Detection of coronary plaque by computed tomography with a novel plaque analysis system, 'Plaque Map', and comparison with intravascular ultrasound and angioscopy.

BACKGROUND: Previous reports suggest that plaque may be characterized by the computed tomography (CT) number, but there is not a comprehensive method for evaluating the gray-scale CT image of the coronary artery obtained by multi-detector row CT (MDCT). METHODS AND RESULTS: Forty-five patients with acute coronary syndrome (ACS) underwent MDCT either 3-4 weeks after the onset of acute myocardial infarction (n=24) or within 1 week after percutaneous coronary intervention in patients with unstable angina (UA; n=21). The cross-sections obtained at intervals of 5 mm were converted to numerical data and a 'plaque map' was drawn using the color-based isometric line method and bird's eye view. 'Plaque map' was compared with the findings of intravascular ultrasound (IVUS) and angioscopy. Of 662 slices of 78 vessels, soft, intermediate or calcified plaque was detected in 144, 134, and 84 slices, respectively. Compared with IVUS, the sensitivities were 92%, 87%, and 89%, respectively, and compared with angioscopy, sensitivity was 80% and specificity was 87%. CONCLUSIONS: MDCT with the 'Plaque Map' system can noninvasively characterize plaque in patients with ACS.     

Pneumocystis jiroveci pneumonia as a complication of glucocorticoid therapy for interstitial pneumonia]

We evaluated the clinical features of pneumocystis jiroveci pneumonia (PCP) as a complication of glucocorticoid therapy for interstitial pneumonia We analyzed 74 interstitial pneumonia patients receiving glucocorticoid therapy, of whom 7 patients developed PCP. At the time of PCP diagnosis, the average duration of the glucocorticoid therapy was 71 days and the average daily dose of predonisolone was 37 mg. Circulating CD4+ lymphocyte counts were 370/microl on the average and more than 200/microl in three cases. PCP cases showed less circulating lymphocyte counts four weeks after the initiation of the therapy. Any cases receiving sulfamethoxazole-trimethoprim (TMP-SMX) did not develop PCP. In conclusion, interstitial pneumonia patients, who are treated with glucocorticoid, are benefit from TMP-SMX as PCP prophylaxis, but CD4 + lymphocyte counts greater than 200/microl is no reason to denying PCP.     

Activation of non-primary motor areas during a complex finger movement task revealed by functional magnetic resonance imaging

We examined the brain activation induced by a complex finger movement task using functional magnetic resonance imaging (fMRI) with echo planar imaging (EPI). Imaging planes were set up for the observation of non-primary motor areas. Among five normal males examined, four subjects naive to the task showed activations in contralateral primary and supplementary motor areas and the ipsilateral superior anterior part of the cerebellar hemisphere. Also, the bilateral premotor areas and the contralateral ventrolateral nucleus of thalamus were occasionally activated. No changes were observed in the putamen and globus pallidus. The subject accustomed to the task showed activation in the narrow areas of the contralateral primary motor and supplementary motor and premotor areas but not in the cerebellum. These results suggest that fMRI has nearly the same degree of detectability to that of positron emission tomography (PET) in regard to motor functions.     

Neurotoxicodynamics of the Interaction between Ciprofloxacin and Foscarnet in Mice

The potential for convulsions induced by the coadministration of ciprofloxacin (CPFX) and foscarnet (PFA) may be due not to a change in the distribution of CPFX to the brain but to a potential CPFX-induced inhibition of γ-aminobutyric acid (GABA)-GABA_A receptor binding in the presence of PFA.     

Effects of 1‐O‐hexyl‐2,3,5‐trimethylhydroquinone on carbon tetrachloride‐induced hepatic cirrhosis in rats

Aim: The present study was undertaken to evaluate the effects of 1‐O‐hexyl‐2,3,5‐trimethylhydroquinone (HTHQ), a synthesized vitamin E derivative, on carbon tetrachloride (CCl₄)‐induced cirrhosis. Methods: Rats were treated with hypodermic injections of CCl₄ twice a week to induce the hepatic cirrhosis, and given drinking water containing HTHQ or solvent. Primary cultures of rat hepatocytes were performed to evaluate the effects of HTHQ on the expression of inducible nitric oxide synthase (iNOS). Results: Masson's staining of rat livers showed fibrosis around pseudo‐lobules in the CCl₄ group, the lesions being reduced in the CCl₄ HTHQ group. Increases in liver tissue hydroxyproline and α₁(I) collagen, α‐smooth muscle actin and iNOS induced by CCl₄, were also markedly diminished by HTHQ. Furthermore, both HTHQ and vitamin E attenuated interleukin‐1β‐induced iNOS protein expression in cultured hepatocytes, the potency of HTHQ being 10‐times higher than that of vitamin E. Conclusion: HTHQ may inhibit development of hepatic cirrhosis in rats, more potently than vitamin E, by inhibiting the iNOS expression in hepatocytes. Because vitamin E has a radical scavenging action, roles of NO and peroxynitrite will be discussed in the effects of HTHQ on the fibrosis.     

