Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of cyclosporine (6 to 8 mg/kg/day) on urinary kallikrein excretion was examined in 10 patients with rheumatoid arthritis by using a radioimmunoassay for kallikrein, a product of renal tubular biosynthesis. All patients had baseline values of serum creatinine and blood urea nitrogen (BUN) within the normal range. The group had a mean baseline kallikrein excretion of 98.30 +/- 29.98 micrograms/24 hours (mean +/- SEM), and 3 and 6 months after therapy was initiated, kallikrein excretion was 44% and 46% of baseline, respectively (p less than 0.01). The five patients who had a normal mean baseline kallikrein excretion rate (106.60 +/- 15.21 micrograms/24 hr) excreted significantly less (p less than 0.05) kallikrein 3 and 6 months after therapy was initiated (56.60 +/- 3.98 micrograms/24 hr and 34.50 +/- 11.02 micrograms/24 hr, respectively), as did one patient with an elevated baseline kallikrein. All six of these individuals completed the protocol. In a subgroup of four patients with low baseline levels (28.25 +/- 5.06 micrograms/24 hr), two individuals experienced elevations of BUN such that cyclosporine was discontinued; in the two who completed the protocol, there was some further decrement in kallikrein excretion. Kallikrein excretion increased in all patients after a 3-month washout period. During a low-dose (3 mg/kg/day) open extension study that followed the initial trial, kallikrein excretion was determined monthly. Seven episodes in which kallikrein excretion decreased in six patients by 44% +/- 18% over a 1-month interval preceded any increase in serum creatinine by 1 to 4 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cyclosporine on urinary kallikrein excretion in patients with rheumatoid arthritis. 341 Nov 94

A radioimmunoassay for the determination of somatostatin-like immunoreactivity (SLI) in plasma has been developed using antibodies raised in rabbits against synthetic somatostatin conjugated to hemocyanin and 125I-Tyr1-somatostatin. The detection limit was 2 pg/ml. A combination of EDTA and aprotinin (0.15 M and 80 Kallikrein Inhibitor Units = KIU/ml) inhibited the tracer degradation, but did not eliminate it completely. In addition somatostatin immunoreactivity in unextracted plasma showed a strong dilution effect and the estimates depended on the antiserum used (e.g. a plasma sample (1 : 5) assayed with antiserum R 141 apparently contained 150 pg/ml, whereas antiserum K 5615 yielded a value of 300 pg/ml). When plasma was extracted with acid ethanol, the values obtained with the two different antisera were practically the same, recovery of somatostatin added to plasma was approx. 80% and dilution of specimens gave proportional readings. Consequently, extraction of plasma is regarded as obligatory to ensure valid results. Mean basal level was 26.5 +/- 1.2 pg/ml (mean +/- SEM). When plasma extracts were subjected to chromatography on Sephadex G-25 at neutral pH, approx. 30% of the SLI was recovered in the MW1600 fraction; whereas the major part of the remaining immunoreactivity (37-60%) eluted earlier in one fraction and the residual immunoreactivity in the void volume.
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PMID:Somatostatin-like immunoreactivity in man. Measurement in peripheral plasma. 612 67

