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Coronary artery disease (CAD) is the leading cause of death and disability worldwide. Despite recent progress in the diagnosis and treatment of CAD, evidence gaps remain, including pathogenesis, the most efficient diagnostic strategy, prognosis of individual patients, monitoring of therapy, and novel therapeutic strategies. These gaps could all be filled by developing novel, minimally invasive, blood-based biomarkers. Potentially, extracellular vesicles (EVs) could fill such gaps. EVs are lipid membrane particles released from cells into blood and other body fluids. Because the concentration, composition, and functions of EVs change during disease, and because all cell types involved in the development and progression of CAD release EVs, currently available guidelines potentially enable reliable and reproducible measurements of EVs in clinical trials, offering a wide range of opportunities. In this chapter, we provide an overview of the associations reported between EVs and CAD, including (1) the role of EVs in CAD pathogenesis, (2) EVs as biomarkers to diagnose CAD, predict prognosis, and monitor therapy in individual patients, and (3) EVs as new therapeutic targets and/or drug delivery vehicles. In addition, we summarize the challenges encountered in EV isolation and detection, and the lack of standardization, which has hampered real clinical applications of EVs. Since most conclusions are based on animal models and single-center studies, the knowledge and insights into the roles and opportunities of EVs as biomarkers in CAD are still changing, and therefore, the content of this chapter should be seen as a snapshot in time rather than a final and complete compendium of knowledge on EVs in CAD., (© 2023. The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd.)

Copyright of SMAD Revista Electronica Salud Mental, Alcohol y Drogas is the property of Universidade de Sao Paulo, Escola de Enfermagem de Ribeirao Preto and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of SMAD Revista Electronica Salud Mental, Alcohol y Drogas is the property of Universidade de Sao Paulo, Escola de Enfermagem de Ribeirao Preto and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cerebral toxoplasmosis is the most common cause of expansive brain lesions in people living with HIV/AIDS (PLWHA) and continues to cause high morbidity and mortality. The most frequent characteristics are focal subacute neurological deficits and ring-enhancing brain lesions in the basal ganglia, but the spectrum of clinical and neuroradiological manifestations is broad. Early initiation of antitoxoplasma therapy is an important feature of the diagnostic approach of expansive brain lesions in PLWHA. Pyrimethamine-based regimens and trimethoprim-sulfamethoxazole (TMP-SMX) seem to present similar efficacy, but TMP-SMX shows potential practical advantages. The immune reconstitution inflammatory syndrome is uncommon in cerebral toxoplasmosis, and we now have more effective, safe, and friendly combined antiretroviral therapy (cART) options. As a consequence of these 2 variables, the initiation of cART can be performed within 2 weeks after initiation of antitoxoplasma therapy. Herein, we will review historical and current concepts of epidemiology, diagnosis, and treatment of HIV-related cerebral toxoplasmosis. [ABSTRACT FROM AUTHOR]

Purpose: While statins are used as first-line treatments for high-risk patients with hypercholesterolemia, statin monotherapy is often insufficient to achieve target low-density lipoprotein cholesterol (LDL-C) levels. Second-line treatment options include up-titration of statin dose, switching to a more potent statin, or combination therapy, e.g., with ezetimibe. The aim of this study was to evaluate the efficacy of adding ezetimibe to simvastatin, atorvastatin, or rosuvastatin monotherapy versus doubling the dosage or switching to a higher-potency statin in a population of patients with hypocholesterolemia at high risk of cardiovascular disease (CVD) and who had been previously treated with a statin. Methods: A systematic literature search was performed and evidence bases were established for populations of atorvastatin-, simvastatin-, and rosuvastatin-experienced patients using eligible randomized controlled trials (RCTs). Based on the available data, we constructed networks of evidence and conducted a Bayesian network meta-analysis (NMA) within each statin population. The primary outcome of interest was percent change from baseline in LDL-C. Changes in total cholesterol were explored as a secondary outcome. Findings: Across all patient populations, 35 RCTs were identified and included in the evidence base. Among patients on simvastatin therapy, the addition of ezetimibe resulted in a mean difference (MD) in LDL-C of − 13.62% (95% CrI − 19.99, − 6.91; see table below) compared to doubling the starting dose of simvastatin. In the population of patients on atorvastatin therapy, the addition of ezetimibe resulted in an MD in LDL-C of − 14.71% (95% CrI − 16.46, − 12.95) compared to doubling the starting dose of atorvastatin. The addition of ezetimibe to rosuvastatin resulted in an MD in LDL-C of − 14.96% (95% CrI − 17.79, − 12.11), compared to doubling the starting rosuvastatin dose. Similar trends were observed for changes in total cholesterol. Implications: Given the available data, the addition of ezetimibe to ongoing simvastatin, atorvastatin, or rosuvastatin monotherapy offers greater reduction in LDL-C among patients at high risk of CVD compared to doubling the initial statin dose. [ABSTRACT FROM AUTHOR]

