High air humidity is sufficient for successful egg incubation and early post‐embryonic development in the marbled crayfish (Procambarus virginalis)

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Improvement of nutritional quality of cultured sobaity sea bream,Sparidentex hasta (Valenciennes) muscle by preharvest feeding of finisher feeds

A 6‐month long study was conducted to improve the nutritional quality of the cultured sobaity bream, Sparidentex hasta by feeding them finisher feeds containing high docosahexaenoic acid (DHA) at the last two months of the grow‐out stage so that the muscle DHA level be increased at par to the wild. A grow‐out feed used from the beginning until the end of the trial was considered as the control (Diet 1). Experimental diets 2 and 3 were formulated to contain 9.0% DHA (e.g. 1.68 g DHA/100 g feed) and 10.5% DHA (2.20 g DHA/100 g feed), by incorporating high DHA tuna oil into a sea bream grow‐out diet. For comparison, a commercial finisher feed (Diet 4) from Skretting, Italy was also used. The results of this study demonstrated that fish fed DHA enriched finisher diets resulted in significantly (p < .05) better growth, feed utilization and higher muscle eicosapentaenoic acid (EPA) and DHA content compared to those fed grow‐out diet. The muscle DHA and EPA of fish fed finisher diets were also higher than those of the whole year average DHA and EPA content of wild sobaity. An organoleptic evaluation showed no significant (p > .05) differences between sensory attributes of muscle from cultured and wild sea bream. The results of the study demonstrated that feeding finisher feed enriched with DHA at the later part of the grow‐out operation, the n‐3 PUFA levels of cultured sobaity can cost‐effectively be increased at par to the wild.     

Which option best estimates the above-ground biomass of mangroves of Bangladesh: pantropical or site- and species-specific models?

Wetlands Ecology and Management - Bangladesh has the single largest tract of naturally growing mangrove forest as well as the world’s largest manmade mangrove forest on newly accreted land in...     

Comparison Study of Allelochemicals and Bispyribac-Sodium on the Germination and Growth Response of Echinochloa crus-galli L.

The phytotoxic effects of two allelochemicals (trans-cinnamic acid and syringaldehyde) at different concentrations (1000, 100, 10, and 1 µM) on seed germination, seedling growth, and physiological and biochemical changes of Echinochloa crus-galli L. were tested by comparison to a commercial herbicide ‘Nominee’ (that is, 100 g/L bispyribac-sodium). trans-Cinnamic acid and the herbicide inhibited seed germination completely at 100 µM, whereas for syringaldehyde, complete inhibition required 1000 µM. However, with 100 µM syringaldehyde, the seed germination of the test species was 53% of the control. Allelochemicals and the herbicide delayed seed germination and significantly affected the speed of germination index (S), speed of cumulative germination index (AS), and coefficient of germination rate (CRG). The roots were more affected when nutrients were not added to the growth bioassay. In general, with the increasing concentration of allelochemicals from 100 to 1000 µM, the inhibitory effects increased. Via microscopy analysis, we found leaf blade wilting and necrosis at concentrations above 100 µM in allelochemical-treated plants. Roots of E. crus-galli treated with 1000 µM allelochemicals had black points on root nodes but had no root hairs. The anatomy of roots treated with allelochemicals (1000 µM) showed contraction or reduction of root pith cells as well as fewer and larger vacuoles compared to the control. The allelochemicals also showed remarkable effects on seedling growth, SPAD index, chlorophyll content, and free proline content in a pot culture bioassay, indicating that trans-cinnamic acid and syringaldehyde are potent inhibitors of E. crus-galli growth and can be developed as herbicides for future weed management strategies.

     

The human sex-determining gene SRY is a direct target of WT1

The product of the Wilms' tumor gene, WT1, is essential for male sex determination and differentiation in mammals. In addition to causing Wilms' tumor, mutations in WT1 often cause two distinct but overlapping urogenital defects in men, Denys-Drash syndrome and Frasier syndrome. In this study we investigated the regulation of the sex determination gene SRY by WT1. Our results showed that WT1 up-regulates the SRY gene through the proximal early growth response gene-1-like DNA-binding sequences in the core promoter. Mutant WT1 proteins in Denys-Drash syndrome patients were unable to activate this promoter. These mutants did not act in a dominant negative manner, as expected over the wild-type WT1 in this promoter. We also found that WT1 could transactivate the endogenous SRY gene. These observations, together with the overlapping expression patterns of WT1 and SRY in human gonads, led us to propose that WT1 regulates SRY in the initial sex determination process in humans and activates a cascade of genes ultimately leading to the complete organogenesis of the testis.     

