coli bacteria were less sensitive with a growth inhibition of 48 ± 8.5% at 5000 ppm. The presence of light did not significantly increase the toxicity. Increase of the particle size to 930 nm or 60,000 nm did not influence toxicity ( Adams et al., 2006). Silica particles (10–20 nm, purity 99.5%, obtained as dry powder from American Elements, USA), stabilised with a non-toxic dispersant (100 mg Dispex A40/L) did not inhibit oxygen uptake by yeast cells up to

the highest tested concentration of 1000 mg/L; however, some damage of the cell membrane was found 17-AAG datasheet (Garcia-Saucedo et al., 2011). Fumed and porous type SiO2 particles (purchased from Sigma Corp., USA) with specific surface areas of 349.71 and 644.44 m2/g, and primary particle sizes of 7 nm (fumed) and 10 nm

(porous type), respectively PS-341 (aggregate sizes not reported), did not affect DNA integrity (as measured in the Comet assay), nor growth or reproduction parameters in Daphnia magna at the only tested concentration of 1 mg/L. An increase in the mortality rate of D. magna was observed after a 96 h-treatment with fumed material (mortality rate 10 ± 8.16%) and porous type material (15 ± 4.08%; controls 5 ± 4.08%). In larvae of the aquatic midge Chironomus riparius, an increase in mortality was observed after exposure to the porous-type SiO2 particles, but growth indicators were not significantly changed ( Lee et al., 2009). Because of the high variability in the results reported by Lee et al. (2009), and because only one dose level (1 mg/L) was tested and therefore no dose–response relationship

can be established, the relevance of these findings is doubtful. Fujiwara et al. (2008) report a non-linear, but size-dependent growth inhibition of algae (Chlorella kessleri) after a 96 h exposure to suspensions of Na2O stabilised SiO2 nanoparticles (Catalloid; 5, 26 and 78 nm). The pH of the culture medium was adjusted to 7.7. The 96 h-EC50 values were 0.8 ± 0.6%, 7.1 ± 2.8%, and 9.1 ± 4.7% for materials with primary particle sizes of 5, 26 and 78 nm, indicating an overall very low level of toxicity, even after exposure concentrations that by Methocarbamol far exceed current standard testing guideline recommendations. Toxicity was independent of illumination with light. The size of cells increased in the presence of 5 nm particles, and, to a lesser extent in the presence of materials composed of 26 and 78 nm-sized primary particles (as shown by flow cytometry). Coagulation of cells was observed after exposure to the material containing 5 nm particles (1.02%; test conditions not specified further). In a study reported by Ji et al. (2011), SiO2-nanoparticles showed no significant toxicity in Chlorella up to the highest tested concentration of 1000 mg/L. A low level of toxicity was found in the alga Scenedesmus obliquus by Wei et al. (2010), using silica “nano”-particles (primary particle sizes of 10–20 nm, purity 99.

In contrast, any potential MR-related effects seem harder to detect and fragile relative to the variability in data. The robustness of WM/inhibition results is an extremely important factor to consider when it comes to testing theories and ABT-199 price diagnosing children at the individual level and remediation of DD. Sixth, our study joins several studies with negative results with regard to the MR theory of DD. To date eight studies could not detect any distance/ratio

effect discrepancy between DD and controls (Landerl et al., 2004, Kucian et al., 2006, Kucian et al., 2011, Rousselle and Noël, 2007, Soltész et al., 2007, Landerl and Kolle, 2009, Mussolin et al., 2010b and Kovas et al., 2009) while four studies reported such a difference (Price et al., 2007, Mussolin et al., 2010a and Piazza et al., 2010; Mazzocco et al., 2011). However, as noted before, none of these four studies used non-numerical control tasks and their crucial non-symbolic number comparison diagnostic task is inevitably

confounded by visual stimulus parameters (Gebuis and Reynvoet, 2012 and Gebuis and Reynvoet, 2012) which particularly seriously affects the computation of ‘w’, a proposed measure of the MR (Szűcs et al. 2013). It is also important to note that sometimes simply worse accuracy on MR tasks in DD than controls is considered evidence for impaired selleck chemicals MR in DD. However, obviously, worse accuracy (especially

