactometry and odor activity values, we identified nonanal, octanal, and dimethyl tetrasulfide as the basic characteristic aroma compounds in chicken meat, present in several breeds. Hexanal, 1-octen-3-ol, (E)-2-nonenal, heptanal, and (E,E)-2,4-decadienal were breed-specific aroma compounds found in native Chinese chickens but not in the meat of white-feathered broilers. Metabolomics analysis showed that L-glutamine was an important metabolic marker of nonanal, hexanal, heptanal, octanal, and 1-octen-3-ol. Exogenous supplementation experiments found that L-glutamine increased the content of D-glucosamine-6-P and induced the degradation of L-proline, L-arginine, and L-lysine to enhance the Maillard reaction and promote the formation of nonanal, hexanal, heptanal, octanal, and 1-octen-3-ol, thus improving the aroma profile of chicken meat.

Multi-Omics Analysis of Genes Encoding Proteins Involved in Alpha-Linolenic Acid Metabolism in Chicken.

Alpha-linolenic acid (ALA, ω-3) is an antioxidant that reduces triglyceride (TG) levels in blood, a component of cell membranes and a precursor compound of eicosapentaenoic acid (EPA, ω-3) and eicosatrienoic acid (DHA, ω-3). Fatty acid content is a quantitative trait regulated by multiple genes, and the key genes regulating fatty acid metabolism have not been systematically identified. This study aims at investigating the protein-encoding genes regulating ω-3 polyunsaturated fatty acid (PUFA) content in chicken meat. We integrated genomics, transcriptomics and lipidomics data of Jingxing yellow chicken (JXY) to explore the interactions and associations among multiple genes involved in the regulation of fatty acid metabolism. Several key genes and pathways regulating ω-3 fatty acid metabolism in chickens were identified. The upregulation of GRB10 inhibited the mTOR signaling pathway, thereby improving the content of EPA and DHA. The downregulation of FGFR3 facilitated the conversion of ALA to EPA. Additionally, we analyzed the effects of ALA supplementation dose on glycerol esters (GLs), phospholipid (PL) and fatty acyl (FA) contents, as well as the regulatory mechanisms of nutritional responses in FFA metabolism. This study provides a basis for identifying genes and pathways that regulate the content of FFAs, and offers a reference for nutritional regulation systems in production.

Enhanced elimination of V5+ in wastewater using zero-valent iron activated by ball milling: The overlooked crucial roles of energy input and sodium chloride.

The ball-milling technology, a highly efficient and cost-effective method, had excellent application prospects for overcoming passivation issues of normal zero-valent iron (ZVI) to enhance the decontamination efficiency. In this work, we investigated the effects and mechanisms of pH, process control agents (PCA), and main process parameters on the removal of V5+ using ball-milled zero-valent iron (ZVIbm). The results showed that ZVI was successfully activated due to mechanochemical action. The enhanced proton conductivity of ZVIbm leaded to the rapid production of more Fe2+, thereby resulting in an order of magnitude higher elimination of V5+ by ZVIbm than by ZVI under near-neutral conditions. In addition, the introduction of NaCl in the ball milling process could not only effectively alleviate the agglomeration phenomenon of ZVIbm, but also effectively enhance its activity. Unexpectedly, due to over-compaction and small size effects, excessive energy input weakened the reactivity of ZVIbm on V5+ elimination. Various characterization results confirmed that the removal of V5+ by ZVIbm was dominated by reduction and supplemented by adsorption. This work updated the basic understanding of the critical effects of process parameters and NaCl on ZVIbm in the remediation of vanadium-containing wastewater.

Involvement of macrophage-derived exosomes in abdominal aortic aneurysms development.

BACKGROUND AND AIMS: Abdominal aortic aneurysm (AAA) is characterized by infiltration of inflammatory cells, extracellular matrix (ECM) degradation, and dysfunction of vascular smooth muscle cells (VSMCs). Recent studies reported that exosomes mediate intercellular communication and are involved in different diseases. Whether exosomes play a role in AAA is poorly understood. Hence, this study evaluated the function of exosomes in AAA development. METHODS: The presence of exosomes in human and calcium phosphate (CaPO4)-induced AAA tissues was determined by immunofluorescence staining of CD63 and Alix. GW4869, an inhibitor of exosome biogenesis, was intraperitoneally injected into CaPO4-induced AAA tissues to evaluate the effects of exosomal inhibition on AAA development. To explore the underlying mechanisms, the human monocytic cell line THP-1 was differentiated into macrophages, and exosomes were collected from macrophages. VSMCs were treated with macrophage-derived exosomes, and the expression of matrix metalloproteinase-2 (MMP-2) was evaluated. The activation of mitogen-activated protein kinases (MAPKs) pathways was also investigated in vitro and in vivo. RESULTS: Exosomes were detected in the adventitia of aneurysmal tissues obtained from humans and mice. They were mainly expressed in clusters of macrophages. Intraperitoneal injection of GW4869 for two weeks significantly attenuated the progression of CaPO4-induced AAA, preserved elastin integrity and decreased MMP-2 expression. Similarly, administration of GW4869 suppressed the systemic and aneurysmal exosome generation. In vitro, treatment with macrophage-derived exosomes elevated MMP-2 expression in human VSMCs, while pre-treatment with GW4869 abolished these effects. It was also found that JNK and p38 pathways mediated the production of MMP-2 in VSMCs following treatment with macrophage-derived exosomes. CONCLUSIONS: This study suggests that exosomes derived from macrophages are involved in the pathogenesis of AAA. Macrophage-derived exosomes trigger MMP-2 expression in VSMC via JNK and p38 pathways. GW4869 supplementation attenuates CaPO4-induced AAA in mice.

