Comparison of bacterial strains and antibiotic susceptibilities in urinary isolates of spinal cord injury patients from the community and hospital.

STUDY DESIGN: A one-year epidemiological survey. OBJECTIVE: To compare bacterial strains and antimicrobial susceptibilities of urinary isolates from hospital and community spinal cord injury (SCI) patients. SETTING: A specialized SCI unit in a freestanding rehabilitation hospital. METHODS: From June 2012 through May 2013, urine cultures were obtained from all of the newly admitted patients. Bacterial strains and antimicrobial susceptibilities were compared between patients from community and hospital settings. RESULTS: The proportion of Enterobacteriaceae in the total urinary isolates from hospital-dwelling patients was smaller than that from community-dwelling patients (66.0 vs. 85.5%, P<0.001), while the proportions of Pseudomonas, Acinetobacter and Enterococcus species were relatively larger (8.7%, 6.0% and 12.0% vs. 2.8%, 0.7% and 2.8%, respectively, P<0.05). The isolates from hospital-dwelling patients showed lower susceptibility to ampicillin, amoxicillin-clavulanic acid, trimethoprim-sulfamethoxazole and all generations of cephalosporin (P<0.05), and a higher prevalence of extended-spectrum beta-lactamase (ESBL)-producers (41.7 vs. 5.4%, P<0.001), compared with those from community-dwelling patients. The susceptibility rates to levofloxacin were lower than 50% in both community and hospital-dwelling patients. CONCLUSION: Broader-spectrum antibiotics should be considered in treating nosocomial urinary tract infection (UTI) of SCI patients because of the relatively wide variety of organisms and higher frequency of antibiotic-resistant strains, including ESBL-producing Enterobacteriaceae in hospital-derived specimens. Furthermore, in areas with high prevalence of fluoroquinolone resistance, fluoroquinolones should be used with caution during empirical treatment for UTI in SCI patients.

Rac and p38 kinase mediate 5-lipoxygenase translocation and cell death.

5-Lipoxygenase (5-LO) is a key enzyme involved in the synthesis of leukotrienes from arachidonic acid, and its activation is usually followed by translocation to the nuclear envelope. The details of mechanisms involved in the translocation of 5-LO are not well understood, though Ca(2+) is known to be essential. Here we show that ionomycin, a Ca(2+) ionophore, induces 5-LO translocation and necrotic cell death in Rat-2 fibroblasts, suggesting a potential relationship between activation of 5-LO and cell death. These effects were markedly attenuated in Rat2-Rac(N17) cells expressing a dominant negative Rac1 mutant. Pretreatment with SB203580, a specific inhibitor of p38 MAP kinase, or EGTA, a Ca(2+) chelator, likewise diminished ionomycin-induced 5-LO translocation and cell death, but PD98059, a MEK inhibitor, did not. Thus, Rac and p38 MAP kinase appear to be components in a Ca(2+)-dependent pathway leading to 5-LO translocation and necrotic cell death in Rat-2 fibroblasts.

Acute gastroparesis in Duchenne's muscular dystrophy.

Duchenne's muscular dystrophy (DMD) is an X-linked recessive disease. Clinical descriptions of the disorder focus principally on skeletal muscle degeneration. Another manifestation, which involves the gastrointestinal tract, may be fatal. But its prevalence remains undefined. We report here a case of acute gastroparesis associated with Duchenne's muscular dystrophy. In our case, the patient's symptoms were improved by prokinetic agents and timely decompression in life-threatening acute gastric dilatation.

Localized form of bronchioloalveolar carcinoma: FDG PET findings.

OBJECTIVE: The aim of our study was to describe 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) findings of a localized form of bronchioloalveolar carcinoma and to compare those findings with other cell types of lung cancer. SUBJECTS AND METHODS: FDG PET was performed in 48 patients with lung cancer. The patients had carcinomas of various cell types: bronchioloalveolar carcinoma (n = 9), squamous cell carcinoma (n = 11), adenocarcinoma (n = 22), and other cell types (n = 6). Using FDG PET, we compared peak standardized uptake values among the various cell types of lung cancer. CT and pathologic findings for patients with bronchioloalveolar carcinoma were also reviewed. RESULTS: Overall, 48 malignant tumors showed a mean peak standardized uptake value of 8.0 +/- 4.1. The mean peak standardized uptake value was 3.5 +/- 2.2 for bronchioloalveolar carcinoma, 10.8 +/- 4.4 for squamous cell carcinoma, and 8.8 +/- 3.2 for adenocarcinoma. The mean peak standardized uptake value for bronchioloalveolar carcinoma was significantly lower than that for adenocarcinoma and squamous cell carcinoma (p < .001). On high-resolution CT scans, bronchioloalveolar carcinomas appeared as areas of ground-glass opacity (n = 4), as nodules (n = 2), as masses (n = 2), and as a ground-glass opacity plus consolidation (n = 1). On pathologic examination, bronchioloalveolar carcinomas were well differentiated, having moderate degrees of nuclear atypism, mild degrees of mitotic figure, desmoplasia, and necrosis. CONCLUSION: The localized form of bronchioloalveolar carcinoma shows significantly lower peak standardized uptake values than do other lung carcinomas. Thus, bronchioloalveolar carcinoma can be a potential cause of false-negative findings of malignancy on FDG PET scans. When bronchioloalveolar carcinoma is suggested, FDG PET results should be interpreted in combination with high-resolution CT findings.

