The effect of stocking size on the first winter survival of whitefish, Coregonus lavaretus (L.), in the Gulf of Bothnia, Baltic Sea

The anadromous whitefish, Coregonus lavaretus (L.), is the most numerous fish species stocked in the Gulf of Bothnia, Baltic Sea. One-summer-old-whitefish fingerlings are mostly 8–10 cm long when released annually in September–October, whereas the wild whitefish are 10–12 cm at that time. About 6 million, one-summer-old, spray-marked, whitefish were released in the northern and central parts of the Gulf in 1995–1998. To study the effect of the stocking length on the survival of the marked fish, the length of the recaptured whitefish as 1-year-olds was back-calculated. Altogether 1106 whitefish recaptured in the Gulf of Bothnia were analysed. The back-calculated length was slightly greater than the stocking length but not as large as the length of the wild fish. In the central part of the Gulf of Bothnia, where the mean stocking length was more than 10 cm, the back-calculated length was 10.5–11.1 cm. In the northern part of the Gulf the mean stocking length varied between 8.8 and 10.0 cm annually, and the corresponding back-calculated mean lengths were 9.3–9.7 cm. It also seemed that bigger fingerlings started their feeding migration earlier or they migrated faster than the smaller ones to the southern parts of the Gulf of Bothnia.     

归参汤对免疫抑制小鼠血清中IL-2、TNF-α和脾细胞Th1/Th2细胞因子的影响

为了探讨归参汤(GST)对免疫抑制小鼠血清中IL-2、TNF-α和脾细胞Th1/Th2细胞因子的影响。本试验采用环磷酰胺制造免疫抑制模型,利用双抗夹心ELISA法,观察归参汤对小鼠血清中IL-2、TNF-α的影响;RT-PCR法观察归参汤对小鼠脾细胞中INF-γ、IL-4、T-bet和GATA-3的mRNA表达的影响。结果显示:归参汤高剂量组可以显著增加免疫抑制小鼠血清中IL-2、TNF-α的含量(P<0.01),提高INF-γ的表达(P<0.05),降低IL-4的含量(P<0.05),升高T-bet(P<0.05),降低GATA-3的表达(P<0.05)。归参汤的免疫增强作用与升高血清中IL-2、TNF-α有关,且升高INF-γ/IL-4纠正免疫抑制小鼠Thl/Th2细胞因子的比例紊乱,其机制可能部分归因于对T-bet和GATA-3的mRNA表达的影响。     

水稻OsNHO1基因cDNA序列分离及表达分析

OsNHO1是一种甘油激酶,受多种因素的诱导,在植物先天免疫反应中起着重要的作用。笔者采用同源序列法,根据已报道的拟南芥NHO1基因序列结合水稻基因组测序结果,筛选水稻OsNHO1基因,采用RT-PCR获得水稻OsNHO1基因全长cDNA(1 590 bp,529AA),并通过半定量RT-PCR方法分析OsNHO1基因在SA,PXO99刺激下的表达模式,结果显示OsNHO1基因的表达受SA,PXO99的诱导,为进一步研究OsNHO1的具体功能和作用机理奠定了基础。     

Chronic alcohol intake-induced epithelial-mesenchymal transition contri-butes to hepatic fibrogenesis in mice

AIM：To evaluate the effect of chronic alcohol intake on the histopathological changes of the liver and to determine the contribution of epithelial-mesenchymal transition (EMT) to hepatic fibrogenesis. METHODS：Thirty male C57BL/6 mice were randomly divided into 3 groups as following: the mice in control group was given (ig) water; the mice in low-dose alcohol group (2.0 g·kg -1·d -1) and high-dose alcohol group (4.0 g·kg -1·d -1) were given (ig) alcohol for 5 months. Alcohol-induced histopathological changes of the liver or development of hepatic fibrosis were evaluated using the histological methods with HE and Masson trichrome staining. The apoptosis of the liver was detected by TUNEL fluorometric staining (counterstained with DAPI). The activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) was measured by an automated biochemical analyzer. The expression of fibroblast-specific protein 1 (FSP-1), α-smooth muscle actin (α-SMA) and E-cadherin in the hepatic tissues was detected by immunofluorescence examination. The protein levels of E-cadherin, α-SMA, FSP-1, transforming growth factor β 1 (TGF-β 1) and hypoxia-inducible factor 1α (HIF-1α) were analyzed by Western blotting. RESULTS：Compared with control, the activity of serum ALT and AST, and apoptotic index of liver tissues were increased in the mice treated with alcohol for 5 months. The histopathological changes of the livers in the mice of low-dose alcohol group included steatosis and mild liver fibrosis, while severe liver fibrosis was observed in the high-dose alcohol-treated mice. Chronic alcohol consumption induced the increase in malondialdehyde (MDA) level, and the decreases in the activity of superoxide dismutase (SOD) and catalase (CAT) in the livers. It also reduced E-cadherin expression and increased α-SMA expression. FSP-1 immunostaining and albumn immunostaining positive cells were co-localized in the hepatocytes of low-dose alcohol group, but only FSP-1 positive hepatocytes were observed in high-dose alcohol group. Chronic alcohol consumption decreased E-cadherin expression and increased α-SMA, FSP-1, TGF-β 1 and HIF-1α expression in a dose-dependent manner, but the HIF-1α expression was not altered between the 2 alcohol-treated groups. CONCLUSION：Chronic alcohol intake induces the progression of hepatic fibrosis. Some fibroblasts derive from hepatocytes in liver fibrosis via EMT. The underlying mechanism is associated with the changes of the redox state, and increased TGF-β 1 generation and HIF-1α expression.     

