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Biomedical subjects

R Shainkin-Kestenbaum

Publications and source records attributed to R Shainkin-Kestenbaum.

35 records · Page 2Linked to original sources
PubMed1986

Serum amyloid A (SAA) variations in patients with cancer: correlation with disease activity, stage, primary site, and prognosis.

Serum amyloid A (SAA) was determined in 160 patients with cancer. Active disease was associated with high titre compared with the titre in non-active condition (31.8 v 5.8 micrograms/ml, respectively; p = 0.0002). SAA value showed a direct correlation with the stage of the disease: it was lowest at stages 1 and 2 and highest at the metastatic stage 4 (stage 1 v 4, p = 0.001; stage 2 v 3, p = 0.05). Cancers of the lung and unknown primary site were characterised by highly increased SAA concentration. Initial SAA value had prognostic significance: a value below 10 micrograms/ml correlated with survival advantage, whereas a higher initial value indicated a greater likelihood of a poor outcome (actuarial survival analysis p less than 0.001). When stage was accounted for, initial SAA value had significant prognostic bearing on survival of patients with advanced disease (stages 3 and 4) but not on that of patients with limited disease (stages 1 and 2). Serial testing showed good concordance between changes in SAA titre and clinical course.

Amyloid↗
PubMed1986

Effect of guanidino-propionic acid on lymphocyte proliferation.

The 'uremic toxin', guanidino propionic acid (GPA), which was detected in uremic serum in correlation with BUN level, modified the mitogenic response of normal lymphocytes to phytohemagglutinin (PHA). Mild modifications can be detected in the concentrations which are found in uremic patients. Other guanidino compounds which have been detected in uremic sera, such as guanidino succinic acid (GSA), guanidino butyric acid (GBA) and guanidino acetic acid (GAA), show similar inhibitory pathways. It is suggested that guanidino compounds contribute to the immunological disturbances in uremia. The complexity of their action on lymphocyte mitogenic response is probably the cause of the conflicting results which have been reported in the literature.

Cell Division↗
PubMed1985

Transitory hypocalcemia complicating measles.

During an epidemic of measles, 12 young adults developed hypocalcemia associated with a decrease in parathyroid hormone level. Calcium and parathyroid hormone levels returned to normal in five of the 12 patients for whom convalescent data were available.

Acute Disease↗
PubMed1984

Importance of serum amyloid A (SAA) level in monitoring disease activity and response to therapy in patients with prostate cancer.

Serum amyloid A (SAA) and acid phosphatase (AcP) levels were determined in serial serum samples of 35 patients in different stages of dissemination and correlated with activity of carcinoma of the prostate. Up to 500-fold increases in SAA level were detected during active periods of cancer with a decrease towards the normal range in remission, in comparison with a 10-fold increase of AcP. The correlation between these two parameters was highly significant (P less than 0.001), but while SAA shows 100% sensitivity during the active stage, AcP shows only 85% sensitivity. It is suggested that although SAA is not a specific marker for any particular illness, due to its characteristic pattern of change in malignant diseases and its high sensitivity, it represents a useful biochemical parameter for the assessment of the activity of the disease to monitor response to therapy during follow-up.

Acid Phosphatase↗
PubMed1984

Degradation of amyloid A and serum amyloid A by red blood cell haemolysate in patients with familial mediterranean fever.

Enzymatic activity for the degradation of serum amyloid A (SAA) and amyloid A (AA) was detected in erythrolysates of normal subjects and patients with familial mediterranean fever. A significant difference between the activity of normal subjects and patients was not found. Serum inhibited the SAA (but not the AA) haemolysate proteolytic activity. Interindividual variation in the susceptibility of SAA to degradation by RBC haemolysates was shown. The original digestible fraction of SAA became gradually resistant to proteolytic cleavage over a 9 month period while the susceptibility of AA to degradation remained unchanged in this time period. These findings suggest that enzymatic degradation of SAA depends on the source of SAA, as well as inhibitory activity in serum.

Amyloid↗
PubMed1984

Parathyroid hormone, calcitonin, and vitamin D metabolites during normal fracture healing in humans. A preliminary report.

