Effect of Mercury on Seed Germination and Seedling Growth of Mungbean (Vigna radiata (L.) Wilczek)

Among the toxic elements release in the environment, mercury is considered highly toxic to the growth of plants. The present studies report the effects of different concentrations (1, 3, 5 and 7 mM) of mercury on seed germination and seedling growth performance of mungbea (Vigna radiata) as compared to control. Mercury treatment in the form of mercuric chloride at 1 mM did not show significant reduction in seed germination of V. radiata as compared to control. Increase in  concentration of mercury to 3 mM produced significant (p<0.05) reduction in seed germination. Mercury treatment at 7 mM-produced significant (p<0.05)  reduction in seedling and root length of the plants. The increase in concentration of mercury treatment at 7 mM was found sufficient to cause significant reductions in seedling dry weight of as compared to control. Mercury treatment at all concentrations decreased seed germination, shoot, and root length and seedling dry weight. Increase in mercury concentration upto 7 mM showed highest percentage of decrease in seed germination (42%), seedling length (70%), root length  (66%) and seedling dry weight (47%) of mungbean as relation to control. V. radiata were more sensitive to mercury stress in seedling growth and root elongation than seed germination. The seedlings of V. radiata showed greater tolerance to mercury at 1 mM (85.83 %) and lowest at 7 mM (34.13%). These results show that there is a negative effect towards germination and growth of mungbean by mercury treatment. Minimum use of the mercury containing compounds in fungicide,  pesticide and nematicide is recommended. Special care should be taken to monitor the toxic pollutants available in the immediate environment. The accumulation of such types of toxic pollutants in larger concentrations by crop can produce harmful effects to crops and ecosystem as well

Low-level laser therapy for carpal tunnel syndrome

BACKGROUND: The role of low-level laser therapy (LLLT) in the management of carpal tunnel syndrome (CTS) is controversial. While some trials have shown distinct advantages of LLLT over placebo and some other non-surgical treatments, other trials have not. OBJECTIVES: To assess the benefits and harms of LLLT versus placebo and versus other non-surgical interventions in the management of CTS. SEARCH METHODS: On 9 December 2016 we searched CENTRAL, MEDLINE, Embase, and Science Citation Index Expanded for randomised controlled trials (RCTs). We also searched clinical trial registries for ongoing studies. We checked the references of primary studies and review articles, and contacted trial authors for additional studies. SELECTION CRITERIA: We considered for inclusion RCTs (irrespective of blinding, publication status or language) comparing LLLT versus placebo or non-surgical treatment for the management of CTS. DATA COLLECTION AND ANALYSIS: Two review authors independently identified trials for inclusion and extracted the data. For continuous outcomes, we calculated the mean difference (MD) or standardised mean difference (SMD) with a 95% confidence interval (CI) using the random-effects model, calculated using Review Manager. For dichotomous data, we reported risk ratio (RR) and 95% CI. MAIN RESULTS: We identified 22 trials randomising 1153 participants that were eligible for inclusion; nine trials (525 participants, 256 randomised to LLLT) compared LLLT with placebo, two (150 participants, 75 randomised to LLLT) compared LLLT with ultrasound, one compared LLLT with placebo and LLLT with ultrasound, two compared LLLT with steroid injection, and one trial each compared LLLT with other non-surgical interventions: fascial manipulation, application of a pulsed magnetic field, transcutaneous electrical nerve stimulation (TENS), steroid injection, tendon gliding exercises, and applying a wrist splint combined with non-steroidal anti-inflammatory drugs. Three studies compared LLLT as part of multiple interventions. Risk of bias varied across the studies, but was high or unclear in most assessed domains in most studies. Most studies were small, with few events, and effect estimates were generally imprecise and inconsistent; the combination of these factors led us to categorise the quality of evidence for most outcomes as very low or, for a small number, low. At short-term follow-up (less than three months), there was very low-quality evidence for any effect over placebo of LLLT on CTS for the primary outcome of Symptom Severity Score (scale 1 to 5, higher score represents worsening; MD -0.36, 95% CI -0.78 to 0.06) or Functional Status Scale (scale 1 to 5, higher score represents worsened disability; MD -0.56, 95% CI -1.03 to -0.09). At short-term (less than three months) follow-up, we are uncertain whether LLLT results in a greater improvement than placebo in visual analogue score (VAS) pain (scale 0 to 10, higher score represents worsening; MD -1.47, 95% CI -2.36 to -0.58) and several aspects of nerve conduction studies (motor nerve latency: higher score represents worsening; MD -0.09 ms, 95% CI -0.16 to -0.03; range 3.1 ms to 4.99 ms; sensory nerve latency: MD -0.10 ms, 95% CI -0.15 to -0.06; range 1.8 ms to 3.9 ms), as the quality of the evidence was very low. When compared with placebo at short-term follow-up, LLLT may slightly improve grip strength (MD 2.58 kg, 95% CI 1.22 to 3.95; range 14.2 kg to 25.23 kg) and finger-pinch strength (MD 0.94 kg, 95% CI 0.43 to 1.44; range 4.35 kg to 5.7 kg); however, the quality of evidence was low. Only VAS pain and finger-pinch strength results reached the minimal clinically important difference (MCID) as previously published. We are uncertain about the effect of LLLT in comparison to ultrasound at short-term follow-up for improvement in VAS pain (MD 2.81, 95% CI 1.21 to 4.40) and motor nerve latency (MD 0.61 ms, 95% CI 0.27 to 0.95), as the quality of evidence was very low. When compared with ultrasound at short-term follow-up, LLLT may result in slightly less improvement in finger-pinch strength (MD -0.71 kg, 95% CI -0.94 to -0.49) and motor nerve amplitude (MD -1.90 mV, 95% CI -3.63 to -0.18; range 7.10 mV to 9.70 mV); however, the quality of evidence was low. There was insufficient evidence to assess the long-term benefits of LLLT versus placebo or ultrasound. There was insufficient evidence to show whether LLLT is better or worse in the management of CTS than other non-surgical interventions. For all outcomes reported within these other comparisons, the quality of evidence was very low. There was insufficient evidence to assess adverse events, as only one study reported this outcome. AUTHORS' CONCLUSIONS: The evidence is of very low quality and we found no data to support any clinical effect of LLLT in treating CTS. Only VAS pain and finger-pinch strength met previously published MCIDs but these are likely to be overestimates of effect given the small studies and significant risk of bias. There is low or very low-quality evidence to suggest that LLLT is less effective than ultrasound in the management of CTS based on short-term, clinically significant improvements in pain and finger-pinch strength. There is insufficient evidence to support LLLT being better or worse than any other type of non-surgical treatment in the management of CTS. Any further research of LLLT should be definitive, blinded, and of high quality

