Prevalence of Toxocara canis, Toxascaris leonina and Dirofilaria immitis in dogs in Chuncheon, Korea (2004)

The intestines and hearts of dogs were examined for Toxocara canis, Toxascaris leonina, and Dirofilaria immitis, after necropsy between June 26 and September 29, 2004 in Chuncheon, Korea. Of the 662 dogs examined, 6 were infected with T. canis (0.9%), 86 with T. leonina (13.0%). Fifty dogs were infected with D. immitis among 500 dogs examined (10.0%). Five were co-infected with T. canis and T. leonina, and three were co-infected with T. leonina and D. immitis. The cumulative positive infection rate for three species was 134/662 (20.2%). Considering previously reported seropositive rates of T. canis excretory-secretory antigen, i.e., 5% in the adult population in Korea, the possibility of toxocariasis caused by T. leonina should be reevaluated.     

Effect of processing time on enteric bacteria survival and on temperature and chemical composition of broiler poultry litter processed by two methods

This study was conducted to evaluate the effects of deepstack processing broiler poultry litter with or without aeration on enteric bacteria survival (Trial 1), and to determine the optimum aeration period (Trial 2) and aeration frequency (Trial 3) to control excessive heating of litter during the deepstacking process. The effects of deepstacked litter temperature on bacteria survival and on chemical compositions of the litter were monitored. In Trial 1, E. coli, Salmonella enteriticis and Shigella sonnei were intentionally inoculated into the litter and their survival was monitored with time of litter processing. In Trial 2, litter was deepstacked and aerated once a day from the initial day or from the day when maximum stack temperature was reached and started to decrease to the end of processing period. In Trial 3, litter was deepstacked and aerated once or twice a day from the day after maximum stack temperature was attained until constant temperature was attained. During the deepstacking process of litter pathogenic bacteria were eliminated between the 2nd and 4th day of deepstacking. This phenomenon occurred apparently not only by high heat generated, but also by other potential factors, such as ammonia and microbial competition. Aeration resulted in the heat dissipation and early temperature reduction of deepstacked litter. The optimum aeration procedure to avoid excessive heating of deepstacked litter was to aerate once a day after the stack temperature reached its maximum at the early stage of deepstacking and for 3 days or until the stack temperature dropped off and reached constancy. This aerating frequency and duration did not negatively affect the chemical composition of deepstacked litter. These results suggest that poultry litter properly deepstacked, with or without aeration, to ensure the elimination of enteric bacterial pathogens may be fed at least 10 days earlier than the 21-day deepstacking period previously recommended.     

Kinetics of the extraction of succinic acid with tri-n-octylamine in 1-octanol solution

Kinetic studies for the extraction of succinic acid from aqueous solution with 1-octanol solutions of tri-n-octylamine (TOA) were carried out using a stirred cell with a microporous hydrophobic membrane. The interfacial concentrations of species were correlated and thus the intrinsic kinetics was obtained. The overall extraction process was controlled by the chemical reaction at or near the interface between the aqueous and organic phases. The formation reaction of succinic acid-TOA complex was found to be first order with respect to the concentration of succinic acid in the aqueous phase and the order of 0.5 with respect to that of TOA in the organic phase with a rate constant of (3.14 +/- 0.6) x 10(-8) m(2.5) x mol(-0.5) x s(-1). The dissociation reaction of succinic acid-TOA complex was found to be the second-order with respect to that of succinic acid-TOA complex in the organic phase and the order of -2 with respect to that of TOA in the organic phase with a rate constant of (1.44 +/- 1.4) x 10(-4) mol x m(-2) x s(-1).     