Effects of synthetic kainic acid on microfilament expression and gap junction in astrocytes

AIM：To study the effects of synthetic kainic acid (SKA) and 1-heptanol (1-Hep), a gap junction blocker, on the cytoskeletal filament expression in the astrocytes. METHODS：The neonatal rat brain was obtained from the Wistar rats (1 day old) and primary purified astrocytes were obtained by differential attachment for removing filamentoblasts and orbital shaker for removing the oligodendrocytes. The effects of SKA and other interventions on the morphologic changes and expression levels of skeleton protein filamentous actin (F-actin) were observed in the astrocytes after 24 h of the exposures by laser scanning confocal microscopy. The effect of 1-Hep on the expression of F-actin was also explored. RESULTS：Compared with control group, the fluorescence intensities in KCl group and KCl+SKA group were increased, and highly increased in KCl+SKA group. The F-actin filaments in the above 2 groups were more intensive, thickened and concentrated than those in control group, and more obvious in KCl+SKA group. l-Hep significantly decreased the expression of F-actin in KCl group and KCl+SKA group as compared with control group, and parts of the filamentous fracture were seen in the astrocytes in all 1-Hep-treated groups, in which some of the filamentous lines were crosscut. CONCLUSION：Increase in the expression of F-actin in the astrocytes affects the structure and function of the intercellular gap junctions, which may be involved in the mechanism of SKA-induced epilepsy.     

Inflammatory response in rat kidney with contrast-induced nephropathy

AIM：To observe the expression of tumor necrosis factor α (TNF-α) and nuclear factor κB (NF-κB) in the renal tissue of the rats with contrast-induced nephropathy (CIN). METHODS：Male Sprague-Dawley rats (n=96) were randomly divided into control group (n=48) and CIN group (n=48). The model rats in CIN group were intravenously injected with iodinated contrast media (76% compound diatrizoate injection,10 mL/kg), while the rats in control group were injected with the same volume of saline. Six rats in each group were sacrificed at 6 h, 12 h, 24 h, 48 h, 72 h, 5 d, 10 d and 15 d after intravenous injection, respectively, and the blood and kidney samples of the rats were obtained. The renal tubular injury was assessed by histological examination (HE staining). The expression of kidney injury molecule-1 (KIM-1), TNF-α and NF-κB at mRNA and protein levels in the renal tissues were semiquantitatively measured by the methods of RT-PCR and immunohistochemistry, respectively. The correlations between the expression of TNF-α, NF-κB and tubular injury score, KIM-1 expression in renal tissue of CIN group were analyzed. RESULTS：The levels of serum creatinine (SCr) and blood urea nitrogen (BUN) in control group were not changed between different time points (P>0.05). The levels of SCr and BUN in CIN group displayed significant increases at different time points (except 15 d) compared with control group (P<0.05). The renal tubular injury score in CIN group was significantly higher at all time points than that in control group (P<0.05). The expression of KIM-1, TNF-α and NF-κB at mRNA and protein levels up-regulated significantly at 6 h and the peaking of KIM-1 expression was at 24 h, while the peaking of TNF-α and NF-κB expression was at 48 h in CIN group. The expression of KIM-1,TNF-α and NF-κB was significantly increased in CIN group compared with control group except at 15 d (P<0.05). The expression of TNF-α and NF-κB at mRNA and protein levels showed close correlations with renal tubular injury score (r=0.843, 0.758, 0.743 and 0.707, P<0.05). The expression of TNF-α and NF-κB at mRNA and protein levels was also positively correlated with KIM-1 expression (r=0.863, 0.807, 0.839 and 0.855, P<0.05). CONCLUSION：The expression of TNF-α and NF-κB at mRNA and protein levels in the renal tissues of CIN group is up-regulated and is closely related with renal tubular injury, indicating that the inflammatory response is involved in the pathogenesis of CIN.     

