Immediate hair transplantation into a newly closed wound to conceal the final scar on the hair-bearing skin

A surgical incision after suturing usually leaves a visible scar on the hair-bearing skin, even after optimal wound conditions. The conspicuousness of such a scar results from its linear continuity and hairlessness. To prevent this effect, a row of micrografts or minigrafts was inserted between the wound edges immediately after wound closure. The hair grafts that were transplanted were dissected from the discharged skin in the same surgical procedure, if feasible. Otherwise, a mini donor strip was harvested from the mastoid scalp to dissect the hair grafts. The final linear scar was interrupted and concealed sufficiently with the growth of the transplanted hairs. Tension-free closure is required to obtain a satisfactory result with this technique.     

Tissue transglutaminase expression is necessary for adhesion,metastatic potential and cancer stemness of renal cell carcinoma

Tissue transglutaminase (TG2) is the ubiquitously expressed member of transglutaminase family and shown to play a critical role in the development and progression of drug resistance malignancies. We have previously showed the association of TG2 upregulation with progression and metastasis of renal cell carcinoma (RCC) and low disease-free survival. In the present study we further investigate the role of TG2 in cell adhesion, migration and invasion of RCC by silencing TG2 expression in Caki-2 and A-498 primary site and Caki-1 and ACHN metastatic site RCC cell lines. Downregulation of TG2 expression led up to a 60% decrease in actin stress fiber formation and adhesion to β 1 integrin (ITGB1) substrates fibronectin, collagen type I and laminin in both primary and metastatic site RCC cell lines. In addition, treatment with siRNAs against TG2 impaired the migration capacity and cellular invasiveness of ITGB1 substrates in all 4 RCC cell lines. Lastly, the knockdown of TG2 in metastatic Caki-1 cells diminished the expression of CD44, CD73-and CD105 cancer stem cell-like markers. We conclude, for the first time, that TG2 expression is critical for cancer cell adhesion, migration, invasiveness and cancer cell-stemness during RCC progression and dissemination. Therefore, combined targeting of TG2 with drugs widely used in the treatment of RCC may be a promising therapeutic strategy for RCC.     

Immobilized Pseudomonas sp. lipase: A powerful biocatalyst for asymmetric acylation of (±)-2-amino-1-phenylethanols with vinyl acetate

Pseudomonas sp. lipase was immobilized onto glutaraldehyde-activated Florisil^® support via Schiff base formation and stabilized by reducing Schiff base with sodium cyanoborohydride. The immobilization performance was evaluated in terms of bound protein per gram of support (%) and recovered activity (%). A 4-factor and 3-level Box–Behnken design was applied for the acylation of (±)-2-(propylamino)-1-phenylethanol, a model substrate, with vinyl acetate and the asymmetric acylations of other (±)-2-amino-1-phenylethanols with different alkyl substituents onto nitrogen atom such as (±)-2-(methylamino)-1-phenylethanol, (±)-2-(ethylamino)-1-phenylethanol, (±)-2-(butylamino)-1-phenylethanol and (±)-2-(hexylamino)-1-phenylethanol were performed under the optimized conditions. The optimal conditions were bulk water content of 1.8%, reaction temperature of 51.5 °C, initial molar ratio of vinyl acetate to amino alcohol of 1.92, and immobilized lipase loading of 47 mg mL^?1. (R)-enantiomers of tested amino alcohols were preferentially acylated and the reaction purely took place on the hydroxyl group of 2-amino-1-phenylethanols. The increase of alkyl chain length substituted onto nitrogen atom caused an increase in the acylation yield and ee values of (S)-enantiomers. Enantiomeric ratio values were >200 for all the reactions. Our results demonstrate that the immobilized lipase is a promising biocatalyst for the preparation of (S)-2-amino-1-phenylethanols and their corresponding (R)-esters via O-selective acylation of (±)-2-amino-1-phenylethanols with vinyl acetate.     

