The type VI secretion system (T6SS) is a multi-protein complex that injects bacterial effector proteins into target cells. It is composed of a cell membrane complex anchored to a contractile bacteriophage tail-like apparatus consisting of a sharpened tube that is ejected by the contraction of a sheath against a baseplate. We present structural and biochemical studies on TssA subunits from two different T6SSs that reveal radically different quaternary structures in comparison to the dodecameric E. coli TssA that arise from differences in their C-terminal sequences. Despite this, the different TssAs retain equivalent interactions with other components of the complex and position their highly conserved N-terminal ImpA_N domain at the same radius from the centre of the sheath as a result of their distinct domain architectures, which includes additional spacer domains and highly mobile interdomain linkers. Together, these variations allow these distinct TssAs to perform a similar function in the complex.

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TssA is a core component of the type VI secretion system, and phylogenetic analysis of TssA subunits from different species has suggested that these proteins fall into three distinct clades. Whilst representatives of two clades, TssA1 and TssA2, have been the subjects of investigation, no members of the third clade (TssA3) have been studied. Constructs of TssA from Burkholderia cenocepacia, a representative of clade 3, were expressed, purified and subjected to crystallization trials. Data were collected from crystals of constructs of the N-terminal and C-terminal domains. Analysis of the data from the crystals of these constructs and preliminary structure determination indicates that the C-terminal domain forms an assembly of 32 subunits in D16 symmetry, whereas the N-terminal domain is not involved in subunit assocation.

Abstract

Objectives: The goal of this study was to determine the correlation of clinicopathological factors and the up-regulation of Int-8 receptors and vascular endothelial growth factor (VEGF) expression in oral squamous cell carcinoma (OSCC).

Materials and Methods: Clinical data (age, gender, size of the tumor, location of the tumor, lymph nodes status,..) were collected from 20 patients with OSCC, tabulated and statistically analyzed (SPSS17).Immunohistochemical stainings of Int-8 receptors, CXCR1 and CXCR2 (united states biological, United Bio, USA) and VEGF (Abcam, Cambridge, MA, USA) were done.

Results: Our immunohistochemical study demonstrated: 1)expression of Int-8 receptors in all cases of OSCC with variable intensities, 2) high-level staining of VEGF In poorly differentiated and invasive oral squamous cell carcinoma. Significant correlation was observed between immunohistochemical expression of Int-8 receptors, VEGF and histologic differentiation and clinical stages(Analysis of variance ANOVA, P<0.05).

Conclusion: Our findings suggest that the reactivity to Int-8 receptors

observed in OSCC cases could be used as a parameter for tumor aggressiveness and as potential prognostic marker. Also, up-regulation of VEGF may play a role in the angiogenesis and progression of oral squamous cell carcinoma.

The effect of the duration of cigarette smoking on liver function

Background:. Interleukin-8 (IL-8) is a pro-inammatory cytokine which exerts its effects via binding to CXCR1 and

is known to promote angiogenesis. CXCR1 represent potential prognostic biomarkers and therapeutic target.

Aim of the study: To evaluate the expression of CXCR1 in OSCC and control tissue as well as correlate the expression of the CXCR1to the

clinicopathologic parameters of OSCC .

Material and Methods: Immunohistochemical analysis of 22 cases OSCC and 7 control cases sections stained by anti-CXCR1antibody.

Immunohistochemical staining will be performed using a Labeled Strept-Avidin Biotin complex method (LSAB).

Results: Expression was recognized in all cases of OSCC and normal control cases and the pattern of expressed in both the cytoplasm and

nucleus of the malignant epithelial cells (total cell reactivity), as well as high expression was noticed in low histological grade and clinical

stage malignancy, whereas decrease of expression was detected in high grade and stage malignancy.

Conclusions: the results show an association between CXCR1and the clinicopathologic parameters, and considered as prognostic marker

in OSCC

Study was to identify DNA repair gene (HexB) from S. pneumoniae in

the public databases, and using available programs to analyse and

compare the sequences between different strains. In this study, we

observe interesting polymorphisms in the sequences of HexB enzyme.

