Bacteremia after supragingival scaling and dental extraction: Culture and molecular analyses.

OBJECTIVE: To study the incidence and magnitude of bacteremia after dental extraction and supragingival scaling. SUBJECTS AND METHODS: Blood samples were taken before and 5 and 30 min after dental extraction and supragingival scaling from individuals at high (n = 44) or negligible risk (n = 51) for infective endocarditis. The former received prophylactic antibiotic therapy. Samples were subjected to aerobic and anaerobic culture and quantitative real-time polymerase chain reaction to determine the incidence of bacteremia and total bacterial levels. RESULTS: Patients who did not receive prophylactic antibiotic therapy had a higher incidence of positive blood cultures (30% 5 min after extraction) than patients who received prophylactic antibiotic therapy (0% 5 min after extraction; p < .01). Molecular analysis did not reveal significant differences in the incidence or magnitude of bacteremia between the two patient groups either 5 or 30 min after each of the procedures evaluated. Extraction was associated with higher incidence of bacteremia than supragingival scaling by blood culture (p = .03) and molecular analysis (p = .05). CONCLUSIONS: Molecular methods revealed that dental extraction and supragingival scaling were associated with similar incidence of bacteremia in groups receiving or not prophylactic antibiotic therapy. However, blood culture revealed that antibiotic therapy reduced viable cultivable bacteria in the bloodstream in the extraction group.

Two-dimensional speckle tracking echocardiography demonstrates no effect of active acromegaly on left ventricular strain.

BACKGROUND: Speckle tracking echocardiography (STE) allows for the study of myocardial strain (ε), a marker of early and subclinical ventricular systolic dysfunction. Cardiac disease may be present in patients with acromegaly; however, STE has never been used to evaluate these patients. OBJECTIVE: To evaluate left ventricular (LV) global longitudinal strain in patients with active acromegaly with normal LV systolic function. DESIGN: Cross-sectional clinical study. METHODS: Patients with active acromegaly with no detectable heart disease and a control group were matched for age, gender, arterial hypertension and diabetes mellitus underwent STE. Global LV longitudinal ε (GLS), left ventricular mass index (LVMi), left ventricular ejection fraction (LVEF) and relative wall thickness (RWT) were obtained via two-dimensional (2D) echocardiography using STE. RESULTS: Thirty-seven patients with active acromegaly (mean age 45.6 ± 13.8; 48.6% were males) and 48 controls were included. The mean GLS was not significantly different between the acromegaly group and the control group (in %, -20.1 ± 3.1 vs. -19.4 ± 2.2, p = 0.256). Mean LVMi was increased in the acromegaly group (in g/m2, 101.6 ± 27.1 vs. 73.2 ± 18.6, p < 0.01). There was a negative correlation between LVMi and GLS (r = -0.39, p = 0.01). CONCLUSIONS: Acromegaly patients, despite presenting with a higher LVMi when analyzed by 2D echocardiography, did not present with impairment in the strain when compared to a control group; this finding indicates a low chance of evolution to systolic dysfunction and agrees with recent studies that show a lower frequency of cardiac disease in these patients.

Nitrogen signalling in plant interactions with associative and endophytic diazotrophic bacteria.

Some beneficial plant-interacting bacteria can biologically fix N2 to plant-available ammonium. Biological nitrogen fixation (BNF) is an important source of nitrogen (N) input in agriculture and represents a promising substitute for chemical N fertilizers. Diazotrophic bacteria have the ability to develop different types of root associations with different plant species. Among the highest rates of BNF are those measured in legumes nodulated by endosymbionts, an already very well documented model of plant-diazotrophic bacterial association. However, it has also been shown that economically important crops, especially monocots, can obtain a substantial part of their N needs from BNF by interacting with associative and endophytic diazotrophic bacteria, that either live near the root surface or endophytically colonize intercellular spaces and vascular tissues of host plants. One of the best reported outcomes of this association is the promotion of plant growth by direct and indirect mechanisms. Besides fixing N, these bacteria can also produce plant growth hormones, and some species are reported to improve nutrient uptake and increase plant tolerance against biotic and abiotic stresses. Thus, this particular type of plant-bacteria association consists of a natural beneficial system to be explored; however, the regulatory mechanisms involved are still not clear. Plant N status might act as a key signal, regulating and integrating various metabolic processes that occur during association with diazotrophic bacteria. This review will focus on the recent progress in understanding plant association with associative and endophytic diazotrophic bacteria, particularly on the knowledge of the N networks involved in BNF and in the promotion of plant growth.

Central kappa opioid receptors modulate salt appetite in rats.