when there is no control task) can appear for various reasons (see e.g. Szűcs et al., 2013). Hence, decreased accuracy cannot be considered evidence for specific MR impairment. Overall, we conclude that DD and control groups were practically indistinguishable on measures of the MR while other tasks strongly and clearly discriminated these groups. The only piece of data from our study which could perhaps call for number-specific explanations is that the counting-range slope (4–6 number range) in accuracy in the subitizing task was less steep in DD than in controls. However, first, this finding appeared because DD children were isothipendyl more accurate for number 6 than controls. Second, there were no effects in RT which is usually considered the main measure in subitizing tasks. Third, when counting-range slope accuracy and the Inhibition measure were entered into a regression together, counting-range slope was a non-significant predictor of mathematical performance. When only WM and Inhibition were entered into regression, the model fit remained practically unchanged. WM and Inhibition were significant predictors even when entered with verbal and non-verbal IQ measures and with processing speed. WM and Inhibition scores were not correlated which suggests their independence.

Animals were deeply anesthetized with ketamine and submitted to neurophysiological evaluation by electromyography of the mandibular branch of the facial nerve aiming at obtaining find protocol compound muscle action potentials (CMAPs). Outcome variables were the CMAP amplitude and latency values. To obtain the CMAPs, we used a portable electromyography system (Neuro-MEP-Micro®, Neurosoft, Dhaka, Bangladesh) connected to a battery-operated Pavilion dv5C portable personal computer (Hewlett-Packard). The Neuro-MEP.NET software (version 2.4.23.0, Neurosoft) was employed to assess the CMAP data obtained under the following configuration of the electromyography

system: 10-Hz high-pass filter, 10-kHz low-pass filter, notch filter off, 60 mV of leading edge signal, and 10-kHz of sampling rate. The electromyography protocol has been established specifically for

evaluation of the rat facial nerve and described in detail by Salomone et al. (2012). Histomorphometric analyses were performed blindly six weeks after surgical procedure, and this method was well established by Costa et al., 2006, Costa et al., 2007 and Costa et al., 2012. After sacrifice, the surgically repaired portion of the facial nerve was cut into four parts, two distally and two proximally related to the graft. One pair of proximal (middle learn more of the autografting) and distal (3 mm distal to autografting) sections was fixed in 2% glutaraldehyde and 1% paraformaldehyde in 0.0031 M phosphate buffer, pH 7.3. After 60 min. in solution A, the tissue was postfixed for 2 h in 2% osmium tetroxide in phosphate buffer, dehydrated in ethanol, infiltrated

in propilene oxide and included in Epoxi® resin (Burlington, VT) until polymerization. Transversal, 1-μm sections were made and stained with 1% toluidine blue. Histological observations were carried out using light microscopy (Nikon Eclipse E 600, Nikon, Japan). The slides were photographed with a digital camera (Nikon Coolpix E 955, Nikon, Japan), and cell measurement taken (Sigma Scan Pro 5.0 software, SPSS Science). Qualitative analyses were performed according to general nerve architecture, pattern of tissue organization and myelination. For quantitative analyses of distal portion of the facial nerve, axons were counted in Bumetanide a partial area of 9.000 μm2 in three random microscopic fields for every fiber displaying its center within it. Total axon density was obtained by the ratio between total axon number and area. The shortest external diameter (including the myelin sheath) of all axons within a partial, randomly selected area (3.000 μm2) of the transversal section of the nerve was measured to evaluate the maturation of myelinated fibers (Mayhew and Sharma, 1984). The second pair of proximal and distal sections was fixed in 4% paraformaldehyde in phosphate-buffered saline.

This indicates that the change in atmospheric horizontal resolution also plays an important role, as explained in Hourdin et al. (2012) and also underlined by Marti et al. (2010). Note also that these numbers highlight the fact that CM5_piStart

(and thus also probably CM5_RETRO) is not in full equilibrium, as the intensity of the flow through the Drake Passage in this simulation (109 Sv) slightly differs from what is found in CM5-piCtrl (98 Sv). Finally, intensification of the ACC in CM5_piStart is consistent with strengthening of the density gradient across the Southern Ocean, as described above (Fig. 10), but this does not allow distinguishing causality. On the other hand, it contrasts with the weaker eastward heat transport seen in Fig. 11, demonstrating the importance of meridional temperature gradients and meanders for this heat transport (Sun and Watts, 2002). Downstream of the Drake Passage, the circumpolar ABT-263 concentration transport of mass is fed BIBW2992 concentration in both simulations by a weak input from the South Atlantic and a stronger one from the Indian Ocean, consistent with inversions from Ganachaud and Wunsch (2000). In both simulations, it thus slightly increases from the Drake Passage to the Cape of Good Hope and Cape Leewin sections. In the Pacific, the net mass transport is northward at all latitudes. This is again consistent with Ganachaud and Wunsch (2000). Their inversion yields an Indonesian Throughflow of 16 Sv, and the latest long-term

