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1.
Evidence has been provided for an increase in baseline serum corticotrophin (ACTH) levels in response to a rise in circulating ionized calcium (Cai) levels within the physiological range. In order to establish whether small Cai increments are also able to modify the basal secretion of arginine vasopressin (AVP), we infused calcium gluconate through an intravenous infusion pump in eight healthy male subjects (25–31 years old). Serum Cai, ACTH and AVP concentrations were measured every 10 min over an infusion period lasting 90 min. A significant progressive rise in serum Cai (baseline: 42 ± 0.9 mg dL−1; 90 min: 47.2 ± 0.9 mg dL−1, P  < 0.001), ACTH (baseline: 30.7 ± 1.3 pg mL−1; mean peak at 80 min: 37.4 ± 2.4 pg mL−1, P  < 0.01) and AVP levels (baseline: 2.1 ± 0.6 pg mL−1; mean peak at 80 min: 3.2 ± 0.5 pg mL−1, P  < 0.01) was observed during calcium infusion. Furthermore, a significant positive correlation ( r  = 0.71; P  < 0.001) was observed between ACTH and AVP responses to calcium infusion at 60, 70, 80 and 90 min. These data demonstrate that AVP secretion is stimulated by a slight rapid increase in serum Cai levels even though absolute serum Cai levels remain within the normal range. In addition, the positive correlation between Cai-induced ACTH and AVP increments suggests that AVP plays a releasing role on ACTH secretion during calcium infusion.  相似文献   

2.
The endothelium-derived peptide endothelin-1 (ET-1) was evaluated in 14 male patients [mean age 52.74 years (SEM 1.10)] affected by coronary artery disease during a bicycle electrocardiographic stress test and dipyridamole echocardiogram. Both tests were performed before and after coronary revascularization. Fourteen healthy male subjects served as controls [mean age 53.21 years (SEM 1.63)]. Baseline plasma endothelin-1 levels were higher ( P  < 0.0001) in ischaemic patients [1.81 pg mL−1 (0.15, n  = 14)] than in control subjects [0.61 pg mL−1 (0.03, n  = 14)], but did not increase with exercise in both groups. Similar results were obtained with dipyridamole infusion. Endothelin-1 levels significantly decreased after coronary revascularization [before: mean 1.81 pg mL−1 (SEM 0.15, n  = 14); after: mean 1.16 pg mL−1 (SEM 0.11), P  < 0.002], without changes in the peptide response to both tests. In conclusion, elevated plasma endothelin-1 concentrations were found in patients with stable angina compared with non-ischaemic subjects. No changes were observed during exercise or dipyridamole infusion in both groups. Coronary revascularization was followed by a significant decrease in plasma endothelin-1 levels.  相似文献   

3.
Concentrations and ex vivo production of interleukin 1β (IL-1), tumour necrosis α (TNF), interleukin 6 (IL-6), interleukin-1 receptor antagonist (IL-1RA) and TNF soluble receptors (sTNF-receptors, P55 and P75) were measured in bronchoalveolar lavage (BAL) fluid and blood in 23 HIV-seropositive (HIV+) patients with Pneumocystis carinii pneumonia (PCP) and compared with values found in healthy HIV-seronegative (HIV−) controls and asymptomatic HIV+ subjects. Concentrations of the proinflammatory cytokine IL-1β were increased in BAL fluid of HIV+ patients with PCP (184 ± 47 pg mL−1) compared with undetectable levels in healthy control subjects ( P  = 0.0001). In plasma of these patients higher concentrations of the anti-inflammatory cytokine IL-1RA were found during acute PCP than after recovery (2.1 ± 0.7 vs. 0.5 ± 0.2 ng mL−1, P  = 0.01). No correlations could be found between cytokine concentrations and clinical severity of the infection. Corticosteroid treatment did not influence cytokine concentrations in BAL or blood, nor did it suppress the production in alveolar cells. In whole-blood cultures, however, lipopolysaccharide (LPS)-stimulated production was significantly suppressed for IL-1 (1.3 vs. 5.5 ng mL−1, P  = 0.009) and for IL-6 (0.6 vs. 2.5 ng mL−1, P  = 0.01). The overall data show that in HIV+ patients with PCP (similar to what we had found previously in HIV− patients with PCP) proinflammatory cytokines are more prominently present in BAL, whereas anti-inflammatory reaction is predominant in the circulation.  相似文献   

