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The present study was conducted to investigate the effects of high dietary lipid levels on growth, metabolism, antioxidant capacity, and immune responses of largemouth bass. Fish (initial body weight 13.38 ± 0.11 g) were fed three isonitrogenous semi-purified diets containing 5%, 10%, and 20% lipid, respectively. The results indicated that fish fed 10% lipid diet showed significantly better final body weight, specific growth rate (SGR), protein efficiency ratio (PER), and feed conversion ratio (FCR) compared with that fed 5% lipid diet. Meanwhile, fish fed 20% lipid diet had a significantly higher viscera ratio (VR), hepatosomatic index (HSI), intraperitoneal fat ratio (IPF), and liver lipid content than those fed the other diets. Higher alanine aminotransferase (ALT) and aspartate transaminase (AST) activities, total cholesterol (TC), triglyceride (TG), free fatty acids (FFA), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) contents, and LDL-C/HDL-C value in plasma were recorded in fish fed 20% lipid diet, while higher insulin contents were obtained in fish fed 5% lipid diet. In addition, the highest carnitine palmitoyltransferase I (CPT1), AMP-activated protein kinase (AMPK), fructose-1,6-bisphosphatase (FBPase), and phosphoenolpyruvate carboxykinase (PEPCK) activities in the liver were also observed in fish fed 20% lipid diet. However, fish fed 20% lipid diet had a significantly lower superoxide dismutase (SOD) and catalase (CAT) activities and higher MDA contents in liver than those fed the other diets. The higher nitric oxide (NO) contents and inducible nitric oxide synthase (iNOS) activity in liver were recorded in fish fed 10% lipid diet. Moreover, the alkaline phosphatase (ALP), inducible nitric oxide synthase (iNOS) and lysozyme activities, and nitric oxide (NO) contents in plasma were higher in fish fed the 10% diets than the other groups. In conclusion, high dietary lipid levels could suppress growth performance and liver anti-oxidative capacity, and reduce immune responses of largemouth bass.

The study was conducted to evaluate the effect of dietary phospholipids (PLs) on growth, lipid metabolism, and antioxidative status of hybrid snakehead (Channa argus × Channa maculata). Five isonitrogenous and isolipidic diets with graded levels of PLs (8.5, 19.3, 30.7, 41.5, and 50.8 g kg−1) were fed to triplicate groups of juveniles (initial body weight 12.6 ± 0.23 g) for 8 weeks. Results showed that dietary PL supplementation significantly improved growth of juveniles. The final body weight (FBW) and specific growth rate (SGR) significantly increased with dietary PLs increasing from 8.5 to 41.5 g kg−1 (P < 0.05). Fish fed with the diet containing 8.5 g kg−1 PLs showed higher feed conversion ratio (FCR) compared to the other treatments (P < 0.05). Survival rate (SR) was not affected by dietary PL levels (P > 0.05). Liver lipid contents, serum triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) contents significantly decreased with the increasing levels of dietary PLs (P < 0.05). However, serum total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) contents and HDL-C/TC and HDL-C/LDL-C value significantly increased with increasing dietary PL levels (P < 0.05). The catalase (CAT), superoxide dismutase (SOD), and carnitine palmitoyl transferase I (CPT-1) activities in the liver significantly increased with incremental dietary PL level (P < 0.05), while the liver malondialdehyde (MDA) contents and fatty acid synthase (FAS) activity significantly reduced (P < 0.05). No significant difference was observed in the glutathione peroxidase (GPx) activity among dietary treatments (P > 0.05).These results confirmed that dietary PL supplementation has beneficial effects on growth performance and antioxidant capacity of juvenile hybrid snakehead. Dietary PLs might reduce lipid deposition in the liver of juvenile hybrid snakehead.

A feeding trial was conducted to evaluate the effect of linseed oil (LO) on growth, plasma biochemistry, hepatic metabolism enzymes, and antioxidant capacity of juvenile largemouth bass, Micropterus salmoides. Four isonitrogenous (crude protein, 45%) and isoenergetic (gross energy, 18 MJ/kg) diets were formulated by replacing 0 (the control), 33.3%, 66.7%, and 100% of fish oil with linseed oil. Each diet was fed to three replicate groups of fish (initial body weight, 22.02 ± 0.61 g) for 8 weeks. The results indicated that fish fed diet with 100% LO substitution level had lower weight gain (WG), specific growth rate (SGR), and protein efficiency ratio (PER) than the other groups (P < 0.05), while feed conversion ratio (FCR) was higher compared to the other groups (P < 0.05). Feed intake (FI) and hepatosomatic index (HSI) of 66.7% LO substitution level were significantly lower than the control groups (P < 0.05). Glycogen, lipid, and non-esterified fatty acid content in the liver decreased significantly with increasing dietary LO levels (P < 0.05). Moreover, the replacement of fish oil (FO) with LO could significantly reduce the content of triglyceride (TG) and total cholesterol (TC) and the activity of alanine amiotransferase (ALT) in plasma of M. salmoides (P < 0.05). There were significant differences in hepatic metabolism enzymes in fish fed diets with different dietary LO levels. Adenosine 5′-monophosphate (AMP)–activated protein kinase (AMPK) and peroxisome proliferator–activated receptor (PPAR-α) activities in liver significantly increased with increasing dietary LO level (P < 0.05). In addition, phosphoenolpyruvate carboxykinase (PEPCK) and fructose-1,6-bisphosphatase (FBPase) activities in the liver significantly increased with decreasing dietary LO level (P < 0.05). Both the lowest superoxide dismutase (SOD) and catalase (CAT) activities in the liver were recorded in the control group (P < 0.05). Moreover, nitric oxide content, glutathione peroxidase (GPx), and inducible nitric oxide synthase (iNOS) activities in the liver significantly increased with increasing dietary LO level, while malondialdehyde (MDA) content significantly reduced. These findings demonstrated that LO can improve liver function and antioxidant ability of M. salmoides. In addition, replacing partial FO with LO cannot affect growth performance, but all substitutions inhibit growth performance of M. salmoides.

