Impact of blood pressure changes and course on hematoma growth in acute intracerebral hemorrhage.

BACKGROUND AND PURPOSE: An association between high blood pressure (BP) in acute intracerebral hemorrhage (ICH) and hematoma growth (HG) has not been clearly demonstrated. Therefore, the impact of BP changes and course on HG and clinical outcome in patients with acute ICH was determined. METHODS: In total, 117 consecutive patients with acute (<6 h) supratentorial ICH underwent baseline and 24-h CT scans, CT angiography for the detection of the spot sign and non-invasive BP monitoring at 15-min intervals over the first 24 h. Maximum and minimum BP, maximum BP increase and drop from baseline, and BP variability values from systolic BP (SBP), diastolic BP and mean arterial pressure (MAP) were calculated. SBP and MAP loads were defined as the proportion of readings >180 and >130 mmHg, respectively. HG (>33% or >6 ml), early neurological deterioration (END) and 3-month mortality were recorded. RESULTS: Baseline BP variables were unrelated to either HG or clinical outcome. Conversely, SBP 180-load independently predicted HG (odds ratio 1.05, 95% CI 1.010-1.097, P = 0.016), whilst both SBP 180-load (odds ratio 1.04, 95% CI 1.001-1.076, P = 0.042) and SBP variability (odds ratio 1.2, 95% CI 1.047-1.380, P = 0.009) independently predicted END. Although none of the BP monitoring variables was associated with HG in the spot-sign-positive group, higher maximum BP increases from baseline and higher SBP and MAP loads were significantly related to HG in the spot-sign-negative group. CONCLUSIONS: In patients with acute supratentorial ICH, SBP 180-load independently predicts HG, whilst both SBP 180-load and SBP variability predict END.

Ultraearly hematoma growth predicts poor outcome after acute intracerebral hemorrhage.

OBJECTIVE: To investigate the impact of the adjustment of initial intracerebral hemorrhage (ICH) volume by onset-to-imaging time (ultraearly hematoma growth [uHG]) on further hematoma enlargement and outcome in patients with acute ICH. METHODS: We studied 133 patients with acute (<6 hours) supratentorial ICH. Patients underwent baseline and 24-hour CT scans for ICH volume measurement, and a CT angiography (CTA) for the detection of the spot sign. We defined uHG as the relation between baseline ICH volume/onset-to-imaging time, hematoma growth (HG) as hematoma enlargement >33% or >6 mL at 24 hours, early neurologic deterioration (END) as increase ≥4 points in the NIH Stroke Scale score or death at 24 hours, and poor long-term outcome as modified Rankin Scale score >2 at 3 months. RESULTS: The uHG was significantly faster in spot sign patients (p < 0.001), as well as in patients who experienced HG (p = 0.021), END (p < 0.001), 3-month mortality (p < 0.001), and poor long-term outcome (p < 0.001). The uHG improved the accuracy of baseline ICH volume in the prediction of END (sensitivity 93.1% vs 82.8%, specificity 85.3% vs 82.4%) and 3-month mortality (sensitivity 77.5% vs 70%, specificity 87.9% vs 84.6%). A uHG >10.2 mL/hour emerged as the most powerful predictor of HG (odds ratio [OR] 3.55, 95% confidence interval [CI] 1.39-9.07, p = 0.008), END (OR 70.22, 95% CI 14.63-337.03, p < 0.001), 3-month mortality (OR 16.96, 95% CI 5.32-54.03, p < 0.001), and poor long-term outcome (OR 6.19, 95% CI 1.32-28.98, p = 0.021). CONCLUSIONS: The uHG represents a powerful and easy-to-use tool for improving the prediction of HG and outcome in patients with acute ICH.

Coma mixedematoso en una herniorrafia urgente / No disponible

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[Clinical effects and pharmacokinetics of ropivacaine and bupivacaine for epidural analgesia during labor]. / Efectos clínicos y farmacocinética de ropivacaína y bupivacaína en la analgesia epidural durante el trabajo de parto.