The role of the central opioid system in the control of water and salt intake is complex, with both stimulatory and inhibitory effects having been observed. The aim of the present study was to investigate the participation of the central κ-opioid receptors in the control of salt appetite. Male Wistar rats were submitted to two different experimental protocols: sodium deficit produced by the diuretic, furosemide, and brain angiotensinergic stimulation in rats under normal sodium balance. Lateral ventricle (LV) injections of Nor-binaltorphimine (Nor-BNI) at different doses (5, 10 and 20 nmol) inhibited hypertonic saline solution (1.5%) intake in sodium-depleted rats. The salt appetite induced by an LV injection of angiotensin II (Ang II) (10 ng) was also blocked by Nor-BNI injections into the LV, while no significant change was observed in water intake. Furthermore, the decrease in salt intake seems not to have been due to a general inhibition of locomotor activity or to any change in palatability, since central administration of Nor-BNI failed to modify the intake of a 0.1% saccharin solution when the animals were submitted to a "dessert test" or to induce any significant locomotor deficit in the open-field test. Also the central administration of Nor-BNI was unable to modify blood pressure in sodium-depleted animals. The present results suggest that activation of endogenous κ-opioid receptors modulates salt appetite induced by sodium depletion and by central angiotensinergic stimulation in rats.

Dealing with initial inconclusive serological results for chronic Chagas disease in clinical practice.

Most guidelines for Chagas disease recommend the performance of two serological tests in order to detect it. However, inconclusive results may arise from this strategy. The aim was to describe whether serological follow-up together with the patient's clinical characteristics could clarify the outcome of patients with initial inconclusive test results. In this retrospective case series, all results of Chagas disease serological tests and outpatient visits recorded from 2004 to 2008 were screened for inclusion. The inclusion criterion was clinical suspicion of chronic Chagas disease and the exclusion criteria were previous diagnosis of Chagas disease, suspicion of acute Chagas disease, and serological tests with no corresponding medical evaluation. A total of 1,732 patients were analyzed. Chronic Chagas disease prevalence was 21.1%. After the initial set of serological tests, 2.9% of patients had inconclusive test results. Most of these patients had definite diagnosis after clinical follow-up and the repetition of serological tests in a new blood sample. Loss to follow-up while partaking in the diagnostic investigation reached 17.7%. The prevalence of initial inconclusive serological tests for chronic Chagas disease is low. Clinical evaluations and follow-up clarify the definite diagnosis. Noncompliance to follow-up is a frequent problem. Strategies to reduce inconclusive results and noncompliance are discussed.

Rats with high left ventricular end-diastolic pressure can be identified by Doppler echocardiography one week after myocardial infarction

The severity of left ventricular (LV) dysfunction in rats with myocardial infarction (MI) varies widely. Because homogeneity in baseline parameters is essential for experimental investigations, a study was conducted to establish whether Doppler echocardiography (DE) could accurately identify animals with high LV end-diastolic pressure as a marker of LV dysfunction soon after MI. Direct measurements of LV end-diastolic pressure were made and DE was performed simultaneously 1 week after surgically induced MI (N = 16) or sham-operation (N = 17) in female Wistar rats (200 to 250 g). The ratio of peak early (E) to late (A) diastolic LV filling velocities and the ratio of E velocity to peak early (Em) diastolic myocardial velocity were the best predictors of high LV end-diastolic pressure (>12 mmHg) soon after MI. Cut-off values of 1.77 for the E/A ratio (P = 0.001) identified rats with elevated LV end-diastolic pressure with 90 percent sensitivity and 80 percent specificity. Cut-off values of 20.4 for the E/Em ratio (P = 0.0001) identified rats with elevated LV end-diastolic pressure with 81.8 percent sensitivity and 80 percent specificity. Moreover, E/A and E/Em ratios were the only echocardiographic parameters independently associated with LV end-diastolic pressure in multiple linear regression analysis. Therefore, DE identifies rats with high LV end-diastolic pressure soon after MI. These findings have implications for using serial DE in animal selection and in the assessment of their response to experimental therapies.

Rats with high left ventricular end-diastolic pressure can be identified by Doppler echocardiography one week after myocardial infarction.