4.
Summary.  Introduction:  In some patients with mild hemophilia A, there are discrepancies between 1-stage (1-st) and 2-stage (2-st) factor VIII (FVIII) clotting assays, and also chromogenic assays for FVIII activity (FVIII:C). We examined whether thrombography could provide a better evaluation of the hemostatic status of these patients. Methods:  Two families with such discrepancies and markedly contrasting clinical histories were studied. Family X had no serious bleedings, in contrast to family Y. Sixty-one moderate/mild hemophiliacs without discrepancy and 15 healthy subjects served as controls. Calibrated automated thrombography was performed with platelet-rich plasma after one freeze-thawing cycle and low tissue factor concentration. Results:  The chromogenic FVIII:C levels were higher (0.90 ± 0.15 and 0.47 ± 0.13 IU mL−1) than the 1-st clotting ones (0.14 ± 0.05 and 0.10 ± 0.05 IU mL−1) in family X and Y, respectively ( P  < 0.001). Mean endogenous thrombin potential (ETP) was 1579 ± 359 n m  min−1 and 1060 ± 450 for healthy controls and hemophilic controls, respectively. For members of family X, the ETP values were 1188, 1317 and 2277 n m  min−1, whereas for those of family Y they ranged from 447 to 1122 n m  min−1. Two novel missense point mutations were evidenced: p.Ile369Thr in family X and p.Phe2127Ser in family Y. In family X, we postulate that the mutation is responsible for a delayed but non-deleterious FVIII activation. Conclusions:  Our results suggest that the hemostatic phenotype assessed by thrombography may be clinically relevant in moderate/mild hemophilic patients with discrepant FVIII:C results.  相似文献   

5.
Microdialysis was used to selectively assess the effect of the paracrine renin–angiotensin system (RAS) on interstitial glucose and lactate concentration profiles in skeletal muscle of healthy volunteers ( n  = 8) during basal and insulin-stimulated conditions. Paracrine RAS was selectively inhibited by local retrodialysis with enalaprilate. Under basal conditions, local administration of enalaprilate (2 μg mL−1) increased interstitial dialysate glucose concentration from 0.71 ± 0.14 mmol L−1 to 0.84 ± 0.14 mmol L−1 and decreased the serum interstitial gradient (SIGglu) compared with baseline ( P  < 0.02). Under clamp conditions, enalaprilate, even at the lowest concentration (0.02 μg mL−1), increased interstitial dialysate glucose concentration from 0.77 ± 0.11 mmol L−1 to 1.02 ± 0.09 mmol L−1 and decreased SIGglu compared with baseline ( P  < 0.01). Interstitial lactate concentrations slightly increased during basal as well as during clamp conditions ( P  < 0.05 vs. baseline). Selective inhibition of paracrine muscle angiotensin-converting enzyme (ACE) increases interstitial glucose and lactate concentrations and decreases SIGglu in muscle by facilitating transcapillary glucose transport. This effect is more pronounced during hyperinsulinaemia and may be of clinical relevance in diabetic patients treated with therapeutic doses of enalapril.  相似文献   

