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C Limas

Publications and source records attributed to C Limas.

At least 109 records · Page 6Linked to original sources
PubMed1978

Tissue blood-group antigens and prognosis in low stage transitional cell carcinoma of the bladder.

The loss of A, B or H blood-group antigens from the surface of neoplastic epithelial cells has been correlated with aggressive tumor behavior. We examined this phenomenon in low stage transitional cell carcinoma of the bladder. In an analysis of biopsy material from 37 patients the absence of these antigens on the original or recurrent tumors correlated with the subsequent development of invasive disease (stage B or greater), while the presence of antigens correlated with failure to develop invasive disease. Analysis of transitional cell surface antigens may help improve the therapy of bladder cancer.

ABO Blood-Group System↗
PubMed1977

Prostaglandin metabolism in the kidneys of spontaneously hypertensive rats.

Renal prostaglandins have been implicated in the regulation of blood pressure. We have therefore compared prostaglandin metabolism in the kidneys of spontaneously hypertensive rats (SHR's) of the Aoki-Okamoto strain and normotensive Wistar-Kyoto (WKY) controls. The microsomal fraction of the renal medulla contained most of the prostaglandin synthetase activity in both groups; SHR's had significantly higher enzymatic activity than their normotensive controls at age 10 wk and thereafter; furthermore, synthetase activity in SHR's increased with age. Two forms of 15-hydroxyprostaglandin dehydrogenases were demonstrated: an NAD+-dependent form which was localized mainly in the cortex and an NADP+-dependent form, higher in the medulla. The activities of these enzymes were lower in the hypertensive animals at all ages studied; this depression was more pronounced for the NAD+-dependent dehydrogenase. The results indicate that, in hypertension, renal prostaglandin metabolism is altered so that enhanced synthesis is accompanied by decreased degradation rate.

Aging↗
PubMed1977

Vascular prostaglandin synthesis in the spontaneously hypertensive rat.

Vascular prostaglandin synthesis was studied in tissues (aorta and inferior vena cava) obtained from spontaneously hypertensive rats (SHRs) of the Aoki-Okamoto strain and age-matched Wistar-Kyoto (WKYs) controls. PGE2 synthesis in aortas from SHRs was significantly enhanced at 10 wk of age (5.3 +/- 0.7 nmol PGE2/mg protein per 10 min vs. 1.9 +/- 0.03 nmol PGE2/mg protein per min in the WKYs, P less than 0.001) and increased progressively until 22 wk of age; PGE2alpha synthesis in SHRs was not significantly different from WKYs. In the venous walls from SHRs, PGF2alpha was the prostaglandin predominantly synthesized (7.1 +/- 0.6 vs. 1.9 +/- 0.05 nmol PGE2alpha/mg protein per 10 min in the WKY controls, P less than 0.01). The activities of 15-hydroxy prostaglandin dehydrogenase and PGE 9-ketoreductase were also compared in the two groups of animals. The only difference detected was a significant increase in venous PGE 9-ketoreductase of SHR's (7.3 +/- 0.06 vs. 4.8 +/- 0.04 nmol PGF2alpha/mg per min, P less than 0.01). The results suggest that increased vascular synthesis of prostaglandins accompanies the development of spontaneous hypertension and may serve to attenuate the effects of blood pressure elevation.

Aging↗
PubMed1977

Histologic changes in preserved cadaveric renal transplants.

The histologic changes in human cadaveric kidneys preserved by either simple hypothermia or continuous pulsatile perfusion were studied by light and electron microscopy and by immunofluorescence in biopsies obtained immediately before (15 kidneys) and approximately 1 hour after (41 kidneys) transplantation. The changes observed in pretransplantation biopsies were largely similar in kidneys preserved by either method with the exception that foreign material was found in the vasculature of perfused kidneys only. Endothelial edema was more frequent and more severe in nonperfused kidneys only. Endothelial edema was more frequent and more severe in nonperfused kidneys. In the 1 hour posttransplantation biopsies, a lesion resembling intravascular coagulation (IVC) was noted in 18 of the 25 perfused kidneys but was absent from all 16 nonperfused kidneys. Transplants with severe IVC lesions failed to function and had extensive cortical necrosis when removed by the end of the first month. In follow-up biopsies, milder lesions appeared to heal fast and were compatible with transplant function. The IVC lesion is probably due to endothelial cell damage during perfusion of the kidneys.

