Assessment of potential indigenous plant species for the phytoremediation of arsenic-contaminated areas of Bangladesh

Soil and water contaminated with arsenic (As) pose a major environmental and human health problem in Bangladesh. Phytoremediation, a plant-based technology, may provide an economically viable solution for remediating the As-polluted sites. The use of indigenous plants with a high tolerance and accumulation capacity for As may be a very convenient approach for phytoremediation. To assess the potential of native plant species for phytoremediation, plant and soil samples were collected from four As-contaminated (groundwater) districts in Bangladesh. The main criteria used for selecting plants for phytoremediation were high bioconcentration factors (BCFs) and translocation factors (TFs) of As. From the results of a screening of 49 plant species belonging to 29 families, only one species of fern (Dryopteris filix-mas), three herbs (Blumea lacera, Mikania cordata, and Ageratum conyzoides), and two shrubs (Clerodendrum trichotomum and Ricinus communis) were found to be suitable for phytoremediation. Arsenic bioconcentration and translocation factors > 1 suggest that these plants are As-tolerant accumulators with potential use in phytoextraction. Three floating plants (Eichhornia crassipes, Spirodela polyrhiza, and Azolla pinnata) and a common wetland weed (Monochoria vaginalis) also showed high BCF and TF values; therefore, these plants may be promising candidates for cleaningup As-contaminated surface water and wetland areas. The BCF of Oryza sativa, obtained from As-contaminated districts was > 1, which highlights possible food-chain transfer issues for As-contaminated areas in Bangladesh.     

MsrA knockout mouse exhibits abnormal behavior and brain dopamine levels

Oxidative stress can cause methionine oxidation that has been implicated in various proteins malfunctions, if not adequately reduced by the methionine sulfoxide reductase system. Recent evidence has found oxidized methionine residues in neurodegenerative conditions. Previously, we have described elevated levels of brain pathologies and an abnormal walking pattern in the methionine sulfoxide reductase A knockout (MsrA(-/-)) mouse. Here we show that MsrA(-/-) mice have compromised complex task learning capabilities relative to wild-type mice. Likewise, MsrA(-/-) mice exhibit lower locomotor activity and altered gait that exacerbated with age. Furthermore, MsrA(-/-) mice were less responsive to amphetamine treatment. Consequently, brain dopamine levels were determined. Surprisingly, relative to wild-type mice, MsrA(-/-) brains contained significantly higher levels of dopamine up to 12 months of age, while lower levels of dopamine were observed at 16 months of age. Moreover, striatal regions of MsrA(-/-) mice showed an increase of dopamine release parallel to observed dopamine levels. Similarly, the expression pattern of tyrosine hydroxylase activating protein correlated with the age-dependent dopamine levels. Thus, it is suggested that dopamine regulation and signaling pathways are impaired in MsrA(-/-) mice, which may contribute to their abnormal behavior. These observations may be relevant to age-related neurological diseases associated with oxidative stress.     

Leucine-enriched essential amino acid and carbohydrate ingestion following resistance exercise enhances mTOR signaling and protein synthesis in human muscle

We recently showed that resistance exercise and ingestion of essential amino acids with carbohydrate (EAA+CHO) can independently stimulate mammalian target of rapamycin (mTOR) signaling and muscle protein synthesis in humans. Providing an EAA+CHO solution postexercise can further increase muscle protein synthesis. Therefore, we hypothesized that enhanced mTOR signaling might be responsible for the greater muscle protein synthesis when leucine-enriched EAA+CHOs are ingested during postexercise recovery. Sixteen male subjects were randomized to one of two groups (control or EAA+CHO). The EAA+CHO group ingested the nutrient solution 1 h after resistance exercise. mTOR signaling was assessed by immunoblotting from repeated muscle biopsy samples. Mixed muscle fractional synthetic rate (FSR) was measured using stable isotope techniques. Muscle protein synthesis and 4E-BP1 phosphorylation during exercise were significantly reduced (P < 0.05). Postexercise FSR was elevated above baseline in both groups at 1 h but was even further elevated in the EAA+CHO group at 2 h postexercise (P < 0.05). Increased FSR was associated with enhanced phosphorylation of mTOR and S6K1 (P < 0.05). Akt phosphorylation was elevated at 1 h and returned to baseline by 2 h in the control group, but it remained elevated in the EAA+CHO group (P < 0.05). 4E-BP1 phosphorylation returned to baseline during recovery in control but became elevated when EAA+CHO was ingested (P < 0.05). eEF2 phosphorylation decreased at 1 and 2 h postexercise to a similar extent in both groups (P < 0.05). Our data suggest that enhanced activation of the mTOR signaling pathway is playing a role in the greater synthesis of muscle proteins when resistance exercise is followed by EAA+CHO ingestion.     