simultaneous measurements within both inflow and outflow passages (INSTANT

2004–2006) estimated a total transport of 14 ± 3 Sv (Sprintall et al., 2009). The intensity of the Indonesian Throughflow in terms of net mass transport in CM5_piStart is lower than these estimates (12.7 Sv Fig. 13), slightly stronger than in CM5_RETRO (12.3 Sv), although the difference is probably not significant. This might be again a consequence from the implementation of the ITF parameterisation developed by Koch-Larrouy et al. (2009) in CM5_piStart. Fig. 14 (left panels) compares the global mean meridional circulation for the years [2200–2291] of each simulation. The major difference lies in intensification by roughly 12 Sv of the Antarctic Bottom Water circulation in the Southern Hemisphere in CM5_piStart as compared to CM5_RETRO. This increase is roughly portioned Autophagy activator among the oceanic basins according to their width, as this cell increases by 4 Sv at the southern bottom of the Indian Ocean, 5 Sv in the Pacific and only 3 Sv in the Atlantic (not shown). As seen above for the forced simulations, this intensification is consistent with the evolution of the oceanic component, and in particular the implementation of the kz-tide parameterization. It is associated with notable temperature and more importantly salinity modifications in the Southern Ocean and along the sea floor, as described above. The shallow subtropical cells are very similar in the two simulations, consistent with comparable mean wind stress field and wind stress curl (not shown).

4 Gy. As of 2002, all patients were treated with intensity-modulated radiotherapy (IMRT) technique where a five- to seven-field treatment plan was used. EBRT was delivered to the prostate gland and seminal vesicles. The lymph nodes were not incorporated beta-catenin inhibitor into the treatment fields. For patients who received neoadjuvant androgen deprivation therapy (ADT; n = 98; 42%), treatment was usually initiated 3 months before the three-dimensional conformal radiotherapy/IMRT and discontinued at the completion of radiotherapy.

The ADT was given to patients with large prostates to achieve pretreatment volume reduction or to high-risk patients, and adjuvant ADT even for high-risk patients was not routinely given. The median duration of ADT used in these patients was 9 months (range, 1–33 months). The median follow-up for the entire cohort of patients was 61.2 months (range, 3–150 find more months). Follow-up examinations consisted of an assessment of serum prostate-specific antigen (PSA), patient symptom assessment, and digital rectal examination. New or worsening acute and late GU and GI toxicities were scored according to the National Cancer Institute Common Terminology Criteria for Adverse Events toxicity scale, version 3. Acute toxicity was defined as symptoms experienced by patients during the course of therapy and up to 90 days from the completion of EBRT. The International Prostate

Symptom Score (IPSS) was used to assess urinary functioning (urinary frequency, hesitancy, urgency, intermittence, weak urinary stream, and nocturia) both before and after the treatment. The patient’s status was determined at the time of

analysis in October 2011. The Phoenix definition of biochemical Oxymatrine failure (absolute nadir plus 2 ng/mL with the corresponding date) was used for this analysis (16). Actuarial likelihood of complication probabilities and disease-specific survival were calculated according to the product-limit estimate (Kaplan–Meier) method. The threshold of statistical significance for differences was set at 0.05. The 7-year PSA relapse-free survival rates were 95% (95% confidence interval [CI], 86.5–100.0%), 90% (95% CI, 84.4–96.9%), and 57% (95% CI, 38.2–80.8%) for low-, intermediate-, and high-risk patients, respectively (Fig. 1). The median follow-up for each risk group was 69 months (range, 11–137 months), 64 months (range, 3–150 months), and 47 months (range, 5–140 months) for low-, intermediate-, and high-risk patients, respectively. In 206 patients who were free of biochemical relapse, 142 patients (69%) were noted to have PSA levels lower than 0.2 ng/mL at the time of last follow-up, and the PSA was undetectable (<0.05 ng/mL) at last follow-up in 85 (36%) of these patients. The 7-year DMs-free survival for low-, intermediate-, and high-risk patients were 95%, 98%, and 83%, respectively.

