Phylogeny and identification of Nocardia species on the basis of multilocus sequence analysis.

Nocardia species identification is difficult due to a complex and rapidly changing taxonomy, the failure of 16S rRNA and cellular fatty acid analysis to discriminate many species, and the unreliability of biochemical testing. Here, Nocardia species identification was achieved through multilocus sequence analysis (MLSA) of gyrase B of the ß subunit of DNA topoisomerase (gyrB), 16S rRNA (16S), subunit A of SecA preprotein translocase (secA1), the 65-kDa heat shock protein (hsp65), and RNA polymerase (rpoB) applied to 190 clinical, 36 type, and 11 reference strains. Phylogenetic analysis resolved 30 sequence clusters with high (>85%) bootstrap support. Since most clusters contained a single type strain and the analysis corroborated current knowledge of Nocardia taxonomy, the sequence clusters were equated with species clusters and MLSA was deemed appropriate for species identification. By comparison, single-locus analysis was inadequate because it failed to resolve species clusters, partly due to the presence of foreign alleles in 22.1% of isolates. While MLSA identified the species of the majority (71.3%) of strains, it also identified clusters that may correspond to new species. The correlation of the identities by MLSA with those determined on the basis of microscopic examination, biochemical testing, and fatty acid analysis was 95%; however, MLSA was more discriminatory. Nocardia cyriacigeorgica (21.58%) and N. farcinica (14.74%) were the most frequently encountered species among clinical isolates. In summary, five-locus MLSA is a reliable method of elucidating taxonomic data to inform Nocardia species identification; however, three-locus (gyrB-16S-secA1) or four-locus (gyrB-16S-secA1-hsp65) MLSA was nearly as reliable, correctly identifying 98.5% and 99.5% of isolates, respectively, and would be more feasible for routine use in a clinical reference microbiology laboratory.

The pathophysiology of intracerebral haemorrhage.

Spontaneous intracerebral haemorrhage carries a high mortality rate and treatment of the disease raises more questions then answers. Mass effect, ischaemia and toxicity of blood components are responsible for brain tissue damage. Initially occurring disturbances of cerebral blood flow have a temporary character and do not play a key role in the pathology of intracerebral haematoma. Oedema formatting in the 24-48 hours after intracerebral bleeding is the result of multidirectional processes. The pathological mechanism that underlines it is the function of activation of systemic complement and cascade of coagulation. In the light of these findings, further clinical and experimental investigations should be focused on these factors.

The technique of inhalation anaethesia in experimental investigation in the rat.

The rat is the most frequently used animal in scientific inquiry conducted for the purpose of advancing basic knowledge that may lead to an improvement in the results of treatment. Understanding of the pharmacological properties of inhalation anaesthetics, in combination with monitoring of their concentration in the inspired and end-tidal gas, together provide safe and precise control of the depth of the anaesthesia. However, accurate application of the inhalation method of anaesthesia requires special equipment for the delivery and effective scavenging of inhalation anaesthetics.

Characterization and sequence analysis of the replicator region of the novel plasmid pALC1 from Paracoccus alcaliphilus.

The replicator region of a low-copy-number plasmid, pALC1, of Paracoccus alcaliphilus JCM 7364 was cloned in a form of the minireplicon pALC100 (3.6 kb). The host range of the minireplicon embraces several species of genus Paracoccus, as well as Agrobacterium tumefaciens, Rhizobium leguminosarum, and Rhodobacter sphaeroides (all belonging to alpha-Proteobacteria), but not Escherichia coli. The complete nucleotide sequence of the replicator region (2276 bp) revealed the presence of one complete open reading frame coding for the 28.4-kDa protein (RepA) with similarity to replication proteins of plasmid pSW500 of Erwinia stewartii and pVS1 of Pseudomonas fluorescens. The iteron-like region was identified upstream of the repA gene and consisted of two clusters of repeated sequences (17 bp long) separated by a putative DnaA box. Analysis of the predicted amino acid sequence of two adjacent incomplete ORFs suggests the localization of repA between genes involved in conjugation (traG) and partitioning (parA) within the pALC1 genome.

[Effects of thrombolysis on left and right ventricular diastolic function in patients after myocardial infraction. One-year follow-up]. / Wplyw leczenia trombolitycznego na czynnosc rozkurczowa lewej i prawej komory u pacjentów po zawale sciany przedniej. Obserwacja roczna.