Laboratory Surveillance for Prospective Plasmid-Mediated AmpC β-Lactamases in the Kinki Region of Japan

Extended-spectrum β-lactamases, plasmid-mediated AmpC β-lactamases (PABLs), and plasmid-mediated metallo-β-lactamases confer resistance to many β-lactams. In Japan, although several reports exist on the prevalence of extended-spectrum β-lactamases and metallo-β-lactamases, the prevalence and characteristics of PABLs remain unknown. To investigate the production of PABLs, a total of 22,869 strains of 4 enterobacterial species, Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, and Proteus mirabilis, were collected during six 6-month periods from 17 clinical laboratories in the Kinki region of Japan. PABLs were detected in 29 (0.13%) of 22,869 isolates by the 3-dimensional test, PCR analysis, and DNA sequencing analysis. PABL-positive isolates were detected among isolates from 13 laboratories. Seventeen of 13,995 (0.12%) E. coli isolates, 8 of 5,970 (0.13%) K. pneumoniae isolates, 3 of 1,722 (0.17%) K. oxytoca isolates, and 1 of 1,182 (0.08%) P. mirabilis isolates were positive for PABLs. Of these 29 PABL-positive strains, 20 (69.0%), 6 (20.7%), 2 (6.9%), and 1 (3.4%) carried the genes for CMY-2, DHA-1, CMY-8, and MOX-1 PABLs, respectively. Pattern analysis of randomly amplified polymorphic DNA and pulsed-field gel electrophoretic analysis revealed that the prevalence of CMY-2-producing E. coli strains was not due to epidemic strains and that 3 DHA-1-producing K. pneumoniae strains were identical, suggesting their clonal relatedness. In conclusion, the DHA-1 PABLs were predominantly present in K. pneumoniae strains, but CMY-2 PABLs were predominantly present in E. coli strains. The present findings will provide significant information to assist in preventing the emergence and further spread of PABL-producing bacteria.β-Lactamase production is the most important factor for β-lactam resistance in Gram-negative rods (16). Plasmid-mediated β-lactamases, such as extended-spectrum β-lactamases (ESBLs), plasmid-mediated AmpC β-lactamases (PABLs), and plasmid-mediated metallo-β-lactamases (MBLs), hydrolyze broad-spectrum β-lactams. Detection of these plasmid-mediated β-lactamase-producing isolates is important for epidemiological studies and hospital infection control, because plasmid-mediated genes can spread to other organisms.The Study of Bacterial Resistance in the Kinki Region of Japan (SBRK) Antimicrobial Surveillance Program was established in 1997 to monitor the predominant pathogens and antimicrobial resistance patterns of nosocomial and community-acquired infections via a broad network of clinical laboratories differing in geographic location and size. Our previously reported survey data from the Kinki region of Japan revealed the prevalence of ESBLs and plasmid-mediated MBLs (21, 30); however, the epidemiology of PABLs remains unknown. For this reason, a laboratory-based surveillance study was conducted to determine the presence and prevalence of PABLs among members of the family Enterobacteriaceae.PABL CMY-1 was first found in a Klebsiella pneumoniae isolate in South Korea in 1989 (4, 5). Since then, additional organisms producing PABLs have been reported worldwide (25). PABLs are a heterogeneous group of enzymes that originated from the chromosomal genes of Enterobacter spp. (ACT-1/MIR-1 type), Citrobacter freundii (CMY/LAT type), Morganella morganii (DHA type), Hafnia alvei (ACC-1), and Aeromonas spp. (CMY/MOX type and FOX type). The most prevalent and most widely distributed PABLs are the CMY/LAT-type enzymes (25). In addition to these enzyme types, DHA-type enzymes have been identified in Taiwan (31) and China (15). In Korea (14, 26), DHA-, CMY/MOX-, and ACT-1/MIR-1-type enzymes have also been identified, while in the United States (1, 17), in addition to the types mentioned above, DHA-, ACT-1/MIR-1-, and FOX-type enzymes have been identified. To date, in Japan, MOX-1 (11), CMY-9 (9, 28), CMY-19 (28), CFE-1 (19), CMY-2 (18), and DHA-1 (18) have been found in clinical isolates. Muratani et al. (18) reported PABL producers among cephem-resistant K. pneumoniae isolates, but this report did not indicate the rate of occurrence of PABLs.For the present study, we collected 22,869 isolates from 17 clinical laboratories in the Kinki region of Japan, and we assessed the prevalence and types of PABL-positive bacteria.     

MBSJ MCC Young Scientist Award 2009REVIEW: Selective autophagy regulates various cellular functions

Autophagy is a self‐eating system conserved among eukaryotes, in which cellular components including organelles are entrapped into a double membrane structure called the autophagosome and then degraded by lysosomal hydrolases. In addition to its role in supplying amino acids in response to nutrient starvation, autophagy is involved in quality control to maintain cell health. Thus, inactivation of autophagy causes the formation of cytoplasmic protein inclusions, which comprise misfolded proteins and the accumulation of many degenerated organelles, resulting in liver injury, diabetes, myopathy and neurodegeneration. Furthermore, although autophagy has been considered nonselective, increasing evidence points to the selectivity of autophagy in sorting vacuolar enzymes and removal of aggregate‐prone proteins and unwanted organelles. Such selectivity allows diverse cellular regulation, similar to the ubiquitin proteasome pathway. In this review, we discuss the physiological roles of selective autophagy and their molecular mechanisms.