esearch (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 25, No. 31. See the NIHR Journals Library website for further project information.[Erratum to BMB Reports 2012; 45(9) 509-514, PMID 23010171] The BMB Reports would like to correct in the Figure 2 of BMB Rep. 2012; 45(9) 509-514 titled “Biphasic effects of TGFβ1 on BMP9-induced osteogenic differentiation of mesenchymal stem cells.” The original version of this article unfortunately contained image assembling error in the Figure 2. The image for “GFP-Day13” group was inadvertently duplicated from that for “BT20-Day 5” group, and an incorrect image was used for “GFP-Day 17” group. This article has been updated to correct this error in Figure 2.Viral latency is an active process during which the host cell environment is optimized for latent carriage and reactivation. This requires control of both viral and host gene promoters and enhancers often at the level of chromatin, and several viruses co-opt the chromatin organiser CTCF to control gene expression during latency. While CTCF has a role in the latencies of alpha- and gamma-herpesviruses, it was not known whether CTCF played a role in the latency of the beta-herpesvirus human cytomegalovirus (HCMV). Here, we show that HCMV latency is associated with increased CTCF expression and CTCF binding to the viral major lytic promoter, the major immediate early promoter (MIEP). Selleck Androgen Receptor Antagonist This increase in CTCF binding is dependent on the virally encoded G protein coupled receptor, US28, and contributes to suppression of MIEP-driven transcription, a hallmark of latency. Furthermore, we show that latency-associated upregulation of CTCF represses expression of the neutrophil chemoattractants S100A8 and S100A9 which we have previously shown are downregulated during HCMV latency. As with downregulation of the MIEP, CTCF binding to the enhancer region of S100A8/A9 drives their suppression, again in a US28-dependent manner. Taken together, we identify CTCF upregulation as an important mechanism for optimizing latent carriage of HCMV at both the levels of viral and cellular gene expression.Nanomaterials have applications in almost every field and among them, green nanomaterials have various biological applications. Green nanomaterials are specifically useful for drug and DNA delivery applications. Considering that cellulose is the most abundant and easily available biomolecules, and it has been used for preparing greener cellulose nanomaterials. Cellulosic nanowhiskers are a cost-effective and green alternative to chemical non-viral gene delivery systems. Cellulose nanowhiskers are commonly extracted from plant sources, and they are generally prepared by sulfuric and hydrochloric acid hydrolysis of plant cellulose. In this review, the topic of cellulose nanowhiskers as green biocompatible materials for gene and drug delivery is discussed with several practical examples.Objectives. The combined role of whole-body vibration (WBV) exposure and awkward posture on musculoskeletal disorders (MSDs) experienced by dumper operators in two metalliferous mines in India was evaluated through a cross-sectional study. Methods. Frequency-weighted root mean square (rms) acceleration was used for WBV exposure assessment. Anthropometry and rapid upper limb assessment (RULA) were used for static and dynamic posture assessment, respectively. Prevalence of MSDs was assessed using the Nordic musculoskeletal questionnaire (NMQ). Logistic regression was used to assess the factors contributing to MSD problems. Results. The rms values revealed that the operators exceeded the lower limit of Standard No. ISO 2631-11997. The dynamic posture study revealed that the majority of dumper operators were taking awkward postures and 58-74% of them were subjected to high and medium levels of MSD risk. The adjusted odds ratio (7.96, 95% confidence interval [1.24, 41.35]) for the most awkward postures revealed WBV exposure as the significant risk factor for MSD problems among the operators. Conclusion. WBV exposure and posture of operators should be regularly monitored and corrective actions implemented to reduce their MSD problems. Ergonomic seat design based on the anthropometry of the operators should be assessed at the time of procuring new equipment.

One-carbon (1C) metabolism is a metabolic network that integrates nutritional signals with biosynthesis, redox homeostasis, and epigenetics. There are sex differences in hepatic 1C metabolism, however, it is unclear whether sex differences in 1C impact the brain. The aim of this study was to investigate if sex modulates the effects of dietary folic acid deficiency, the main component of 1C, in brain tissue using a mouse model.

Male and female C57Bl/6J mice were placed on a folic acid deficient (FD) or control diet (CD) at six weeks until six months of aged. After which brain tissue and serum were collected for analysis. In brain tissue, hippocampal volume, morphology, and apoptosis as well as cortical acetylcholine metabolism were measured.

Male and female FD mice had reduced serum levels of folate. Both males and females maintained on a FD showed a decrease in the thickness of the hippocampal CA1-CA3 region. Interestingly, there was a sex difference in the levels of active caspase-3 within the CA3 region of the hippocampus. In cortical tissue, there were increased levels of neuronal ChAT and reduced levels of AChE in FD females and male mice.

The results indicated that FD impacts hippocampal morphology and cortical neuronal acetylcholine metabolism. The data from our study indicate that there was only one sex difference and that was in hippocampal apoptosis. Our study provides little evidence that sex modulates the effects of dietary folate deficiency on hippocampal morphology and cortical neuronal acetylcholine metabolism.

The results indicated that FD impacts hippocampal morphology and cortical neuronal acetylcholine metabolism. The data from our study indicate that there was only one sex difference and that was in hippocampal apoptosis. Our study provides little evidence that sex modulates the effects of dietary folate deficiency on hippocampal morphology and cortical neuronal acetylcholine metabolism.