Search

Syndromic management of sexually transmitted diseases (STDs) is strongly promoted in Namibia. However, no data are available on rates of asymptomatic reproductive tract infections (RTIs) which would remain undetected and thus untreated in the general population. This study was aimed at assessing the prevalence of RTIs in a young rural population and to gain an insight into their health-care seeking behaviour for RTIs. A total of 97 patients (44 male, 53 female)30 years of age attending the outpatient clinic of a rural hospital in Northern Namibia for problems unrelated to RTIs were interviewed and examined. Specimens were taken for investigation of RTIs according to a non-invasive diagnostic schedule. Laboratory examinations revealed 58 infections of the reproductive tract in 42 of the 97 patients (43%). In addition, HIV infection was detected in 13 cases (13%). RTI rates were highest in female teenagers (68%), but no infections were detected in their male counterparts. Of those 42 patients with a laboratory-diagnosed infection, 7 had both symptoms and signs (symptomatic), 16 had neither symptoms nor signs (asymptomatic), and 19 had signs on examination but no symptoms (inapparent). Awareness and perception of symptoms and signs of RTIs were low in the studied population. Provision of adequate treatment for RTIs alone is unlikely to have a major impact on the overall burden of disease since the largest burden of disease was found among those patients (predominantly females) with inapparent infections. Health education on RTIs including STDs and the symptoms they cause together with the importance of early attendance at health facilities and improved access to treatment need to be addressed urgently.Findings are reported from a study conducted to assess the prevalence of reproductive tract infections (RTIs) in a young rural population in northern Namibia. 44 men and 53 women aged 16-29 years attending the outpatient clinic of Engela District Hospital during March-May 1997 for problems unrelated to RTIs were interviewed and examined. Specimens were taken to determine the presence of RTIs using a non-invasive diagnostic schedule. Laboratory examinations identified 58 infections of the reproductive tract in 42 of the 97 patients (43%). HIV infection was detected in 13 cases (13%). 68% of female teenagers had at least 1 RTI, while no infections were detected among male teens. Of the 42 patients with a laboratory-diagnosed infection, 7 had both symptoms and signs of infection, 16 had neither signs nor symptoms, and 19 had signs on examination but no symptoms (inapparent). The study subjects were poorly aware and poorly perceived the signs and symptoms of RTIs. Providing adequate treatment for RTIs alone will probably have no major effect upon the overall burden of disease since the largest such burden was found among those patients with inapparent infections.

Contains fulltext : 52859.pdf (Publisher’s version ) (Closed access)

Anaplastic large cell lymphomas (ALCLs) can be subdivided into two subgroups on the basis of their expression of the ALK protein. ALK protein expression leads to activation of signal transducer and activator of transcription (STAT) 3, which is more commonly expressed in ALK-positive than in ALK-negative tumours. Activated STAT3 leads to the induction of several genes such as Mcl-1, Bcl-2 and Bcl-X-L, and tissue inhibitor of metalloproteinase (TIMP)-1. In this study, we analysed TIMP-1 expression in five ALCL cell lines and 11 tumours by quantitative RT-PCR and immunohistochemistry. We identified high-level TIMP-1 expression by RT-PCR in three ALK-positive ALCL-derived cell lines and in all ALK-positive ALCLs, whereas ALK-negative ALCLs generally demonstrated a lower level of TIMP-1 expression. Concordant with these results, we observed TIMP-1 immunostaining in all ALK-positive ALCLs and in only two of six ALK-negative ALCLs. No relationship was observed between the levels of ALK and TIMP-1 expression in the ALK-positive tumours. STAT3 expression levels were similar in all ALCL samples. Double staining with either CD30 or CD68 demonstrated that TIMP-1 expression was restricted to macrophages in the majority of TIMP-1-positive tumours. Expression of the TIMP-1 substrate MMP-2 was more prominent in ALK-negative tumours, while MMP-9 levels were low in all cases. Expression levels of IL-6 and TGF-beta 1, which are cytokines known to induce TIMP-1 were higher in ALK-negative ALCLs and moderate in ALK-positive tumours. No clear relationship was observed between IL-10 expression and ALK positivity. Overall, no correlation was seen in ALCLs between the expression of TIMP-1 and that of cytokines that induce TIMP-1. Lack of TIMP-I expression in the tumour cells of ALK-positive ALCLs argues against a direct role for ALK-induced activation of STAT3 in the regulation of TIMP-1 expression in ALCL. Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

no abstract

no abstract

Laser dissection microscopy was applied to isolate endothelial cells from tumors obtained from mice treated with TNF-alpha. RNA integrity was demonstrated from whole sections and dissected cells after acetone fixation and hematoxylin staining. RT-PCR for GAPDH, CD31, VCAM-1, ICAM-1 and E-selectin was successfully performed on these samples. These data demonstrate the feasibility of analyzing local endothelial cell responses in diseased tissues at the level of gene expression.