Near-infrared (NIR) emissive metal complexes have shown potential applications in optical communication, chemosensors, bioimaging, and laser and organic light-emitting diodes (OLEDs) due to their structural tunability and luminescence stability. Among them, complexes with bridging ligands that exhibit unique emission behavior have attracted extensive interests in recent years. The target performance can be easily achieved by NIR light-emitting metal complexes with bridging ligands through molecular structure design. In this review, the luminescence mechanism and design strategies of NIR luminescent metal complexes with bridging ligands are described firstly, and then summarize the recent advance of NIR luminescent metal complexes with bridging ligands in the fields of electroluminescence and biosensing/bioimaging. Finally, the development trend of NIR luminescent metal complexes with bridging ligands are proposed, which shows an attractive prospect in the field of photophysical and photochemical materials.

Background Lung cancer is the most prevalent cancer, and the leading cause of cancer-related deaths in China. The aim of this study was to estimate the direct medical expenditure incurred for lung cancer care and analyze the trend therein for the period 2002–2011 using nationally representative data in China Methods This study was based on 10-year, multicenter retrospective expenditure data collected from hospital records, covering 15,437 lung cancer patients from 13 provinces diagnosed during the period 2002–2011. All expenditure data were adjusted to 2011 to eliminate the effects of inflation using China’s annual consumer price index. Results The direct medical expenditure for lung cancer care (in 2011) was 39,015 CNY (US$6,041) per case, with an annual growth rate of 7.55% from 2002 to 2011. Drug costs were the highest proportionally in the total medical expenditure (54.27%), followed by treatment expenditure (14.32%) and surgical expenditure (8.10%). Medical expenditures for the disease varied based on region, hospital level, type, and stage. Conclusion The medical expenditure for lung cancer care is substantial in China. Drug costs and laboratory test are the main factors increasing medical costs.

The study reported here is the first to systematically investigate the postprandial change in glucose metabolism in the adipose tissue (AT) of an omnivorous fish. Sub-adult Genetically Improved Farmed Tilapia (GIFT) Oreochromis niloticus were sampled at 0, 1, 3, 8 and 24 h after feeding (HAF), and the time course of changes in glucose transport and glycolipid metabolism at the transcript level were analyzed in the AT. The plasma glucose level increased between 1 and 8 HAF, and the expression of glucose transporter 1a (glut1a) and glut4 in the AT were stimulated at the same time. Concomitantly, the mRNA levels of glycolytic genes, such as hexokinase 1a (hk1a), hk1b, glucokinase and liver type of phosphofructokinase, were upregulated. The expression of glycogen synthase 1 and glycogen level in the AT increased between 3 and 8 HAF, suggesting that AT has the capacity to store excess glucose in tilapia. The decreased glycogen level together with upregulated transcription of glucose-6-phosphatase catalytic subunit a2 (g6pca2) at 24 HAF suggests that glycogen breakdown and glucose release from AT might contribute to circular glucose in tilapia. The opposite expression patterns between g6pca2 and phosphoenolpyruvate carboxykinase (pck) paralogs suggest that pck might participate in glyceroneogenesis rather than gluconeogenesis in the AT of tilapia. The mRNA levels of both cytosolic pck1 and mitochondrial pck2 increased during the period 1–8 HAF, and the expressions of lipogenic genes, such as acetyl-CoA carboxylase α and fatty acid synthase, were upregulated between 3 and 8 HAF, suggesting that glyceroneogenesis was probably stimulated as a source of glyceride–glycerol for triglyceride synthesis in the AT of tilapia. Taken together, our preliminary data suggest that AT plays an important role in the regulation of postprandial glucose homeostasis in the omnivorous tilapia, at least at the molecular level.