The amino acid sequences of HexB were identified from 16 strains

and differ by 1% from R6 HexB. At nucleotide level of HexB the

region 801-1000 may represent mosaic gene, as it differ by 10%. This

result suggests that the HexB proteins are highly conserved which

may indicates that these proteins perform a common essential role in repair process

T he conclusion from this present review would indicate that there were insufficient RCTs to adequately address the original research question, although a number of suggestions may be recommended. There was no doubt from the evidence presented in the published literature that in the the accumulation of the plaque which may in turn lead to gingival inflammation. Furthermore, there also appears to be a higher risk of dental caries (particularly root caries) in RPD wearers in the absence of good oral hygiene measures The importance of an integrated prosthodontics maintenance programme with regular recall visits to include both oral and denture hygiene care of a RPD cannot be under-estimated and should be adopted as a gold standard in general dental practice.absence of good oral hygiene measures a RPD may promote 

Abstract

Our previous study showed that circulating microvesicles (cMVs) of diabetic mice have negative effects on the function of endothelial progenitor cells (EPCs). Whether this is true in diabetic patients deserves further study. In this study, the effects of cMVs and EPC-derived MVs (EPC-MVs) on EPC migration, apoptosis, and reactive oxygen species (ROS) production in healthy controls, well-controlled, and uncontrolled diabetic patients were investigated. The levels of miR-126 and vascular endothelial growth factor receptor 2 (VEGFR2) in cMVs, EPC-MVs, and/or EPCs were analyzed. Moreover, miR-126 inhibitor or mimic was applied to EPCs to modulate the miR-126 level in EPC-MVs. We found the following: 1) the circulating EPC level was reduced but the circulating EPC-MV level increased in uncontrolled diabetic patients; 2) the cMVs and EPC-MVs of healthy controls had beneficial effects on EPCs (migration, apoptosis, ROS), whereas the effects were reversely changed in the cMVs and EPC-MVs of uncontrolled diabetic patients; and 3) the cMVs and EPC-MVs of uncontrolled diabetic patients carried less miR-126 and had downregulated VEGFR2 expression in EPCs. Manipulating the miR-126 level in EPC-MVs with inhibitor or mimic changed their function. The effects of cMVs and EPC-MVs are compromised in diabetes due to the reduction of their carried miR-126, which might provide a therapy target for diabetic vascular complications.

diabetes mellitus (DM) is considered one of the major risk factors for various cardiovascular complications. Endothelium dysfunction is a key initiator for vascular disease, which results from increased oxidative stress in the vascular cells (39). Endothelial progenitor cells (EPCs) are known to play important roles in maintaining vascular function and structure by repairing or replacing dysfunctional or injured endothelial cells (ECs) (33). Impaired EPC proliferation, differentiation, adhesion, mobilization, and survival have been reported in DM (1, 26). Our previous study has demonstrated that the circulating EPC level is decreased and the function of EPCs impaired in db/db diabetic mice (8). Moreover, we found that the circulating microvesicles (cMVs) of db/db diabetic mice compromised the functions of EPCs. Investigation on the regulatory effects of cMVs on EPCs in diabetic patients could provide novel therapeutic avenues for vascular complications of diabetes.

Extracellular MVs are submicrometric fragments released from the cells in response to activation and apoptosis (22, 37). cMVs are the MVs released from the cells in the blood and from the vascular wall. An elevation of cMV levels has been reported in vascular diseases such as thrombotic diseases, diabetes, and cardiovascular diseases (2, 8, 25). Furthermore, one study has shown that the level of cMVs could predict the severity of vascular diseases (30). MVs released from EPCs (EPC-MVs) have been reported to serve as an index for EPC loss and functional incompetence (27). Moreover, the level of circulating EPC-MVs can predict aortic stiffness in atherosclerotic patients (27). Therefore, circulating MV and EPC-MV levels could serve as biomarkers and predictors for vascular diseases. On the other hand, accumulating evidence suggests that MVs mediate cell-cell communication via transferring proteins, mRNAs, and miroRNAs (miRs) from their parent cells to the target cells (5, 17, 29). The functions of MVs are complex and multifactorial, depending on the stimulator and origin. Previously, we demonstrated that cMVs of diabetic mice impair the function of EPCs, whereas cMVs of healthy controls do not have detrimental effects on EPCs (8). However, whether this is true in diabetic patients remains unclear.

Previous studies have shown that miR-126 governs vascular integrity (35) and is a biomarker or mediator of vascular diseases (11, 32). Downregulation of miR-126 impairs EPC function (23). EPC-MVs have been shown to improve ischemia-reperfusion injury of hindlimb and kidney through the transfer of miR-126 to target cells (6, 28). In the meantime, miR-126 has been reported to regulate angiogenic process and EC/EPC function by modulating vascular endothelial growth factor receptor 2 (VEGFR2) (13, 15). Our previous study found that EPC-MVs affect EC functions and apoptosis via their carried miR-126 (34). However, it is unknown whether EPC-MVs, as one type of MVs, would affect EPC functions through the miR-126 and its downstream VEGFR2 pathway.

In the present study, we determined the effects of cMVs and EPC-MVs of diabetic patients on EPC survival and functions and explored whether miR-126/VEGFR2 is involved in the mechanism.