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Jin Wei Mia Madel Alfajaro Peter C. DeWeirdt Ruth E. Hanna William J. Lu-Culligan Wesley L. Cai Madison S. Strine Shang-Min Zhang Vincent R. Graziano Cameron O. Schmitz Jennifer S. Chen Madeleine C. Mankowski Renata B. Filler Neal G. Ravindra Victor Gasque Fernando J. de Miguel Ajinkya Patil Huacui Chen Craig B. Wilen 《Cell》2021,184(1):76-91.e13
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T Faraggiana D Villari J Jagirdar J Patil 《The journal of histochemistry and cytochemistry》1986,34(6):811-816
Lung alveoli are coated by a thin layer of extracellular material rich in anionic charges. The nature of this acid layer and its relationship to the phospholipid surfactant are not known. We investigated the possible presence of sialic acid groups by light and electron microscopy in tissues from normal fetal and adult lungs, using neuraminidase treatment followed by staining with the galactose-binding lectin from peanut, labeled with peroxidase. Our results showed that adult lung does not bear peanut lectin-reactive sites but that a very thin and distinct reactive layer becomes evident after neuraminidase treatment, especially on type II pneumocytes. In fetal lung, the entire surface of the developing respiratory tree is outlined by a strongly peanut lectin-reactive layer even if neuraminidase digestion is not performed. We conclude that the acid coat of the alveolar lining is in part composed of sialic acid residues and that sialic acid is added to the fetal lung as the alveoli mature. 相似文献
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Sheila Polakoff 《BMJ (Clinical research ed.)》1987,294(6578):1031-1032
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Isolation and expression of an anther-specific gene from tomato 总被引:31,自引:0,他引:31
David Twell Rod Wing Judy Yamaguchi Sheila McCormick 《Molecular & general genetics : MGG》1989,217(2-3):240-245
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Robert M. Levin Penelope A. Longhurst Sheila S. Levin Niels Haugaard Alan J. Wein 《Molecular and cellular biochemistry》1990,97(2):153-159
The urinary bladder depends on intracellular ATP for the support of a number of essential intracellular processes including contraction. The concentration of ATP is maintained constant primarily via the rapid transfer of a phosphate from creatine phosphate (CP) to ADP catalyzed by the enzyme creatine kinase (CK). Since muscular pathologies associated with diabetes are in part related to intracellular alterations in metabolism, we have characterized the CK activity in both skeletal muscle and urinary bladder from control and streptozotocin-diabetic rats.The following is a summary of the results: 1) Bladder tissue from control rats showed linear kinetics with a Vmax = 390 nmoles/mg protein/min, and a Km = 275 µM. 2) Urinary bladder tissue isolated from diabetic rats displayed biphasic kinetics with Vmax = 65 and 324 nmoles/mg protein/min, and Km's = 10 µM and 190 µM respectively. 3) Skeletal muscle isolated from control rats showed linear kinetics with an approximate Vmax of 800 nmoles/mg protein/min and a Km of 280 µM CP. 4) Homogenates of skeletal muscle from diabetic rats showed complex kinetics not separable into distict component forms. 5) The Km for ADP for both skeletal muscle and bladder was approximately 10 µM.These studies demonstrate that whereas bladders isolated from both control and diabetic rats possess a low-affinity isomer(s) of CK with similar maximum enzymatic activity, there is a high affinity isomer present within the urinary bladder muscle of diabetic rats that is not present in bladder tissue isolated from control rats. Skeletal muscle isolated from both diabetic and control rats exhibited a maximal activity 2 to 3 times higher than that of the bladder. 相似文献
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A child with normal growth and development and the abnormal karyotype 46,XY,17ps, was analyzed using molecular probes localized to 17p13. The results indicated the presence of two copies of the probes YNZ22.1 (D17S5) and YNH37.3 (D17S28), previously shown to be deleted in all Miller-Dieker (MDS) patients studied. However, the patient was hemizygous for probe p144D6 (D17S34), which is absent in approximately 75% of the MDS patients. As the patient is active at 9 months of age, with no clinical signs of MDS, the results confirm that the absence of locus D17S34 does not lead to the phenotypic expression of MDS. Furthermore, this deletion should assist in defining the distal limits of this contiguous gene syndrome. 相似文献