The severity of left ventricular (LV) dysfunction in rats with myocardial infarction (MI) varies widely. Because homogeneity in baseline parameters is essential for experimental investigations, a study was conducted to establish whether Doppler echocardiography (DE) could accurately identify animals with high LV end-diastolic pressure as a marker of LV dysfunction soon after MI. Direct measurements of LV end-diastolic pressure were made and DE was performed simultaneously 1 week after surgically induced MI (N = 16) or sham-operation (N = 17) in female Wistar rats (200 to 250 g). The ratio of peak early (E) to late (A) diastolic LV filling velocities and the ratio of E velocity to peak early (Em) diastolic myocardial velocity were the best predictors of high LV end-diastolic pressure (>12 mmHg) soon after MI. Cut-off values of 1.77 for the E/A ratio (P = 0.001) identified rats with elevated LV end-diastolic pressure with 90% sensitivity and 80% specificity. Cut-off values of 20.4 for the E/Em ratio (P = 0.0001) identified rats with elevated LV end-diastolic pressure with 81.8% sensitivity and 80% specificity. Moreover, E/A and E/Em ratios were the only echocardiographic parameters independently associated with LV end-diastolic pressure in multiple linear regression analysis. Therefore, DE identifies rats with high LV end-diastolic pressure soon after MI. These findings have implications for using serial DE in animal selection and in the assessment of their response to experimental therapies.

Incidence of heart failure in infarcted rats that die spontaneously

The present study reports for the first time the incidence of congestive heart failure (CHF) in previously infarcted rats that died spontaneously. Previously, pulmonary (PWC) and hepatic (HWC) water contents were determined in normal rats: 14 control animals were evaluated immediately after sacrifice, 8 placed in a refrigerator for 24 h, and 10 left at room temperature for 24 h. In the infarcted group, 9 rats died before (acute) and 28 died 48 h after (chronic) myocardial infarction. Thirteen chronic animals were submitted only to autopsy (N = 13), whereas PWC and HWC were also determined in the others (N = 15). Seven rats survived 48 h and died during anesthesia. Notably, PWC differed in normal rats: ambient (75.7 ± 1.3 percent) < control (77.5 ± 0.7 percent) < refrigerator (79.1 ± 1.4 percent) and there were no differences with respect to HWC. No clinical signs of CHF (dyspnea, lethargy or foot edema) were observed in infarcted rats before death. PWC was elevated in all chronic and anesthetized rats. HWC was increased in 48 percent of chronic and in all anesthetized rats. Our data showed that PWC needs to be evaluated before 24 h post mortem and that CHF is the rule in chronic infarcted rats suffering natural death. The congestive syndrome cannot be diagnosed correctly in rats by clinical signs alone, as previously proposed.

Incidence of heart failure in infarcted rats that die spontaneously.

The present study reports for the first time the incidence of congestive heart failure (CHF) in previously infarcted rats that died spontaneously. Previously, pulmonary (PWC) and hepatic (HWC) water contents were determined in normal rats: 14 control animals were evaluated immediately after sacrifice, 8 placed in a refrigerator for 24 h, and 10 left at room temperature for 24 h. In the infarcted group, 9 rats died before (acute) and 28 died 48 h after (chronic) myocardial infarction. Thirteen chronic animals were submitted only to autopsy (N = 13), whereas PWC and HWC were also determined in the others (N = 15). Seven rats survived 48 h and died during anesthesia. Notably, PWC differed in normal rats: ambient (75.7 +/- 1.3%) < control (77.5 +/- 0.7%) < refrigerator (79.1 +/- 1.4%) and there were no differences with respect to HWC. No clinical signs of CHF (dyspnea, lethargy or foot edema) were observed in infarcted rats before death. PWC was elevated in all chronic and anesthetized rats. HWC was increased in 48% of chronic and in all anesthetized rats. Our data showed that PWC needs to be evaluated before 24 h post mortem and that CHF is the rule in chronic infarcted rats suffering natural death. The congestive syndrome cannot be diagnosed correctly in rats by clinical signs alone, as previously proposed.

A routine electrocardiogram cannot be used to determine the size of myocardial infarction in the rat.

Nine lead electrocardiograms of non-infarcted (N = 61) and infarcted (N = 71) female Wistar rats (200-250 g) were analyzed in order to distinguish left ventricle myocardial infarction (MI) larger than 40% (LMI) from MI smaller than 40% (SMI). MI larger than 40% clearly caused a deviation of AQRS and AT from normal values of 270-360 degrees to 90-270 degrees. Infarcted rats showed Q wave in D1 larger than 1 mm with 94% sensitivity and 100% specificity. The sum of QRS positivity in V1, V2 and V6 lower than 10 mm identified MI with 82% sensitivity and 100% specificity. The data showed that MI can be easily and reliably diagnosed by electrocardiogram in the rat. However, contradicting what is frequently believed, when specificity and sensitivity were analyzed focusing on MI size, none of these current electrocardiographic indices of MI size adequately discriminates LMI from SMI.

