BACKGROUND: Antibiotic dosing in critically ill patients is complicated by variations in the pharmacokinetics of antibiotics in this group. The dosing of imipenem/cilastatin is usually determined by severity of illness and renal function OBJECTIVES: To determine the correlation between estimated glomerular filtration rates (eGFRs) calculated with the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation and imipenem trough levels in critically ill patients METHODS: This prospective observational study was done in the surgical intensive care unit (ICU) at Steve Biko Academic Hospital, Pretoria, South Africa. Imipenem trough levels were measured by high-performance liquid chromatography and compared with eGFRs calculated with the CKD-EPI equation. Correlation was evaluated by the Pearson product-moment correlation coefficient RESULTS: The study population consisted of 68 critically ill patients aged between 18 and 81 years; 43 (63%) were male, and the mean weight was 78 kg (range 40 - 140). On admission, 30 patients (44%) had sepsis, 16 (24%) were admitted for trauma, and 22 (32%) were admitted for miscellaneous surgical conditions. Acute Physiology and Chronic Health Evaluation II (APACHE II) scores ranged from 4 to 39 (mean 18). The 28-day mortality rate was 29%. The mean albumin level was 16 g/L (range 7 - 25), the mean creatinine level 142 μmol/L (range 33 - 840), and the mean eGFR 91 mL/min/1.73 m² (range 6 - 180). Imipenem trough levels ranged between 3.6 and 92.2 mg/L (mean 11.5). The unadjusted Pearson product-moment correlation coefficient between eGFR and imipenem trough level was -0.04 (p=0.761 CONCLUSION: Considering the high mortality rate of sepsis in ICUs and the rapid global increase in antimicrobial resistance, it is crucial to dose antibiotics appropriately. Owing to the variability of antibiotic pharmacokinetics in critically ill patients, this task becomes almost impossible when relying on conventional dosing guidelines. This study found that eGFRs do not correlate with imipenem blood levels in critically ill patients and should not be used to determine the dose of imipenem/cilastatin. Instead, the dose should be individualised for patients through routine therapeutic drug monitoring

BACKGROUND. The drug levels and clearances of imipenem in critically ill patients are not comprehensively described in current literature, yet it is vital that adequate levels be achieved for therapeutic success. OBJECTIVES. To determine the proportion of critically ill patients treated with imipenem/cilastatin with sub-therapeutic imipenem plasma levels, and to compare the clinical outcomes of those patients with therapeutic levels with those who had sub-therapeutic levels. Methods. Trough imipenem plasma levels of 68 critically ill patients from a surgical intensive care unit were measured using a validated high-performance liquid chromatography method. Imipenem trough levels were compared with the minimum inhibitory concentration (MIC) of the causative bacterial agents, based on a target value of 100% time above MIC (/T >MIC). RESULTS. The proportion of participants with sub-therapeutic imipenem levels was 22% (95% confidence interval (CI) 13% - 34%). The 14- and 28-day mortality rates in the sub-therapeutic group were 33% and 40%, respectively, compared with 19% (p=0.293) and 26% (p=0.346), respectively, in the therapeutic group. Sub-therapeutic imipenem plasma levels are associated with adjusted hazard ratio of 1.47 (95% CI 0.55 - 3.91). CONCLUSIONS. The lower proportion of critically ill patients with sub-therapeutic imipenem plasma levels in this study compared with previous studies may be attributed to the practice of higher dosages and the administration method of extended infusions of imipenem/ cilastatin in our setting. The results demonstrate a trend of higher mortality in patients with sub-therapeutic imipenem levels, although the results were not statistically significant at this sample size.

INTRODUCTION: Lathes and pumice slurry are commonly used without change or disinfection for polishing both new and old, repaired dentures PURPOSE: To identify and quantify any microorganisms harboured in these components in the laboratories of an academic teaching institution where the machines are in constant daily use. MATERIAL AND METHODS: Two machines were identified and labelled in each laboratory, one for exclusive use for new dentures and the other for dentures which had been exposed to any form of patient oral contact. Users were so informed. Samples were collected twice daily on alternate days over a period of one week and tested for the presence and type of microorganisms, and whether the levels of contamination increased with usage. RESULTS: Pumice throughout was contaminated with a variety of bacteria, yeasts and moulds. notably Aspergillus, which will hover in the abundant aerosol during polishing. Cross-contamination can thus occur between dentures, posing danger to patients. Consultation between the dental staff and the Department of Medical Microbiology established a standardised disinfection protocol for the polishing wheels, machinery and pumice slurry. CONCLUSION: Prevention of cross contamination is crucial to avoid inadvertent but nevertheless culpable infection of denture-wearing patients, as well as for personal protection.

