Periodontal Conditions in Human Immunodeficiency Virus–Positive Patients Under Highly Active Antiretroviral Therapy From a Metropolitan Area of Rio De Janeiro

Background: The aim of this study is to evaluate the periodontal status and the presence of opportunistic oral lesions in human immunodeficiency virus–positive (HIV+) patients under highly active antiretroviral therapy (HAART) and their association with cluster of differentiation (CD)4+ and CD4+ nadir T‐cell counts and viral load levels. Methods: Clinical periodontal parameters and the presence of opportunistic oral lesions along with records of CD4+ counts and viral load levels were evaluated in 29 individuals (16 females; mean age: 42.7 years) with previous serologic diagnosis of HIV, from the acquired immunodeficiency syndrome program of the Health Center of Duque de Caxias, Rio de Janeiro, Brazil. Results: All individuals presented gingivitis or periodontitis. A higher non‐significant prevalence of periodontitis was found in smokers (93.8%) compared with non‐smokers (76.9%). A significant weak positive correlation was observed between CD4+ counts and missing teeth (ρ = 0.380, P <0.05), CD4+ nadir and periodontal diagnosis (ρ = 0.418, P <0.005), and CD4+ nadir and moderate probing depth (PD) (ρ = 0.424, P <0.05). When only non‐smokers were analyzed, a significant moderate positive association was found between viral load and moderate clinical attachment level (CAL) (ρ = 0.638, P <0.05), CD4+ nadir and diagnosis (ρ = 0.586, P <0.05), and CD4+ nadir and moderate CAL (ρ = 0.680, P <0.05). Analysis considering only smokers found no correlations between serologic parameters and demographic or clinical parameters. Conclusions: The current investigation demonstrates that HIV+ individuals under HAART presents a high prevalence of mild to moderate periodontal disease. Viral load levels, CD4+ nadir, and CD4+ counts may present a weak to moderate correlation to the number of missing teeth, periodontal diagnosis, moderate PD, and moderate CAL, which may also reflect some effect of these systemic conditions on the periodontal status.     

Fas ligand-dependent inflammatory regulation in acute myocarditis induced by Trypanosoma cruzi infection

Fas/Fas ligand (Fas-L) engagement, a potent inducer of apoptosis, is also important for cellular activation, regulation of effector and chemotactic activity, and secretion of chemokines and cytokines. We evaluated the relevance of Fas/Fas-L in the regulation of myocarditis induced by Trypanosoma cruzi infection and observed that in Fas-L(-/-) mice (gld/gld), cardiac infiltration was significantly reduced, accordingly showing less cardiomyocyte destruction. Fluorescence-activated cell sorting analysis of cardiac inflammatory cells showed higher numbers of CD8(+) T cells in BALB/c compared with gld/gld mice but similar levels of lymphocyte function-associated antigen-1, intercellular adhesion molecule, CD2, and CD69 expression; MAC-1(+) myeloid cells and mast cells were increased in BALB/c mice, whereas gld/gld mice exhibited an enrichment of CD4(+/low) T cells. Intracellular labeling of cytokines revealed no clear cardiac skewing of Th1 or Th2 responses, but we found a higher number of interleukin-10(+) cells in gld/gld mice and a deficient expression of vascular cell adhesion molecule-1 on cardiac endothelial cells in gld/gld mice. Finally, we found a population of CD3(+) but CD4/CD8 double negative cardiac T cells in both groups of infected mice, but down-regulation of some adhesion molecules and surface receptors was only observed in gld/gld mice, indicating a targeted T-cell population mostly affected by the lack of Fas-L engagement. These results point to a role for myocarditis regulation by Fas/Fas-L beyond its possible direct relevance in cellular death.     

Effect of <Emphasis Type="Italic">Myracrodruon urundeuva</Emphasis> leaf lectin on survival and digestive enzymes of <Emphasis Type="Italic">Aedes aegypti</Emphasis> larvae

Aedes aegypti transmits the viruses that cause yellow and dengue fevers. Vector control is essential, since a vaccine for dengue has not as yet been made available. This work reports on the larvicidal activity of Myracrodruon urundeuva leaf lectin (MuLL) against A. aegypti fourth-stage larvae (L₄). Also, the resistance of MuLL to digestion by L₄ gut proteases and the effects of MuLL on protease, trypsin-like and α-amylase activities from L₄ gut were evaluated to determine if lectin remains active in A. aegypti gut and if insect enzyme activities can be modulated by MuLL. MuLL promoted mortality of L₄ with LC₅₀ of 0.202 mg/ml. Haemagglutinating activity of MuLL was detected even after incubation for 96 h with L₄ gut preparation containing protease activity. MuLL affected the activity of gut enzymes, inhibiting protease and trypsin activities and stimulating α-amylase activity. The results suggest that MuLL may become a new biodegradable larvicidal agent for dengue control. Larvicidal activity of MuLL may be linked to its resistance to proteolysis by larval enzymes and interference in the activity of digestive larval enzymes.     