Copyright of Itinerários - Revista de Literatura is the property of Itinerarios - Revista de Literatura and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Penicillium and Talaromyces species have a worldwide distribution and are isolated from various materials and hosts, including insects and their substrates. The aim of this study was to characterize the Penicillium and Talaromyces species obtained during a survey of honey, pollen and the inside of nests of Melipona scutellaris. A total of 100 isolates were obtained during the survey and 82% of those strains belonged to Penicillium and 18% to Talaromyces. Identification of these isolates was performed based on phenotypic characters and β-tubulin and ITS sequencing. Twenty-one species were identified in Penicillium and six in Talaromyces, including seven new species. These new species were studied in detail using a polyphasic approach combining phenotypic, molecular and extrolite data. The four new Penicillium species belong to sections Sclerotiora (Penicillium fernandesiae sp. nov., Penicillium mellis sp. nov., Penicillium meliponae sp. nov.) and Gracilenta (Penicillium apimei sp. nov.) and the three new Talaromyces species to sections Helici (Talaromyces pigmentosus sp. nov.), Talaromyces (Talaromyces mycothecae sp. nov.) and Trachyspermi (Talaromyces brasiliensis sp. nov.). The invalidly described species Penicillium echinulonalgiovense sp. nov. was also isolated during the survey and this species is validated here. [ABSTRACT FROM AUTHOR]

The evolutionary processes underlying the high diversity and endemism in the Cerrado, the most extensive Neotropical savanna, remain unclear, including the factors promoting the presence and evolution of savanna enclaves in the Amazon forest. In this study, we investigated the effects of past climate changes on genetic diversity, dynamics of species range and the historical connections between the savanna enclaves and Cerrado core for Qualea grandiflora, a tree species widely distributed in the biome. Totally, 40 populations distributed in the Cerrado core and Amazon savannas were analyzed using chloroplast and nuclear DNA sequences. We used phylogeographic, coalescent and ecological niche modeling approaches. Genetic data revealed a phylogeographic structure shaped by Pleistocene climatic oscillations. An eastern-western split in the Cerrado core was observed. The central portion of the Cerrado core harbored most of the sampled diversity for cpDNA. Ecological niche models predicted the presence of a large historical refuge in this region and multiple small refuges in peripheral areas. Relaxed Random Walk (RRW) models indicated the ancestral population in the north-western border of the central portion of the Cerrado core and cyclical dynamics of colonization related to Pleistocene climatic oscillations. Central and western ancient connections between Cerrado core and Amazonian savannas were observed. No evidence of connections among the Amazonian savannas was detected. Our study highlights the importance of Pleistocene climatic oscillations for structuring the genetic diversity of Q. grandiflora and complex evolutionary history of ecotonal areas in the Cerrado. Our results do not support the recent replacement of a large area in the Amazon forest by savanna vegetation. The Amazonian savannas appear to be fragmented and isolated from each other, evolving independently a long ago. [ABSTRACT FROM AUTHOR]