Meta-analysis of human methylation data for evidence of sex-specific autosomal patterns

Background

Several individual studies have suggested that autosomal CpG methylation differs by sex both in terms of individual CpG sites and global autosomal CpG methylation. However, these findings have been inconsistent and plagued by spurious associations due to the cross reactivity of CpG probes on commercial microarrays. We collectively analysed 76 published studies (n = 6,795) for sex-associated differences in both autosomal and sex chromosome CpG sites.

Results

Overall autosomal methylation profiles varied substantially by study, and we encountered substantial batch effects. We accounted for these by conducting random effects meta-analysis for individual autosomal CpG methylation associations. After excluding non-specific probes, we found 184 autosomal CpG sites differentially methylated by sex after correction for multiple testing. In line with previous studies, average beta differences were small. Many of the most significantly associated CpG probes were new. Of note was differential CpG methylation in the promoters of genes thought to be involved in spermatogenesis and male fertility, such as SLC9A2, SPESP1, CRISP2, and NUPL1. Pathway analysis revealed overrepresentation of genes differentially methylated by sex in several broad Gene Ontology biological processes, including RNA splicing and DNA repair.

Conclusions

This study represents a comprehensive analysis of sex-specific methylation patterns. We demonstrate the existence of sex-specific methylation profiles and report a large number of novel DNA methylation differences in autosomal CpG sites between sexes.

Electronic supplementary material

The online version of this article (doi:10.1186/1471-2164-15-981) contains supplementary material, which is available to authorized users.     

No genotoxic effect in exfoliated bladder cells of rat under the exposure of 1800 and 2100 MHz radio frequency radiation

In this study, we aimed to investigate the effects of 1800 and 2100?MHz Radio Frequency (RF) radiation on the number of micronucleus (MN) in exfoliated bladder cells of rat which shows the genotoxic damage. Exposure period was 30?min/day, 6 days/week for a month and two months exposure periods. Thirty male wistar albino rats were used for five groups: Group I (n?=?6): 1800?MHz RF exposed animals for one month, Group II (n?=?6): 2100?MHz RF exposed animals for one month, Group III (n?=?6): 2100?MHz RF exposed for two months, Group IV (n?=?6): control group for one month, Group V (n?=?6): control group for two months. Rats of the control groups were housed in their home cages during the entire experimental period without subjecting to any experimental manipulation. 1800 and 2100?MHz RF exposures did not result in any significant MN frequencies in rat bladder cells with respect to the control groups (p?>?0.05). There was no statistically significant difference between 2100?MHz RF exposed groups, either. Further studies are needed to demonstrate if there is any genotoxic effect, micronucleus formation in other tissues of rats.     

Molecularly defined unfolded protein response subclasses have distinct correlations with fatty liver disease in zebrafish

The unfolded protein response (UPR) is a complex network of sensors and target genes that ensure efficient folding of secretory proteins in the endoplasmic reticulum (ER). UPR activation is mediated by three main sensors, which regulate the expression of hundreds of targets. UPR activation can result in outcomes ranging from enhanced cellular function to cell dysfunction and cell death. How this pathway causes such different outcomes is unknown. Fatty liver disease (steatosis) is associated with markers of UPR activation and robust UPR induction can cause steatosis; however, in other cases, UPR activation can protect against this disease. By assessing the magnitude of activation of UPR sensors and target genes in the liver of zebrafish larvae exposed to three commonly used ER stressors (tunicamycin, thapsigargin and Brefeldin A), we have identified distinct combinations of UPR sensors and targets (i.e. subclasses) activated by each stressor. We found that only the UPR subclass characterized by maximal induction of UPR target genes, which we term a stressed-UPR, induced steatosis. Principal component analysis demonstrated a significant positive association between UPR target gene induction and steatosis. The same principal component analysis showed significant correlation with steatosis in samples from patients with fatty liver disease. We demonstrate that an adaptive UPR induced by a short exposure to thapsigargin prior to challenging with tunicamycin reduced both the induction of a stressed UPR and steatosis incidence. We conclude that a stressed UPR causes steatosis and an adaptive UPR prevents it, demonstrating that this pathway plays dichotomous roles in fatty liver disease.KEY WORDS: Unfolded protein response, Steatosis, Zebrafish, Tunicamycin, Thapsigargin, ER stress, Fatty liver disease