Biopsy↗
PubMed1976

Perfusion nephropathy in human transplants.

To determine whether perfusion preservation affected the structure and survival of kidney transplants, we correlated clinical and histologic data in 77 kidneys biopsied one hour after transplantation. Twenty-one of 36 perfusion-preserved kidneys had a glomerular capillary lesion suggestive of intravascular coagulation. None of 41 kidneys preserved by hypothermia alone had this lesion. Presence of the lesion did not correlate with donor or recipient characteristics, warm or cold ischemia time, HLA match, percentage of preformed lymphocytotoxic antibody titers or perfusion characteristics. Of 21 transplants with the lesion, nine required nephrectomy by one month, and one-month serum creatinine was less than 2.0 mg per deciliter in only three of the remaining 12 transplants. We conclude that perfusion preservation may cause pathologic changes that may adversely affect kidney-transplant function. The causes of the pathologic process remain unclear.

Cadaver↗
PubMed1976

Effects of indomethacin on renomedullary interstitial cells.

The effects of indomethacin, an inhibitor of prostaglandin synthesis, on rat renomedullary interstitial cells were studied. Indomethacin, 5 mg. per kg. intravenously in divided doses over 48 hours, resulted in reduced granularity of interstitial cells (5.56+/-1.37 versus 9.85+/-1.07 granules per cell, (p is less than 0.001) and, at the same time, inhibited the incorporation of 14C-arachidonate into renomedullary phospholipids (715 + 11 versus 1299 + 42 c.pm.per mug. of lipid orthophosphate; p is less than 0.001) 14C-arachidonate incorporation into cortical phospholipids was not affected by indomethacin. There was a close correlation between individual granule counts and 14C-arachidonate incorporation into medullary phospholipids for both control (r=0.85) and indomethacin-treated animals (r=0.9). Radioactivity in the cytosol fraction was depressed by indomethacin reflecting inhibition of prostaglandin synthesis; cytosol radioactivity correlated closely with individual granule count (r=0.81) in the indomethacin-treated but not in the control rats. Indomethacin given as a single dose 4 hours prior to sacrifice resulted in a significant depression of 14C-arachidonate incorporation but did not affect granularity of interstitial cells. The results suggest that granularity of renomedullary interstitial cells reflects the activity of prostaglandin synthesis and the rate of prostaglandin precursor delivery from microsomal phospholipids.

Animals↗
PubMed1976

Renomedullary interstitial cells in the spontaneously hypertensive rat.

Renomedullary interstitial cells (RIC) are known to synthesize and release prostaglandins which may play a significant role in the development or severity of hypertension. The medulla of the spontaneously hypertensive rat contains RIC which are morphologically very similar to those previously described in the normotensive rat. The granularity of the RIC, however, was increased in the spontaneously hypertensive rat compared to normotensive Wistars (9.6 +/- 2.34 versus 5.3 +/- 2.05 granules per cell, respectively, p less than 0.001) or treated spontaneously hypertensive rats (7.2 +/- 1.65 granules per cell, p less than 0.001). Granule counts also increased in the presence of mild and moderate degrees of renal arteriolar sclerosis, but decreased in long standing hypertension with more severe and extensive lesions involving both arteries and arterioles. These results are consistent with the hypothesis that the RIC respond to an elevation of blood pressure in the spontaneously hypertensive rats by increased release of antihypertensive substances. In addition, the decrease in granularity of the RIC in the presence of extensive renal arteriolar and arterial damage suggests reduced ability to compensate for the elevated blood pressure and thus may contribute to the acceleration of hypertension.

Aging↗
PubMed1975

Bone and joint involvement in primary amyloidosis.