Angiotensin type 1 (AT1) and type 2 (AT2) receptors mediate the increase in TGF-β1 in thyroid hormone-induced cardiac hypertrophy

Increased thyroid hormone (TH) levels are known to induce cardiac hypertrophy. Some studies have provided evidence for a functional link between angiotensin II (ANG II) and transforming growth factor β1 (TGF-β1) in the heart, both being able to also induce cardiac hypertrophy. However, the contribution of this growth factor activated directly by TH or indirectly by ANG II in cardiac hypertrophy development remains unknown. To analyze the possible role of TGF-β1 in cardiac hypertrophy induced by TH and also to evaluate if the TGF-β1 effect is mediated by ANG II receptors, we employed Wistar rats separated into control, hypothyroid (hypo) and hyperthyroid (T4 − 10) groups combined or not with ANG II receptor blockers (losartan or PD123319). Serum levels of T3 and T4, systolic pressure and heart rate confirmed the thyroid state of the groups. The T4 − 10 group presented a significant increase in cardiac TGF-β1 levels; however, TGF-β1 levels in the hypo group did not change in relation to the control. Inhibition of the increase in cardiac TGF-β1 levels was observed in the groups treated with T4 in association with losartan or PD123319 when compared to the T4 − 10 group. These results demonstrate for the first time the TH-modulated induction of cardiac TGF-β1 in cardiac hypertrophy, and that this effect is mediated by ANG II receptors.     

Time course of hydrogen peroxide-thioredoxin balance and its influence on the intracellular signalling in myocardial infarction

We investigated the myocardial thioredoxin-1 and hydrogen peroxide concentrations and their association with some prosurvival and pro-apoptotic proteins, during the transition from myocardial infarction (MI) to heart failure in rats. Male Wistar rats were divided into the following six groups: three sham-operated groups and three MI groups, each at at 2, 7 and 28 days postsurgery. Cardiac function was analysed by echocardiography; the concentration of H(2)O(2) and the ratio of reduced to oxidized glutathione were measured spectrophotometrically, while the myocardial immunocontent of thioredoxin-1, angiotensin II, angiotensin II type 1 and type 2 receptors, p-JNK/JNK, p-ERK/ERK, p-Akt/Akt, p-mTOR/mTOR and p-GSK3β/GSK3β was evaluated by Western blot. Our results show that thioredoxin-1 appears to make an important contribution to the reduced H(2)O(2) concentration. It was associated with lower JNK expression in the early period post-MI (2 days). However, thioredoxin-1 decreased, while renin-angiotensin system markers and levels of H(2)O(2) increased, over 28 days post-MI, in parallel with some signalling proteins involved in maladaptative cardiac remodelling and ventricular dysfunction. These findings provide insight into the time course profile of endogenous antioxidant adaptation to ischaemic injury, which may be useful for the design of therapeutical strategies targeting oxidative stress post-MI.     

Low plasma levels of l-arginine,impaired intraplatelet nitric oxide and platelet hyperaggregability: Implications for cardiovascular disease in depressive patients

BackgroundObsessive–compulsive disorder (OCD) is a chronic condition that normally presents high rates of psychiatric comorbidity. Depression, tic disorders and other anxiety disorders are among the most common comorbidities in OCD adult patients. There is evidence that the higher the number of psychiatric comorbidities, the worse the OCD treatment response. However, little is known about the impact of OCD treatment on the outcome of the psychiatric comorbidities usually present in OCD patients. The aim of this study was to investigate the impact of exclusive, conventional treatments for OCD on the outcome of additional psychiatric disorders of OCD patients, detected at baseline.MethodsSeventy-six patients with primary OCD admitted to the treatment protocols of the Obsessive–Compulsive Spectrum Disorders Program between July 2007 and December 2009 were evaluated at pre-treatment and after 12 months. Data were analyzed to verify possible associations between OCD treatment response and the outcome of psychiatric comorbidities.ResultsResults showed a significant association between OCD treatment response and improvement of major depression and dysthymia (p-value = 0.002), other anxiety disorders (generalized anxiety disorder, social phobia, specific phobia, posttraumatic stress disorder, panic disorder, agoraphobia and anxiety disorder not otherwise specified) (p-value = 0.054) and tic disorders (p-value = 0.043).LimitationsThis is an open, non-blinded study, without rating scales for comorbid conditions. Further research is necessary focusing on the possible mechanisms by which OCD treatment could improve these specific disorders.ConclusionsOur results suggest that certain comorbid disorders may benefit from OCD-targeted treatment.     

Drug and multidrug resistance among Mycobacterium leprae isolates from Brazilian relapsed leprosy patients

Skin biopsy samples from 145 relapse leprosy cases and from five different regions in Brazil were submitted for sequence analysis of part of the genes associated with Mycobacterium leprae drug resistance. Single nucleotide polymorphisms (SNPs) in these genes were observed in M. leprae from 4 out of 92 cases with positive amplification (4.3%) and included a case with a mutation in rpoB only, another sample with SNPs in both folP1 and rpoB, and two cases showing mutations in folP1, rpoB, and gyrA, suggesting the existence of multidrug resistance (MDR). The nature of the mutations was as reported in earlier studies, being CCC to CGC in codon 55 in folP (Pro to Arg), while in the case of rpoB, all mutations occurred at codon 531, with two being a transition of TCG to ATG (Ser to Met), one TCG to TTC (Ser to Phe), and one TCG to TTG (Ser to Leu). The two cases with mutations in gyrA changed from GCA to GTA (Ala to Val) in codon 91. The median time from cure to relapse diagnosis was 9.45 years but was significantly shorter in patients with mutations (3.26 years; P = 0.0038). More than 70% of the relapses were multibacillary, including three of the mutation-carrying cases; one MDR relapse patient was paucibacillary.