The present study was performed to investigate the roles of anterior intestine in the postprandial glucose homeostasis of the omnivorous Genetically Improved Farmed Tilapia (GIFT). Sub-adult fish (about 173 g) were sampled at 0, 1, 3, 8 and 24 h post feeding (HPF) after 36 h of food deprivation, and the time course of changes in intestinal glucose transport, glycolysis, glycogenesis and gluconeogenesis at the transcription and enzyme activity level, as well as plasma glucose contents, were analyzed. Compared with 0 HPF (fasting for 36 h), the mRNA levels of both ATP-dependent sodium/glucose cotransporter 1 and facilitated glucose transporter 2 increased during 1-3 HPF, decreased at 8 HPF and then leveled off. These results indicated that intestinal uptake of glucose and its transport across the intestine to blood mainly occurred during 1-3 HPF, which subsequently resulted in the increase of plasma glucose level at the same time. Intestinal glycolysis was stimulated during 1-3 HPF, while glucose storage as glycogen was induced during 3-8 HPF. Unexpectedly, intestinal gluconeogenesis (IGNG) was also strongly induced during 1-3 HPF at the state of nutrient assimilation. The mRNA abundance and enzyme activities of glutamic-pyruvic and glutamic-oxaloacetic transaminases increased during 1-3 HPF, suggesting that the precursors of IGNG might originate from some amino acids. Taken together, it was concluded that the anterior intestine played an important role in the regulation of postprandial glucose homeostasis in omnivorous tilapia, as it represented significant glycolytic potential and glucose storage. It was interesting that postprandial IGNG was stimulated by feeding temporarily, and its biological significance remains to be elucidated in fish.

p53 is the major mediator of the tumor suppressor response. It participates in apoptosis and senescence and can respond to DNA damage. As a crucial sequence-specific transcription factor, p53 regulates the expression of many genes, such as small noncoding RNAs (ncRNAs), microRNAs, and long ncRNAs (lncRNAs). Given the emergence of novel and high-throughput sequencing technologies, many lncRNAs have been discovered. LncRNAs may function as vital gene regulators in a variety of biological processes through extensive mechanisms. Recently, lncRNAs have been demonstrated to be associated with the p53 regulatory pathway. In this review, we discuss the current and fast growing knowledge about the influence of lncRNAs to the p53 signaling pathway, the different mechanisms by which they affect gene expression in cancer. Our findings show that p53-associated lncRNAs may be used as biomarkers for cancer diagnosis or targets for disease therapy.

Background The carboxyl terminus of Hsp70-interacting protein (CHIP) is a member of E3 ubiquitin ligase, functioning as a link between the chaperone (heat shock protein 70/90) and proteasome systems, playing a vital role in maintaining the protein homeostasis in the cytoplasm. CHIP has been demonstrated to be involved in tumorigenesis, proliferation and invasion in several malignancies, regulating a number of oncogenic proteins. However, CHIP has also been implicated in the modulation of tumor suppressor proteins. The pathogenic mechanism of CHIP expression in human malignancy is not yet clear, and a number of studies have suggested that CHIP may have opposing roles in different cancers. Therefore, many studies have focused on the relationship between CHIP and carcinoma. Methods A literature search focusing on regulation network, biological function and clinical significance of CHIP in connection with its role in cancer development was performed on the MEDLINE databases. Results and conclusions CHIP may be a potential diagnostic biomarker and therapeutic target for human cancer, and may play different roles in different human cancers. This inconsistence might be induced by the diversity of CHIP downstream targeting proteins. Therefore, the phenotypes determined by CHIP should be dependent on the function of its specific targets in a specific type of cancer cells. Whether CHIP contributes to tumor progression or suppression in various human cancers remains unclear, suggesting the necessity of further extensive investigation of its role in tumorigenesis.

CHIP (c-terminal Hsp70-interacting protein) is an E3 ligase which may play different roles in different cancers. The elucidation of the VHL-HIF-1α(hypoxia inducible factor-1α)-VEGF (vascular endothelial growth factor) pathway has led to the development of targeted therapy in renal cell carcinoma (RCC). However, little is known about the role of CHIP and the relationship between CHIP and VEGF-VEGFR2 (VEGF receptor 2) pathway in RCC. In this study, we found that the expression of CHIP was downregulated and significantly correlated with pT status ( P  = 0.022) and TNM stage ( P  = 0.022) in 304 RCC and 35 normal renal tissues using tissue microarray. Moreover, low expression of CHIP is a strong and independent negative prognostic value for RCC. In vitro , CHIP negatively regulated RCC cell migration, invasion and angiogenesis. In addition, ELISA tests showed that restoration of CHIP inhibited, while knockdown promoted, the secreted level of VEGF. Furthermore, western blot indicated that the VEGFR2 protein level was reduced after CHIP overexpression. Our findings demonstrate for the first time that CHIP may be involved in RCC angiogenesis through regulating VEGF secretion and expression of VEGFR2. CHIP may serve as promising prognostic biomarker of angiogenesis and may constitute a potential therapeutic target in RCC.