The metabolism of calcium is regulated by hormones: parathyroid hormone, (PTH) calcitonin (CT), and vitamin D metabolites. To study the physiologic role of these hormones during the process of fracture healing in humans, the blood levels of PTH, CT, 25-(OH)-D3, 24,25-(OH)2-D3, and calcium were determined in 13 young patients with fractures of long bones. The parameters were measured first on admission and again after six to eight weeks. A group of healthy volunteers of similar age and sex served as control subjects. Plasma calcium level on the day of fracture was significantly reduced, 8.50 +/- 0.23 mg% (p less than 0.001). Serum CT level on the day of fracture was significantly increased, 0.18 +/- 0.02 ng/ml (p less than 0.05), and it continued to increase during the healing period, up to 0.23 +/- 0.02 ng/ml (p less than 0.001) after six to eight weeks. A significant rise was noted in plasma level of 24,25-(OH)2-D3, from 2.02 +/- 0.42 ng/ml on the day of fracture to 2.84 +/- 0.41 ng/ml six weeks later (p less than 0.05). No significant changes were found in serum PTH and plasma 25-(OH)-D3 levels on the day of fracture or during the healing process. The results suggest a possible physiologic active role for CT and 24,25-(OH)2-D3 in fracture healing in humans.

Adult↗
PubMed1982

The toxicity of guanidino compounds in the red blood cell in uremia and the effects of hemodialysis.

The presence of creatine, guanidinopropionic acid (GPA) and guanidinobutyric acid (GBA) was demonstrated in red blood cells from uremic patients; they were found only in trace amounts in red blood cells of normal controls. The levels of creatine, GPA and GBA in the red cell did not change during dialysis in contrast to the simultaneous decrease in plasma level. Both creatine and GPA inhibited glucose-6-phosphate dehydrogenase (G6PD) in vitro in physiological concentration, while creatine also activated erythrocyte transketolase (ETK). These effects are consistent with the low red cell G6PD level and high ETK activity that were observed in our uremic patients. The unchanging levels of creatine and GPA in the red cell despite hemodialysis may explain the continuing autohemolysis in otherwise adequately hemodialyzed end-stage renal failure patients.

Adult↗
PubMed1982

Serum amyloid A (SAA) in viral infection: rubella, measles and subacute sclerosing panencephalitis (SSPE).

Serum amyloid A (SAA) levels were determined in the serial serum samples of eight rubella, 10 measles and seven subacute sclerosing panencephalitis (SSPE) patients. An early rise in SAA levels was detected in the acute phase in rubella and measles, followed by a prompt decrease in the convalescent phase. In a number of measles and rubella patients from whom early serum samples were available, the rise of SAA levels could be demonstrated before specific viral antibodies could be detected by complement fixation (CF) (measles) and haemagglutination inhibition (HI) (rubella). In only one rubella and one measles patient was no rise of SAA level detected. In SSPE only a moderate increase in SAA levels was noted except in one patient during a temporary deterioration, at which time the SAA level was very high; it returned to close to normal shortly thereafter. The possibility that SAA levels might be of value in monitoring the severity of infections, the recovery process and effects of anti-viral agents is discussed.

Adult↗
PubMed1981

Hypercalcemia in carcinoma of the breast without evidence of bone destruction: beneficial effect of hormonal therapy.

A premenopausal woman with soft tissue metastases from a carcinoma of the breast developed hypercalcemia with hypophosphatemia, reduced tubular reabsorption of phosphate, elevated urinary cyclic AMP levels and normal serum PTH levels was observed. Hormonal therapy with testosterone followed by tamoxifen induced normalization of her serum calcium concomitant with the disappearance of the pleural effusion and reduction in the size of her lung metastases. The correlation between the efficacy of antitumor treatment on pleural effusion, lung metastases, and normalization of serum calcium, as well as the elevated PTH level in the pleural effusion, suggest that this breast carcinoma secreted a PTH-like substance.

Adult↗
PubMed1979

25 Hydroxycholecalciferol levels in Beduin women in labor and in cord blood of their infants.

25 Hydroxycholecalciferol levels were measured in eight Beduin mothers in labor and in the cord blood of their infants, and compared with values in 42 Sephardi Israeli women in labor and the cord blood of their offspring. Beduin baby cord blood had a mean 25 hydroxycholecalciferol concentration of 3.78 ng/ml +/- 3.22 (SD) being about half of their mothers' level in labor. Values in Sephardi women and cord blood were 3 times higher. PTH levels were lower and calcium concentrations were higher in cord blood (P less than 0.001) in both groups when compared to their mothers' blood. The relevance of these findings to the high incidence of infantile rickets and hyypocalcemia in Beduin children is discussed.

Calcium↗
PubMed1977

Plasma calcitonin in chronic renal failure: relation to other factors of importance in bivalent ion metabolism.

1. Plasma concentrations of human calcitonin were measured in groups of patients with chronic renal failure, treated either conservatively or by haemodialysis, and compared with a normal group of persons. 2. Plasma calcitonin was statistically significantly elevated in both groups with renal failure. 3. When the data from the three groups were pooled, plasma calcitonin was found to be inversely correlated with total calcium and directly correlated with plasma creatinine.