Numerous studies demonstrate the significant role of central β‐endorphin and its receptor, the μ‐opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high‐NaCl intake and brain endogenous MOR functioning. We examined whether short‐term (4 days) obligatory salt intake (2% NaCl solution) in rats induces changes in MOR mRNA expression, G‐protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G‐protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G‐protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G‐protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload‐induced anorexia. [ABSTRACT FROM AUTHOR]

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Copyright of Acta Paulista de Enfermagem is the property of Universidade Federal de Sao Paulo, Escola Paulista de Enfermagem and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Due to the biological importance of sodium and its relative scarcity within many natural environments, 'salt appetite' has evolved whereby dietary salt is highly sought after and palatable when tasted. In addition to peripheral responses, salt depletion is detected within the brain via circumventricular organs and 11β-hydroxysteroid dehydrogenase type 2 (HSD2) neurons to increase salt appetite. Salt appetite is comprised of two main components. One component is the incentive salience or motivation for salt (i.e. how much salt is 'wanted'). Incentive salience is dynamic and largely depends on internal homeostatic conditions in combination with the detection of relevant cues. It involves the mesolimbic system and structures such as the central amygdala, and opioid signalling within these regions can increase salt intake in rodents. A second key feature is the hedonic palatability of salt (i.e. how much it is 'liked') when it is tasted. After detection on the tongue, gustatory information passes through the brainstem nucleus of the solitary tract and thalamus, before being consciously detected within the gustatory cerebral cortex. The positive or negative hedonic value of this stimulus is also dynamic, and is encoded by a network including the nucleus accumbens, ventral pallidum, and lateral parabrachial nucleus. Opioid signalling within these areas can alter salt intake, and 'liking'. The overconsumption of dietary salt likely contributes to hypertension and associated diseases, and hence further characterising the role played by opioid signalling has important implications for human health. [ABSTRACT FROM AUTHOR]

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Copyright of Texto & Contexto Enfermagem is the property of Universidade Federal de Santa Catarina, Programa de Pos-Graduacao de Enfermagem and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Early reperfusion of the occluded coronary artery during acute myocardial infarction is considered crucial for reduction of infarcted mass and recovery of ventricular function. Effective microcirculation and the balance between protective and harmful lymphocytes may have roles in reperfusion injury and may affect final ventricular remodeling.Methods/design: BATTLE-AMI is an open-label, randomized trial comparing the effects of four therapeutic strategies (rosuvastatin/ticagrelor, rosuvastatin/clopidogrel, simvastatin plus ezetimibe/ticagrelor, or simvastatin plus ezetimibe/clopidogrel) on infarcted mass and left ventricular ejection fraction (LVEF) (blinded endpoints) in patients with ST-segment elevation myocardial infarction submitted to fibrinolytic therapy before coronary angiogram (pharmacoinvasive strategy). All patients (n = 300, 75 per arm) will be followed up for six months. The effects of treatment on subsets of B and T lymphocytes will be determined by flow-cytometry/ELISPOT and will be correlated with the infarcted mass, LVEF, and microcirculation perfusion obtained by cardiac magnetic resonance imaging. The primary hypothesis is that the combined rosuvastatin/ticagrelor therapy will be superior to other therapies (particularly for the comparison with simvastatin plus ezetimibe/clopidogrel) for the achievement of better LVEF at 30 days (primary endpoint) and smaller infarcted mass (secondary endpoint) at 30 days and six months. The trial will also evaluate the improvement in the immune/inflammatory responses mediated by B and T lymphocytes. Omics field (metabolomics and proteomics) will help to understand these responses by molecular events.Discussion: BATTLE-AMI is aimed to (1) evaluate the role of subsets of lymphocytes on microcirculation improvement and (2) show how the choice of statin/antiplatelet therapy may affect cardiac remodeling after acute myocardial infarction with ST elevation.Trial Registration: ClinicalTrials.gov, NCT02428374 . Registered on 28 September 2014. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Nursing UFPE / Revista de Enfermagem UFPE is the property of Revista de Enfermagem UFPE and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background Extracellular vesicles ( EVs) are submicron cellular fragments that mediate intercellular communication. EVs have in the last decade attracted major interest as biomarkers or platforms for biomarkers of health and disease. To better understand the reasons why despite great expectations and considerable effort, EV-based methods have not yet been introduced into clinical practice, we present a systematic analysis of published results of clinical studies. Materials and methods Clinical studies on populations of body fluid samples, published from 2010 to including 2015, applying centrifugation of fluid human samples with centrifuge accelerations up to about 25 000 g and flow cytometry for detection of EVs were analysed with respect to statistical significance ( p), statistical power ( P), clinical significance ( CS), defined as the difference between the means divided by the sum of standard deviations, and size of the populations ( Nmin), defined as the number of samples in the smaller group. Results Final analysis included 65 publications with 716 comparisons reporting 308 (43%) statistically significant differences ( P < 0·05), 242 (34%) had statistical power P > 0·8 and 88 (12%) had clinical importance CS > 1·96. None of comparison with CS > 1·96 included populations in which the smaller group consisted of 50 or more samples. Conclusions To fulfil claimed expectations for EV-based methods as promising diagnostic tools, more evidence on EV-based mechanisms of diseases should be gathered. Also, the methods of EV harvesting and assessment should be improved to yield better repeatability and thus allow clinical studies with larger number of samples. [ABSTRACT FROM AUTHOR]