OBJECTIVE: To compare the analgesic efficacy, pharmacokinetics and histamine release of ropivacaine and bupivacaine with fentanyl in continuous epidural perfusion during labor and childbirth. MATERIAL AND METHODS: Prospective study of 40 women at full-term pregnancy who requested epidural analgesia. The patients were randomly assigned to 2 groups of 20: group R received an initial bolus dose of 10 mL of 0.25% ropivacaine and group B received 0.25% bupivacaine, followed in both groups by epidural infusion of the assigned drugs at a concentration of 0.125% plus 0.30 mg of fentanyl at a rate of 5 mL/h through a patient-controlled analgesia device that allowed additional bolus doses. The studied variables were age, weight, height, sensory and motor block, mean blood pressure and maternal-fetal heart rates, number of bolus doses, total local anesthetic administered, duration and type of delivery, oxytocin increase, Apgar at 1 and 5 minutes, plasma levels of local anesthetic (30 minutes after the initial dose, at the end of dilation, in the umbilical vein, and 30 minutes after switching off the perfusion pump), time to clearance, elimination half-life, and a test of histamine release by radioimmunoassay. RESULTS: No significant differences were observed in the course of labor or in Apgar scores. The plasma concentrations of ropivacaine were higher than those of bupivacaine (p<0.03). Clearance of both drugs was similar. The elimination half-life of ropivacaine was significantly less than that of bupivacaine (5.2 +/- 0.7 h vs. 10.8 +/- 1.06 h). CONCLUSIONS: Analgesia was equally effective in both groups, without adverse maternal-fetal effects, with spontaneous micturition and absence of motor blockade in both groups. The plasma concentrations were higher with ropivacaine but were not toxic.

Trombosis de seno cavernosopostraumática / Posttraumatic cavernous sinus thrombosis

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Empleo del estimulador de cordones posteriores en un paciente con angina de pecho refractaria a tratamiento / Use of the stimula tor of medullary posterior cords in a patient with angina pectoris refractory to treatment

La electroestimulación medular es una de las terapias alt e rnativas en el tratamiento de la angina de pecho refractaria. Presentamos el caso clínico de un paciente con angina de pecho refractaria al cual se le colocó un electrodo tetrapolar en el espacio epidural (a nivel de C6) para estimular los cordones posteriores de la médula espinal. El electrodo se conecta a una bateria, tras ser tunelizado subdérmicamente, colocada en un bolsillo subcutáneo a nivel subcostal. La estimulación utilizada fue continua. Se indicó su colocación siguiendo unos criterios de inclusión y exclusión, lo que contribuyó a que la técnica fuese efectiva y a mejorar la calidad de vida de dicho paciente (AU)

Development of a plasmid vector for easy selection of strong promoters.

A promoter vector pACPR33 for Escherichia coli based on the promotorless ampicillin-resistance gene from pBR322 has been constructed. The promoter of the ampicillin-resistance gene was deleted and replaced by a suitable multiple cloning site. Molecular cloning of promoters into the polylinker resulted in activation of the ampicillin resistance in E. coli. The plasmid contains a functional origin of DNA replication and a tetracycline resistance gene for E. coli, and a chloramphenicol resistance gene for S. aureus. The vector permitted direct detection of promoter activity, especially strong promoters, by easy iodometric determination of beta-lactamase activity in liquid or solid media.

DNA bending by the TrpI protein of Pseudomonas aeruginosa.

TrpI protein, the activator of transcription of the trpBA operon of fluorescent pseudomonads, bends the DNA when it forms either of two well-characterized complexes with the trpBA regulatory region. In complex 1, with TrpI bound only to its strong binding site (site I), the calculated bending angle is 65 to 67 degrees and the center of bending is in the middle of site I. In complex 2, which is required for activation of the trpBA promoter, with TrpI bound both to site I and to the weaker site II, the bending angle is increased to 89 to 90 degrees and the center of bending is at the site I-site II boundary. Indoleglycerol phosphate (InGP), which strongly stimulates formation of complex 2 and is required for activation, does not affect the bending angle of either complex. However, a mutation (-10C/11C) shown previously to affect activation has a small but detectable effect on bending, reducing the calculated bending angle to 83 to 86 degrees. These results suggest a way that DNA bending and InGP may be important for activation.

Bis[(E)-2-(2,4-dichloro-5-nitrostyryl)-1,3-benzothiazole] hydrate.

