Occurrence of blood-feeding terrestrial leeches (Haemadipsidae) in a degraded forest ecosystem and their potential as ecological indicators

Blood-feeding invertebrates are emerging model taxa in biodiversity assessments, both as indicators of mammal abundance and also as sources of mammal DNA for identification. Among these, terrestrial leeches arguably offer the greatest promise; they are abundant and widespread in the humid tropics, and their blood meals can be easily assayed to establish diet. Unfortunately, terrestrial leeches are understudied, with little known about their ecology and behavior. Such information is needed to evaluate their utility as ecological indicators and to account for potential sampling biases that might arise from habitat preferences. By combining occupancy modeling and thermal tolerance assays, we determined the factors affecting species occurrence in the related terrestrial brown (Haemadipsa sumatrana) and tiger leech (Haemadipsa picta), both of which are widespread in tropical forests in Southeast Asia. We sampled both species across a degraded forest landscape in Sabah, Borneo, in wet and dry seasons, associating occurrence with habitat-level metrics. We found that, for both species, detection probability increased with canopy height regardless of season. Additionally, increased vegetation heterogeneity had a strong negative influence on brown leech occurrence in the dry season, implying an interaction between vegetation structure and climate. However, we found no difference in physiological thermal tolerance (CT_MAX) between the two species. Finally, using a reduced dataset, we found a small improvement in brown leech model fit when including mammal abundance. Our results suggest that the presence of terrestrial leeches may act as useful ecological indicators of habitat quality and potentially mammalian abundance. Abstract in Indonesia is available with online material.     

β-Lapachone induces programmed necrosis through the RIP1-PARP-AIF-dependent pathway in human hepatocellular carcinoma SK-Hep1 cells

β-Lapachone activates multiple cell death mechanisms including apoptosis, autophagy and necrotic cell death in cancer cells. In this study, we investigated β-lapachone-induced cell death and the underlying mechanisms in human hepatocellular carcinoma SK-Hep1 cells. β-Lapachone markedly induced cell death without caspase activation. β-Lapachone increased PI uptake and HMGB-1 release to extracellular space, which are markers of necrotic cell death. Necrostatin-1 (a RIP1 kinase inhibitor) markedly inhibited β-lapachone-induced cell death and HMGB-1 release. In addition, β-lapachone activated poly (ADP-ribosyl) polymerase-1(PARP-1) and promoted AIF release, and DPQ (a PARP-1 specific inhibitor) or AIF siRNA blocked β-lapachone-induced cell death. Furthermore, necrostatin-1 blocked PARP-1 activation and cytosolic AIF translocation. We also found that β-lapachone-induced reactive oxygen species (ROS) production has an important role in the activation of the RIP1-PARP1-AIF pathway. Finally, β-lapachone-induced cell death was inhibited by dicoumarol (a NQO-1 inhibitor), and NQO1 expression was correlated with sensitivity to β-lapachone. Taken together, our results demonstrate that β-lapachone induces programmed necrosis through the NQO1-dependent ROS-mediated RIP1-PARP1-AIF pathway.     

Microsatellite analysis as a tool for discriminating an interfamily hybrid between olive flounder and starry flounder

An interspecific artificial hybrid was produced between two economically important aquaculture flatfish: olive flounder (Paralichthys olivaceus) and starry flounder (P. stellatus). This hybrid displays the rapid growth characteristic of the former and tolerance to low temperatures and low salinity of the latter, but the genetics of inheritance in this hybrid have not been elucidated. Polymorphic microsatellite markers developed for P. olivaceus and P. stellatus were tested to determine if these markers can be used for analysis of parentage and genetic inheritance. Multiplex PCR using two primer sets that were specific to each species produced PCR products of different sizes; these could be used for the identification of interspecific hybrids. Among the 192 primers derived from olive flounder, 25.5% of the primer sets successfully amplified genomic DNA from starry flounder, and 23% of the 56 primer sets originating from starry flounder amplified DNA from olive flounder. Analysis of genetic inheritance in the hybrid using seven of the 62 microsatellite markers common to both species demonstrated classic Mendelian inheritance of these markers in the hybrid progeny, with the exception of one locus identified as a null allele in the hybrid. These results demonstrate that cross-specific microsatellite markers can be used tools for parentage analysis of hybrid flatfish, for mapping quantitative trait loci, for marker-assisted selective breeding, and for studies of the evolution of fish.     

Consequences of changing rainfall for fungal pathogen-induced mortality in tropical tree seedlings

Most general circulation models predict that most tropical forests will experience lower and less frequent rainfall in future as a result of climate change, which may reduce the capacity of fungal pathogens to drive density-dependent tree mortality. This is potentially significant because fungal pathogens are thought to play a key role in promoting and structuring plant diversity in tropical forests through the Janzen-Connell mechanism. Therefore, we hypothesize that the drying of tropical forests will negatively impact species coexistence. To test one prediction of this hypothesis, we imposed experimental watering regimes on the seedlings of a tropical tree, Pleradenophora longicuspis, and measured mortality induced by fungal pathogens under shade house conditions. The frequency of watering had a strong impact on survival. Seedlings watered daily experienced significantly higher mortality than those watered every three or every six days, while increasing the volume of water applied also led to increased mortality, although this relationship was less pronounced. These results suggest that the capacity of fungal pathogens to drive density-dependent mortality may be reduced in drier climates and when rainfall is less frequent, with potential implications for the diversity enhancing Janzen-Connell mechanism.     