Degenerative aortic stenosis (AS) is the most frequent form of acquired valvular heart disease. AS is known to entail endothelial dysfunction caused by increased mechanical shear stress leading to elevated circulatory levels of microparticles. Endothelial and platelet microparticles (EMP and PMP) are small vesicles that originate from activated cells and thrombocytes. We sought to evaluate whether transcatheter aortic valve implantation (TAVI) procedure would elicit effects on circulating EMP and PMP. 92 patients undergoing TAVI procedure for severe AS were included in this study. Samples were obtained at each visit before TAVI, 1 week post-procedure and at 1, 3 and after 6 months after TAVI and were evaluated using flow cytometry. A 12 month clinical follow-up was also performed. CD62E+ EMP concentration before TAVI was 21.11 % (±6.6 % SD) and declined to 20.99 % (±6.8 % SD) after 1 week, to 16.63 % (±5.4 % SD, p < 0.0001) after 1 month, to 17.08 % (±4.6 % SD, p < 0.0001) after 3 months and to 15.94 % (±5.4 % SD, p < 0.0001) after 6 months. CD31+/CD42b−, CD31+/Annexin+/− EMP remained unchanged. CD31+/CD41b+ PMP evidenced a slight, but statistically significant increase after TAVI and remained elevated during the entire follow-up. Apart from a procedure-related improvement in echocardiographic parameters, TAVI procedure led also to a decline in CD62E+ EMP. The reduction in pressure gradients with less hemodynamic shear stress seems also to have beneficially affected endothelial homeostasis. [ABSTRACT FROM AUTHOR]

Objectives The objective of this study was to perform a systematic review and meta-analysis of the literature to evaluate the efficacy and safety of therapies for cerebral toxoplasmosis in HIV-infected adults. The pyrimethamine plus sulfadiazine (P-S) combination is considered the mainstay therapy for cerebral toxoplasmosis and pyrimethamine plus clindamycin (P-C) is the most common alternative treatment. Although trimethoprim-sulfamethoxazole ( TMP- SMX) has potential advantages, its use is infrequent. Methods We searched PubMed and four other databases to identify randomized controlled trials ( RCTs) and cohort studies. Two independent reviewers searched the databases, identified studies and extracted data. Risk ratios ( RRs) were pooled across studies using random-effects models. Results Nine studies were included (five RCTs, three retrospective cohort studies and one prospective cohort study). In comparison to P-S, treatment with P-C or TMP- SMX was associated with similar rates of partial or complete clinical response [P-C: RR 0.87; 95% confidence interval ( CI) 0.70-1.08; TMP- SMX: RR 0.97; 95% CI 0.78-1.21], radiological response (P-C: RR 0.92; 95% CI 0.82-1.03), skin rash (P-C: RR 0.81; 95% CI 0.56-1.17; TMP- SMX: RR 0.17; 95% CI 0.02-1.29), gastrointestinal impairment (P-C: RR 5.16; 95% CI 0.66-40.11), and drug discontinuation because of adverse events (P-C: RR 0.32; 95% CI 0.07-1.47). Liver impairment was more frequent with P-S than P-C (P-C vs. P-S: RR 0.48; 95% CI 0.24-0.97). Conclusions The current evidence fails to identify a superior regimen in terms of relative efficacy or safety for the treatment of HIV-associated cerebral toxoplasmosis. Use of TMP- SMX as preferred treatment may be consistent with the available evidence and other real-world considerations. Larger comparative studies are needed. [ABSTRACT FROM AUTHOR]