A routine electrocardiogram cannot be used to determine the size of myocardial infarction in the rat

Nine lead electrocardiograms of non-infarcted (N = 61) and infarcted (N = 71) female Wistar rats (200-250 g) were analyzed in order to distinguish left ventricle myocardial infarction (MI) larger than 40 percent (LMI) from MI smaller than 40 percent (SMI). MI larger than 40 percent clearly caused a deviation of AQRS and AT from normal values of 270-360 degrees to 90-270 degrees. Infarcted rats showed Q wave in D1 larger than 1 mm with 94 percent sensitivity and 100 percent specificity. The sum of QRS positivity in V1, V2 and V6 lower than 10 mm identified MI with 82 percent sensitivity and 100 percent specificity. The data showed that MI can be easily and reliably diagnosed by electrocardiogram in the rat. However, contradicting what is frequently believed, when specificity and sensitivity were analyzed focusing on MI size, none of these current electrocardiographic indices of MI size adequately discriminates LMI from SMI.

Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure

Infarct-induced heart failure is usually associated with cardiac hypertrophy and decreased beta-adrenergic responsiveness. However, conflicting results have been reported concerning the density of L-type calcium current (I Ca(L)), and the mechanisms underlying the decreased beta-adrenergic inotropic response. We determined I Ca(L) density, cytoplasmic calcium ([Ca2+]i) transients, and the effects of beta-adrenergic stimulation (isoproterenol) in a model of postinfarction heart failure in rats. Left ventricular myocytes were obtained by enzymatic digestion 8-10 weeks after infarction. Electrophysiological recordings were obtained using the patch-clamp technique. [Ca2+]i transients were investigated via fura-2 fluorescence. beta-Adrenergic receptor density was determined by [ H]-dihydroalprenolol binding to left ventricle homogenates. Postinfarction myocytes showed a significant 25 percent reduction in mean I Ca(L) density (5.7 + or - 0.28 vs 7.6 + or - 0.32 pA/pF) and a 19 percent reduction in mean peak [Ca2+]i transients (0.13 + or - 0.007 vs 0.16 + or - 0.009) compared to sham myocytes. The isoproterenol-stimulated increase in I Ca(L) was significantly smaller in postinfarction myocytes (Emax: 63.6 + or - 4.3 vs 123.3 + or - 0.9 percent in sham myocytes), but EC50 was not altered. The isoproterenol-stimulated peak amplitude of [Ca2+]i transients was also blunted in postinfarction myocytes. Adenylate cyclase activation through forskolin produced similar I Ca(L) increases in both groups. beta-Adrenergic receptor density was significantly reduced in homogenates from infarcted hearts (Bmax: 93.89 + or - 20.22 vs 271.5 + or - 31.43 fmol/mg protein in sham myocytes), while Kd values were similar. We conclude that postinfarction myocytes from large infarcts display reduced I Ca(L) density and peak [Ca2+]i transients. The response to Beta-adrenergic stimulation was also reduced and was probably related to Beta-adrenergic receptor down-regulation and not to changes in adenylate cyclase activity

Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure.

Infarct-induced heart failure is usually associated with cardiac hypertrophy and decreased -adrenergic responsiveness. However, conflicting results have been reported concerning the density of L-type calcium current (I Ca(L)), and the mechanisms underlying the decreased -adrenergic inotropic response. We determined I Ca(L) density, cytoplasmic calcium ([Ca2+]i) transients, and the effects of -adrenergic stimulation (isoproterenol) in a model of postinfarction heart failure in rats. Left ventricular myocytes were obtained by enzymatic digestion 8-10 weeks after infarction. Electrophysiological recordings were obtained using the patch-clamp technique. [Ca2+]i transients were investigated via fura-2 fluorescence. -Adrenergic receptor density was determined by [ H]-dihydroalprenolol binding to left ventricle homogenates. Postinfarction myocytes showed a significant 25% reduction in mean I Ca(L) density (5.7 0.28 vs 7.6 0.32 pA/pF) and a 19% reduction in mean peak [Ca2+]i transients (0.13 0.007 vs 0.16 0.009) compared to sham myocytes. The isoproterenol-stimulated increase in I Ca(L) was significantly smaller in postinfarction myocytes (Emax: 63.6 4.3 vs 123.3 0.9% in sham myocytes), but EC50 was not altered. The isoproterenol-stimulated peak amplitude of [Ca2+]i transients was also blunted in postinfarction myocytes. Adenylate cyclase activation through forskolin produced similar I Ca(L) increases in both groups. -Adrenergic receptor density was significantly reduced in homogenates from infarcted hearts (Bmax: 93.89 20.22 vs 271.5 31.43 fmol/mg protein in sham myocytes), while Kd values were similar. We conclude that postinfarction myocytes from large infarcts display reduced I Ca(L) density and peak [Ca2+]i transients. The response to -adrenergic stimulation was also reduced and was probably related to -adrenergic receptor down-regulation and not to changes in adenylate cyclase activity.

