This study indicated that changes occurring during the menstrual cycle influence the periodontium and induce inflammatory conditions.

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Background The aim of the present study was to determine whether postprocedural antibiotic reduces the risk of infection related to the cardiac implantable electronic device (CIED) implantations. Methods The present investigation is a randomized, prospective, single‐blinded controlled trial. All consecutive patients who presented for new CIED implantation, generator replacement, or upgrade were randomized into the following three groups: (A) no antibiotic, (B) intravenous (IV) antibiotic for 1 day, (C) 1 day IV plus 7 days oral antibiotic. Follow‐up was performed on 10‐12 days; 1, 3, 6 months; and then every 6 months for 2 years. The primary endpoint was any evidence of infection at the generator pocket or systemic infection related to the procedure at short‐term (6‐month) and long‐term (2‐year) follow‐ups. Results Of the 450 patients (72 patients with cardiac resynchronization device) included in the study, the primary endpoint of short‐term infection was reached in one patient (0.2%) in group A and no patients in groups B and C. The endpoint of long‐term infection was reached in nine patients (2%) with equal frequency between three randomized groups (three patients in each group). On multivariable analysis, the only independent predictor of infection was defibrillator implantation (odds ratio, 8.5; 95% confidence interval, 1.6‐45). Conclusions The results of this prospective study showed no benefit for the postoperative antibiotic for the prevention of CIED infection.

Multiple sclerosis (MS) is an inflammatory and demyelinating disease of the central nervous system (CNS) that leads to disability in middle‐aged individuals. High rates of apoptosis and inappropriate homing are limitations for the application of stem cells in cell therapy. Preconditioning of bone marrow mesenchymal stem cells (BMSCs) with stromal cell‐derived factor 1α (SDF‐1α), also called C‐X‐C motif chemokine 12 (CXCL12), is an approach for improving the functional features of the cells. The aim of this study was to investigate the therapeutic efficacy of intranasal delivery of SDF‐1α preconditioned BMSCs in the cuprizone‐induced chronically demyelinated mice model. BMSCs were isolated, cultured, and preconditioned with SDF‐1α. Then, intranasal delivery of the preconditioned cells was performed in the C57BL/6 mice receiving cuprizone for 12 weeks. Animals were killed at 30 days after cell delivery. SDF‐1α preconditioning increased C‐X‐C chemokine receptor type 4 (CXCR4) expression on the surface of BMSCs, improved survival of the cells, and decreased their apoptosis in vitro. SDF‐1α preconditioning also improved CXCL12 level within the brain, and enhanced spatial learning and memory (assessed by Morris water maze [MWM]), and myelination (assessed by Luxol fast blue [LFB] and transmission electron microscopy [TEM]). In addition, preconditioning of BMSCs with SDF‐1α reduced the protein expressions of glial fibrillary acidic protein and ionized calcium‐binding adapter molecule (Iba‐1) and increased the expressions of oligodendrocyte lineage transcription factor‐2 (Olig‐2) and adenomatous polyposis coli (APC), evaluated by immunofluorescence. The results showed the efficacy of intranasal delivery of SDF‐1α‐preconditioned BMSCs for improving remyelination in the cuprizone model of MS.

Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system (CNS). Despite introducing multiple immunomodulatory approaches for MS, there are still major concerns about possible ways for improving remyelination in this disease. Microglia exert essential roles in regulation of myelination processes, and interaction between colony-stimulating factor 1 (CSF1) with its receptor CSF1R is considered as a key regulator of microglial differentiation and survival. The aim of this study was to investigate possible roles for a CSF1R inhibitor PLX3397 in recovery of central myelination processes. Chronic demyelination was induced in mice by addition of 0.2% cuprizone to the chow for 12 weeks. Next, animals were undergoing a diet containing 290 mg/kg PLX3397 to induce microglial ablation. The PLX3397 treatment caused a significant decrease in the rate of expression for the CSF1/CSF1R axis, and a reduction in the protein expressions for the microglial marker Iba-1 and for the oligodendrocyte marker Olig-2. Findings from Luxol fast blue (LFB) staining and transmission electron microscopy (TEM) showed an increase in the rate of myelination for the mice receiving PLX3397. The rate of destruction in the nerve fibers and the extent of the gaps formed between layers of myelin sheaths was also reduced after the treatment with PLX3397. In addition, animals experienced an improvement in recovery of motor deficit after receiving PLX3397 (for all P < 0.05). It could be concluded that PLX3397 could retain myelination in the MS model possibly through regulation of the myelin environment. K E Y W O R D Scolony-stimulating factor 1 (CSF1), CSF1R, cuprizone, demyelination, microglia, multiple sclerosis (MS), PLX3397 Effect of the CSF1R inhibitor PLX3397 on remyelination of corpus callosum in a cuprizoneinduced demyelination mouse model.

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Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system with symptoms such as neuroinflammation, astrocytosis, microgliosis, and axonal degeneration. Mesenchymal stem cells (MSCs) with their immunomodulation, differentiation, and neuroprotection abilities can influence the remyelination process. The goal of this study is to investigate the impact of microglial ablation and MSCs transplantation on remyelination processes in the corpus callosum (CC) of the cuprizone demyelination model. For the induction of a chronic demyelination model, C57BL6 mice were fed with chow containing 0.2% cuprizone (wt/wt) for 12 weeks. For the depletion of microglia, PLX3397 was used as a colony‐stimulating factor 1 receptor inhibitor for 21 days. MSCs were injected to the right lateral ventricle and after 2 weeks, the mice were killed. We assessed glial cells using specific markers such as APC, Iba‐1, and GFAP using the immunohistochemistry method. Remyelination was evaluated by Luxol fast blue (LFB) staining and transmission electron microscope (TEM). The specific genes of microglia and MSCs were evaluated by a quantitative real‐time polymerase chain reaction. According to the results of the study, 21 days of PLX3397 treatment significantly reduced microglial cells, and MSCs transplantation decreased the number of astrocytes, whereas the oligodendrocytes population increased significantly in PLX + MSC group in comparison with the cuprizone mice. Furthermore, PLX and MSC treatment elevated levels of remyelination compared with the cuprizone group, as confirmed by LFB staining and TEM analysis. The molecular results showed that MSC transplantation significantly decreased the number of microglia through the CX3CL1/CX3CR1 axis. These results revealed that PLX3397 treatment and MSCs injection reduced microgliosis and astrocytosis. It also increased the oligodendrocytes population by enhancing remyelination in the CC of the cuprizone model of MS.

Phage display of many nanobodies via filamentous phage in combination with helper phage has been reported by many scientists. The aim of this study was to produce lambda (λ) bacteriophage displaying high-affinity nanobody against HER-2 expressing breast carcinoma cells. Bacteriophage λ is a temperate phage with inherent biological safety in mammalian cells. Here we report the construction of a recombinant λ phage that efficiently expresses specific nanobody towards third domain of HER-2 target on SKBR-3 and MCF-7 cell lines in vitro. We constructed recombinant λ phage particles containing a mammalian expression cassette, C-Myc tagged, encoding VHH gene of camelid anti HER-2 third domain epitope using λ ZAP-cytomegalic virus (CMV) vector. The SKBR-3, MCF-7 and human endometrial stem cells were treated by the nanobody displayed recombinant λ phage. The cell growth inhibition assay was performed by MTT Cell Viability Assay Kit. After the fourth round of biopanning there was a significant enrichment in the phage specifically binding to the antigen. The ratio of targeted phage increased approximately 1,000-fold in the fifth round. The nanobody expressed by λ ZAP-CMV-VHH phagemid cloned in λ bioparticles significantly inhibited the proliferation of HER-2 positive SKBR-3 and MCF-7 cells. Recombinant bacteriophage λ ZAP-CMV-VHH-cDNA could be used efficiently for construction of nanobodies to mortify HER-2 positive breast carcinoma cells as a nanomedical therapeutic.