UNLABELLED: It has been shown, that successful reperfusion of the infarctrelated artery by thrombolysis can prevent left ventricular (LV) dilatation and dysfunction. To date no study has shown the impact of thrombolytic therapy on LV and RV diastolic filling. The aim of the study was to assess the effects of thrombolysis on LV and RV diastolic inflow and systolic function of LV in patients (pts) after anterior myocardial infarction MI. METHODS: Echocardiographic and Doppler-derived measurements of LV systolic function, RV and LV diameters and diastolic function at rest and after treadmill exercise test (TET) were assessed prospectively in 21 patients (pts) after MI treated with streptokinase and 10 pts treated without thrombolysis during one-year follow-up. They were compared with 31 age-matched controls. RESULTS: LV and RV filling indices in both groups of pts after MI were impaired compared to controls but in pts without thrombolysis were more abnormal compared to pts treated with thrombolysis. Among several echocardiographic variables most consistent alteration was shortening of E-deceleration time of mitral as well as RV inflow, more abnormal in pts without thrombolysis. There was strong inverse relation between degree of impairment of diastolic variables and exercise capacity. CONCLUSIONS: These data indicates beneficial effect of thrombolysis on RV and LV diastolic function in patients after AMI. E-deceleration was the most sensitive marker of diastolic dysfunction.

[Neurohumoral factors in hypertensive patients with and without left ventricular hypertrophy]. / Czynniki neurohumoralne u chorych na nadcisnienie tetnicze pierwotne z przerostem miesnia lewej komory i bez przerostu.

Increased pressure load and neurohumoral activation are main factors involved in pathomechanism of left ventricular hypertrophy (LVH) in hypertension (HT). To gain insight into the involvement of neurohumoral factors responsible for cardiac hypertrophy, plasma level of aldosterone (Aldo), plasma renin activity (PRA), insulin-like growth factor-1 (IGF-1), pro-endothelin-1 (pro-ET) and atrial natriuretic peptide (ANP) were measured in HT patients (pts) and compared between pts with and without LVH. Also relationships between neurohormones and LV mass index (LVMI), mean blood pressure (MBP) were assessed separately in HT pts with and without LVH. 121 HT patients (pts) of age 17-79 (mean 48 +/- 15.3) were divided into three groups: 1-53 pts with mild HT, 2-44 pts with moderate HT and 3-24 pts with severe HT. Each of the group was divided into pts with and without LVH further all HT pts were divided into two groups; with and without LVH. Control group consisted of 39 healthy normotensives. LV mass was assessed echocardiographically and plasma levels of IGF-1, PRA, Aldo, pro-ET, and ANP were measured by radioimmunoassay in each pts and controls. LVH was found in 35.8% pts with mild HT, in 68.18% pts with moderate HT and in 100% pts with severe HT. The level of all measured neurohormones were significantly higher in pts with LVH compared to pts without LVH (p < 0.001). In pts with LVH there was significant correlation between LVMI and IGF-1, PRA, Aldo, pro-ET-1 and ANP, contrary to pts without LVH in which such correlations was not found. In pts with LVH there was also significant correlation between MBP and IGF-1, PRA, ANP and pro-ET-1. Increased plasma level of PRA, Aldo, IGF-1, pro-ET-1 and ANP in HT pts with LVH and significant correlation between measured neurohormones and LVMI suggests their contribution to LVH in HT pts. Significant correlation between LVMI, MBP and IGF-1 level, PRA and ANP indicate interplay between hemodynamic and neuroendocrine factors in pathomechanism of LVH.

[The influence of 3-month treatment with molsidomine on structure, function and some neurohormonal parameters in patients with chronic heart failure treated with digoxin, diuretic and angiotensin converting enzyme inhibitors]. / Wplyw trzymiesiecznego leczenia molsidomina na strukture i czynnosc serca oraz wybrane parametry neurohumoralne u chorych na zastoinowa niewydolnosc krazenia leczonych inhibitorem enzymu konwertujacego angiotensyne, srodkiem moczopednym i digoksyna.