Copyright of Salud Pública de México is the property of Instituto Nacional de Salud Publica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Toxoplasma gondii is an obligate intracellular parasite belonging to the phylum Apicomplexa. It has a worldwide distribution and can infect a wide variety of intermediate hosts, including humans. In South America, toxoplasmosis shows high health impacts, and the incidence of the disease is frequently reported and more severe than in other regions, such as Europe. Although most T. gondii infections are asymptomatic, severe manifestations can occur in cases of congenital toxoplasmosis and immunocompromised individuals. In South America, the ocular disease in immunocompetent individuals is also frequently reported. Treatment for any clinical manifestation of toxoplasmosis consists of the combination of sulfadiazine (SDZ) and pyrimethamine (PYR). However, failures in the treatment of toxoplasmosis have been reported, especially in South America, suggesting the acquisition of resistance against SDZ and PYR. Another paradigm present in the literature is that once infected with T. gondii, the host is immunologically protected from further reinfections. However, some studies indicate cases of congenital transmission of T. gondii from immunocompetent pregnant women with chronic infection, suggesting the possibility of reinfection in humans. Thus, in this review, we will cover several aspects of South American T. gondii isolates, such as genetic characterization, disease manifestation, host reinfection and drug resistance., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background Increased levels of endothelial cell microparticles ( EMP) are known to reflect endothelial dysfunction ( ED). In diabetes mellitus type 2 (T2DM), the expression of endothelin ( ET)-1 is increased. As treatment with an ET-1 antagonist significantly inhibited atherosclerosis in animal models, we sought to investigate whether treatment with ET-1 antagonists affects EMP levels in vitro and in vivo in patients with T2DM. Materials and methods In vitro study: Human umbilical vein endothelial cells ( HUVEC) were stimulated with ET-1 alone and ET-1 in combination with a dual ET-A and ET-B endothelin receptor blocker. In vivo study: Patients with T2DM were randomized to treatment with the ET receptor antagonist bosentan or placebo. After 4 weeks, the patients were re-examined and blood samples were obtained. EMP counts in supernatants and plasma samples were determined using flow cytometry. Results In vitro study: In supernatants of ET-1-stimulated HUVECs, the increased release of EMP was reduced significantly by co-incubation with an ET-1 receptor antagonist (e.g. CD31+/CD42b- EMP decreased from 37·1% ± 2·8 to 31·5% ± 2·8 SEM, P = 0·0078). In vivo study: No changes in EMP levels in blood samples of patients with T2DM were found after 4 weeks of bosentan treatment ( n = 36, P = ns). Conclusions Our in vitro results suggest that ET-1 stimulates the release of EMP from HUVECs via a receptor-dependent mechanism. Co-incubation with an endothelin receptor blocker abolished ET-1-dependent EMP release. However, treatment with bosentan for 4 weeks failed to alter EMP levels in patients with T2DM. Other factors seem to have influenced EMP release in patients with T2DM independent of ET-1 receptor-mediated mechanisms. [ABSTRACT FROM AUTHOR]