We studied prostaglandins and kallikrein urinary excretion in 14 children with acute poststreptococcal glomerulonephritis within 48 hours of hospital admission (period A), and again, 4-6 weeks later, when they were clinically recovered (period B). Seventeen apparently healthy children were studied as controls. The results (mean +/- SEM) indicate that PGE2 urinary excretion (ng/kg/day) was diminished during both periods of study (control group = 2.06 +/- 0.43, patients = period A 0.91 +/- 0.28 [P less than 0.02], period B 0.92 +/- 0.21 [P less than 0.02]). PGF2 alpha urinary excretion (ng/kg/day) was also suppressed during period A, but not during period B when large individual variability existed (control group = 7.10 +/- 1.07, patients period A 3.56 +/- 0.66 [P less than 0.001], period B 10.51 +/- 5.01 [NS]). Kallikrein urinary excretion (EU/kg/day) was also depressed during the acute phase and remained low during convalescence (control group = 0.492 +/- 0.1, patients period A 0.143 +/- 0.044 [P less than 0.001], period B 0.265 +/- 0.093 [P less than 0.02]). There was no difference in PGE/PGF ratio between controls and patients in the periods of study (control 0.328 +/- 0.055, period A 0.395 +/- 0.144, period B 0.384 +/- 0.128). Urine volume (ml/day) was lower in period A (582 +/- 75.8) but comparable in period B (1020 +/- 140.2) and control children (1210 +/- 80.2). No correlation could be found between the urinary excretion of PGE2, PGF2 alpha and kallikrein with any of the following parameters: urinary or serum sodium and potassium, serum or urinary osmolality, Cosm, urine flow, plasma renin activity, plasma or urinary aldosterone, hypertension or fluid retention.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary excretion of prostaglandins (PGE2 and PGF2 alpha) and kallikrein in acute glomerulonephritis. 658 Sep 82

Two recent studies have shown decreased blood loss in patients given aprotinin undergoing primary hip replacement surgery. Because patients undergoing bilateral (bTHA) or revision total hip arthroplasty (rTHA) suffer more blood loss than those undergoing primary THA, we studied consecutive patients undergoing bTHA or rTHA who were randomized to receive either a blinded solution of 3.8 x 10(6) Kallikrein inactivation units (KIU) aprotinin (n = 29) or placebo (n = 24) throughout the surgical procedure. Total blood loss, measured as intraoperative suction losses, weight of sponges, and postoperative volumetric drainage, was compared between groups. Aprotinin patients had significantly less total blood loss 1498 +/- 110 mL (mean +/- SEM) versus 2096 +/- 223 (P = 0.022), and transfused patients in the aprotinin group received fewer packed red blood cells than placebo-treated patients (confidence interval for the difference -1.69, -0.07). In addition, assessment of biochemical markers of hepatic and renal function did not disclose any clinically important differences between groups. Patients were also assessed for development of deep venous thrombosis (DVT) by preoperative and predischarge bilateral lower limb compression ultrasound. None of the aprotinin-treated patients and three placebo-treated patients demonstrated DVT. Unless this trend for decreased DVT with aprotinin can be confirmed, it is questionable whether the slight reduction in blood loss justifies routine use of this expensive drug.
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PMID:Aprotinin decreases blood loss in patients undergoing revision or bilateral total hip arthroplasty. 752 67

Uterine homogenates of cycling and early pregnant Sprague Dawley rats and purified rat urinary kallikrein showed similar curves of displacement of 125I-kallikrein binding to a polyclonal antibody. Uterine kallikrein concentration measured by RIA was 8.7 +/- 2 SEM ng/g wet weight during the cycle (n = 6 in diestrus and metestrus) and 20.8 +/- 2 SEM (n = 7) ng/g wet weight on Day 7 of pregnancy (P7) (p < 0.001). On P7, kallikrein concentration was increased 12.4-fold in the implantation nodes, as compared to the interimplantation segments. Uterine homogenates of rats on P7, submitted to DEAE-cellulose chromatography and Sephadex gel filtration, yielded two fractions containing kallikrein immunoreactivity and kininogenase activity, with molecular masses that ranged from 120-125 kDa and 39-43 kDa, respectively. In the RIA, both fractions displayed parallelism with purified kallikrein. Enzymatic activity was expressed after activation by trypsin. It was inhibited by aprotinin, PMSF, p-amino-benzamidine, and leupeptin, but not by soybean or ovomucoid trypsin inhibitors. Kallikrein mRNA was demonstrated by reverse transcriptase/polymerase chain reaction in uteri of nonpregnant and P7 rats. These results show that rat uterus synthesizes one or more serine proteases that are immunologically and enzymatically related to tissue kallikrein in the implantation node on P7--determined both by an increment of whole uterus kallikrein content and a depletion of the interimplantation segments--suggests that kallikrein may play a role in the vasoactive changes of implantation.
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PMID:Uterine kallikrein in the early pregnant rat. 821 45