Epigenetic deregulation of multiple S100 gene family members by differential hypomethylation and hypermethylation events in medulloblastoma

Deregulated expression of genes encoding members of the S100 family of calcium-binding proteins has been associated with the malignant progression of multiple tumour types. Using a pharmacological expression reactivation approach, we screened 16 S100 genes for evidence of epigenetic regulation in medulloblastoma, the most common malignant brain tumour of childhood. Four family members (S100A2, S100A4, S100A6 and S100A10) demonstrated evidence of upregulated expression in multiple medulloblastoma cell lines, following treatment with the DNA methyltransferase inhibitor, 5′-aza-2′-deoxycytidine. Subsequent analysis revealed methylation of critical CpG sites located within these four genes in an extended cell line panel. Assessment of these genes in the non-neoplastic cerebellum (from which medulloblastomas develop) revealed strong somatic methylation affecting S100A2 and S100A4, whereas S100A6 and S100A10 were unmethylated. Assessed against these normal tissue-specific methylation states, S100A6 and S100A10 demonstrated tumour-specific hypermethylation in medulloblastoma primary tumours (5 out of 40 and 4 out of 35, respectively, both 12%) and cell lines (both 7 out of 9, 78%), which was associated with their transcriptional silencing. Moreover, S100A6 hypermethylation was significantly associated with the aggressive large cell/anaplastic morphophenotype (P=0.026). In contrast, pro-metastatic S100A4 displayed evidence of hypomethylation relative to the normal cerebellum in a significant proportion primary tumours (7 out of 41, 17%) and cell lines (3 out of 9, 33%), which was associated with its elevated expression. In summary, these data characterise complex patterns of somatic methylation affecting S100 genes in the normal cerebellum and demonstrate their disruption causing epigenetic deregulation of multiple S100 family members in medulloblastoma development. Epigenetic events affecting S100 genes have potential clinical utility and merit further investigation as molecular biomarkers for this disease

Host Genetics and Environmental Factors Regulate Ecological Succession of the Mouse Colon Tissue-Associated Microbiota

Background: The integration of host genetics, environmental triggers and the microbiota is a recognised factor in the pathogenesis of barrier function diseases such as IBD. In order to determine how these factors interact to regulate the host immune response and ecological succession of the colon tissue-associated microbiota, we investigated the temporal interaction between the microbiota and the host following disruption of the colonic epithelial barrier. Methodology/Principal Findings: Oral administration of DSS was applied as a mechanistic model of environmental damage of the colon and the resulting inflammation characterized for various parameters over time in WT and Nod2 KO mice. Results: In WT mice, DSS damage exposed the host to the commensal flora and led to a migration of the tissue-associated bacteria from the epithelium to mucosal and submucosal layers correlating with changes in proinflammatory cytokine profiles and a progressive transition from acute to chronic inflammation of the colon. Tissue-associated bacteria levels peaked at day 21 post-DSS and declined thereafter, correlating with recruitment of innate immune cells and development of the adaptive immune response. Histological parameters, immune cell infiltration and cytokine biomarkers of inflammation were indistinguishable between Nod2 and WT littermates following DSS, however, Nod2 KO mice demonstrated significantly higher tissue-associated bacterial levels in the colon. DSS damage and Nod2 genotype independently regulated the community structure of the colon microbiota

