Platelets affect different stages of the angiogenic response with a trend to a pro-angiogenic net effect despite the presence of angiogenesis inhibitors such as platelet factor 4. While a concomitant effect of bFGF and VEGF seemed to be essential for the entire process of vessel formation (aortic ring and matrigel models), PDGF and heparanase were effective only at the migration stage.
Dermatophytes are common pathogens of skin but rarely cause invasive disease. We present a case of deep infection by Trichophyton rubrum in an immunocompromised patient. T. rubrum was identified by morphological characteristics and confirmed by PCR. Invasiveness was apparent by histopathology and immunohistochemistry. The patient was treated successfully with itraconazole. CASE REPORTA 56-year-old male was admitted for evaluation of elevated erythrocyte sedimentation rate (ESR), anemia, and multiple subcutaneous nodules on both legs. The patient was under close medical supervision due to an autoimmune disease with liver, cardiac, and lung involvement.His medical history included pericarditis (27 years before admission), and a profound jaundice after a respiratory infection treated with cefuroxime (3 years before admission). Serology was negative for hepatitis viruses and positive for antiparietal, antinuclear, and antineutrophil cytoplasmic antibodies. Liver biopsy revealed a profound destruction of liver architecture, fibrosis, active inflammation, and cholestasis. Treatment with steroids was followed by a good clinical response and normalization of liver enzymes. Attempts to wean the patient from steroids including administration of azathioprine and cyclosporine failed, and during the 2 years prior to admission he received both prednisone and cyclosporine. Several weeks before admission, he was evaluated for a chronic cough. He had undergone a transbronchial biopsy that disclosed chronic inflammation and thickening of the basement membrane, without any specific diagnosis, but responded to an increase of the dose of steroids. A few weeks later, while trying to taper the steroids, he developed multiple, hard cutaneous nodules, distributed mainly on the lower limbs. Some later softened and discharged caseous material spontaneously.Other underlying conditions included glucose-6-phosphate dehydrogenase deficiency, nephrolithiasis, benign prostate hypertrophy, bilateral inguinal hernia repair, and osteoporosis.On admission, medications included prednisone (10 mg once a day [QD]), cyclosporine (100 mg QD), ursodeoxycholic acid (300 mg twice a day), alendronate (10 mg QD), omeprazole (20 mg QD), and calcium (600 mg) and vitamin D (0.25 g) once daily. On physical examination, rhonchi were heard over both lungs. A few hard, mobile subcutaneous nodules were present on both lower limbs, mainly around the knees and thighs (Fig. 1a), and the sacral area. Some of these nodules were purplish and soft. Onychomycosis was present on the feet and both hands (Fig. 1b and c).Laboratory test results were as follows: ESR, 80; hemoglobin level, 10.8 g/dl; leukocyte count, 7,900/l (42% granulocytes); albumin level, 34 g/liter; total protein level, 83 g/liter; liver enzyme levels, normal.Two of the patient's nodules were excised. A granulomatous inflammatory reaction was present in the dermis and hypodermis. It was composed of monocytes, macrophages, multinucleated giant cells, and rare neutrophils (Fig. 2). Septate hyphae were revealed...
Our survey emphasizes the high rate of pregnancy-related listeriosis in Israel and shows that specific clones might account for this.
HIV/AIDS causes severe dysfunction of the immune system through CD4+ T cell depletion, leading to dysregulation of both the adaptive and innate immune arms. A primary target for viral infection is the gastrointestinal tract, which is a reservoir of CD4+ T cells. In addition to being a major immune hub, the human gastrointestinal tract harbors trillions of commensal microorganisms, the microbiota, which have recently been shown to play critical roles in health. Alterations in the composition and function of microbiota have been implicated in a variety of ‘multi-factorial’ disorders, including infectious, autoimmune, metabolic, and neoplastic disorders. It is widely accepted that, in addition to its direct role in altering the gastrointestinal CD4+ T cell compartment, HIV infection is characterized by gut microbiota compositional and functional changes. Herein, we review such alterations and discuss their potential local and systemic effects on the HIV-positive host, as well as potential roles of novel microbiota-targeting treatments in modulating HIV progression and associated adverse systemic manifestations.
Rhinocerebral mucormycosis is a rare disease, affecting almost exclusively patients with known predisposing conditions such as diabetes mellitus, immunocompromised status, haemochromatosis or major trauma. Subsequent to a case of rhinocerebral mucormycosis in a 78-year-old woman without any known risk factor, we reviewed the published English-language literature and found an additional 72 cases. Reviewing all the published case series of mucormycosis involving any site, the proportion of apparently normal hosts among cases of rhinocerebral mucormycosis was found to be 9.06% (95% confidence interval 6.7-11.8). These findings suggest that rhinocerebral mucormycosis in patients without known predisposing factors is more prevalent than was previously believed.
Productive replication of human immunodeficiency virus type 1 (HIV-1) occurs efficiently only in humans. The posttranscriptional stages of the HIV-1 life cycle proceed poorly in mouse cells, with a resulting defect in viral assembly and release. Previous work has shown that the presence of human chromosome 2 increases HIV-1 production in mouse cells. Recent studies have shown that human chromosome region maintenance 1 (hCRM1) stimulates Gag release from rodent cells. Here we report that expressions of hCRM1 in murine cells resulted in marked increases in the production of infectious HIV-1 and feline immunodeficiency virus (FIV). HIV-1 production was also increased by hSRp40, and a combination of hCRM1 and hSRp40 resulted in a more-than-additive effect on HIV-1 release. In contrast, the overexpression of mouse CRM1 (mCRM1) minimally affected HIV-1 and FIV production and did not antagonize hCRM1. In the presence of hCRM1 there were large increases in the amounts of released capsid, which paralleled the increases in the infectious titers. Consistent with this finding, the ratios of unspliced to spliced HIV-1 mRNAs in mouse cells expressing hCRM1 and SRp40 became similar to those of human cells. Furthermore, imaging of intron-containing FIV RNA showed that hCRM1 increased RNA export to the cytoplasm.By testing chimeras between mCRM1 and hCRM1 and comparing those sequences to feline CRM1, we mapped the functional domain to HEAT (Huntingtin, elongation factor 3, protein phosphatase 2A, and the yeast kinase TOR1) repeats 4A to 9A and a triple point mutant in repeat 9A, which showed a loss of function. Structural analysis suggested that this region of hCRM1 may serve as a binding site for viral or cellular factors to facilitate lentiviral RNA nuclear export.
Hepatic abscesses are a rare complication of inflammatory bowel disease (IBD). Despite the fact that certain hepatobiliary complications of IBD, including cholelithiasis, primary sclerosing cholangitis (PSC) and cholangiocarcinoma predispose patients with IBD to ascending cholangitis, previously published data does not demonstrate that biliary infection is an important mechanism underlying liver abscess development in these patients. We describe two patients with inflammatory bowel disease, both with PSC, who developed multiple liver abscesses, and review the literature on liver abscesses in association with inflammatory bowel disease.
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