Calcitonin↗
PubMedDate not supplied

Effect of serum amyloid A, HDL-apolipoprotein, on endothelial cell proliferation. Implication of an enigmatic protein to atherosclerosis.

The possible contribution of apo-HDL serum amyloid A (SAA) to the protective effect of HDL against atherosclerosis was studied by evaluating its effect on bovine aortic endothelial cell (BAEC) proliferation. Our results suggest that human SAA, both purified and recombinant, in concentrations relevant to mild acute phase events, significantly inhibit endothelial cell proliferation in a dose-dependent manner (e.g., 50 micrograms/ml causes approximately 88% inhibition; p < 0.001). This inhibition was attenuated by addition of fibroblast growth factor (FGF), which antagonized the SAA-mediated effect. As levels of TNF may be highly elevated during the acute phase response, its effect on BAEC proliferation was evaluated and found, at concentrations of > 1 pg/ml, to be substantially inhibitory Co-incubation of cells with both SAA and TNF was inhibitory, albeit neither additive nor synergistic. FGF antagonized the effect of both proteins. Amyloidic deposit (AA, i.e. SAA 1-76), derived from pathological proteolysis of SAA, practically retains the inhibitory activity (e.g. 50 micrograms/ml causes approximately 66% inhibition; p < 0.001) but apparently lacks the regulatory site towards FGF. In contrast to the above inhibitory effect, synthetic SAA-related peptide corresponding to the sequence 29-33 of SAA enhances BAEC proliferation (50 micrograms/ml causes approximately 64% increase; p < 0.001). The present data, coupled with our previous observations in which SAA was found to induce endothelial PGI2 formation and to inhibit overproduction of PGI2 by TNF and LPS as well as platelet aggregation, may suggest that SAA contributes to the protective effect of HDL against atherosclerosis. This, by means of its modulatory effect on endothelial cell and platelet activation, primarily in the presence of other regulatory proteins. SAA-derived peptides may, potentially, be used as therapeutic agents in the treatment of atherosclerosis and cardiovascular diseases.

Amino Acid Sequence↗
PubMedDate not supplied

Modulation of prostaglandin I2 production from bovine aortic endothelial cells by serum amyloid A and its N-terminal tetradecapeptide.

The study was aimed to explore the possible involvement of the acute phase HDL apolipoprotein, serum amyloid A (SAA) in the regulation of PGI2 production by endothelial cells. This, in view of the recent detection of SAA mRNA in endothelial cells of human atherosclerotic lesions. Human SAA induces PGI2 formation in bovine aortic endothelial cells culture in a concentration relevant to moderate acute phase events. 50 micrograms/ml of purified human SAA increases PGI2 production from a mean basal level of 2,490 +/- 330 pg/ml by 1.80 +/- 0.1 fold (n = 10; p < 0.01). The PGI2 inducing activity resides apparently in the N-terminal, i.e. amino acid residues 1-14, of the SAA molecule, 50 micrograms/ml of the peptide induces 2.9 +/- 0.5 fold increase of PGI2 production (n = 4; p < 0.03). TNF and LPS each induce PGI2 production in a concentration and time dependent manner. TNF in concentration of 10 ng/ml induces, in the presence of calf serum, an increase of 24.9 +/- 2.3 fold (n = 4; p < 0.001) and LPS in concentration of 1 microgram/ml causes a 18.3 +/- 1.3 fold increase, (n = 4; p < 0.01). In serum-free cultures, only a 2.5 +/- 0.3 fold increase was detected by 10 ng/ml TNF (n = 4), and a 5.9 +/- 0.4 by 1 microgram/ml of LPS. Thus, serum has a strong effect on PGI2 induction. When 50 micrograms/ml SAA is coadministered with 1 ng/ml TNF it reduces the TNF-induction of PGI2 from 7.7 +/- 2.8 to 3.3 +/- 1.2 fold (n = 4; p < 0.01). SAA attenuates, as well, LPS-mediated activity, although in a less pronounced manner. Our finding suggest a potential physiological function for SAA in regulation of basal and cytokine-induced PGI2 production by vascular endothelium. The capacity of SAA to markedly moderate PGI2 induction by TNF and LPS suggest that it may play a role in defending against vessel damage, in cases of atherosclerosis, bacterial infection or septic shock. The induction of PGI2 by SAA through its N-terminal domain, which also exhibits an anti-platelet aggregation activity, suggests a potential therapeutical use for this peptide as an anti-hypertensive and an anti-aggregatory agent.

Amino Acid Sequence↗