Curcumin suppresses migration and invasion of human endometrial carcinoma cells.

Curcumin, a widely used Chinese herbal medicine, has historically been used in anti-cancer therapies. However, the anti-metastatic effect and molecular mechanism of curcumin in endometrial carcinoma (EC) are still poorly understood. The purpose of this study was to detect the anti-metastatic effects of curcumin and the associated mechanism(s) in EC. Based on assays carried out in EC cell lines, it was observed that curcumin inhibited EC cell migration and invasion in vitro. Furthermore, following treatment with curcumin for 24 h, there was a decrease in the expression levels of matrix metalloproteinase (MMP)-2 and -9 as well as proteinase activity in EC cells. Moreover, curcumin treatment significantly decreased the levels of the phosphorylated form of extracellular signal-regulated kinase (ERK) 1/2. MEK1 overexpression partially blocked the anti-metastatic effects of curcumin. Combined treatment with ERK inhibitor U0126 and curcumin resulted in a synergistic reduction in MMP-2/-9 expression; the invasive capabilities of HEC-1B cells were also inhibited. In conclusion, curcumin inhibits tumor cell migration and invasion by reducing the expression and activity of MMP-2/9 via the suppression of the ERK signaling pathway, suggesting that curcumin is a potential therapeutic agent for EC.

Long-term effect of agricultural reclamation on soil chemical properties of a coastal saline marsh in Bohai Rim, northern China.

Over the past six decades, coastal wetlands in China have experienced rapid and extensive agricultural reclamation. In the context of saline conditions, long-term effect of cultivation after reclamation on soil chemical properties has not been well understood. We studied this issue using a case of approximately 60-years cultivation of a coastal saline marsh in Bohai Rim, northern China. The results showed that long-term reclamation significantly decreased soil organic carbon (SOC) (-42.2%) and total nitrogen (TN) (-25.8%) at surface layer (0-30 cm) as well as their stratification ratios (SRs) (0-5 cm:50-70 cm and 5-10 cm:50-70 cm). However, there was no significant change in total phosphorus (TP) as well as its SRs under cultivation. Cultivation markedly reduced ratios of SOC to TN, SOC to TP and TN to TP at surface layer (0-30 cm) and their SRs (0-5 cm:50-70 cm). After cultivation, electrical conductivity and salinity significantly decreased by 60.1% and 55.3% at 0-100 cm layer, respectively, suggesting a great desalinization. In contrast, soil pH at 20-70 cm horizons notably increased as an effect of reclamation. Cultivation also changed compositions of cations at 0-10 cm layer and anions at 5-100 cm layer, mainly decreasing the proportion of Na+, Cl- and SO4(2-). Furthermore, cultivation significantly reduced the sodium adsorption ratio and exchangeable sodium percentage in plow-layer (0-20 cm) but not residual sodium carbonate, suggesting a reduction in sodium harm.

Human tissue kallikrein promoted activation of the ipsilesional sensorimotor cortex after acute cerebral infarction.

BACKGROUND/AIMS: Kallikrein, a serine proteinase, has been reported to have many functions, such as selectively dilating arterioles in the ischemic area and enhancing angiogenesis and neurogenesis. Therefore, it may promote cerebral poststroke reorganization. We observed the effect of human tissue kallikrein on the brain motor activation of acute ischemic stroke patients and evaluated patient condition severity and prognosis. METHODS: Forty-four cases suffering from cerebral infarction between 6 and 72 h of onset were randomly assigned into the kallikrein group (n = 24) and the control group (n = 20). The control group was given conventional treatment, whereas the kallikrein group was given both conventional treatment and human tissue kallikrein over the course of 12-14 days. The activation of the sensorimotor cortex (SMC) and cerebellum, the affected forefinger strength and the NIHSS scores were evaluated before and after treatment. The MBI and MRS scores were assessed at 30 and 90 days after stroke onset. RESULTS: There were no differences between the two groups in activation volume, patient condition and scores before treatment. After treatment, the ipsilesional SMC activation volume was significantly larger and the increase in the volume was significantly greater in the kallikrein group than in the control group (p < 0.05 for both). The NIHSS score was significantly smaller and the improvement in the score was significantly greater in the kallikrein group after treatment (p < 0.05 for both). Moreover, the MBI scores at 30 days were significantly higher, whereas the MRS scores at 30 days were significantly lower in the kallikrein group than in the control group (p < 0.05 for both). CONCLUSIONS: Kallikrein improved neural function effectively and quickly after stroke, and promoting cerebral reorganization might be an important mechanism for kallikrein in the treatment of acute cerebral infarction.

Expression of Pkd2l2 in testis is implicated in spermatogenesis.

Pkd2l2 is a novel member of the polycystic kidney disease (PKD) gene family in mammals. Prominently expressed in testis, this gene is still poorly understood. In this study, reverse transcription polymerase chain reaction (RT-PCR) results showed a time-dependent expression pattern of Pkd2l2 in postnatal mouse testis. Immunohistochemical analysis revealed that Pkd2l2 encoded a protein, polycystin-L2, which was predominantly detectable in the plasma membrane of spermatocytes and round spermatids, as well as in the head and tail of elongating spermatids within seminiferous tubules in mouse testis tissue sections of postnatal day 14 and adult mice. A green fluorescent fusion protein of Pkd2l2 resided in the plasma membrane of HEK 293 and MDCK cells, suggesting that it functions as a plasma membrane protein. Overexpression of Pkd2l2 increased the intracellular calcium concentration of MDCK cells, as detected by flow cytometry. Collectively, these data indicated that Pkd2l2 may be involved in the mid-late stage of spermatogenesis through modulation of the intracellular calcium concentration.