BACKGROUND. Group B streptococcus (GBS) is a leading cause of invasive disease, particularly in newborns. Seventy-five percent of neonates will be colonised by mothers carrying the organism. Confirmation of maternal colonisation with GBS is essential for prompt treatment and prevention of neonatal sepsis. The current gold standard of culture for isolation of GBS has a disadvantage of long turnaround time (24 -72 hours). Rapid assays are required to determine maternal carriage of GBS. OBJECTIVES. To determine the usefulness of the Xpert GBS technology v. culture methods to detect GBS carriage in pregnant women. METHODS. This was a prospective observational study of 284 pregnant women between 26 and 37 weeks' gestation. Two vaginorectal swabs were collected from each participant. One swab was processed using the gold-standard culture method, while the second swab was processed using the Xpert GBS assay. The performance of the Xpert GBS assay was then compared with that of the culture method. RESULTS. Two swabs were processed from each of 284 pregnant women between 26 and 37 weeks' gestation. Culture detected 70 GBS isolates from a total of 279 specimens (25.1%), whereas the Xpert GBS detected 66 positive specimens (23.7%). The Xpert GBS assay had a sensitivity of 87% and specificity of 98%, with a positive predictive value of 92% and a negative predictive value of 96%. CONCLUSIONS. The Xpert GBS assay is a rapid and sensitive tool for prenatal detection of GBS. The assay should ideally be available in every labour ward, where women can be screened for GBS on arrival.

Anodic limiting currents were measured in an unstirred divided cell at an inclined small scale anode using a large scale cathode with angles of inclination from vertical axis as 45, 60 and 75°. Anode heights (II) vary from 1 cm to 6 cm and phosphoric acid concentration from 6 to 10 moles. Limiting currents for electropolishing of copper were between 5 and 58 mA.cm-2 depending on the operating conditions. A general correlation of data of all inclinations was obtained using the equation: I = 28.57(Θ0.520.C -0.89.H -0.91) with an average deviation of ±4%.

The sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a) is under the control of an SR protein named phospholamban (PLN). Dephosphorylated PLN inhibits SERCA2a, whereas phosphorylation of PLN at either the Ser16 site by PKA or the Thr17 site by CaMKII reverses this inhibition, thus increasing SERCA2a activity and the rate of Ca2+ uptake by the SR. This leads to an increase in the velocity of relaxation, SR Ca2+ load and myocardial contractility. In the intact heart, ß-adrenoceptor stimulation results in phosphorylation of PLN at both Ser16 and Thr17 residues. Phosphorylation of the Thr17 residue requires both stimulation of the CaMKII signaling pathways and inhibition of PP1, the major phosphatase that dephosphorylates PLN. These two prerequisites appear to be fulfilled by ß-adrenoceptor stimulation, which as a result of PKA activation, triggers the activation of CaMKII by increasing intracellular Ca2+, and inhibits PP1. Several pathological situations such as ischemia-reperfusion injury or hypercapnic acidosis provide the required conditions for the phosphorylation of the Thr17 residue of PLN, independently of the increase in PKA activity, i.e., increased intracellular Ca2+ and acidosis-induced phosphatase inhibition. Our results indicated that PLN was phosphorylated at Thr17 at the onset of reflow and immediately after hypercapnia was established, and that this phosphorylation contributes to the mechanical recovery after both the ischemic and acidic insults. Studies on transgenic mice with Thr17 mutated to Ala (PLN-T17A) are consistent with these results. Thus, phosphorylation of the Thr17 residue of PLN probably participates in a protective mechanism that favors Ca2+ handling and limits intracellular Ca2+ overload in pathological situations.