Synthesis of 6-[1-[4-(benzoxazol-2-yl)thiobuthyl]-1,2,3-triazole-4-yl]methylenepenam as beta-lactamase inhibitors.

The 6,6-dibromopenam6 was treated with CH(3)MgBr and carbaldehyde5 to afford the 6-bromo-6-(1-hydroxy-1-methyl)penicillanate7, which was reacted with acetic anhydride to give acetoxy compound8. The deacetobromination of8 with zinc and acetic acid gave 6-exomethylenpenams, Z-isomer9 and E-isomer10, which were oxidized to sulfones11 and12 by m-CPBA. The p-methoxybenzyl compounds were deprotected by AlCl(3) and neutralized to give the sodium salts13, 14, and15.

Numerical simulations of the 1960 Chilean tsunami propagation and inundation at Hilo, Hawaii

An explicit staggered leap-frog finite difference models is used to simulate the transoceanic propagation of the 1960 Chilean Tsunami and the associated inundation at Hilo, Hawaii. In computing the transoceanic tsunami propagation, linear shallow water equations with coriolis force are solved. However, spatial grid sizes and time step sizes are chosen in such a way that the numerical dispersion introduced by the leap-frog finite difference scheme is almost the same as the frecuency dispersion in the linear Boussinesq equations. Because the grid size and the time step depend on the local depth, a nested multiple - grid system is developed for the numerical model. In the inundation model, nonlinear shallow water equations including bottom friction are solved. A moving boundary treatment is developed to track the shoreline movement. The maximun inundation area at Hilo Bay, Hawaii is generated and compared with the observed record. Good agreement is observed (AU)

Carnitine-acylcarnitine translocase in ischemia: evidence for sulfhydryl modification.

After coronary occlusion and reflow, carbohydrate catabolism is enhanced, whereas fatty acid utilization is delayed. To test the hypothesis that "stunning" of fatty acid use by ischemic heart reflects reduced fatty acid transport into the mitochondria, two activities involved in the transport were examined: carnitine-acylcarnitine translocase and carnitine palmitoyltransferase II (CPT II). The maximal velocity for carnitine exchange of the translocase is reduced 55% in mitochondria isolated from ischemic canine heart (60-min left circumflex occlusion). Mitochondria from ischemic heart show 50% depletion in total matrix glutathione, a 200% increase in glutathione disulfide (GSSG), and an 80% decrease in the ratio of reduced glutathione (GSH) to GSSG, suggesting that the loss of translocase activity may be a consequence of protein sulfhydryl modifications. In support of this, treatment of these mitochondria with the sulfhydryl-reducing agents, GSH or dithiothreitol, restores carnitine exchange to control. Partial return of mitochondrial GSH and a decrease in GSSG are observed with a 20-min reperfusion of the ischemic myocardium. Continued depression in carnitine exchange with reperfusion suggests that other mechanisms may prevent restoration of activity. Import of palmitoylcarnitine on the translocase is coupled to palmitoyl-CoA production by CPT II. Mitochondria from ischemic heart with decreased coupling activity also have the lowest palmitoylcarnitine-supported respiratory rates, suggesting that in severely ischemic tissue the translocation-transesterification sequence may become rate limiting to fatty acid oxidation.

Protection by verapamil of mitochondrial glutathione equilibrium and phospholipid changes during reperfusion of ischemic canine myocardium.