The aim of the study was to estimate the influence of long-term treatment with molsidomine on structure, systolic function and neurohormonal parameters in patients with chronic heart failure (CHF). Investigations were carried out in 30 patients (mean age 63.0 +/- 10.9) in NYHA class III and IV. The cause of CHF was: coronary artery disease in 60% of patients, hypertension in 20% and dilated cardiomyopathy in 20% of patients. Molsidomine was administrated in dose of 2 mg tid for 3 months. During the study the previous treatment with ACEI, diuretics and digitalis was maintained. Using echocardiographic method left atrial dimension (LA), left ventricular end diastolic (LVEDD) and end systolic diameter (LVESD), interventricular septum (IVSDD) and posterior wall end diastolic diameter (LVPWDD), ejection fraction (LVEF) and fraction of shortening (LVFS) were measured. Plasma level of atrial natriuretic peptide, endotelin, neuropeptide Y and aldosterone and plasma renin activity were estimated radioimmunologically. All echocardiographic and neurohormonal measures were performed 4 times: before therapy, after 3 days, 2 weeks and 3 months of treatment with molsidomine. We observed significant increase in LVEF, which at baseline was 33.8% and after 3 months 44.8% (p < 0.05). None of the other echocardiographic parameters nor any of neurohormonal factors changed significantly during the 3-months treatment with molsidomine.

[Right ventricular diastolic disfunction and its relation to left ventricular performance in patients with hypertension]. / Dysfunkcja rozkurczowa prawej komory i jej relacja do czynnosci lewej komory u chorych na nadcisnienie tetnicze.

Abnormalities in left ventricular (LV) diastolic function may be the earliest indications of hypertensive heart disease. Because the two ventricles influence each other's performance this study was designed to investigate the impact of chronic LV pressure overload in essential hypertension (HT) on diastolic function of right ventricle (RV). RV and LV diastolic function was evaluated in 74 patients with mild-to-moderate essential HT using pulsed wave Doppler echocardiography. Fifty-five normotensive patients without heart disease acted as control subjects. In studied group, 17 patients (23%) had normal mitral (MV) and tricuspid (TV) flow parameters, 28 (38%) had impaired LV filling parameters [MV early (E) to late (A) peak flow velocity ratio (MV E/A) 0.81 +/- 0.12 vs control 1.19 +/- 0.18, p < 0.001] while 29 patients (39%) had abnormal both mitral [MV E/A) 0.72 +/- 0.15 vs control 1.19 +/- 0.18, p < 0.001] and tricuspid flow parameters (TV E/A) 0.8 +/- 0.19 vs control 1.23 +/- 0.1, p < 0.001). In group with impaired diastolic filling of both ventricles indices of mitral flow were significantly more abnormal compared to group with normal TV flow parameters (MV E/A 0.72 +/- 0.15 vs control 0.81 +/- 0.12, p < 0.05). RV filling parameters correlated with filling parameters. There was good correlation between TV A and MV E (r = -0.56, p < 0.01), the time velocity integral of early mitral inflow (MV E-VTI) (r = -0.64, p < 0.001) and positive correlation with MV A (r = 0.78, p < 0.0001). Also there was good correlation between LV mass and TV E (r = -0.56, p < 0.01) and the time velocity integral of early tricuspid inflow (r = -0.72, p < 0.001). Data indicate that RV diastolic function is abnormal in essential hypertension and these abnormalities are closely related to those of LV diastolic function and LV mass.

[The effect of amlodipine on structure and function of the heart and exercise tolerance in patients with hypertension]. / Wplyw amlodypiny na strukture i funkcje serca oraz tolerancje wysilku fizycznego u chorych na nadcisnienie tetnicze.

UNLABELLED: The aim of the study was to assess whether the hypotensive activity of amlodipine is associated with regression of left ventricular hypertrophy and improvement of impaired LV or right ventricular (RV) diastolic function or increasing of tolerance of physical activity in hypertensive patients. Assessment of left ventricular structure, systolic and diastolic function as well as RV diastolic dimension and diastolic function were performed in 24 patients with mild-to-moderate hypertension before administration of amlodipine and 3, 6 and 9 months of the treatment. In order to assess the tolerance of physical activity, incremental treadmill exercise testing was performed at baseline and after 6 and 9 months of the therapy with amlodipine. RESULTS: During 9 months of the therapy with amlodipine no significant change in indexes of LV mass or in LVM was observed. Similarly amlodipine did not influence the parameters of LV or RV diastolic function in studied patients. However, amlodipine treatment resulted in significant increase in total exercise time (p < 0.05), total workload (p < 0.01) measured in METs and decrease in diastolic blood pressure during exercise test. CONCLUSION: The nine months of the therapy with amlodipine resulted in significant improvement in exercise tolerance. Total exercise duration and total workload measured in METs significantly increased. During this time of the therapy no significant changes in LV structure or LV and RV diastolic function were observed. One can make an assumption that amlodipine inhibits progression of structural and functional derangement in hypertensive patients.