Nonproliferating bystander CD4+ T cells lacking activation markers support HIV replication during immune activation

HIV replicates primarily in lymphoid tissue and immune activation is a major stimulus in vivo. To determine the cells responsible for HIV replication during Ag-driven T cell activation, we used a novel in vitro model employing dendritic cell presentation of superantigen to CD4(+) T cells. Dendritic cells and CD4(+) T cells are the major constituents of the paracortical region of lymphoid organs, the main site of Ag-specific activation and HIV replication. Unexpectedly, replication occurred in nonproliferating bystander CD4(+) T cells that lacked activation markers. In contrast, activated Ag-specific cells were relatively protected from infection, which was associated with CCR5 and CXC chemokine receptor 4 down-regulation. The finding that HIV replication is not restricted to highly activated Ag-specific CD4(+) T cells has implications for therapy, efforts to eradicate viral reservoirs, immune control of HIV, and Ag-specific immune defects.     

High affinity binding between lipoprotein lipase and lipoproteins involves multiple ionic and hydrophobic interactions, does not require enzyme activity, and is modulated by glycosaminoglycans

Lipoprotein lipase (LPL) physically associates with lipoproteins and hydrolyzes triglycerides. To characterize the binding of LPL to lipoproteins, we studied the binding of low density lipoproteins (LDL), apolipoprotein (apo) B17, and various apoB-FLAG (DYKDDDDK octapeptide) chimeras to purified LPL. LDL bound to LPL with high affinity (K(d) values of 10(-12) m) similar to that observed for the binding of LDL to its receptors and 1D1, a monoclonal antibody to LDL, and was greater than its affinity for microsomal triglyceride transfer protein. LDL-LPL binding was sensitive to both salt and detergents, indicating the involvement of both hydrophobic and hydrophilic interactions. In contrast, the N-terminal 17% of apoB interacted with LPL mainly via ionic interactions. Binding of various apoB fusion peptides suggested that LPL bound to apoB at multiple sites within apoB17. Tetrahydrolipstatin, a potent enzyme activity inhibitor, had no effect on apoB-LPL binding, indicating that the enzyme activity was not required for apoB binding. LDL-LPL binding was inhibited by monoclonal antibodies that recognize amino acids 380-410 in the C-terminal region of LPL, a region also shown to interact with heparin and LDL receptor-related protein. The LDL-LPL binding was also inhibited by glycosaminoglycans (GAGs); heparin inhibited the interactions by approximately 50% and removal of trace amounts of heparin from LPL preparations increased LDL binding. Thus, we conclude that the high affinity binding between LPL and lipoproteins involves multiple ionic and hydrophobic interactions, does not require enzyme activity and is modulated by GAGs. It is proposed that LPL contains a surface exposed positively charged amino acid cluster that may be important for various physiological interactions of LPL with different biologically important molecules. Moreover, we postulate that by binding to this cluster, GAGs modulate the association between LDL and LPL and the in vivo metabolism of LPL.     

Endothelial cell survival and apoptosis in the tumor vasculature

Angiogenesis is essential for the growth and metastasis of solid tumors. The balance of endothelial cell (EC) proliferation and apoptosis is a major determinant in tumor angiogenesis. Recently, several studies demonstrated that numerous angiogenic factors not only induce angiogenesis but also function as EC survival factors. Vascular endothelial growth factor (VEGF), a potent angiogenic factor, is also an EC survival factor in embryonic vasculogenesis and tumor angiogenesis. VEGF activates specific intracellular survival pathways in ECs including Bcl-2, A1, IAP, Akt, and Erk. Integrins may function as EC survival factors by preventing anoikis by enhancing binding to the extracellular matrix. In addition, integrins may function in concert with VEGF to promote EC survival. Angiopoietin-1 (Ang-1) has recently been shown to stabilize EC networks by binding to the EC-specific tyrosine kinase receptor Tie-2. Pericytes also function as EC survival factors, by cell-cell contact, secretion of survival factors, or both. Targeting any of the above mechanisms for EC survival may provide novel antineoplastic strategies.     

