21 research outputs found

    Probable Donor-Derived Human Adenovirus Type 34 Infection in 2 Kidney Transplant Recipients From the Same Donor.

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    Human adenovirus type 34 (HAdV-34) infection is a recognized cause of transplant-associated hemorrhagic cystitis and, in rare cases, tubulointerstitial nephritis. The source of such infections is often difficult to assess, that is, whether acquired as a primary infection, exposure to a pathogen in the transplanted organ, or reactivation of an endogenous latent infection. We present here 2 cases of likely transplant-acquired HAdV-34 infection from the same organ donor, manifesting as tubulointerstitial nephritis in 1

    Early Third Molar Extraction: When Germectomy Is the Best Choise

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    Third molars are often removed in order to prevent complications and various other problems associated..

    TLR2-Dependent Modulation of Antigen Presenting Cell Functions by Mycobacterial Lipoproteins

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    Histological evaluation of the root apices of failed endodontic cases

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    Aim: The aim of this histological study was to evaluate the different causes of the failures of the endodontic treatment. Materials and Methods: Adult patients who were referred for endodontic surgery and for whom root-end resection was considered suitable were invited to participate in this study. The inclusion criteria were: (1) Patients aged between 18 and 65 years; (2) teeth with apical periodontitis that was diagnosed radiographically; (3) the tooth could not be adequately and better managed by root-canal retreatment; and (4) the crown of the tooth was adequately restored. One hundred root apices were surgically removed together with the periapical pathological tissue from 92 patients (56 males and 36 women).Histological sectioning was performed on calcified specimens that were embedded in a suitable medium. Results: The causes of endodontic failure identified through histological evaluation were as follows: Presence of bacterial and debris into canals (51%), apex transposition and overfilling (3%), presence of the isthmus (21%), bacterial colonization of root surface (2%), untreated canals (11%), and filling material outside root canal (4%). There was no significant difference between the distribution of teeth and the causes of endodontic failures (P = 0.32). Conclusions: The present study demonstrated that the most common cause of endodontic failure is the insufficient cleaning of the root canal system. It also explores the effectiveness of histological evaluation of the root apex following root-end resection in exploring the causes of endodontic failures

    Mycobacterium tuberculosis Promotes HIV trans-Infection and Suppresses Major Histocompatibility Complex Class II Antigen Processing by Dendritic Cellsâ–¿

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    Mycobacterium tuberculosis is a leading killer of HIV-infected individuals worldwide, particularly in sub-Saharan Africa, where it is responsible for up to 50% of HIV-related deaths. Infection by HIV predisposes individuals to M. tuberculosis infection, and coinfection accelerates the progression of both diseases. In contrast to most other opportunistic infections associated with HIV, an increased risk of M. tuberculosis infection occurs during early-stage HIV disease, long before CD4 T cell counts fall below critical levels. We hypothesized that M. tuberculosis infection contributes to HIV pathogenesis by interfering with dendritic cell (DC)-mediated immune control. DCs carry pathogens like M. tuberculosis and HIV from sites of infection into lymphoid tissues, where they process and present antigenic peptides to CD4 T cells. Paradoxically, DCs can also deliver infectious HIV to T cells without first becoming infected, a process known as trans-infection. Lipopolysaccharide (LPS)-activated DCs sequester HIV in pocketlike membrane invaginations that remain open to the cell surface, and individual virions are delivered from the pocket into T cells at the site of contact during trans-infection. Here we report that M. tuberculosis exposure increases HIV trans-infection and induces viral sequestration within surface-accessible compartments identical to those seen in LPS-stimulated DCs. At the same time, M. tuberculosis dramatically decreases the degradative processing and major histocompatibility complex class II (MHC-II) presentation of HIV antigens to CD4 T cells. Our data suggest that M. tuberculosis infection promotes a shift in the dynamic balance between antigen processing and intact virion presentation, favoring DC-mediated amplification of HIV infections

    TLR2 and its co-receptors determine responses of macrophages and dendritic cells to lipoproteins of Mycobacterium tuberculosis

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    Mycobacterium tuberculosis (Mtb) signals through Toll-like receptor 2 (TLR2) to regulate antigen presenting cells (APCs). Mtb lipoproteins, including LpqH, LprA, LprG and PhoS1, are TLR2 agonists, but their co-receptor requirements are unknown. We studied Mtb lipoprotein-induced responses in TLR2(-/-), TLR1(-/-), TLR6(-/-), CD14(-/-) and CD36(-/-) macrophages. Responses to LprA, LprG, LpqH and PhoS1 were completely dependent on TLR2. LprG, LpqH, and PhoS1 were dependent on TLR1, but LprA did not require TLR1. None of the lipoproteins required TLR6, although a redundant contribution by TLR6 cannot be excluded. CD14 contributed to detection of LprA, LprG and LpqH, whereas CD36 contributed only to detection of LprA. Studies of lung APC subsets revealed lower TLR2 expression by CD11b(high)/CD11c(low) lung macrophages than CD11b(low)/CD11c(high) alveolar macrophages, which correlated with hyporesponsiveness of lung macrophages to LpqH. Thus, lung APC subsets differ in TLR expression, which may determine differences in responses to Mtb
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