Copyright of Colombia Medica is the property of Universidad del Valle and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Despite the huge body of research on social support, literature has been primarily focused on its beneficial role for both physical and mental health. It is still unclear why people with mental and neurological disorders experience low levels of social support. The main objective of this study was to explore what are the strongest factors related to social support and how do they interact with each other in neuropsychiatric disorders. The study used cross-sectional data from 722 persons suffering from dementia, depression, epilepsy, migraine, multiple sclerosis, Parkinson's disease, schizophrenia, stroke, and substance use disorders. Multiple linear regressions showed that disability was the strongest factor for social support. Extraversion and agreeableness were significant personality variables, but when the interaction terms between personality traits and disability were included, disability remained the only significant variable. Moreover, level of disability mediated the relationship between personality (extraversion and agreeableness) and level of social support. Moderation analysis revealed that people that had mental disorders experienced lower levels of support when being highly disabled compared to people with neurological disorders. Unlike previous literature, focused on increasing social support as the origin of improving disability, this study suggested that interventions improving day-to-day functioning or maladaptive personality styles might also have an effect on the way people perceive social support. Future longitudinal research, however, is warranted to explore causality. [ABSTRACT FROM AUTHOR]

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The Kölliker-Fuse region (KF) and the lateral parabrachial nucleus (LPBN) have been implicated in the maintenance of cardiorespiratory control. Here, we evaluated the involvement of the KF region and the LPBN in cardiorespiratory responses elicited by chemoreceptor activation in unanesthetized rats. Male Wistar rats (280-330 g; n = 5-9/group) with bilateral stainless-steel guide cannulas implanted in the KF region or the LPBN were used. Injection of muscimol (100 and 200 pmol/100 nl) in the KF region decreased resting ventilation (1,140 ± 68 and 978 ± 100 vs. saline: 1,436 ± 155 ml·kg-1·min-1), without changing mean arterial pressure (MAP) and heart rate (HR). Bilateral injection of the GABA-A antagonist bicuculline (1 nmol/100 nl) in the KF blocked the inhibitory effect on ventilation (1,418 ± 138 vs. muscimol: 978 ± 100 ml·kg1·min1) elicited by muscimol. Muscimol injection in the KF reduced the increase in ventilation produced by hypoxia (8% O2) (1,827 ± 61 vs. saline: 3,179 ± 325 ml·kg-1·min-1) or hypercapnia (7% CO2) (1,488 ± 277 vs. saline: 3,539 ± 374 ml·kg-1·min-1) in unanesthetized rats. Bilateral injection of bicuculline in the KF blocked the decrease in ventilation produced by muscimol in the KF during peripheral or central chemoreflex activation. Bilateral injection of muscimol in the LPBN did not change resting ventilation or the increase in ventilation elicited by hypoxia or hypercapnia. The results of the present study suggest that the KF region, but not the LPBN, has mechanisms to control ventilation in resting, hypoxic, or hypercapnic conditions in unanesthetized rats. [ABSTRACT FROM AUTHOR]

In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review. [ABSTRACT FROM AUTHOR]

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Copyright of Acta Paulista de Enfermagem is the property of Universidade Federal de Sao Paulo, Escola Paulista de Enfermagem and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In order to determine whether serotonergic (5HT) dorsal raphe nucleus (DRN) cells are involved in body sodium status regulation, the effect of a s.c. infusion of either 2 M or 0.15 M NaCl on 5HT DRN neuron firing was studied using single unit extracellular recordings. In separate groups of 2 M and 0.15 M NaCl-infused rats, water intake, oxytocin (OT) plasma concentration, urine and plasma sodium and protein concentrations were also measured. Also, to determine the involvement of particular brain nuclei and neurochemical systems in body sodium overload (SO), animals from both groups were perfused for brain immunohistochemical detection of Fos, Fos-OT and Fos-5HT expression. SO produced a significant increase in serotonergic DRN neuron firing rate compared to baseline and 0.15 M NaCl-infused rats. As expected, 2 M NaCl s.c. infusion also induced a significant increase of water intake, diuresis and natriuresis, plasma sodium concentration and osmolality, even though plasma volume did not increase as indicated by changes in plasma protein concentration. The distribution of neurons along the forebrain and brainstem expressing Fos after SO showed the participation of the lamina terminalis, extended amygdala, supraoptic and paraventricular hypothalamic nuclei in the neural network that controls osmoregulatory responses. Both Fos-OT immunoreactive and plasma OT concentration increased after s.c. hypertonic sodium infusion. Finally, matching the “in vivo” electrophysiological study, SO doubled the number of Fos-5HT immunolabeled cells within the DRN. In summary, the results characterize the behavioral, renal and endocrine responses after body sodium overload without volume expansion and specify the cerebral nuclei that participate at different CNS levels in the control of these responses. The electrophysiological approach also allows us to determine in an “in vivo" model that DRN 5HT neurons increase their firing frequency during an increase in systemic sodium concentration and osmolality, possibly to modulate sodium and water intake/excretion and avoid extracellular volume expansion. [ABSTRACT FROM AUTHOR]