Organ and detriment-weighted dose rate coefficients for exposure to radionuclide-contaminated soil considering body morphometries that differ from reference conditions: adults and children

Radiation and Environmental Biophysics - The system of protection established by the International Commission on Radiological Protection (ICRP) provides a robust framework for ionizing radiation...     

Mechanisms of palatal epithelial seam disintegration by transforming growth factor (TGF) beta3

TGFbeta3 signaling initiates and completes sequential phases of cellular differentiation that is required for complete disintegration of the palatal medial edge seam, that progresses between 14 and 17 embryonic days in the murine system, which is necessary in establishing confluence of the palatal stroma. Understanding the cellular mechanism of palatal MES disintegration in response to TGFbeta3 signaling will result in new approaches to defining the causes of cleft palate and other facial clefts that may result from failure of seam disintegration. We have isolated MES primary cells to study the details of MES disintegration mechanism by TGFbeta3 during palate development using several biochemical and genetic approaches. Our results demonstrate a novel mechanism of MES disintegration where MES, independently yet sequentially, undergoes cell cycle arrest, cell migration and apoptosis to generate immaculate palatal confluency during palatogenesis in response to robust TGFbeta3 signaling. The results contribute to a missing fundamental element to our base knowledge of the diverse roles of TGFbeta3 in functional and morphological changes that MES undergo during palatal seam disintegration. We believe that our findings will lead to more effective treatment of facial clefting.     

Autosomal recessive nonsyndromic deafness locus DFNB63 at chromosome 11q13.2–q13.3

A genome wide linkage analysis of nonsyndromic deafness segregating in a consanguineous Pakistani family (PKDF537) was used to identify DFNB63, a new locus for congenital profound sensorineural hearing loss. A maximum two-point lod score of 6.98 at θ = 0 was obtained for marker D11S1337 (68.55 cM). Genotyping of 550 families revealed three additional families (PKDF295, PKDF702 and PKDF817) segregating hearing loss linked to chromosome 11q13.2-q13.3. Meiotic recombination events in these four families define a critical interval of 4.81 cM bounded by markers D11S4113 (68.01 cM) and D11S4162 (72.82 cM), and SHANK2, FGF-3, TPCN2 and CTTN are among the candidate genes in this interval. Positional identification of this deafness gene should reveal a protein necessary for normal development and/or function of the auditory system.     

Prediction of survival ratios of Cadra cautella (Lepidoptera: Pyralidae) different life stages after treated with ultraviolet radiation in dates

Date palm, is a tree of economic importance which is grown around the world, including Saudi Arabia. Its fruit is nutritious and possesses medicinal benefits. Almond moth, is a serious date fruits pest in the field as well as in the storage and causes severe economic losses. In the given research, ultraviolet radiation type B (UV-B, 315 nm) harmful effects were evaluated against all developmental stages of C. cautella. One and 3-d-old eggs, 12 and 18-d-old larvae, 1-d and 6-d-old pupae, and 1-d-old adults, were exposed to UV-B for different intervals. Eggs were exposed for 0–30 min and 0% hatchability was achieved both for 1-d and 3-d-old eggs after 30 min. The larvae were exposed for 6–24 h, and after 24 h, mortality was 100 and 97% for 12 and 18-d-old larvae, respectively. Similarly, the pupae were exposed for 0–30 h, and 100% mortality was achieved after 30 h for 1-d-old pupae. Furthermore, none of the 6-d-old pupae emerged as an adult after 12 h of exposure. When adults were exposed for 1–4 d, no mortality was observed; however, UV-B reduced fecundity and hatchability in the treated adults. The susceptibility order was as follows: eggs > larvae > pupae > adults. Several uncharacteristic behaviors of C. cautella were noted, such as females depositing eggs openly on food items and containers, mature larvae exiting from food, larvae starting to wander for pupation, and pupation occurring typically outside the food. The application of UV-B could be an effective management strategy because all developmental stages of C. cautella were susceptible to UV-B that might be helpful to protect the dates from C. cautella infestation.