RASSF1A expression mediated by lentivirus inhibits growth of small-cell lung cancer cell line H446

AIM：To explore the inhibitory effect of Ras-association domain family 1A (RASSF1A) on the small-cell lung cancer cell growth. METHODS：The lentiviral expression vector containing RASSF1A gene was constructed and used to infect the small-cell lung cell line H446. The growth curve and cell cycle were detected by MTT assay and flow cytometry. The mRNA and protein levels of cell cycle-associated proteins were determined by real-time PCR and Western blotting. RESULTS：We obtained the H446 cells in which RASSF1A was stably expressed (named RASSF1A-H446). Compared with normal cell group and negative cell group, RASSF1A inhibited the proliferation of H446 cells, and arrested H446 cells in G1 phase. The expression of p21 and p27 was significantly increased, and E2F1 was significantly decreased in RASSF1A-H446 cells. CONCLUSION：RASSF1A inhibits the H446 cell growth by increasing the expressions of p21 and p27, and decreasing the expression of E2F1.     

紫色马铃薯新品种桂彩薯1 号的选育

桂彩薯1 号是以日本北海道岛系571 号为母本,以日本北海道岛系568 号为父本经有性杂交系统选育而成。早中熟,生育期（出苗至成熟）85～95 d（天）。块茎长椭圆形,中等大小,紫皮紫肉,表皮光滑,芽眼少而浅,结薯集中,单薯质量100 g 左右,鲜薯产量1 000～1 500 kg· （ 667 m²）^-1,最高可达2 000 kg（ 667 m²）^-1。块茎淀粉含量9.07%,粗蛋白质2.45%,还原糖0.67%,VC 137.0 mg·kg^-1（FW）,花色苷1 786.0 mg·kg^-1（FW）。适宜广西、广东、福建、云南、湖南等地秋冬种植。     

Vasonatrin peptide attenuates injuries of dopaminergic neurons induced by 1-methyl-4-phenylpyridinium

AIM：To investigate the neuroprotective effects of vasonatrin peptide (VNP) on the injury of dopaminergic neurons induced by 1-methyl-4-phenylpyridinium (MPP+). METHODS：Cultured dopaminergic neurons from the mouse ventral mesencephalon were exposed to MPP+, and the effects of VNP on the neurotoxicity of MPP+ were eva-luated by cell viability analysis and immunofluorescence staining. Various kinds of agonists and antagonists were used to clarify the mechanism underlying the effects of VNP. RESULTS：MPP+ caused injuries in the dopaminergic neurons. VNP significantly increased the viability, axon number and axon length of the dopaminergic neurons. The MPP+-induced depolymerization of β-tubulin Ⅲ was also attenuated by the treatment with VNP. In addition, VNP significantly increased the intracellular levels of cGMP. These effects of VNP were mimicked by 8-Br-cGMP (a cell-permeable analog of cGMP), whereas inhibited by HS-142-1 ［the antagonist of the particulate guanylyl cyclase-coupled natriuretic peptide receptors (NPR)］, or KT-5823 ［a cGMP-dependent protein kinase (PKG) inhibitor］. CONCLUSION：VNP attenuates the neurotoxicity of MPP+ via guanylyl cyclase-coupled NPR/cGMP/PKG pathway, indicating that VNP might be a new effective reagent in the treatment of neural degeneration of dopaminergic neurons in Parkinson disease.     

Effect of idazoxan on permeability of blood-brain barrier and expression of MMP-9/TIMP-1 in mouse experimental autoimmune encephalomyelitis

AIM：To study the effect of idazoxan (IDA) on the permeability of blood-brain barrier (BBB) and the expression of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) in mouse experimental autoimmune encephalomyelitis (EAE).METHODS：Female C57BL/6 mice (n=36) were randomly divided into control group, EAE group and IDA group, with 12 mice in each group. EAE was induced by myelin oligodendrocyte glycoprotein 35-55 (MOG35-55). IDA (2 mg/kg, ip, bid) was administered for 15 d after immunization. The neurological defects of the mice were observed daily and scored. The pathological changes were observed under microscope with HE staining and LFB myelin staining. The BBB permeability was detected by Evans blue extravasation. The expression of MMP-9 and TIMP-1 in the brain of EAE mice was determined by Western blotting.RESULTS：Compared with EAE group, the score of neurological defects in IDA group was decreased, the inflammation was relieved, the BBB permeability was reduced, and the expression MMP-9 and the ratio of MMP-9/TIMP-1 were decreased (P<0.05).CONCLUSION：The neuroprotective effect of IDA on mouse EAE might be related to the down-regulation of MMP-9 and the ratio of MMP-9/TIMP-1, thus reducing the degradation of BBB and the permeability of BBB, and ameliorating the pathologic process of EAE.