After intravenous injection of a low dose (25 mug/kg) in rats, the anti HIV-1 compound succinylated human serum albumin (Suc-HSA) is taken up mainly in the liver and spleen and is proteolytically degraded. Ten minutes after injection of I-125-Suc-HSA, 72 and 14% of the dose were found in the liver and spleen, respectively. With immunohistochemistry we demonstrated that in both organs, Suc-HSA was specifically endocytosed in endothelial cells. In the isolated perfused rat liver preparation, liver uptake was shown to be saturable, with a K(m) of 2.9 10(-8) M and a V(max) of 2.4 mug/min/100 g body weight. The apparent K(m) and V(max) in vivo were 2.2 10(-7) M and 10.3 mug/min/100 g, respectively. Uptake in liver and spleen was inhibited by preadministration of an excess of formaldehyde-treated albumin and with polyinosinic acid, indicating the involvement of the scavenger receptor, as anticipated for such polyanionic compounds. Suc-HSA is not absorbed intact from the colon and the ileum. After injecting (i.v.) rats with a high dose of Suc-HSA (10 mg/kg), the elimination t1/2 was 3 hr, and therefore, sustained plasma levels above the concentration needed for in vitro anti-HIV-1 activity can be achieved.

We synthesized several para-aminophenyl (pap-) mannose-terminated albumins with varying sugar density (Man7-HSA, Man22-HSA, and Man40-HSA) and compared hepatic uptake with (thio-)mannose-terminated bovine serum albumin (Man-43-AI-BSA) The rate of uptake in isolated perfused rat livers was found to be positively correlated with the sugar density (Man40-HSA = Man22-HSA > Man7-HSA > HSA). Immunohistochemical staining of liver sections showed for both types of neoglycoproteins that uptake occurred in nonparenchymal cells only. Competition experiments with a 500-fold excess of mannan, a known ligand for the mannose/N-acetylglucosamine receptor, that is predominantly localized in endothelial cells, showed complete inhibition of the (thio-)Man43-AI-BSA uptake. In the case of (pap-)mannose-terminated albumins, however, the extent of inhibition by mannan was moderate and decreased markedly with increasing sugar density, being only 20% for (pap-)Man40-HSA. Therefore, we hypothesized that one or more additional removal systems contributed to the clearance of these (pap-)mannose glycoproteins. We found that net negative charge of the (pap-)mannose albumins clearly increased with increasing sugar density, as shown on fast protein liquid chromatography anion-exchange chromatograms. To determine whether the scavenger receptor system that is also mainly present on endothelial cells is involved, we performed competition studies with strongly negatively charged substrates, such as dextran sulfate and formaldehyde-treated human serum albumin (fHSA). An excess of dextran sulfate (500 kDa), indeed blocked the (pap-)mannose-albumin uptake for more than 95%. Dextran sulfate completely inhibited the hepatic uptake of mannan as well, indicating that the polyanion does not discriminate between the scavenger system and the mannose receptor system and should be regarded as an aspecific inhibitor of receptor-mediated endocytotic pathways. Surprisingly, a 500-fold excess of fHSA only moderately (20%) inhibited the clearance of (pap-)Man40-HSA in spite of its high affinity for the scavenger receptor. However, a combination of mannan and fHSA strongly inhibited the uptake of (pap-)Man22-HSA (90%) and to a lesser extent (pap-)Man40-HSA (80%), indicating that a third uptake mechanism may exist that recognizes both mannose groups (or other sugars) and net negative charge. This so far unnoticed receptor system apparently is strongly affected by dextran sulfate and, as shown by immunohistochemistry, is mainly localized on Kupffer cells rather than on the endothelial cells of the liver.