Prosaposin is an AR-target gene and its neurotrophic domain upregulates AR expression and activity in prostate stromal cells

Recent studies have introduced prosaposin (PSAP) as a pleiotrophic growth factor for prostate cancer (PCa). We have previously reported that PSAP or one of its known active molecular derivatives, saposin C functions as an androgen-agonist and androgen-regulated gene (ARG) for androgen-sensitive (AS) PCa cell lines. Due to the potential significance of androgen receptor (AR)-expressing stroma in PCa, we evaluated a possible bi-directional paracrine regulatory interactions between DHT and PSAP in AR-positive prostate stromal (PrSt) cells. We report that saposin C in a ligand-independent manner increased AR expression, its nuclear content, and tyrosine phosphorylation. DHT treatment of PrSt cells increased PSAP expression. We also demonstrated both serum- and androgen-inducibility of a previously characterized hormone-responsive element (HRE) located in the proximal region of PSAP promoter. In addition, conditioned-media derived from PrSt cells and bone fibroblasts (i.e., MSF) differentially increased PSAP-promoter activity in androgen-independent (AI) PC-3 and AS LNCaP cells. Our data for the first time demonstrate that not only saposin C or PSAP regulates AR expression/activity, but also function as an ARG in PrSt. Ligand-independent activation of AR by PSAP or saposin C in PCa and stromal cells may contribute not only to prostate carcinogenesis at an early stage, but also in AI progression of the disease in an androgen-deprived tumor microenvironment.     

Metabolic profiling of plasma from discordant schizophrenia twins: correlation between lipid signals and global functioning in female schizophrenia patients

(1)H NMR spectroscopy-based metabonomic analysis was employed to investigate plasma samples from 21 pairs of monozygotic twins discordant for schizophrenia and 8 pairs of age-matched healthy twins in an effort to disentangle genetic and epigenetic components of schizophrenia. We identified alterations in the lipid profile of both affected and unaffected schizophrenia twins. Additionally, there is a close association of VLDL/LDL signals and Global Functioning Scores in female twins suffering from schizophrenia. Our results further support a link between metabolic disturbances and the etiopathology of schizophrenia.     

Abnormal liver function associated with occupational exposure to dimethylformamide and glutathione S-transferase polymorphisms.

Dimethylformaide (DMF) is a major solvent predominately used in synthetic leather and resin production. Many human and animal studies have linked the cause of hepatoxicity to DMF. Previously, the authors demonstrated the significant dose-response relationship between abnormal liver function tests and DMF exposure and the interaction with hepatitis B virus (HBV) infection in Taiwanese workers. Because the toxic effect of various chemicals can be modified by metabolic traits, the study also investigated the influence of the glutathione S-transferases (GSTM1 and GSTT1) on the toxic effect of DMF. The average DMF exposure concentration was 23.87 ppm (range 5.2-86.6 ppm) in the high-exposure (>/=5 ppm) group and 2.41 ppm (range 0.9-4.3 ppm) in the low-exposure (<5 ppm) group. There were 13 of 44 (29.6%) abnormal liver function tests (elevations of either glutamate oxaloacetate transaminase (GOT) or glutamate pyruvate transaminase (GPT)) among the high DMF exposure workers, two of 22 (9.1%) abnormal liver function tests among the low DMF exposure workers. Chronic liver disease as determined by ultrasonography was present in seven of 44 (15.9%) high DMF exposure workers, and 0 of 22 (0%) low DMF exposure workers. There were 11 of 34 (32.4%) abnormal liver function tests among the GSTT1 null genotype workers, and four of 32 (12.5%) abnormal liver function tests among the GSTT1-positive genotype workers. Compared with the low DMF exposure workers, the adjusted odds ratio and 95% confidence intervals for abnormal liver function tests was 6.78 (0.94-48.7) for the high DMF exposure workers. Compared with the GSTT1-positive genotype workers, the adjusted odds ratio and 95% confidence intervals for abnormal liver function tests was 4.41 (1.15-16.9) for the GSTT1 null genotype workers. Compared with the low DMF group with GSTT1-positive genotype workers, the odds ratio (adjusted for HBV status) of abnormal liver function test was 12.38, 95% CI=(1.04-146.9) for the high DMF group with GSTT1 null genotype workers. This study indicates that abnormal liver function and chronic liver disease are associated with DMF exposure, and there are more than multiplicative interaction effects on abnormal liver function tests between the DMF exposure and the GSTT1 genotype.