Primary amyloidosis is an interesting clinical entity in which amyloid is deposited in various organs, particularly mesodermderived tissues such as heart, skeletal muscle, skin, connective tissue and bone. A case with multiple lytic bone lesions is presented. Comparison to previous similar cases is made with attention being directed to the typical distribution of lesions about large joints with associated soft-tissue prominence and increase in the articular space. The differentiating radiologic features are compared to those of rheumatoid arthritis, hyperparathyroidism, and lytic metastatic lesions, with particular attention being given to the osteolytic lesions of plasmacytomas associated with multiple myeloma.

Aged↗
PubMedDate not supplied

Effect of salt on the vascular lesions of spontaneously hypertensive rats.

High salt intake accelerates hypertension in humans and increases cardiovascular morbidity and mortality. The temporal relation between blood pressure (BP) elevation and appearance of vascular lesions during salt-loading was studied in the spontaneously hypertensive rat (SHR). Starting at 5 weeks of age, SHRs and normotensive Wistar-Kyoto rats (WKYs) were given 1% NaCl in their drinking water SHRs and WKYs on tap water served as controls. Animals from each group were sacrificed at 10 and 20 weeks of age, and the aorta and intrarenal vessels were studied by light and electron microscopy. Neither BP nor vascular morphology of WKYs were affected by 1% NaCl. In SHRs, the course of BP was not affected by the addition of salt for at least 11 weeks, but vascular changes were significantly aggravated within 5 weeks. Thus, aortic intimal lesions progressed more rapidly so that, by 20 weeks of age, 50% of the animals had 3+lesions while, in control SHRs, they did not exceed the 2+grade. Salt-loading resulted in significant thickening of the aortic media between the 10th and 20th week of age while control SHRs showed no increment within the same time interval. Also, small intrarenal arterial vessels of salt-treated SHRs had significantly narrower lumina and greater wall thickness at both 10 and 20 weeks of age. In addition, they showed intimal proliferations and necrotizing lesions which were absent from control SHRs at these ages. These results show that, in this experimental model, the aggravation of vascular changes is not merely a sequela of further elevation of BP. Since the adverse effect of salt on the vessels was not seen in WKYs, it is likely that this effect is related to genetic factors or to higher susceptibility of hypertensive vessels.

Animals↗
PubMedDate not supplied

Effect of salt on prostaglandin metabolism in hypertension-prone and -resistant Dahl rats.

The effect of high salt intake on vascular and renomedullary prostaglandin (PG) synthesis was compared in Sprague-Dawley and salt-sensitive (S) and -resistant (R) Dahl rats. Animals were given a diet containing either 0.6% or 8% NaCl starting at 5 weeks of age, and were sacrificed 6 weeks later. Systolic blood pressure of S rats increased to 220 +/- 7 mm Hg but was unaffected in R and Sprague-Dawley rats. Prostaglandin synthesis was studied in aortic rings and renomedullary microsomes using 14C-arachidonate as substrate. [3H]PGE2 degradation was measured in the renocortical cytosol. In Sprague-Dawley and R rats, aortic PGI2 synthesis was not affected by high salt intake, while a significant increase compared to animals on 0.6% NaCl (from 608 +/- 84 to 992 +/-108 pmoles/60 min, p less than 0.05) was noted in S rats. Enhancement of PGI2 synthesis in S rats may be secondary to the hypertension. Salt-loading consistently stimulated renomedullary PGE2 synthesis in all three animal groups. S rats, however, had the lowest PG synthesis in renal medullas compared to Sprague-Dawley and R rats when placed on either diet. Thus, even after 6 weeks on high salt, S rats did not reach the levels of PGE2 synthesis seen in R or Sprague-Dawley rats on regular diet. The activity of cortical 15-hydroxyprostaglandin dehydrogenase was increased by salt-loading in S and Sprague-Dawley, but not in R rats. R rats had lower dehydrogenase activity than the other two groups when placed on either diet. The observed differences in PG synthesis and catabolism will tend to maintain the net output of renal PGs highest in R and lowest in S rats. These differences correlate with the reported differences in renal papillary flow between these two rat strains and may be relevant to their susceptibility or resistance to hypertension in response to salt.

Animals↗