No abstract

Based on Box-Behnken experimental design and response surface method, the joint effect of temperature (16-36°C), salinity (0-22 ppt) and rearing density (200-1000 fish.m À3 ) on the specific growth rate (SGR) and feed conversion rate (FCR) of Nile tilapia juveniles were studied under laboratory conditions. The entire experiment lasted for 1 month (30 days). Results showed that the linear and quadratic effects of temperature, salinity on both growth and feed utilization were highly statistically significant (P < 0.01). The linear and quadratic effect of rearing density on the growth was highly significant (P < 0.01); the linear effect of rearing density on feed utilization was significant (P < 0.05), but the quadratic effect nonsignificant (P > 0.05). Interactions between temperature and salinity, and between salinity and rearing density on the growth statistically differed from zero (P < 0.05). Interactions between temperature and salinity, between temperature and density on feed utilization was significant (P < 0.05). Model equations of the growth and feed utilization on temperature, salinity and density were established, with the coefficient of determination being 98.34% for growth and 98.11% for feed utilization, and could be applied to projection. The optimal temperature/salinity/density combination was obtained utilizing statistical optimization approach: 29°C/6 ppt/500 fish.m À3 , at which the maximal specific growth and feed utilization reached 4.228%.d À1 and 0.520 respectively, with the desirability being 0.989.

Acute hepatopancreatic necrosis disease (AHPND) is a major debilitating disease that causes massive shrimp death resulting in substantial economic losses in shrimp aquaculture. The Pir toxin proteins secreted by a unique strain of Vibrio parahaemolyticus play an essential role in the pathogenesis of AHPND. At present, most studies on the effects of Pir toxin proteins in shrimp focus on digestive tissues or organs such as hepatopancreas, stomach, etc., with none on the immune organs. In the present study, two recombinant Pir toxin proteins (rPirA and rPirB) of V. parahaemolyticus were expressed with rPirB shown to enter shrimp hemocytes. Employing pull-down and LC-MS/MS analysis, GST-rPirB was found to interact with 13 proteins in hemocytes, including histone H3 and histone H4 and among which histone H4 had the highest protein score. Further analysis using GST pull-down and Far-Western blot analysis revealed that rPirB could interact with histone H4. In addition, using the purified nucleosome protein from Drosophila S2 cells, it was found that PirB protein could specifically bind to histones. When flow cytometry was applied, it was observed that the interaction between PirB and histones in shrimp hemocytes induces apoptosis, which results in the dephosphorylation of Serine 10 in histone H3. Collectively, the current study shows that in addition to its effect on the digestive tract of shrimp, the PirB toxin protein interacts with histones to affect the phosphorylation of histone H3-S10, thereby inducing apoptosis.

The respiratory glycoprotein hemocyanin has been implicated in immune‐related functions. Using lectin blotting, we show that the binding of shrimp (Litopenaeus vannamei) hemocyanin to concanavalin A decreases markedly with O‐glycosidase treatment but not with PNGase F. Twelve O‐glycosylation sites, three on the large hemocyanin subunit and nine on the small hemocyanin subunit (HMCs), were identified by LC‐MS/MS. Importantly, when the glycosylation sites at Thr‐537, Ser‐539, and Thr‐542 on the C terminus of HMCs were replaced with alanine, the resultant mutant hemocyanin had reduced carbohydrate content, coupled with a fourfold reduction in bacterial agglutination and 0.2‐fold reduction in antibacterial activities toward Vibrio parahaemolyticus and Staphylococcus aureus. These results suggest that the glycosylation sites on shrimp hemocyanin are closely related to its immunological functions.

Macrophages have emerged as a key player in tumor biology. However, their number and phenotype in human bone marrow of biopsy (BMB) samples of chronic myeloid leukemia (CML) and their association with disease progression from an initial chronic phase (CP) to accelerated phase (AP) to advanced blast phase (BP) are still unclear. BMB samples from 127 CML patients and 30 patients with iron-deficiency anemia (IDA) as control group were analyzed by immunohistochemistry. The expression levels of CD68, CD163, and CD206 in BMB samples of CML patients were significantly higher than those in the patients of control group (P < 0.01), and we observed that their positive expression was gradually elevated during the transformation of CML-CP to AP to BP (P < 0.01). However, the expressions of CD68, CD163, and CD206 in released group were downregulated and contrasted to these in control group; there exists statistical significance (P < 0.01). The percentage ratio of CD163 and CD206 to CD68 was pronounced to be increasing from CML-CP to AP to BP (P < 0.01). Hence, the higher proportion of CD68+, CD163+ and CD206+ macrophages in BMB samples can be considered a key factor for disease progression of CML patients. Targeting macrophages, especially the M2 phenotype may help in designing therapeutic strategies for CML.