ISSN:0884-0431    

DOI:10.1002/jbmr.5650010102

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010103

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractA method for the long‐term culture of rabbit newborn bone marrow has been developed. It is characterized by the rapid appearance of an adherent, adipocyte‐containing stromal layer, proliferation of mature myeloid cells, and the formation of numerous, large multinucleate giant cells. By the combined use of morphological, immunological, and functional criteria these giant cells have been characterized as macrophage polykaryons and not osteoclastic giant cells. We conclude that long‐term bone marrow culture in the rabbit favors the proliferation, maturation, and fusion of macrophage, but not osteoclast, precursors — new experimental models will have to be developed to enable the developmental biology of osteoclasts to be studied in the

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010104

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractDespite the fact that the scanning electron microscope (SEM) offers a number of unique advantages for the investigation of bone structure, this instrument has seldom been applied in studies of the iliac crest bone biopsy. Here we describe a very simple method of preparing iliac crest biopsies for examination in the SEM after the routine histomorphometric analysis has been performed. With observations on biopsies from normal subjects and patients with osteoporosis, the paper illustrates the potential of the method for performing correlative light and scanning electron microscopical studies and for gaining new information on the three‐dimensional architecture of trabecular bon

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010105

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractWe investigated the stimulation of creatine kinase (CK) and ornithine decarboxylase (ODC) by 1,25‐dihydroxyvitamin D3[1,25(OH)2D3] and 24R,25‐dihydroxyvitamin D3[24R,25(OH)2D3] in doses ranging from 1.625 to 6500 pmol in 4‐week‐old vitamin D‐deficient chicks. Enzyme activities were monitored for 72 h. 1,25(OH)2D3but not 24R,25(OH)2D3enhanced the activity of ODC in duodenum and bone. The time course of ODC activity in bone was biphasic, with an increase after 1 h and a higher peak after 24 h. Diaphyses and epiphyses responded equally well after a dose of 6500 pmol. The kidney, liver, and lung showed 1.5–3.8‐fold increase in CK activity following 1,25(OH)2D3, reaching a maximum between 3–5 h. However, sustained stimulation of CK activity could still be demonstrated after 72 h, and the 48‐h levels in the lung even exceeded the 5‐h values. No change of activity of either enzyme was noted in heart and brain after application of 1,25(OH)2D3. There was no coincidence of stimulation of ODC and CK by 1,25(OH)2D3in the same tissue, and the dose‐responsiveness of both enzymes differed considerably. Near maximum activities of ODC were achieved with 19.5 pmol 1,25(OH)2D3in duodenum and pancreas, while maximum responses of CK occurred in the liver at 195 pmol and in lung and kidney at 6500 pmol. 24R,25(OH)2D3failed to produce any consistent effects of either enzyme in all tissues examined. These results, particularly the lack of response to 24R,25(OH)2D3, are different from t

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010106

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractRenal adaptation to low dietary phosphorus (P) can occur within 4 h. To characterize events preceding adaptation, rats were gavaged with 0.6% P (+P) or 0.03% P (‐P) diet and killed 1, 2, or 4 h later. Brush border membrane vesicles were prepared and Na‐dependent phosphate (Pi), glucose, and 1‐proline transport were measured. In intact rats, 1 h after gavage, serum P in +P was 8.0 ± 0.5 and in ‐P, 6.1 ± 0.4 mg/dl, p<0.01. One and 2 h after gavage, Pi uptake was similar between groups; at 4 h, 0.25 min Pi uptake was increased by 59.3% ± 14.8 in ‐P, p<0.02, n = 11. In thyroparathyroidectomized rats, Pi uptake increased in ‐P by 40.1% ± 7.4 compared to +P at 2.5 h after gavage, and by 51.3 ± 9.3 at 4 h, p<0.025, n = 11. When actinomycin D or cycloheximide were administered both 16 h prior to and at gavage, 0.25 min Pi uptake 4 h after gavage was 59.1% ± 14 and 60.6% ± 19 higher in ‐P than +P, respectively, p<0.025. The adaptation was detected only when measured with an inward‐directed Na‐gradient. Na‐dependent glucose and proline uptakes were not changed by ‐P diet.These studies demonstrate that early renal adaptation to low dietary P is preceded by a fall in serum P, is independent of parathyroid hormone, and does not require protein synthesis. Early adaptation may represent an increased rate of carrier movement or a change in availability of already synthesized carrier. The signal for adaptation may be the decrease in serum P, or

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010107

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractThe effects of the cytosol activator protein obtained from rat reticulocytes (RCAP) were investigated in a heterologous membrane system — partially purified cell membranes from dog renal cortex. RCAP enhanced the response of dog renal cortical adenylate cyclase to bovine parathyroid hormone (1–34) [bPTH (1–34)] from two‐ to three‐fold. RCAP also enhanced the response to 5 μMarginine vasopressin, 10 μMglucagon, and 10 μMisoproterenol. Analysis of double‐reciprocal plots of substrate concentration and enzyme activity indicated that bPTH (1–34) alone and together with RCAP increased the Vmaxof the adenylate cyclase enzyme and did not alter the apparent Kmof the enzyme for MgATP. Membranes from dog renal cortex contain 42K and 39K proteins that are ADP‐ribosylated by cholera toxin and pertussis toxin, respectively, and appear to be the stimulatory (Ns) and inhibitory (Ni) guanine nucleotide binding proteins described in many other hormone‐responsive membrane preparations. Similar to its effects in rat reticulocytes, RCAP inhibited ADP‐ribosylation of Nsand enhanced ADP‐ribosylation of Ni. The muscarinic agonist, carbachol, inhibited PTH‐responsive adenylate cyclase activity in dog renal cortical membranes and this inhibition was reversed by RCAP. These results indicate that RCAP enhances stimulation of adenylate cyclase by a variety of hormones in a heterologous membrane preparation and supports the hypothesis that RCAP's site of action is common to all adenylate cyclase systems. RCAP may facilitate coupling between Nsand the catalytic unit of adenylate cyclase by a pertussis toxin‐like effect to inactivate Ni. The dual effects of RCAP upon ADP‐ribosylation of Niand Nsα subunits suggest that a binding site for RCAP may exist at a site

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010108

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

摘要:

AbstractBinding of calcitonin (CT) and calcitonin gene‐related peptide (CGRP) to rat hemicalvariae and renal membranes was examined in an effort to determine whether CT and CGRP interact with the same bone cell binding site, and to see whether the binding pattern was similar for bone and renal cortex. Specific binding of125I‐salmon CT to rat calvariae was inhibited by unlabeled salmon, porcine, or human CT, but not by rat CGRP. Binding of125I‐rat CGRP to calvariae was inhibited by CGRP and high doses of salmon CT, but not by human or porcine CT. Binding of125I‐salmon CT to renal membranes was inhibited by unlabeled salmon CT or rat CGRP, but no specific binding of125I‐rat CGRP could be detected. The results suggest that separate bone cell receptors for CT and CGRP exist and that CGRP can interact with renal recepto

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010109

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010110

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY

ISSN:0884-0431    

DOI:10.1002/jbmr.5650010101

出版商:John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR)    

年代:1986

数据来源: WILEY