Bioencapsulation of five forms of erythromycin by adult Artemia salina (L.)

Uptake of five chemical forms of erythromycin by adult Artemia salina (L.) (erythromycin phosphate – EP, erythromycin stearate – ES, erythromycin estolate – EE, erythromycin hydrate – EH and crystalline erythromycin – CE) was investigated in two trials. In each trial, final erythromycin concentration in Artemia tissue and survival after a 12‐h bioencapsulation period were determined. In the first trial, Artemia tissue concentration after a 12‐h bioencapsulation period was significantly (P < 0.05) affected by erythromycin form with ES (68.5 ± 3.3 μg mL^?1, mean ± SEM) ≈ EH (61.2 ± 3.4 μg mL^?1) > CE (37.1 ± 10.7 μg mL^?1) > EP (16.4 ± 7.7 μg mL^?1) > control. In trial 2, Artemia tissue concentration was also significantly (P < 0.05) affected by erythromycin form with EE (111.4 ± 9.6 μg mL^?1) > CE (89.1 ± 1.7 μg mL^?1) > ES (78.9 ± 1.6 μg mL^?1) > EP (33.4 ± 5.2 μg mL^?1) > control. Survival was significantly affected by erythromycin form in trial 1 with EP=control (100 ± 0.0%) > ES (74.4 ± 2.0%) > CE (32.2 ± 0.3%) > EH (8.8 ± 4.4%). In trial 2, survival was also significantly affected by erythromycin form with EP=control (100 ± 0.0%) > ES (67.1 ±3.7%) > CE (52.5 ± 7.7%) > EE (5.0 ± 2.5%). Based on both uptake and survival, EP and ES appear to be appropriate compounds for bioencapsulation of erythromycin using live adult Artemia.     

Fusarium incarnatum isolated from black tiger shrimp, Penaeus monodon Fabricius, with black gill disease cultured in Vietnam

Fusarium incarnatum was isolated from gill lesions of cultured black tiger shrimp, Penaeus monodon, in every crop during 2000-2002 in Nghe An province, Vietnam. Infected shrimps showed typical signs of black gill disease and mortalities about a month prior to harvest. Detailed morphological examinations, as well as molecular phylogenic analyses based on partial nucleotide sequences of ribosomal DNA, were made on the isolates. An artificial infection of kuruma prawn, Penaeus japonicus, using two selected isolates was also conducted and their pathogenicity determined.     

黄颡鱼的生物学特性与养殖技术

通过对黄颡鱼的生物学特性、繁殖技术、苗种培育技术、养殖技术、放养模式、病害防治技术的系统研究，探明了黄颡鱼的食性、溶氧需求、温度适应性、盐度耐受性等生物学特性，报道了黄颡鱼繁殖与苗种培育措施，提出池塘养殖所需配套技术及常见病害防治技术。     

中草药防治寄生性鱼病的研究进展

通过查阅近年来国内有关中草药防治寄生性鱼病的文献,系统的介绍了常见的鱼类寄生虫病,并就中草药对该病害的防治研究与应用进行阐述,以期为寄生性鱼病的防治提供一定的参考。     

Protective effect of emodin on lung injury induced by hepatic fibrosis in rats

AIM:To explore the protective effect of emodin on lung injury induced by hepatic fibrosis in rats. METHODS:The hepatic fibrosis rat model was established with multiple pathogenic factors (CCl 4, ethanol, high fat, high cholesterol and low choline) and treated with different doses (20 mg/kg and 40 mg/kg) of emodin for 4 weeks. The hepatic index was measured. The biochemical indexes, endotoxin, homocysteine, albumin, aspartate aminotransferase,alanine aminotransferase, total bilirubin, total cholesterol and triglyceride, and hepatic fibrosis indexes, hyaluronic acid, laminin, collagen IV and procollagen Ⅲ, were detected. The histopathological changes of the liver were observed. The pulmonary index was determined. The histopathological changes of the lungs were observed. The levels of tumor necrosis factor α (TNF-α), malondialdehyde (MDA), nitric oxide (NO) and peroxynitrite (ONOO-) in the lung tissues were analyzed. RESULTS:The rat hepatic fibrosis model was successfully established. In model group, lung edema and inflammation occurred, and the pulmonary index and the levels of TNF-α, MDA, NO and ONOO- in the lung tissues were increased significantly. In emodin treatment groups, the pulmonary indexes were lower than that in model group. The pathological injury of the lung tissues was alleviated. The levels of TNF-α, MDA, NO and ONOO- in the lung tissues were decreased. CONCLUSION:Emodin has a protective effect on lung injury induced by hepatic fibrosis in rats.     

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.     

Effect of DADLE on lung injury in rats with acute global cerebral ischemia-reperfusion

AIM：To observe the effects of δ opioid receptor agonist DADLE on acute lung injury (ALI) induced by acute global cerebral ischemia-reperfusion in rats. METHODS：SD rats (n=30) were randomly divided into sham group, model (I/R) group and DADLE treatment group. Global cerebral ischemia-reperfusion model was established by a modified 2-vessel occlusion plus hypotension. DADLE (5 mg/kg) treatment was performed via the left jugular injection before reperfusion. After 120-min reperfusion, the pathological changes of the lung tissues were observed under light microscope and electronic microscope. The activity of superoxide dismutase (SOD) and malondialdehyde (MDA) level were detected. The partial pressure of arterial oxygen (PaO2) was also measured. RESULTS：In I/R group, widened alveolar septum, capillary dilatation and congestion, endovascular and perivascular cells in the lung with neutrophil infiltration, and significantly reduced type II epithelial cell surface microvilli, alveolar lumen cavity and trachea with serous exudate were observed. SOD activity decreased, but the MDA level increased. Compared with I/R group, the SOD activity increased and MDA level decreased in DADLE treatment group, with significantly reduced lung congestion, the degree of lung injury, and the infiltration of neutrophils. Compared with I/R group, the PaO2 and oxygenation index in DADLE treatment group were increased. CONCLUSION：Various degrees of pulmonary injury were observed in acute global cerebral ischemia reperfusion model. DADLE might have a protective effect on lung tissues of ALI in rats.     

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.     

Expression of stem cell factor in mast cells isolated from patients with chronic periapical diseases

AIM:To investigate the expression of stem cell factor (SCF) in tryptase -positive mast cells (MCs) in different types of human periapical diseases for determining the role of SCF and MCs in the pathogenesis of periapical diseases. METHODS:A total 50 cases of specimens were involved in this study, including healthy control (n=20), periapical cyst (n=15) and periapical granuloma (n=15). The tissue material was fixed in 10% formalin for at least 48 h, stained with hematoxylin and eosin for the observation of histopathology, stained with immunohistochemistry for identifying MCs and MCs degranulation, and stained with double immunofluorescence for identification of tryptase-SCF double positive MCs. RESULTS:Compared with healthy control, significantly higher densities of both total and degranulated MCs in human periapical lesions were observed. The densities of both total and degranulated MCs in the periapical cyst were significantly higher than that in the periapical granuloma. The density of tryptase-SCF double positive MCs in the periapical lesions was significantly higher than that in the healthy controls. The density oftryptase-SCF double positive MCs in the periapical cyst was significantly higher than that in periapical granuloma. No significant difference in the density of MCs between immunohistochemistry staining and double immunofluorescence staining was observed. CONCLUSION: The tryptase-SCF double positive MCs play an active role in the pathogenesis of the periapical inflammatory lesions, particularly in the formation of fibrous tissue in periapical cyst. The potential role of the tryptase-SCF double positive MCs relates with the initiation, development, and persistence of the periapical inflammatory process.