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To determine the prevalence rate of and risk factors for depression in Croatian Type 2 diabetic patients. Depressive mood was examined in 384 randomly selected outpatients with Type 2 diabetes. Center for Epidemiological Studies Depression Scale (CES-D) and Structured Clinical Interview for DSM-IV Axis I Disorders (SCID) were used to identify depressive disturbances. The groups with CES-D ≥ 16 and < 16 were compared with respect to demographic, psychological and clinical characteristics. Regression analysis was used to determine risk factors for depression. Of the examined patients, 22% had CES-D scores ≥ 16, and in 33% of them clinical depression was confirmed by the psychiatric interview. Depressed patients compared with the non-depressed ones reported more diabetes-related problems and poorer well-being ( t = 6.71, P < 0.001 and t = 11.98, P < 0.001, respectively). Multiple regression analysis indicated female gender, experienced support and the level of emotional well-being to predict depression ( R = 0.74, F = 15.3, P < 0.001). The obtained data indicate that the prevalence rate in Croatian Type 2 diabetic patients is comparable to findings from other cultural settings. Depressive symptoms can be predicted by psychological rather than disease-related variables. Psychological care for diabetic patients may be necessary to prevent depressive symptomatology. Diabet. Med. 22, 942–945 (2005) [ABSTRACT FROM AUTHOR]

1The Graduate Hospital, 2UPHS/Presbyterian Medical Center, and 3Philadelphia Fight, Philadelphia, PA, 4Central Texas Medical Foundation, Austin, TX, 5Christiana Care, Wilmington Hospital, Wilmington, DE, 6Central Florida Research Initiative, Altamonte Springs, FL, and 7The Immune Response Corporation, Carlsbad, CA, USA Objective We examined the activity of an HIV-1 immunogen (Remune) on viral load, CD4 cells and HIV-1 specific immunity. Methods Plasma and peripheral blood mononuclear cells were obtained in a predefined random subset of subjects (n = 252) from a multicentre, double-blind, adjuvant-controlled phase III clinical endpoint study. Results The subjects treated with the HIV-1 immunogen had a significantly greater decline in viral load at multiple time points (P < 0.05), a trend towards increased CD4+ T cell counts and significantly enhanced HIV-1 specific immune responses as measured by HIV-1 lymphocyte proliferation (P < 0.001) compared to the adjuvant control group. Furthermore, in the HIV-1 immunogen treated group, enhanced HIV-1 specific lymphocyte proliferative immune responses were associated with decreased HIV-1 plasma RNA. Conclusion These results suggest that, in a predefined, random subset of subjects, a beneficial effect of the HIV-1 immunogen was observed on viral load, CD4+ T cells, and HIV-specific immunity. These differences were observed in a background of multiple drug therapies. Ongoing trials are evaluating the effect of the combination of this HIV-1 specific, immune-based therapy with potent antiviral drug therapy on virological outcomes. [ABSTRACT FROM AUTHOR]

This review is focused on recent investigations demonstrating a pharmacological and patho­ physiologic role in gastroduodenal ulceration for growth factors such as basic fibroblast growth factor (bFGF), platetet­derived growth factor (PDGF) and vascular endothelial growth factor (VEGFL) as well as for transcription factors. Our experiments revealed accelerated healing, without decreased gastric acid secretion, of chronic cysteamine­induced duodenal ulcers in rats treated daily for 3weeks with intragastric administration of bFGF. PDGF or VEGF. Our recent studies also indicate a pathophysiologlcal role of endogenous growth factors in the natural history of experimental duodenal ulcer development and healing. More recently, we investigated the genetic regulation of these growth factors in experimental duodenal ulceration. Since gene expression is most effectively controlled by transcription factors, proteins that bind to cis­acting elements of DNA and guide the binding of polymerase II to start the transcription of specific mRNA, we tested the hypothesis that the expression of IEGs and their transcription factor products, such as Egr­I and Spl, might precede the Increased synthesis of BFGF, PDGF and VEGF in duodenal ulcer healing. Indeed, the duodenal ulcerogen cysteamine, but not its nonulcerogen and toxic analogue ethanolamine, rapidly increased duodenal (but not gastric) murosal levels of ET­1, which was followed by enhanced expression of Egr­I and a decrease in Sp1 in the preulcerogenic stage of duodenal ulceration. These changes in levels of ET­1 and expression of transcription factors were also accompanied by Increased expression of the CDK inhibitor p21. Thus, not only growth factors such as bFGF, PDGF and VEGF, but also transcription factors such as Egr­1 and Spl and the cell cycle regulator p21, may play a role in the natural history of experimental duodenal ulceration. [ABSTRACT FROM AUTHOR]

