Does plastic incise drape prevent recolonization of endogenous skin flora during lumbar spine procedures?

Background: The aim of this study was to compare the PID with bare skin (without PID) regarding bacterial recolonization and bacterial regrowth of the adjacent skin of surgical incision in lumbar spine surgery patients. Methods: This quasi-experimental study was conducted from February to May 2018 on 88 patients who were candidate for lumbar spine surgery. Patients were assigned to one of two groups, treatment (with PID) and control (without PID). Skin sampling (adjacent of surgical incision) for bacterial culture was done in two steps, immediately after surgical skin prep (IASSP) and immediately after surgical wound closure (IASWC) by researcher. Finally, samples were sent to the laboratory. Results: The mean total bacterial count of patient's skin in stage IASSP was not significantly different between treatment and control groups (0.34 vs 0.27, P = 0.68). However, mean total bacterial count in stage IASWC in treatment group was significantly higher than control group (2.2 vs 0.93, P = 0.03). The frequency distribution of S. aureus (P = 0.04) and S. epidermidis (P = 0.02) was significantly higher in treatment group compared with control group in stage IASWC. Conclusions: The results showed that using PID is unable to reduce recolonization and regrowth of bacteria on patients' skin adjacent to surgical wound in clean lumbar spine surgeries. However, making a definite decision about using or not using of PID requires further studies. © 2019 Wolters Kluwer Medknow Publications. All rights reserved

A defect in the CLIP1 gene (CLIP-170) can cause autosomal recessive intellectual disability

In the context of a comprehensive research project, investigating novel autosomal recessive intellectual disability (ARID) genes, linkage analysis based on autozygosity mapping helped identify an intellectual disability locus on Chr.12q24, in an Iranian family (LOD score=3.7). Next-generation sequencing (NGS) following exon enrichment in this novel interval, detected a nonsense mutation (p.Q1010*) in the CLIP1 gene. CLIP1 encodes a member of microtubule (MT) plus-end tracking proteins, which specifically associates with the ends of growing MTs. These proteins regulate MT dynamic behavior and are important for MT-mediated transport over the length of axons and dendrites. As such, CLIP1 may have a role in neuronal development. We studied lymphoblastoid and skin fibroblast cell lines established from healthy and affected patients. RT-PCR and western blot analyses showed the absence of CLIP1 transcript and protein in lymphoblastoid cells derived from affected patients. Furthermore, immunofluorescence analyses showed MT plus-end staining only in fibroblasts containing the wild-type (and not the mutant) CLIP1 protein. Collectively, our data suggest that defects in CLIP1 may lead to ARID