Primary malignant melanoma of the urinary bladder diagnosed by urine cytology: a case report

BACKGROUND: Primary melanoma of the urinary bladder is a rare neoplasm, and there have been no prior reports in which the initial diagnosis was made by urinary cytology. CASE: An 82-year-old woman presented with vaginal spotting, gross hematuria and dysuria. Voided urine cytology revealed malignant cells, several of which exhibited cytoplasmic melanin pigment and were accompanied by many macrophages also containing melanin. Cystoscopy revealed a darkly pigmented, polypoid mass at the bladder neck. Biopsy confirmed the diagnosis. CONCLUSION: Primary melanoma of the urinary bladder is rare. The diagnosis can be made on cytologic examination of voided urine if careful study of exfoliated malignant cells reveals cytoplasmic melanin pigment. Macrophages may also harbor melanin pigment, and their presence should alert the cytopathologist to search carefully for pigmented malignant cells. Clinical and radiologic studies are essential to rule out melanoma metastatic to the bladder.     

Disruption of gap junctional communication by the platelet-derived growth factor is mediated via multiple signaling pathways

The platelet-derived growth factor (PDGF) mediates its cellular functions via activation of its receptor tyrosine kinase followed by the recruitment and activation of several signaling molecules. These signaling molecules then initiate specific signaling cascades, finally resulting in distinct physiological effects. To delineate the PDGF signaling pathway responsible for the disruption of gap junctional communication (GJC), wild-type PDGF receptor beta (PDGFRbeta) and a series of PDGFRbeta mutants were expressed in T51B rat liver epithelial cells. In cells expressing wild-type PDGFRbeta, PDGF induced disruption of GJC and phosphorylation of a gap junctional protein, connexin-43 (Cx43), which required activation of mitogen-activated protein kinase, although involvement of additional factors was also evident. In the F5 mutant lacking binding sites for phosphatidylinositol 3-kinase, GTPase-activating protein, SHP-2, and phospholipase Cgamma1 (PLCgamma1), PDGF induced mitogen-activated protein kinase, but failed to affect GJC or Cx43, indicating involvement of additional signals presumably initiated by one or more of the mutated binding sites. Examination of the single-site mutants revealed that PDGF effects were not mediated via a single signaling component. This was confirmed by the "add-back" mutants, which showed that restoration of either SHP-2 or PLCgamma1 binding was sufficient to propagate the GJC inhibitory actions of PDGF. Further analysis showed that activation of PLCgamma1 is involved in Cx43 phosphorylation, which surprisingly failed to correlate with GJC blockade. The results of our study demonstrate that PDGF-induced disruption of GJC can be mediated by multiple signaling pathways and requires participation of multiple components.     

Excessive ATP hydrolysis in ischemic myocardium by mitochondrial F1F0-ATPase: effect of selective pharmacological inhibition of mitochondrial ATPase hydrolase activity

Mitochondrial F(1)F(0)-ATPase normally synthesizes ATP in the heart, but under ischemic conditions this enzyme paradoxically causes ATP hydrolysis. Nonselective inhibitors of this enzyme (aurovertin, oligomycin) inhibit ATP synthesis in normal tissue but also inhibit ATP hydrolysis in ischemic myocardium. We characterized the profile of aurovertin and oligomycin in ischemic and nonischemic rat myocardium and compared this with the profile of BMS-199264, which only inhibits F(1)F(0)-ATP hydrolase activity. In isolated rat hearts, aurovertin (1-10 microM) and oligomycin (10 microM), at concentrations inhibiting ATPase activity, reduced ATP concentration and contractile function in the nonischemic heart but significantly reduced the rate of ATP depletion during ischemia. They also inhibited recovery of reperfusion ATP and contractile function, consistent with nonselective F(1)F(0)-ATPase inhibitory activity, which suggests that upon reperfusion, the hydrolase activity switches back to ATP synthesis. BMS-199264 inhibits F(1)F(0) hydrolase activity in submitochondrial particles with no effect on ATP synthase activity. BMS-199264 (1-10 microM) conserved ATP in rat hearts during ischemia while having no effect on preischemic contractile function or ATP concentration. Reperfusion ATP levels were replenished faster and necrosis was reduced by BMS-199264. ATP hydrolase activity ex vivo was selectively inhibited by BMS-199264. Therefore, excessive ATP hydrolysis by F(1)F(0)-ATPase contributes to the decline in cardiac energy reserve during ischemia and selective inhibition of ATP hydrolase activity can protect ischemic myocardium.     

Benzodiazepine-based selective inhibitors of mitochondrial F1F0 ATP hydrolase

A series of benzodiazepine-based inhibitors of mitochondrial F(1)F(0) ATP hydrolase were prepared and evaluated for their ability to selectively inhibit the enzyme in the forward direction. Compounds from this series showed excellent potency and selectivity for ATP hydrolase versus ATP synthase, suggesting a potentially beneficial profile useful for the treatment of ischemic heart disease.