Concurrent membranous glomerulopathy and diabetes mellitus.
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Adult↗
Biomedical subjects
J C Jennette
Publications and source records attributed to J C Jennette.
Insulin resistance due to receptor antibodies: a complication of progressive systemic sclerosis.
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Adult↗
Consistent fluctuations in quantities of circulating immune complexes during progressive and regressive phases of tumor growth.
Circulating immune complexes (CIC) were quantitated by a Raji cell radioimmunoassay in sera from Brown Norway rats bearing progressing or regressing methylcholanthrene-induced sarcomas. Quantitative profiles of CIC over time were related to tumor dose, tumor mass, and the regressive or progressive course of tumor growth. Animals bearing progressing tumors demonstrated an initial peak of CIC levels by 7 weeks but thereafter displayed a persistent decline in quantities of CIC despite continued tumor growth. Animals bearing regressing tumors were found to have a more directly proportional relationship between the tumor mass and the levels of CIC, but the appearance and disappearance of CIC lagged slightly behind the appearance and disappearance of the tumor. These data are almost identical to data previously published detailing quantities of CIC in BN and Lewis rats bearing Moloney sarcomas and are similar to fluctuations in CIC observed in animals and humans hosting a number of disparate neoplasms.
Animals↗
Experimental meningococcal septicemia. Effect of aspirin therapy.
In previous studies we have presented morphological evidence that the terminal shock-like phase of fatal meningococcemia is caused by the occlusion of the pulmonary microcirculation with thrombi composed of platelets, leukocytes, and fibrin. We have also shown that in experimental meningococcemia, pretreatment of rabbits with heparin sodium prevents fibrin formation but does not influence the cellular pulmonary thrombi and does not prolong survival. If our theory is correct, drugs that inhibit platelet aggregation and leukocyte adhesion in rabbits should prolong life. The present experiment demonstrates that pretreatment with a small dose of aspirin doubles the survival time without altering the mortality.
Animals↗
p30-Anti-p30 immune complexes: intravascular clearance and extravascular sequestration in rats bearing Moloney sarcoma.
Complexes of 125I p30, a viral core polypeptide, and rat anti-p30 antibody, preformed in vitro, were injected into the heart of BN rats bearing Moloney sarcomas (MST) and of BN rats bearing an unrelated tumor or unexposed to tumor. Complexes were cleared from the circulation of MST-bearing rats more rapidly than from sera of controls and were almost completely eliminated after 30 hr. There was no relationship between rate of disappearance and size of tumor or levels of circulating complexes. Disappearance rates in rats with progressing and regressing tumors were similar. Uncomplexed labeled p30 was cleared from the circulation of tumor-bearing and control rats with kinetics similar to those of labeled complexes. Complexes were localized in the spleen of tumor-bearing and control rats, but much more in spleens of MST-bearing rats. No other tissues, including tumor, concentrated complexes, nor was there binding to peripheral blood and spleen cells. The data suggest that augmented clearance and sequestration were due to the formation of large insoluble complexes that were rapidly removed by the reticulo-endothelial system.
Animals↗
Sequential quantitation of circulating immune complexes in syngeneic and allogeneic rats bearing Moloney sarcomas.
A Raji cell radioimmunoassay was employed to quantitate serially circulating immune complexes (CIC) in the sera of syngeneic BN rats and allogeneic Lewis rats bearing BN Moloney sarcomas. In syngeneic BN hosts the levels of CIC attained and the time-course of detection were related to the tumor dose, tumor mass, and regressive or progressive course of the tumor. In general, syngeneic rats that received larger tumor doses developed larger tumors and greater maximum levels of CIC. However, the amount of CIC was not always directly proportional to the tumor size, although this was nearly the case with regressor BN and Lewis rats. In rats with regressing tumors, CIC decreased to insignificant levels as the tumors disappeared. Progressor BN rats that received 20 and 10 X 10(6) tumor cells had higher and more sustained levels of CIC, but, shortly before the hosts died, despite an increase of tumor size, there was a decline of CIC. Progressor BN rats that received an initial inoculum of 0.5 X 10(6) tumor cells that grew to 44 mm maximum mean diameter had levels of CIC which were only slightly above levels of control rats. All allogeneic Lewis hosts rejected BN Moloney sarcomas, but had transient low levels of CIC coincident with tumor growth. Lewis rats had lower levels of CIC than BN rats bearing comparable masses of sarcoma.
Animals↗
Fatal meningococcal septicemia.
The morphologic and clinical findings in seven fatal cases of meningococcal septicemia are described and interpreted in light of recent experimental and clinical studies. We include evidence that suggests the disease has two distinct pathogenetic mechanisms. First, a shock-like terminal phase is associated with the development of widespread pulmonary microvascular thrombosis. These thrombi, composed largely of platelets and leukocytes, produce severe cor pulmonale that cannot be prevented with heparin sodium treatment. Meningococcal endotoxin also produces disseminated intravascular coagulation, which includes the rapid consumption of fibrinogen and the formation of fibrin thrombi in adrenal and renal glomerular capillaries, causing hemorrhagic infarction of the adrenal glands and renal cortical necrosis. This secondary phase of the disease can be modified with heparin therapy, but its control does not improve survival because the parenchymal lesions produced are not immediately life threatening.
Adolescent↗
Inhibition of the membrane transport of folates by anions retained in uremia.
Previous studies from this laboratory indicated that inorganic and organic anions inhibit the unidirectional influx and net transport of the folate analog methotrexate in mammalian cells. Studies were undertaken to establish whether anions retained in uremia might inhibit the membrane transport of folates. Methotrexate was utilized as a model folate compound and its transport was determined in the Ehrlich ascites tumor cell. Influx of methotrexate was inhibited when cells were suspended into sera or ultrafiltrates of sera (pH adjusted to 7.4 by regulation of PCO2) from uremic patients, an effect that was decreased after the patient underwent hemodialysis or peritoneal dialysis. The inhibitory effect of uremic sera correlated well with the level of retained anions as estimated from the "anion gap," but could not be related to changes in osmolality, blood urea nitrogen (BUN), sodium, potassium, calcium, or magnesium. While inhibiting the influx of methotrexate, inorganic anions did not displace methotrexate from albumin binding sites. Anionic inhibition of the membrane transport of 5-methyl [14C] tetrahydrofolate was also demonstrated and this was shown to be accompanied by a depression in the rate of incorporation of the labeled 14C moiety into nucleic acids and protein. The data suggested that transport of folates is impaired in uremia and raises the possibility that whatever the measured blood folate level in the uremic individual with retained anions, the rate of uptake of folates into folate-dependent tissues which this blood folate level will sustain may be reduced.
Animals↗