Pretreatment of the ischemic myocardium with verapamil protects against mitochondrial respiratory depression observed during ischemic arrest as well as during reperfusion. Since ischemic mitochondrial function appears not to be altered further by reperfusion, the purpose of this study is to identify a biochemical event affecting mitochondria that is specifically associated with reperfusion injury. It has been proposed that increased cellular Ca2+ influx and oxygen toxicity may result from reintroduction of coronary flow. Increased cytosolic Ca2+ is transmitted to the mitochondria with subsequent activation of Ca2+-dependent events, including phospholipase A2. Net production of lysophospholipids (and loss of total diacylphospholipids from the mitochondria) will proceed when reacylation mechanisms are inhibited. Since acyl-CoA:lysophospholipid acyltransferase is a sulfhydryl-sensitive enzyme and since increased activity of glutathione peroxidase shifts the levels of the mitochondrial sulfhydryl buffer, glutathione, towards oxidation, levels of glutathione and its oxidation state were measured during reperfusion in the absence or presence of verapamil pretreatment. Ischemia lowers total glutathione and reduces the redox ratio (reduced glutathione: oxidized glutathione) by 85%. Reperfusion partially returns the redox ratio to control by causing oxidized glutathione to disappear from the matrix. Verapamil maintains both the concentration and the redox potential of glutathione at control levels. Concomitant with alterations in reduced glutathione:oxidized glutathione is a decrease in ischemic mitochondrial phospholipid content. During reperfusion, phosphatidylethanolamine and its major constituent fatty acids (C 18:0 and C 20:4) are specifically lost from the mitochondrial membrane. Accompanying the significant loss of arachidonic acid during reperfusion is the decreased content of 11-OH, 12-OH, and 15-OH arachidonate. These lipid peroxidation products are not increased in ischemia. It is proposed that oxidation of matrix glutathione to glutathione disulfide during ischemia results in formation of glutathione-protein mixed disulfides and inhibition of sulfhydryl-sensitive proteins, including acyl-CoA lysophosphatide acyltransferase. Thus, metabolic events occurring within the ischemic period set the stage for prolonged dysfunction during reperfusion.

Protection of canine cardiac mitochondrial function by verapamil-cardioplegia during ischemic arrest.

Hemodynamic and mitochondrial function recover following 60 minutes of ischemic arrest and reperfusion in hearts pretreated with verapamil. The present study was carried out to determine whether verapamil prevents the onset of mitochondrial oxidative impairment after 60 minutes of ischemic arrest without reperfusion. Two preparations of mitochondria isolated following Polytron homogenization and subsequent treatment of the myofibrillar pellet with Nagarse were examined for phosphorylating respiration. The Polytron mitochondria were more sensitive to ischemic arrest than were the Nagarse mitochondria with either glutamate-malate (57% vs. 22% inhibition), succinate (+ rotenone) (41% vs. 14% inhibition), or palmitoylcarnitine (57% vs. 27% inhibition) as respiratory substrates. Verapamil pretreatment significantly increased oxidation of all substrates by the subsequently isolated Polytron mitochondria, but only succinate-supported respiration returned to control levels. In contrast, the small amount of respiratory inhibition exhibited by the Nagarse mitochondria after ischemic arrest was insensitive to verapamil pretreatment. We conclude that the Polytron preparation of mitochondria is more susceptible to ischemia than the Nagarse mitochondria, and this susceptibility correlates with a striking sensitivity to verapamil protection. In general, oxidation of NADH-linked substrates, including palmitoylcarnitine, is more affected by ischemic arrest than succinate, and only oxidation of the latter substrate is totally protected by verapamil. The beneficial action of verapamil on mitochondrial function occurs prior to reperfusion. The data suggest that alterations in calcium homeostasis occur during the ischemic period, as well as in the subsequent reperfusion period.

DNA-induced transformation in Drosophila: genetic analysis of transformed stocks.

The exosome model of transformation in Drosophila melanogaster proposes that DNA fragments enter the cells of treated individuals and become firmly associated with their homologous chromosome segments, but are never integrated into the linear structure of the chromosome. This paper reports results that validate two central predictions of the model: (a) the introduced genetic information usually maps precisely at the site of the target locus, and (b) the original chromosomal information is still present at that site.

DNA-induced transformation in Drosophila: evidence for transmission without integration.

A key feature of the exosome model of transformation in Drosophila melanogaster is that the DNA segments responsible for the phenomenon are not integrated into the linear structure of the chromosomes. This feature is confirmed by the failure to find whole-body transformants in a series of large-scale experiments, and by the absence of evidence for integration under conditions favoring genetic exchange between chromosomes and introduced DNA.

DNA-induced transformation in Drosophila: locus-specificity and the establishment of transformed stocks.

The genetic changes induced in Drosophila melanogaster by DNA obtained from flies differing at specified genetic loci exhibit the general features of transformation, namely locus specificity and heritability. These properties have provided the basis for the establishment of transformed stocks. The phenomenon also exhibits striking special features, prominent among which is the observation that transformed individuals are always mosaics and that whole-body transformants are absent even in established stocks. The exosome model (which proposes that DNA segments enter the cells of treated individuals and become firmly associated with their homologous chromosome segments, but are never integrated into the linear structure of the chromosome) is formulated to fit these observations.