The title compound, bis[(E)-2-(2,4-dichloro-5-nitrostyryl)-1,3-benzothiazole] hydrate, 2C15H8Cl2N2O2S.-H2O, was obtained from the condensation of 2-methyl-benzothiazole with 2,4-dichloro-5-nitrobenzaldehyde. Single-crystal X-ray analysis showed that the asymmetric unit contains two crystallographically unique but structurally similar molecules. The dihedral angle between the benzothiazole fragment and the phenyl ring is 6.1 (4) degrees in molecule A and 19.5 (4) degrees in molecule B.

The emergence of resistance to amikacin in Serratia marcescens isolates from patients with nosocomial infection.

Administration of either amikacin (1985) or gentamicin (1984, 1986-1991) as first-choice aminoglycoside did not decrease the high incidence of amikacin-resistant Serratia marcescens (ARSm) isolates responsible for nosocomial infections at the J.A. Fernández Hospital of Buenos Aires (42% in 1984, 31% in 1985 and 41% in 1987, differences not significant). In addition, a significant peak (P = 0.003) was detected in 1986, with an ARSm incidence of 70%. The incidence of ARSm decreased by 1988-1991 for reasons not related to aminoglycoside use. In the period 1984-1987 all S. marcescens isolates carried the 6'-aminoglycoside-acetyltransferase-Ic [aac(6')-Ic] gene, while in addition 20% of the isolates contained the plasmid-encoded 3'-aminoglycoside-phosphotransferase-VIa[aph(3')-VIa] and 2% the 6'-aminoglycoside-acetyltransferase-Ib [aac(6')-Ib] genes. From 1988 to 1992 resistance to amikacin was associated with only 4 ARSm isolates and correlated with the appearance of Tn1331-related sequences in these isolates. This transposon or related sequences, however, was not widely spread in the S. marcescens population under investigation. Combined use of restriction fragment length polymorphism (RFLP), ribotyping and plasmid profile analysis revealed that S. marcescens strains of the same genotype, including isolates either expressing or not the aac(6')-Ic gene, were involved in outbreaks occurring in May 1984, May 1985 and May 1986. Furthermore, these epidemiological tools permitted discrimination of different S. marcescens clones, each bearing a particular amikacin-resistance marker.

Sequences related to Tn1331 associated with multiple antimicrobial resistance in different Salmonella serovars.

Serovars of Salmonella resistant to ampicillin, third-generation cephalosporins and aminoglycosides but sensitive to chloramphenicol, cefoxitin and ceftibuten emerged in one pediatric hospital of Buenos Aires. All isolates expressed AAC(6')-I and AAC(3)-V enzyme activities, making them resistant to all aminoglycosides marketed in Argentina by the time this investigation was performed. The cefotaxime resistance marker, the AAC(3)-V enzyme activity and Tn1331-related sequences were associated with plasmid DNAs from different Salmonella serovars.

An 8-year study of resistance to amikacin in gram-negative bacilli isolates from patients with nosocomial infection at one hospital in Argentina.

Administration of either gentamicin or amikacin induced an increase in the number of amikacin-resistant (AR) isolates of certain Enterobacteriaceae and Acinetobacter species in a hospital in Buenos Aires. A total of 127 AR isolates was selected to study the molecular mechanisms of resistance involved. The aac(6')-Ic gene was found by dot-blot hybridisation in every Serratia marcescens isolate. A gene different from aac(6')-Ia, aac(6')-Ib and aac(6')-Ic encoding the AAC(6')-I activity was found in a 15.5-kb plasmid in Acinetobacter spp. Plasmids from 27 Enterobacteriaceae contained and aac(6')-Ib gene and 26 of these carried sequences related to the Tn1331 transposon, whereas one Escherichia coli plasmid showed homology in another fragment of the Tn1331 transposase. Because plasmids bearing the aac(6')-Ib gene were heterogeneous, dissemination of the aac(6')-Ib gene may have been due to transposition of Tn1331 rather than the spread of an epidemic plasmid. The rate of AR isolates varied within each species in spite of the presence of Tn1331, and it is likely, therefore, that this transposon may not be the sole factor responsible for the observed variation. The aph(3')-VIa gene (originally described in Acinetobacter spp.) was found with high frequency (80%) in this Acinetobacter population. Furthermore, this gene was found also in plasmids from 20% of other gram-negative organisms commonly involved in nosocomial infections in this hospital.