CD34+/M-cadherin+ Bone Marrow Progenitor Cells Promote Arteriogenesis in Ischemic Hindlimbs of ApoE−/− Mice

BACKGROUND: Cell-based therapy shows promise in treating peripheral arterial disease (PAD); however, the optimal cell type and long-term efficacy are unknown. In this study, we identified a novel subpopulation of adult progenitor cells positive for CD34 and M-cadherin (CD34⁺/M-cad⁺ BMCs) in mouse and human bone marrow. We also examined the long-lasting therapeutic efficacy of mouse CD34⁺/M-cad⁺ BMCs in restoring blood flow and promoting vascularization in an atherosclerotic mouse model of PAD. METHODS AND FINDINGS: Colony-forming cell assays and flow cytometry analysis showed that CD34⁺/M-cad⁺ BMCs have hematopoietic progenitor properties. When delivered intra-arterially into the ischemic hindlimbs of ApoE⁻/⁻ mice, CD34⁺/M-cad⁺ BMCs alleviated ischemia and significantly improved blood flow compared with CD34⁺/M-cad⁻ BMCs, CD34⁻/M-cad⁺ BMCs, or unselected BMCs. Significantly more arterioles were seen in CD34⁺/M-cad⁺ cell-treated limbs than in any other treatment group 60 days after cell therapy. Furthermore, histologic assessment and morphometric analyses of hindlimbs treated with GFP⁺ CD34⁺/M-cad⁺ cells showed that injected cells incorporated into solid tissue structures at 21 days. Confocal microscopic examination of GFP⁺ CD34⁺/M-cad⁺ cell-treated ischemic legs followed by immunostaining indicated the vascular differentiation of CD34⁺/M-cad⁺ progenitor cells. A cytokine antibody array revealed that CD34⁺/M-cad⁺ cell-conditioned medium contained higher levels of cytokines in a unique pattern, including bFGF, CRG-2, EGF, Flt-3 ligand, IGF-1, SDF-1, and VEGFR-3, than did CD34⁺/M-cad⁻ cell-conditioned medium. The proangiogenic cytokines secreted by CD34⁺/M-cad⁺ cells induced oxygen- and nutrient-depleted endothelial cell sprouting significantly better than CD34⁺/M-cad⁻ cells during hypoxia. CONCLUSION: CD34⁺/M-cad⁺ BMCs represent a new progenitor cell type that effectively alleviates hindlimb ischemia in ApoE⁻/⁻ mice by consistently improving blood flow and promoting arteriogenesis. Additionally, CD34⁺/M-cad⁺ BMCs contribute to microvascular remodeling by differentiating into vascular cells and releasing proangiogenic cytokines and growth factors

Direct Identification of the Meloidogyne incognita Secretome Reveals Proteins with Host Cell Reprogramming Potential

The root knot nematode, Meloidogyne incognita, is an obligate parasite that causes significant damage to a broad range of host plants. Infection is associated with secretion of proteins surrounded by proliferating cells. Many parasites are known to secrete effectors that interfere with plant innate immunity, enabling infection to occur; they can also release pathogen-associated molecular patterns (PAMPs, e.g., flagellin) that trigger basal immunity through the nematode stylet into the plant cell. This leads to suppression of innate immunity and reprogramming of plant cells to form a feeding structure containing multinucleate giant cells. Effectors have generally been discovered using genetics or bioinformatics, but M. incognita is non-sexual and its genome sequence has not yet been reported. To partially overcome these limitations, we have used mass spectrometry to directly identify 486 proteins secreted by M. incognita. These proteins contain at least segmental sequence identity to those found in our 3 reference databases (published nematode proteins; unpublished M. incognita ESTs; published plant proteins). Several secreted proteins are homologous to plant proteins, which they may mimic, and they contain domains that suggest known effector functions (e.g., regulating the plant cell cycle or growth). Others have regulatory domains that could reprogram cells. Using in situ hybridization we observed that most secreted proteins were produced by the subventral glands, but we found that phasmids also secreted proteins. We annotated the functions of the secreted proteins and classified them according to roles they may play in the development of root knot disease. Our results show that parasite secretomes can be partially characterized without cognate genomic DNA sequence. We observed that the M. incognita secretome overlaps the reported secretome of mammalian parasitic nematodes (e.g., Brugia malayi), suggesting a common parasitic behavior and a possible conservation of function between metazoan parasites of plants and animals