This article reviews current society guidelines, highlighting similarities and differences, in an attempt to form a general consensus on

surveillance for patients with IBD, while drawing attention to controversial areas in need of further research. Most societies agree that all patients with a history of UC (even isolated proctitis) and Crohn’s colitis should be offered a screening colonoscopy approximately 8 to 10 years after the onset of clinical symptoms to re-stage extent of disease and evaluate for endoscopic features that confer a higher risk for IBD-associated Venetoclax clinical trial CRN (IBD-CRN). The exception is the NICE guideline,6 which recommends only offering colonoscopic surveillance to patients with Crohn’s colitis involving more than 1 segment of the colon or left-sided or more extensive UC, but not isolated ulcerative proctitis. All societies recommend that patients with PSC and UC should be enrolled in a surveillance program at the time of diagnosis. During the initial screening examination, restaging biopsies are recommended to determine disease extent and severity. The HDAC inhibitor extent of disease is defined by the maximum documented extent of disease on any colonoscopy. All societies recommend surveillance colonoscopy for UC patients with

left-sided or extensive colitis (thus excluding patients with isolated proctitis),1, 2, 3, 4, 5, 6 and 8 and for Crohn’s C59 chemical structure colitis involving more than 1 segment of the colon6 and 18 or at least one-third of the colon.2, 3, 5 and 8 The BSG considers patients with Crohn’s disease of less than 50% of colonic involvement, regardless of grade of inflammation, as lower risk, but does offer surveillance at the longest (5-year) intervals.1 The ACG guidelines recognize the possible increased risk of cancer in long-standing Crohn’s disease, but state that surveillance guidelines have yet to be defined, and do not endorse a screening or surveillance

strategy.19 All patients with UC and Crohn’s colitis should be offered a screening colonoscopy to restage the extent of disease and evaluate for endoscopic features that confer a higher risk for IBD-CRN. Current guidelines base screening for IBD-CRN primarily on duration of disease. The risk of IBD-CRN increases over time, although estimates of risk vary in the literature. Meta-analysis of older studies estimated an increase in risk over time, with a cumulative CRC risk of 2% at 10 years, 8% at 20 years, and 18% after 30 years of colitis.20 More recent population-based studies have demonstrated a lower overall risk, from 2.5% at 20 years, to 7.6% at 30 years, and 10.8% at 40 years of extensive UC.

Few labeled fibers

were seen in the olfactory tubercle, ventral border of the nucleus of the horizontal limb of the diagonal band, fundus striati, caudal accumbens, lateral septal nucleus (Figs. 3A and B), infralimbic cortex and anterior olfactory nucleus. The accessory olfactory bulb is devoid of labeling. Fibers from the posterior BST proceed ventrocaudally in the direction to the hypothalamus to innervate very lightly, at the preoptic anterior hypothalamic level, the rostral part of the medial preoptic nucleus and medial preoptic area (Figs. 3B and C) and, more substantially, the retrochiasmatic area (Fig. 3D). Labeled fibers in the anterior hypothalamic nucleus Selleckchem CDK inhibitor have largely spaced varicosities and seemingly provide only a sparse input to this nucleus (Figs. 3C–E). A few fibers were found

in the periventricular zone including the paraventricular nucleus, which shows a modest number of terminals in the anterior parvo- and magnocellular parts (Figs. 3C and D). At the tuberal level, the MeAV provides a particularly dense input to the selleckchem dorsomedial and central parts of the ventromedial nucleus, but the anterior and ventrolateral parts are also labeled (Figs. 3E–G, 7A). Curiously, the caudal extent of the ventrolateral part, which in Nissl-stained sections shows more densely-packed and darkly-stained neurons than the rest of the ventrolateral part (Coolen et al., 1996), is almost completely avoided. Terminal labeling was also observed in the subfornical region of the lateral hypothalamus, but ventral to it, the tuberal nucleus many is sparsely labeled (Figs. 3F,G, 7A). In addition, a few varicose axons were found in the dorsomedial hypothalamic nucleus and intermediate periventricular nucleus (Figs. 3F–H). At the mammillary level, a rather modest terminal field was observed in the ventral premammillary