Background: Activation of GABAB receptors with baclofen into the lateral parabrachial nucleus (LPBN) induces ingestion of water and 0.3 M NaCl in fluid replete rats. However, up to now, no study has investigated the effects of baclofen injected alone or combined with GABAB receptor antagonist into the LPBN on water and 0.3 M NaCl intake in rats with increased plasma osmolarity (rats treated with an intragastric load of 2 M NaCl). Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. Results: In fluid replete rats, baclofen (0.5 nmol/0.2 μl), bilaterally injected into the LPBN, induced ingestion of 0.3 M NaCl (14.3 ± 4.1 vs. saline: 0.2 ± 0.2 ml/210 min) and water (7.1 ± 2.9 vs. saline: 0.6 ± 0.5 ml/210 min). In cell-dehydrated rats, bilateral injections of baclofen (0.5 and 1.0 nmol/0.2 μl) into the LPBN induced an increase of 0.3 M NaCl intake (15.6 ± 5.7 and 21.5 ± 3.5 ml/210 min, respectively, vs. saline: 1.7 ± 0.8 ml/210 min) and an early inhibition of water intake (3.5 ± 1.4 and 6.7 ± 2.1 ml/150 min, respectively, vs. saline: 9.2 ± 1.4 ml/150 min). The pretreatment of the LPBN with 2-hydroxysaclofen (GABAB antagonist, 5 nmol/0.2 μl) potentiated the effect of baclofen on 0.3 M NaCl intake in the first 90 min of test and did not modify the inhibition of water intake induced by baclofen in cell-dehydrated rats. Baclofen injected into the LPBN did not affect blood pressure and heart rate. Conclusions: Thus, injection of baclofen into the LPBN in cell-dehydrated rats induced ingestion of 0.3 M NaCl and inhibition of water intake, suggesting that even in a hyperosmotic situation, the blockade of LPBN inhibitory mechanisms with baclofen is enough to drive rats to drink hypertonic NaCl, an effect independent of changes in blood pressure. [ABSTRACT FROM AUTHOR]

Copyright of SMAD Revista Electronica Salud Mental, Alcohol y Drogas is the property of Universidade de Sao Paulo, Escola de Enfermagem de Ribeirao Preto and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

During independent surveys for freshwater ascomycetes in Brazil and Costa Rica, two new species, Torrentispora pilosa and Vertexicola ascoliberatus, and nine previously described species were recovered. Among the described species, Annulatascus biatriisporus, Anthostomella aquatica, Tamsiniella labiosa and Torrentispora crassiparietis are reported for the first time from the western hemisphere, Aniptodera chesapeakensis, Chaetosphaeria lignomollis and Jahnula seychellensis are new records for South America and Annulatascus velatisporus and Ophioceras venezuelensis are reported for the first time for Brazil. The description of the genus Torrentispora is emended to accommodate T. pilosa. The new species are described and illustrated and a brief description is provided for all new records. [ABSTRACT FROM AUTHOR]