Outward potassium current oscillations in macrophage polykaryons: extracellular calcium entry and calcium-induced calcium release

Outward current oscillations associated with transient membrane hyperpolarizations were induced in murine macrophage polykaryons by membrane depolarization in the absence of external Na+. Oscillations corresponded to a cyclic activation of Ca2+ -dependent K+ currents (IKCa) probably correlated with variations in intracellular Ca2+ concentration. Addition of external Na+ (8mM) immediately abolished the outward current oscillations, suggesting that the absence of the cation is necessary not only for their induction but also for their maintenance. Oscillations were completely blocked by nisoldipine. Ruthenium red and ryanodine reduced the number of outward current cycles in each episode, whereas quercetin prolonged the hyperpolarization 2- to 15-fold. Neither low molecular weight heparin nor the absence of a Na+ gradient across the membrane had any influence on oscillations. The evidence suggests that Ca+ entry through a pathway sensitive to Ca2+ channel blockers is elicited by membrane depolarization in Na+ -free medium and is essential to initiate oscillations, which are also dependent on the cyclic release of Ca2+ from intracellular Ca2+ -sensitive stores; Ca2+ ATPase acts by reducing intracellular Ca2+, thus allowing slow deactivation of IKCa. Evidence is presented that neither a Na+/Ca2+ antiporter nor Ca2+ release from IP3 -sensitive Ca2+ stores participate directly in the mechanism of oscillation.

Outward potassium current oscillations in macrophage polykaryons: extracellular calcium entry and calcium-induced calcium release.

Outward current oscillations associated with transient membrane hyperpolarizations were induced in murine macrophage polykaryons by membrane depolarization in the absence of external Na+. Oscillations corresponded to a cyclic activation of Ca(2+)-dependent K+ currents (IKCa) probably correlated with variations in intracellular Ca2+ concentration. Addition of external Na+ (8 mM) immediately abolished the outward current oscillations, suggesting that the absence of the cation is necessary not only for their induction but also for their maintenance. Oscillations were completely blocked by nisoldipine. Ruthenium red and ryanodine reduced the number of outward current cycles in each episode, whereas quercetin prolonged the hyperpolarization 2- to 15-fold. Neither low molecular weight heparin nor the absence of a Na+ gradient across the membrane had any influence on oscillations. The evidence suggests that Ca2+ entry through a pathway sensitive to Ca2+ channel blockers is elicited by membrane depolarization in Na(+)-free medium and is essential to initiate oscillations, which are also dependent on the cyclic release of Ca2+ from intracellular Ca(2+)-sensitive stores; Ca2+ ATPase acts by reducing intracellular Ca2+, thus allowing slow deactivation of IKCa. Evidence is presented that neither a Na+/Ca2+ antiporter nor Ca2+ release from IP3-sensitive Ca2+ stores participate directly in the mechanism of oscillation.

Mal epilético como apresentaçäo de síndrome de Melas: relato de um caso / Status epilepticus as the presentation of Melas syndrome: a case report

É relatado e discutido o caso de uma paciente admitida no CTI devido a estado de mal epiléptico, atribuído a síndrome de Melas (miopatia mitocondrial, encefalopatia, acidose lática e episódios AVC-símile). A paciente era uma mulher jovem, com história pregressa de hopoacusia bilateral, crises episódicas de enxaqueca com vômitos, que apresentou-se em como, com sinais de irritaçäo meníngea e sem sinais de localizaçäo. Causas estruturais, infecciosas e auto-imunes foram afastadas através de exames laboratoriais e de imagem. Ao invés disso, demonstravam acidose lática grave, aumento de enzimas musculares, azotemia, hiperglicemia e leucocitose e presença de calcificaçöes dos gânglios da base e áreas isquêmicas na tomografia de crânio. Foi levantada a hipótese de Melas, a qual foi confirmada através de biópsia muscular que demonstrou fibras "ragged red" fortemente coradas pelo succinato desidrogenase (SDH). Os autores dirigem atençäo ao fato de uma síndrome rara também deve ser incluída no diagnóstico diferencial de um paciente jovem com convulsäo e acidose lática mesmo quando de uma apresentaçäo inicial.