nucleus and a lighter one in the ventrolateral part of the dorsal premammillary nucleus (Figs. 3I, J, 7C). Some varicose fibers were also noted in the posterior periventricular nucleus, lateral hypothalamic area (Fig. 3I) and, still fewer, in the posterior hypothalamic nucleus and supramammillary region (Figs. 3I–K, 7C). Some labeled fibers enter the periventricular gray to innervate very lightly the dorsolateral periaqueductal gray (Fig. 3L) and dorsal raphe nucleus. Only occasional fibers were found in the nucleus reuniens, paraventricular nucleus and mediodorsal nucleus of the thalamus. A few labeled fibers cross the midline in the anterior, supraoptic and posterior commissures and in the supramammillary region. The ventromedial hypothalamic nucleus is the sole structure on the contralateral side of the brain which shows an appreciable number of terminals (Figs. 3F–G). The pattern of anterograde labeling observed after injections in the MeAD and MePV is similar to that described in male rats by Canteras et al. (1995).

In order to address these concerns, we propose the

use of peripheral monocytes as NGF delivery vehicles Dinaciclib solubility dmso to the AD brain. We and others have shown that Aβ deposits can stimulate monocyte recruitment and infiltration into the brain (Fiala et al., 1998, Giri et al., 2000 and Humpel, 2008). Furthermore, recent studies have shown that bone marrow-derived or blood-derived monocytic cells are recruited to the diseased AD brain and play an important role in the clearance of Aβ deposits and plaques (El Khoury et al., 2007, Gate et al., 2010 and Lebson et al., 2010). This selective transmigration to amyloid plaques confers a gross advantage for the use of these cells as therapeutic delivery vehicles to the AD brain (Malm et al., 2010 and Schwartz and Shechter, 2010). We hypothesize that following BBB insult (e.g. activation or breakdown) or stimuli

from disease-associated lesion sites (i.e. Aβ plaque), monocytes can transmigrate across the BBB and enter the diseased AD brain (Fig. 5). Monocytes are then attracted to the lesion site by a chemotactic gradient (e.g. monocyte chemotactic Pim inhibitor protein-1 (MCP-1/CCL2)) where they can secrete NGF to support the survival of degenerating cholinergic neurons as well as to reduce amyloid tetracosactide burden by differentiating into macrophages and phagocytosing Aβ (Fig. 5). Although a number of recent

studies have reported on the therapeutic potential of monocytes in AD (Lebson et al., 2010), the role of these cells in contributing to further inflammatory activity and disease aggrevation should still be considered. Their response to neurodegeneration can be beneficial, but ultimately become detrimental once dysregulated and persistent (Shechter and Schwartz, 2013). Other hurdles will include generating large populations of healthy functioning monocytes since these cells are short-lived, exhibit limited numbers in vivo, and are ineffective at Aβ phagocytosis in Alzheimer’s patients (Fiala et al., 2005). In the rat brain, physiological levels of NGF have been reported at 1.01 ng/g tissue and 0.2 ng/g tissue in the hippocampus and cortex, respectively (Whittemore et al., 1986). In mice, reducing NGF brain levels from 13–17 ng/mg in wildtype animals to 6 ng/mg in transgenic anti-NGF animals results in AD-like neurodegeneration (Capsoni et al., 2010). The mechanisms of NGF secretion has been studied extensively in hippocampal neurons and a previous investigation has also shown that monocytes can produce, store, and release NGF (Rost et al., 2005). However, the cellular pathway involved in its release has not been fully characterized.

The expression of COX-2 in NCI-H1299 was low compared to the control, and it is known that COX-2 is frequently up-regulated in tumors (Wolff et al., 1998), so that selective downregulation of COX-2 is an important strategy in the development buy LDK378 of anti-tumor agents. Russell et al. (2004) presented a solution to increase melittin efficiency against tumors. Tumor-specific antibodies can be used to target melittin to tumor cells. In the study, administration of an immunoconjugate

containing a melittin-like peptide (peptide 101), improved the survival of immune-deficient mice bearing subcutaneous human prostate carcinoma xenografts. The specific antibody-peptide 101 conjugate also significantly FAK inhibitor inhibited tumor growth compared to the controls: unconjugated antibody or peptide alone. These new strategies can be used to decrease the non-specificity of some toxins and also to increase the action potential, since the immunoconjugates showed a greater anti-cancer potential than the peptide alone. Hu et al. (2006) showed that BV displays a cytostatic effect in a dose- and time-dependent manner, inhibits proliferation and induces apoptosis of SMMC-7721 human hepatoma cells. The study demonstrated that treatment with BV reduced expression of Ki67, a protein that