[Comparative study to assess the efficacy and adverse effects of amlodipine and nifedipine retard in patients with stable exertional angina and hypertension]. / Badania porównawcze skutecznosci i dzialania niepozadanego amlodypiny i nifedypiny retard u chorych na dlawice piersiowa stabilna z wspólistniejacym nadcisnieniem tetniczym.

The purpose of the study was to compare the antianginal and hypotensive efficacy and tolerability of 8 weeks of treatment with amlodipine taken once daily and nifedipine taken twice daily in patients with stable exertional angina pectoris and mild-to-moderate hypertension. Following a 2-week placebo run-in-period 13 patients were randomized to receive amlodipine (5 to 10 mg once daily) and 8 patients to receive nifedipine (20 or 40 mg twice daily) in an 8-week treatment phase. Antianginal efficacy was assessed with angina diares, investigators, and patients global evaluations and with treadmill exercise test during placebo run-in-period and after 8 weeks of the therapy. Amlodipine significantly reduced both weekly anginal attacks and consumption of glyceryl trinitrate tablets. This effect was more pronounced compared to efficacy of nifedipine. Exercise tolerance was also improved more markedly after amlodipine than after nifedipine treatment. Amlodipine treatment resulted in significant increase in total exercise time, increase the exercise time to angina onset, increase time to ST segment depression, decrease in ST segment depression, decrease in total duration of ST segment depression and decrease in duration of pain. In patients treated with nifedipine only favourable effect was significant decrease in total duration of ST segment depression, without significant changes of other examined parameters. Both drugs decreased blood pressure with no significant change in heart rate. No serious adverse events occurred in any patients during therapy with amlodipine as well as with nifedipine. The results of the study demonstrate that amlodipine has markedly better anti-anginal efficacy than nifedipine with respect to the most of the parameters examined. However both drugs showed comparable antihypertensive action and both were well tolerated by angina patients. The good anti-anginal and hypotensive efficacy and safety of amiodipine with once daily dosage regimen makes this drug an excellent choice of treatment for hypertensive patients with severe coronary artery disease.

[Relationship between systolic and diastolic function of the left ventricle in patients with impaired relaxation of the left ventricle without symptoms of heart failure. Attempt at quantitative estimation of diastolic function in the impaired relaxation stage]. / Zaleznosc miedzy funkcja skurczowa i rozkurczowa lewej komory serca u chorych z uposledzona relaksacja lewej komory bez objawów niewydolnosci krazenia. Próba ilosciowego podzialu dysfunkcji o typie uposledzonej relaksacji.