Smith-Lemli-Opitz syndrome (SLOS), or RSH, is an autosomal recessive disorder caused by mutations of the gene encoding 7-dehydrocholesterol reductase (DHCR7). The utility of maternal serum screens and ultrasound as prenatal screening methods for SLOS is presently undetermined. We report the clinical, cytogenetic, biochemical, and molecular findings of a stillborn with SLOS. The diagnosis was made postnatally on the basis of physical findings and confirmed by biochemical and DNA analyses of fetal tissue. Although abnormalities were detected by maternal serum triple screen and prenatal ultrasonography, a diagnosis of SLOS was not suspected before delivery. This study demonstrates that patients with SLOS may escape prenatal diagnosis despite the presence of multiple anomalies and abnormal maternal serum screen results, and lends support for consideration of prenatal biochemical testing for SLOS in pregnancies with these findings. As SLOS is a severe autosomal recessive disorder with a recurrence risk of 25%, ultrasonographic, cytogenetic, and biochemical analyses in the second trimester should be considered if abnormal maternal serum screening results, specifically low levels of unconjugated estriol, are detected., ((c) 2005 Wiley-Liss, Inc.)

Tenofovir is a nucleotide reverse transcriptase inhibitor for treatment of human immunodeficiency virus (HIV) infection. Several cases of renal failure associated with tenofovir therapy recently have been reported. A 54-year-old man with HIV experienced decreasing renal function and Fanconi's syndrome secondary to tenofovir therapy. His condition gradually improved after discontinuation of the drug. The available medical literature for reported cases of tenofovir-related nephrotoxicity indicates that this complication is apparently rare. However, our case report and literature review underscore the importance of monitoring renal function when treating patients with any nucleotide reverse transcriptase inhibitor.

Reboxetine is a non-tricyclic antidepressant with selective noradrenergic (NA) reuptake-blocking effects. The effects of acute and sustained administration of reboxetine, on the firing activity of locus coeruleus NA neurons and dorsal raphe 5-HT neurons, were assessed using in vivo extracellular unitary recording in rats anaesthetized with chloral hydrate. Reboxetine (0.1-1.25 mg/kg, i.v.) dose-dependently decreased the firing activity of NA neurons (ED50 = 480 +/- 14 microg/kg). A 2-day treatment with reboxetine at 1.25, 2.5, 5, or 10 mg/kg per day (using osmotic minipumps implanted subcutaneously) produced significant decreases of 52%, 68%, 81%, and 83%, respectively, of NA firing activity. When the reboxetine treatment (2.5 mg/kg per day) duration was prolonged to 7 days, a 66% decrease in NA firing activity was observed which further decreased to 80% after 21 days of treatment. In contrast, 5-HT neuron firing rate remained unaltered following short- and long-term reboxetine treatments. The suppressant effect of the alpha2-adrenoceptor agonist clonidine on the firing activity of NA neurons was unchanged in long-term reboxetine-treated rats, but its effect on the firing activity of 5-HT neurons was blunted. The enhancement of NA firing activity by the 5-HT1A agonist 8-OH-DPAT was abolished in long-term reboxetine-treated rats, whereas, the inhibitory effect of the 5-HT2 agonist DOI was attenuated by about three-fold. In conclusion, sustained NA reuptake blockade by reboxetine lead to profound alterations in the function of NA neurons and of 5-HT receptors modulating their firing activity.