Collaborative study of antibiotic medium 3 and flow cytometry for identification of amphotericin B-resistant Candida isolates

Center 1 used the National Committee for Clinical Laboratory Standards M27-A2 method and antibiotic medium 3 (AM3) test to determine amphotericin B resistance in 5 of 30 Candida isolates. These isolates were tested at center 2 by AM3 test and flow cytometry (FC). The agreements (C1-C2) were 90% for AM3 test and FC and 73% for the AM3 tests.     

Diblock Copolymers Based on 1,4‐Dioxan‐2‐one and ε‐Caprolactone: Characterization and Thermal Properties

Summary: Various poly(ε‐caprolactone‐block‐1,4‐dioxan‐2‐one) (P(CL‐block‐PDX)) block copolymers were prepared according to the living/controlled ring‐opening polymerization (ROP) of 1,4‐dioxan‐2‐one (PDX) as initiated by in situ generated ω‐aluminium alkoxides poly(ε‐caprolactone) (PCL) chains in toluene at 25 °C. 1 ¹H NMR, PCS and TEM measurements have attested for the formation of colloids attributed to a growing PPDX core surrounded by a solvating PCL shell during the polymerization of PDX promoted by ω‐Al alkoxide PCL chains in toluene. The thermal behavior of the P(CL‐block‐PDX) copolymers was studied by DSC; showing two distinct melting temperatures (as well as two glass transition temperatures) similar to those of the respective homopolyesters. Finally, the thermal degradation of the P(CL‐block‐PDX) block copolymers was investigated by TGA simultaneously coupled to a FT‐IR spectrometer and a mass spectrometer for evolved gas analysis (EGA). The degradation occurred in two consecutive steps involving a first unzipping depolymerization of the PPDX blocks followed by the degradation of the PCL blocks via both ester pyrolysis and unzipping reactions.

TEM observation of P(CL‐block‐PDX) block copolyesters ( = 11 600 and = 22 100) as formed by vaporization starting from a diluted suspension in toluene/TCE mixture solvent (50/50 v/v).     

Asbestos exposure in lung carcinoma: a necropsy-based study of 414 cases.

BACKGROUND: The prerequisites necessary for attributing lung carcinoma to asbestos, represent a controversial issue. METHODS: Three parameters (occupational history, pleural plaques, and lung asbestos bodies) were investigated in 414 consecutive cases of lung carcinoma, examined at necropsy at the Hospital of Monfalcone, Italy. Occupational data were obtained from the patients' relatives by personal or telephone interviews. Pleural plaques were classified into three classes (small, moderate, large). Routine lung sections were examined for asbestos bodies in all cases; isolation and counting were performed in 408 cases. RESULTS: The series included 353 men, and 61 women, aged between 38 and 97 years. The male patients had worked in industries in 74% of cases (60% in shipbuilding). Men showed pleural plaques in 82% of cases (moderate or large plaques in 58.7%). Asbestos bodies were observed in routine lung sections in 34.8%, and in 31% exceeded the value of 5,000 bodies per gram of dried tissue. Among women the principal features were: history or domestic exposure to asbestos in 36% of the cases, prevalence of pleural plaques 34% (moderate or large plaques 15%), asbestos bodies in routine lung sections in 3.3% and there was no case with an asbestos body burden over 5,000/g. The fraction of asbestos-related carcinomas among male patients varied between 24.7 and 61%, depending on the criteria used for attribution. CONCLUSIONS: Different criteria indicated about 60% of the present lung carcinomas among men as plausibly attributable to asbestos.     

Raising plasma phosphorus levels by phosphorus-enriched, bicarbonate-containing dialysate in hemodialysis patients

In 6 hemodialysis patients, enriching the "base concentrate" of a bicarbonate-containing dialysate-generating system with phosphorus succeeded in raising plasma phosphorus levels.     

Validation of serotonin (5-hydroxtryptamine) as an in vitro substrate probe for human UDP-glucuronosyltransferase (UGT) 1A6.

Investigation of human UDP-glucuronosyltransferase (UGT) isoforms has been limited by a lack of specific substrate probes. In this study serotonin was evaluated for use as a probe substrate for human UGT1A6 using recombinant human UGTs and tissue microsomes. Of the 10 commercially available recombinant UGT isoforms, only UGT1A6 catalyzed serotonin glucuronidation. Serotonin-UGT activity at 40 mM serotonin concentration varied more than 40-fold among human livers (n = 54), ranging from 0.77 to 32.9 nmol/min/mg of protein with a median activity of 7.1 nmol/min/mg of protein. Serotonin-UGT activity kinetics of representative human liver microsomes (n = 7) and pooled human kidney, intestinal and lung microsomes and recombinant human UGT1A6 typically followed one enzyme Michaelis-Menten kinetics. Serotonin glucuronidation activity in these human liver microsomes had widely varying V(max) values ranging from 0.62 to 51.3 nmol/min/mg of protein but very similar apparent K(m) values ranging from 5.2 to 8.8 mM. Pooled human kidney, intestine, and lung microsomes had V(max) values (mean +/- standard error of the estimates) of 8.8 +/- 0.4, 0.22 +/- 0.00, and 0.03 +/- 0.00 nmol/min/mg of protein (respectively) and apparent K(m) values of 6.5 +/- 0.9, 12.4 +/- 2.0, and 4.9 +/- 3.3 mM (respectively). In comparison, recombinant UGT1A6 had a V(max) of 4.5 +/- 0.1 nmol/min/mg of protein and an apparent K(m) of 5.0 +/- 0.4 mM. A highly significant correlation was found between immunoreactive UGT1A6 protein content and serotonin-UGT activity measured at 4 mM serotonin concentration in human liver microsomes (R(s) = 0.769; P < 0.001) (n = 52). In conclusion, these results indicate that serotonin is a highly selective in vitro probe substrate for human UGT1A6.     

Cytochrome oxidase deficiency presenting as birth asphyxia

Hypoxic-ischaemic encephalopathy (HIE) was diagnosed in an infant with acidosis. At 7 weeks of age further investigations revealed abnormal neuroimaging (CT and MRI scans) and a raised plasma and CSF lactate. A skeletal-muscle biopsy at 2 months of age confirmed the diagnosis of cytochrome oxidase deficiency. The course of the patient's disorder has taken that of a static encephalopathy (cerebral palsy). Inborn disorders of the respiratory chain should be considered in the differential diagnosis of HIE.