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307 results on '"Hofmann, Wolfgang"'

1. 3.5 Organisationswandel

Author

Müller-Christ, Georg, primary, Czichos, Reiner, additional, Hofmann, Wolfgang, additional, and Neuburger, Rahild, additional

Published
2021
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10. Limnology of the Plußsee

Author

Krambeck, Hans-Jürgen, Albrecht, Dieter, Hickel, Barbara, Hofmann, Wolfgang, Arzbach, Hans-Hermann, Lange, O. L., editor, Mooney, H. A., editor, Remmert, H., editor, Overbeck, Jürgen, editor, and Chróst, Ryszard J., editor

Published
1994
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24. CCR3 and CCR5 are co-receptors for HIV-1 infection of microglia

Author

He, Jianglin, Chen, Youzhi, Farzan, Michael, Choe, Hyeryun, Ohagen, Asa, Gartner, Suzanne, Busciglio, Jorge, Yang, Xiaoyu, Hofmann, Wolfgang, Newman, Walter, Mackay, Charles R., Sodroski, Joseph, and Gabuzda, Dana

Subjects
HIV infection -- Research, Cell receptors -- Research, Central nervous system -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The central nervous system (CNS) can be infected by HIV-1, causing dementia associated with AIDS. A study indicates that microglia, the major target cells for HIV-1 infection in the CNS, express both CCR3 and CCR5. HIV-1 infection of microglia is inhibited by CCR3 ligand, eotaxin, and CCR5 ligand, MIP-1beta. The results show that both CCR3 and CCR5 facilitate efficient infection of the CNS by HIV-1.

Published
1997

50. Increased mitochondrial proton leak in skeletal muscle mitochondria of UCP1-deficient mice

Author

MONEMDJOU, SHADI, HOFMANN, WOLFGANG E., KOZAK, LESLIE P., and HARPER, MARY-ELLEN

Subjects
Physiology -- Research, Striated muscle -- Research, Rats -- Research, Mitochondria -- Research, Biological sciences
Abstract

Monemdjou, Shadi, Wolfgang E. Hofmann, Leslie P. Kozak, and Mary-Ellen Harper. Increased mitochondrial proton leak in skeletal muscle mitochondria of UCP1-deficient mice. Am J Physiol Endocrinol Metab 279: E941-E946, 2000.--Mice having targeted inactivation of uncoupling protein 1 (UCP1) are cold sensitive but not obese (Enerback S, Jacobsson A, Simpson EM, Guerra C, Yamashita H, Harper M-E, and Kozak LP. Nature 387: 90-94, 1997). Recently, we have shown that proton leak in brown adipose tissue (BAT) mitochondria from UCP1-deficient mice is insensitive to guanosine diphosphate (GDP), a well known inhibitor of UCP1 activity (Monemdjou S, Kozak LP, and Harper M-E. Am J Physiol Endocrinol Metab 276: E1073-E1082, 1999). Moreover, despite a fivefold increase of UCP2 mRNA in BAT of UCP1-deficient mice, we found no differences in the overall kinetics of this GDP-insensitive proton leak between UCP1-deficient mice and controls. Based on these findings, which show no adaptive increase in UCP1-independent leak in BAT, we hypothesized that adaptive thermogenesis may be occurring in other tissues of the UCP1-deficient mouse (e.g., skeletal muscle), thus allowing them to maintain their normal resting metabolic rate, feed efficiency, and adiposity. Here, we report on the overall kinetics of the mitochondrial proton leak, respiratory chain, and ATP turnover in skeletal muscle mitochondria from UCP1-deficient and heterozygous control mice. Over a range of mitochondrial protonmotive force ([Delta]p) values, leak-dependent oxygen consumption is higher in UCP1-deficient mice compared with controls. State 4 (maximal leak-dependent) respiration rates are also significantly higher in the mitochondria of mice deficient in UCP1, whereas state 4 [Delta]p is significantly lower. No significant differences in state 3 respiration rates or [Delta]p values were detected between the two groups. Thus the altered kinetics of the mitochondrial proton leak in skeletal muscle of UCP1-deficient mice indicate a thermogenic mechanism favoring the lean phenotype of the UCP1-deficient mouse.

Published
2000

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