Copyright of Experimental Physiology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: HIV-associated subacute meningitis is mostly caused by tuberculosis or cryptococcosis, but often no etiology can be established. In the absence of CT or MRI of the brain, toxoplasmosis is generally not considered as part of the differential diagnosis. Methodology/Principal Findings: We performed cerebrospinal fluid real time PCR and serological testing for Toxoplasma gondii in archived samples from a well-characterized cohort of 64 HIV-infected patients presenting with subacute meningitis in a referral hospital in Indonesia. Neuroradiology was only available for 6 patients. At time of presentation, patients mostly had newly diagnosed and advanced HIV infection (median CD4 count 22 cells/mL), with only 17.2% taking ART, and 9.4% PJP-prophylaxis. CSF PCR for T. Gondii was positive in 21 patients (32.8%). Circulating toxoplasma IgG was present in 77.2% of patients tested, including all in whom the PCR of CSF was positive for T. Gondii. Clinically, in the absence of neuroradiology, toxoplasmosis was difficult to distinguish from tuberculosis or cryptococcal meningitis, although CSF abnormalities were less pronounced. Mortality among patients with a positive CSF T. Gondii PCR was 81%, 2.16-fold higher (95% CI 1.04–4.47) compared to those with a negative PCR. Conclusions/Significance: Toxoplasmosis should be considered in HIV-infected patients with clinically suspected subacute meningitis in settings where neuroradiology is not available. Author Summary: If HIV-infected patients present with seizures, focal neurological symptoms or confusion, a CT-scan or MRI of the brain is normally made. If mass lesions are found (and the CD4 cell count is sufficiently low), cerebral toxoplasmosis is suspected, and often treated empirically. However, some of the symptoms of cerebral toxoplasmosis may mimic those of subacute meningitis. Therefore, in settings where no cerebral imaging can be performed, HIV-associated cerebral toxoplasmosis may be under-diagnosed. We retrospectively looked for toxoplasmosis in a cohort of HIV-infected patients presenting with subacute meningitis in an Indonesian hospital, where neuroradiology was not available for most patients. Patients mostly came with newly diagnosed and advanced HIV infection and few were on HIV-treatment or PJP-prophylaxis. Molecular testing of cerebrospinal fluid (CSF) was positive for Toxoplasma gondii in 32% of patients, serology was positive in 78%. Clinically, in the absence of neuroradiology, toxoplasmosis was difficult to distinguish from tuberculosis or cryptococcal meningitis. A positive CSF T. gondii PCR was associated with a two-fold increased mortality. We conclude that toxoplasmosis should be considered in HIV-infected patients with clinically suspected subacute meningitis in settings where neuroradiology is not available. [ABSTRACT FROM AUTHOR]

Toxoplasmosis caused by Toxoplasma gondii is an opportunistic infection. In healthy individuals, the infection is largely asymptomatic, but in immunocompromised people the parasite can become widely disseminated, causing severe toxoplasmosis. In patients undergoing haemodialysis, the phagocytic process shows a highly significant impairment. Therefore, this study aimed to investigate toxoplasmosis in patients with end-stage renal disease (ESRD) undergoing haemodialysis in Ahvaz hospitals, southwest of Iran. A total of 280 patients and 100 healthy subjects participated in this study. The presence of serum IgM and IgG antibodies against T. gondii was detected by ELISA and the presence of Toxoplasma parasites in whole blood was evaluated by GRA6 PCR. Anti- T. gondii IgG antibodies were detected in 82 (29.3 %) haemodialysis patients and 26 (26 %) controls. In addition, anti- T. gondii IgM antibodies were detected in 7.9 % of patients and in 4 % of controls. For both the antibodies, the differences were statistically significant ( P < 0.05). PCR was performed with DNA extracted from blood samples of all patients and controls. PCR gave positive results with four of the 280 blood samples from patients but none for the control blood samples. The results revealed a high percentage of positivity for Toxoplasma antibodies in patients with ESRD undergoing haemodialysis and also confirmed the parasite in whole blood, indicating disseminated infection in these patients. Patients undergoing dialysis have a higher rate of active infection with Toxoplasma likely due to reactivation of a chronic infection. Thus, parasitological examinations of ESRD patients should be periodically carried out for monitoring and evaluating the possible dissemination of toxoplasmosis during haemodialysis. [ABSTRACT FROM AUTHOR]