Junctional membrane inositol 1,4,5-trisphosphate receptor complex coordinates sensitization of the silent EGF-induced Ca2+ signaling

Ca(2+) is a highly versatile intracellular signal that regulates many different cellular processes, and cells have developed mechanisms to have exquisite control over Ca(2+) signaling. Epidermal growth factor (EGF), which fails to mobilize intracellular Ca(2+) when administrated alone, becomes capable of evoking [Ca(2+)](i) increase and exocytosis after bradykinin (BK) stimulation in chromaffin cells. Here, we provide evidence that this sensitization process is coordinated by a macromolecular signaling complex comprised of inositol 1,4,5-trisphosphate receptor type I (IP(3)R1), cAMP-dependent protein kinase (PKA), EGF receptor (EGFR), and an A-kinase anchoring protein, yotiao. The IP(3)R complex functions as a focal point to promote Ca(2+) release in two ways: (1) it facilitates PKA-dependent phosphorylation of IP(3)R1 in response to BK-induced elevation of cAMP, and (2) it couples the plasmalemmal EGFR with IP(3)R1 at the Ca(2+) store located juxtaposed to the plasma membrane. Our study illustrates how the junctional membrane IP(3)R complex connects different signaling pathways to define the fidelity and specificity of Ca(2+) signaling.     

Subcellular distribution of chromogranins A and B in bovine adrenal chromaffin cells

The major secretory granule proteins chromogranins A (CGA) and B (CGB) have recently been shown to play critical roles in inositol 1,4,5-trisphosphate-dependent intracellular Ca(2+) mobilizations. We determined here the subcellular distribution of CGA and CGB based on 3D-images of chromaffin cells, and found that approximately 95% of cellular CGA was present in secretory granules while approximately 5% was in the endoplasmic reticulum (ER), whereas approximately 57% of cellular CGB was in secretory granules while approximately 24% and approximately 19% were in the ER and nucleus, respectively. These results suggest that chromogranins are at the center of intracellular Ca(2+) homeostasis in secretory cells.     

Cytosolic NADP+-dependent isocitrate dehydrogenase plays a key role in lipid metabolism

NADPH is an essential cofactor for many enzymatic reactions including glutathione metabolism and fat and cholesterol biosynthesis. We have reported recently an important role for mitochondrial NADP(+)-dependent isocitrate dehydrogenase in cellular defense against oxidative damage by providing NADPH needed for the regeneration of reduced glutathione. However, the role of cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) is still unclear. We report here for the first time that IDPc plays a critical role in fat and cholesterol biosynthesis. During differentiation of 3T3-L1 adipocytes, both IDPc enzyme activity and its protein content were increased in parallel in a time-dependent manner. Increased expression of IDPc by stable transfection of IDPc cDNA positively correlated with adipogenesis of 3T3-L1 cells, whereas decreased IDPc expression by an antisense IDPc vector retarded adipogenesis. Furthermore, transgenic mice with overexpressed IDPc exhibited fatty liver, hyperlipidemia, and obesity. In the epididymal fat pads of the transgenic mice, the expressions of adipocyte-specific genes including peroxisome proliferator-activated receptor gamma were markedly elevated. The hepatic and epididymal fat pad contents of acetyl-CoA and malonyl-CoA in the transgenic mice were significantly lower, whereas the total triglyceride and cholesterol contents were markedly higher in the liver and serum of transgenic mice compared with those measured in wild type mice, suggesting that the consumption rate of those lipogenic precursors needed for fat biosynthesis must be increased by elevated IDPc activity. Taken together, our findings strongly indicate that IDPc would be a major NADPH producer required for fat and cholesterol synthesis.     

Rb is required for progression through myogenic differentiation but not maintenance of terminal differentiation

To investigate the requirement for pRb in myogenic differentiation, a floxed Rb allele was deleted either in proliferating myoblasts or after differentiation. Myf5-Cre mice, lacking pRb in myoblasts, died immediately at birth and exhibited high numbers of apoptotic nuclei and an almost complete absence of myofibers. In contrast, MCK-Cre mice, lacking pRb in differentiated fibers, were viable and exhibited a normal muscle phenotype and ability to regenerate. Induction of differentiation of Rb-deficient primary myoblasts resulted in high rates of apoptosis and a total inability to form multinucleated myotubes. Upon induction of differentiation, Rb-deficient myoblasts up-regulated myogenin, an immediate early marker of differentiation, but failed to down-regulate Pax7 and exhibited growth in low serum conditions. Primary myoblasts in which Rb was deleted after expression of differentiated MCK-Cre formed normal multinucleated myotubes that did not enter S-phase in response to serum stimulation. Therefore, Rb plays a crucial role in the switch from proliferation to differentiation rather than maintenance of the terminally differentiated state.