UNLABELLED: Diastolic dysfunction of left ventricle appears very often in patients with coronary artery disease (CAD) and hypertension (HT) and is a main cause of heart failure in 30-40% of all cases. Relation between systolic and diastolic function of left ventricle (LV) is commonly known but not documented well enough. Moreover, no quantitative classification of diastolic dysfunction is still available. AIM OF THE STUDY: To find out the relations between the parameters of systolic and diastolic function of LV in patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure and to make up the quantitative classification of diastolic dysfunction in the stage of impaired relaxation of LV. METHODS: Investigations were carried out in 57 patients (mean age 55.5 +/- 11.5) with angiographically proven CAD and in 91 patients (mean age 56.3 +/- 10.6) with HT and angiographically excluded CAD, all without regional myocardial contractility abnormalities and valvular heart diseases. Control group consisted of 54 healthy subjects (mean age 55.4 +/- 11.4). During 2D echocardiography examination left ventricular end-diastolic (LVEDD) and end-systolic diameters (LVESD) and left atrial dimension (LA) were obtained. Using Doppler method transmitral inflow indices: E velocity (E), A velocity (A), E velocity integral (E-VTI), A velocity integral (A-VTI), total velocity integral (T-VTI), E deceleration time (DT), isovolumic relaxation time (IVRT) and aortic flow velocity integral (Ao-VTI) were measured. Only patients with E/A < or = 1 and--to exclude pseudonormalization of mitral inflow--with DT > or = 140 ms were qualified to the study. We proposed diastolic dysfunction ratio (DDR) calculated from formula: DDR = E/A x E-VTI/T-VTI. Using AFVI, LV outflow diameter, heart rate (HR) and body surface area cardiac index (CI) was calculated. RESULTS: In studied group there were significantly higher values of LA, A, IVRT, DT and lower values of E, E/A, E-VTI and DDR compared to controls. There were no significant differences between these groups in HR, LVEDD, LVESD, T-VTI and CI. No significant differences in any of studied parameters were found between subgroups with CAD and HT. Among healthy subjects in subgroup with abnormal mitral inflow pattern (E/A < or = 1) there were significantly higher values of LA, IVRT, DT and lower values of DDR than in sugroup with normal one. Both subgroups did not differ in LVEDD, LVESD, CI. In the studied group there was positive correlation between DDR and CI (r = 0.69, p < 0.001), DDR and IVRT (r = 0.71, p < 0.001), DDR and DT (r = 0.61, p < 0.001), CI and E (r = 0.34, p < 0.01), CI and IVRT (r = 0.52, p < 0.001), CI and DT (r = 0.42, p < 0.001), CI and E/A (r = 0.54, p < 0.001), CI and E-VTI (r = 0.43, p < 0.001). In the control group significant correlation was found only between DDR and IVRT (r = 0.64, p < 0.02) and between DDR and DT (r = 0.52, p < 0.02) but not between DDR and CI. Using DDR DD was divided into 3 classes: class I with DDR > 0.47, class II with 0.47 > or = 0.30, and class III with DDR < 0.30. Applying of such intervals of values of DDR determined the groups which significantly differed between themselves in CI, IVRT and DT. CONCLUSIONS: (1) In patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure there is relation between parameters of systolic and diastolic function of LV: the more advanced diastolic dysfunction, the more impaired systolic function. (2) In healthy subjects there is no relation between parameters of systolic and diastolic function of LV. (3) DDR is a good indicator of quantitative estimation of diastolic dysfunction in the stage of impaired relaxation of LV.

[The effect of hypotensive drugs on left ventricular mass and diastolic function]. / Wplyw leków hipotensyjnych na mase miesnia i funkcje rozkurczowa lewej komory serca.

Chronic left ventricular hypertrophy (LVH) is associated with depressed contractile performance, abnormal compliance of the chamber, and ultimately, the development of a left ventricular failure. Thus the presence of LVH carries a particularly ominous prognosis in patients with essential hypertension. Finally, regression of LVH appears to be a worthwhile goal of an antihypertensive therapy along with blood pressure control. Of particular importance, is whether the functional derangements associated with hypertrophy will also be reversed. The present study was undertaken to determine whether antihypertensive therapy reduced ventricular mass, and whether these changes were accompanied by improved diastolic function. 47 patients with mild-to-moderate essential hypertension were divided into two groups. Group I--included 21 patients whose blood pressure responded to nifedipine monotherapy. Group II--included 26 patients whose normalization of blood pressure required combined therapy with nifedipine and metoprolol. 40 healthy volunteers comprised a control group. To assess the effects of antihypertensive therapy on the heart, left ventricular mas (LVM), systolic and diastolic function, by M-mode, 2-D and pulsed wave Doppler echocardiography had been evaluated. Measurements were performed before therapy and every 3rd month during first year, and every 40th month during the second year of observation. RESULTS. At baseline all hypertensive patients had significantly increased LVM compared to the controls. Indexes of systolic function in studied patients were normal, while indexes of LV diastolic filling were significantly abnormal compared to the controls. In the group treated with nifedipine, starting from the 9th month of observation, small but significant decrease in posterior wall thickness was noted but LVM did not change during the whole time of the observation. Similarly, there was no significant change in indexes of left ventricular diastolic filling. Contrary to patients treated with nifedipine, in group of patients treated with combination of nifedipine and metoprolol, significant reduction of LVM and improvement of LV diastolic filling was observed. Of particular interest was the fact, that improvement in diastolic, performance appeared earlier, and preceded regression of LVM. Most striking was the improvement in Ev/Av ratio which increased by 16% after 6 months and by 35% after 24 months of the therapy. CONCLUSION. 1. Combined therapy with nifedipine and metoprolol contrary to monotherapy with nifedipine alone, results in the regression of left ventricular mass and the improvement of left ventricular diastolic function. 2. Improvement of left ventricular diastolic function appears earlier, preceding the regression of left ventricular hypertrophy.