is expressed in proliferating cells, and the proliferation rate of treated cells went from 97.0% to 10.2%. In vivo experiments with balb/c nude mice showed that treatment with 1.5 or 3 mg/kg of BV resulted in a significant retardation of SMMC-7721 cell growth, with a tumor inhibition of 31.4% and 48.2%, respectively. In the latest years, PLA2 isolated from BV has become of great interest due to its great anti-cancer potential. Putz et al. (2006) reported that the adjuvant treatment with bee venom-sPLA2 and phosphatidylinositol-(3,4)-bisphosphate (PtdIns(3,4)P2) was more effective 4-Aminobutyrate aminotransferase than any of the single components in the blocking of tumor cell growth. This adjuvant treatment had a synergistic effect together with potent cell lysis. The authors suggest that the observed cytotoxicity is due to the disruption of the membrane integrity, the abrogation of signal

transduction and the generation of cytotoxic lyso-PtdIns(3,4)P2. They further demonstrated a reduction in the proliferation of the human cell kidney carcinoma cell line (A498) employing the adjuvant treatment with sPLA2 and PtdIns(3,4)P2, associated with a complete downregulation of PKB/Akt phosphorylation. The PI3-kinase/PKB/Akt pathway represents a central survival-related signal transduction pathway and its activation enhances cell survival and promotes tumor invasion (Coffer et al., 1998). Furthermore, treated cells exhibited a decrease of the epidermal growth factor receptor (EGFr). The tumor lysates formed after treating the cells with bv-sPLA2 and PtdIns(3,4)P2 enhanced the maturation of immunostimulatory human monocyte-derived dendritic cells.

Zuanazzi et al. 7 reported that the most prevalent bacteria in the saliva of hospitalized individuals were Staphylococcus spp. (85.7%), Pseudomonas spp. (83.8%), and Acinetobacter

spp. (53.3%). The results of another study suggested a possible peroral route for staphylococci, as the provision of microorganisms from the nasal cavity was shown. 8 Staphylococcus species are amongst the most frequent causes of bacteremia in mechanically ventilated patients.9 Further work in this area NVP-BKM120 in vitro may lead to benefits such as improved decolonization regimens for eradication of MRSA and acknowledgement of the mouth as a source of bacteremia-causing staphylococci.10 Microorganisms of the Enterobacteriaceae and Pseudomonadaceae families have been thoroughly investigated by the medical field

and are known for their pathogenicity in humans; however, these bacteria have not been considered pathogenic in the oral cavity. Despite this, the presence of these bacteria in the oral cavity can serve as a reservoir, and can severely compromise the lives of immunocompromised individuals. 11, 12, 13 and 14 Some studies have reported an association between Enterobacteriaceae and oral ulcerations in HIV-positive patients, but this association may not Ferroptosis inhibitor necessarily be causal, as enterobacteria may be secondary invaders. 15 and 16 Local and systemic factors appear to be correlated with increased oral prevalence of Enterobacteriaceae and/or Pseudomonas. However, the percentage of oral isolates containing these species differs amongst reports from different groups and remains controversial. 3, 14, 17 and 18

Despite the importance of this subject, few studies of Enterobacteriaceae and/or Pseudomonas in the oral cavities of HIV-positive patients have been performed in Brazil. Most of the published studies have focused on Candida spp. Because oral reservoirs of potential pathogens such as enterobacteria and staphylococci may also cause local or systemic infections and compromise the lives of immunosuppressed individuals, the aim of this study was to evaluate the presence of Staphylococcus spp., Enterobacteriaceae and Pseudomonadaceae in the oral cavities Interleukin-3 receptor of HIV-positive patients. This study was approved by the Local Ethics Committee (protocol number 012-PH/CEP) and was undertaken with the informed written consent of each subject. Forty-five individuals (23 female and 22 male), aged 22–66 years, HIV-positive as diagnosed by ELISA and confirmed by Western blot, undergoing treatment at the Day Hospital of Taubaté Medical School or Medical Specialties Center (São Paulo State; ARE), and having undergone anti-retroviral therapy for at least 1 year were included in the study. Of the total, 43% of the patients were undergoing highly active antiretroviral therapy (HAART), and the remaining patients were treated only with a protease inhibitor.