摘要:

Some project‐oriented biosciences have been promoted cooperatively by three governmental agencies in Japan: the Ministry of Education, Science and Culture, the Ministry of Health and Welfare, and the Science and Technology Agency. All three agencies have increased their budgetary requests for human genome analyses for FY 1991. The Panel on Life Sciences (chaired by Dr. W. Mori, former president of the University of Tokyo) of the Science and Technology Council of Japan which is chaired by the Prime Minister has decided to organize a working group to suggest how best to coordinate efforts in human genome analyses in Japan. The genome project was initially promoted by the Science and Technology Agency through a program for the design and construction of automated machines for DNA sequencing. Work is ongoing at the Institute of Physical and Chemical Research to integrate, by system engineering, instruments that can separate DNA fragments, perform plaque selection, carry out dideoxy reaction, and read the resulting DNA sequence. However, scientists now realize the enormity of the tasks of compiling DNA sequence data and of mapping the genes and fragments obtained, and efforts are being made to solve these problems. Academic societies have organized symposia to promote general interest in this subject. The most important way for Japan to contribute to research on human genome analyses, however, may be in the evaluation of supporting mechanisms (technical assistance and research resources) and in the recognition and preparation of the transition of biology to a big science approach.—Ikawa, Y. Human genome efforts in Japan.FASEB J.5: 66–69; 1991.

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991587

出版商:Wiley    

年代:1991

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991588

出版商:Wiley    

年代:1991

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991589

出版商:Wiley    

年代:1991

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991590

出版商:Wiley    

年代:1991

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991591

出版商:Wiley    

年代:1991

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991592

出版商:Wiley    

年代:1991

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991593

出版商:Wiley    

年代:1991

数据来源: WILEY

摘要:

Cytotoxic T lymphocytes (CTL) and natural killer (NK) cells are cytolytic lymphocytes known to produce a pore‐forming protein, named perforin or cytolysin, that lyses target cells by creating large pores on the target plasma membrane. Besides perforin, the granules of CTL and NK cells contain a family of serine esterases. Perforin has also been localized in granulated metrial gland (GMG) cells of the murine embryo implantation site by light microscopic immunostaining. Ultrastructural immunogold labeling with antibodies against perforin and a serine esterase (MTSP 1 or granzyme A) shows that GMG cells contain both perforin and serine esterases in the fine granular matrix of their granules. Perforin has been located in all of the granules, whereas gold particles corresponding to serine esterases have been found in most of the granules. Results from the double immunogold technique indicate that perforin and serine esterases colocalize to most of the same granules in GMG cells. This study supports the view that GMG cells are related to cytolytic lymphocytes.—Zheng, L. M.; Ojcius, D. M.; Liu, C.‐C., Kramer, M. D.; Simon, M. M.; Parr, M. L.; Young, J. D.‐E. Immunogold labeling of perforin and serine esterases in granulated metrial gland cells.FASEB J.5: 79–85; 1991.

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991594

出版商:Wiley    

年代:1991

数据来源: WILEY

摘要:

We recently demonstrated a rapid up‐regulation of serum retinol‐retinol binding protein‐transthyretin concentration in rats with short‐term acute renal failure. We examine the effect of retinoic acid and apo‐retinol binding protein (apo‐RBP) on the up‐regulation of serum retinol in renal failure. Injection of retinoic acid (10 μg) into rats with acute renal failure or sham‐operated rats increased circulatory retinoic acid concentration 29‐fold within 2 h but did not influence serum retinol concentration in either group. Injection of a large dose of retinoic acid (100 μg) decreased serum retinol concentration in rats with acute renal failure (19%) and sham‐operated rats (29%). These results suggest that changes in serum retinoic acid concentration within the near‐physiological range have no effect on regulation of hepatic retinol release. Injection of a large dose of retinoic acid may depress serum retinol indirectly via a retinol sparing effect in target tissues. In rats with renal failure the serum retinol concentration, elevated 44–52% above that of sham‐operated controls, was also increased to 70–164% above controls by the injection of 52–63 μg of apo‐RBP. This suggests that circulatory apo‐RBP can upregulate serum retinol. Circulatory apo‐RBP may be a positive physiological feedback signal from peripheral tissues for hepatic release of retinol.—Gerlach, T. H.; Zile, M. H. Effect of retinoic acid and apo‐RBP on serum retinol concentration in acute renal failure.FASEB J.5: 86–92; 1991.

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1991596

出版商:Wiley    

年代:1991

数据来源: WILEY

摘要:

Benzodiazepine discontinuation can lead to a behavioral syndrome in animals and humans. In a mouse model, this syndrome is associated with benzodiazepine receptor up‐regulation. The protein‐modifying reagent, N‐ethoxycarbonyl‐2‐ethoxy‐1,2‐dihydroquinoline (EEDQ), has been used to irreversibly inactivate a number of neurotransmitter receptors including benzodiazepine receptors, and thus allows estimation of receptor recovery in vivo. To assess benzodiazepine receptor recovery after benzodiazepine discontinuation, we treated mice with lorazepam (LRZ), 2 mg·kg–1·day–1for 1 wk. After 24 h, EEDQ (12.5 mg/kg) was administered, and benzodiazepine binding in the cortex and cerebellum was determined after 4–144 h. EEDQ treatment decreased receptor density in the cortex in both LRZ‐ and vehicle‐treated groups by approximately 50%, with no change in apparent affinity as previously reported. Binding in both groups returned to control values after 96 h. Kinetic analysis indicated a more rapid increase in binding in LRZ‐compared with vehicle‐treated animals, witht1/2for LRZ 19.1 h, and for vehicle, 30.8 h (P<0.05). Receptor density was decreased in the cerebellum after EEDQ by approximately 40% in both treatment groups, with no change in apparent affinity. Receptor density returned to control values at 96 h, with no difference in kinetics in LRZ‐ compared with vehicle‐treated mice. The decrease in receptort1/2associated with lorazepam discontinuation is consistent with the observed increase in benzodiazepine receptors in this setting.—Miller, L. G.; Lumpkin, M.; Greenblatt, D. J.; Shader, R. I. Accelerated benzodiazepine receptor recovery after lorazepam discontinuation.FASEB J.5: 93–97; 1991.

ISSN:0892-6638    

DOI:10.1096/fasebj.5.1.1846834

出版商:Wiley    

年代:1991

数据来源: WILEY