6.
Summary.  Background: Racial differences in coagulation are poorly understood. While some studies suggest a 'prothrombotic' coagulation profile in blacks compared with whites, others report an increased bleeding risk for blacks in various clinical settings. Moreover, preclinical data suggest a link between the Duffy antigen (= DARC, Duffy antigen receptor of chemokines) and coagulation. Objectives: Based on our previous research in Duffy antigen negative Africans, we hypothesized that Africans have an attenuated procoagulant response compared with Caucasians in a model of lipopolysaccharide (LPS)-induced, tissue factor (TF)-triggered coagulation activation. Patients/methods: Healthy male volunteers (16 Duffy-negative Africans, 16 Duffy-positive Caucasians) received 2 ng kg−1 LPS, and outcome parameters were measured using enzyme immunoassays and real-time polymerase chain reaction (RT-PCR, Taqman). Results: LPS increased microparticle (MP)-associated TF procoagulant activity (PCA) less in Africans than Caucasians. Africans had reduced in vivo thrombin formation compared with Caucasians: they generated less thrombin–antithrombin (TAT) complexes (10.4 pg mL−1 vs. 23.0 pg mL−1, P  < 0.0001) and less prothrombin fragments (F1+2) (337 pmol mL−1 vs. 819 pmol mL−1, P  < 0.0001). Consistently, Africans also had decreased fibrin formation ( d -dimer: 0.3 pg mL−1 vs. 0.5 pg mL−1, P  = 0.02). Conclusion: Duffy-negative subjects of African descent have a markedly reduced procoagulant response in a model of LPS-induced, TF-triggered coagulation activation compared with Duffy-positive healthy Caucasians.  相似文献   

7.
Background : We tested the hypothesis that plasma levels of plasminogen activator inhibitor-1 (PAI-1) are influenced by percutaneous coronary intervention (PCI) with the implantation of drug eluting stents (DES) and are able to predict the occurrence of in-stent restenosis (ISR). Methods and results : PAI-1 active antigen plasma levels were determined in 75 patients before and 24 h after PCI with DES implantation. Patients with ISR after six to eight months (16%) showed significantly lower PAI-1 plasma levels before PCI (ISR, 11.7 ± 8.1 ng mL−1; non-ISR, 22.8 ± 18.8 ng mL−1; P  < 0.05). PAI-1 levels in the lowest tertile were associated with a 9.5-fold increased risk of ISR, independent of clinical risk factors, angiographic or procedural characteristics, compared to the highest tertile ( P  <   0.05). The induced change of PAI-1 active antigen 24 h after PCI was significantly higher in patients with ISR (ISR, +5.6 ± 8.0 ng mL−1; non-ISR, −3.2 ± 12.1 ng mL−1; P  <   0.05) with positive correlation to late lumen loss ( r  =   0.30; P  <   0.05). Conclusions : ISR after DES implantation is significantly related to plasma levels of PAI-1 active antigen before and after PCI. If confirmed by larger multicenter studies, the determination of PAI-1 plasma levels might be clinically helpful in the identification of patients at high risk of developing of ISR, even after DES implantation.  相似文献   

8.
Background   In the sera of liver, colorectal and prostate cancer patients, several biomarkers may be detected as IgM immune complexes. To determine whether the presence of immune complexes was correlated to an increase of IgMs, we measured the IgM content in the sera of patients with hepatocellular carcinoma (HCC) and cirrhosis, and evaluated the occurrence of des-gamma-carboxy prothrombin (DCP) as immune complexes ( DCP-IgM ) compared to the levels of DCP and alpha-fetoprotein (AFP).
Patients and methods   Serum samples from 31 patients with cirrhosis, 33 untreated HCC patients diagnosed by ultrasound, computed tomography and/or magnetic resonance and confirmed by histopathology, when indicated, and 30 healthy controls were analysed. Concentrations of IgM and DCP-IgM were determined by ELISAs.
Results   Circulating IgM in patients with HCC (median level = 1·79 mg mL−1) and cirrhosis (1·09 mg mL−1) were not significantly different ( P  = 0·1376) while DCP-IgM were significantly higher in HCC patients (median level = 2171·2 AU mL−1) than in those with cirrhosis (1152 AU mL−1, P  = 0·0047). No correlation was found between DCP-IgM and IgM in HCC ( r  = 0·227) and cirrhosis patients ( r  = 0·475). DPC-IgM was positive in 55% (18/33) of HCC patients and in 26% (8/31) of cirrhosis patients compared to 39% and 26% for DCP and 48% and 13% for AFP. DCP-IgM, DCP and AFP tests had 100% specificity in healthy controls.
Conclusions   DCP-IgM in HCC patients was not associated with an increase in IgM concentration. DCP-IgM was more frequently detected in HCC patients than DCP and AFP, strengthening the diagnostic role of IgM immune complexes for liver cancer.  相似文献   

9.
Upon stimulation, polymorphonuclear leucocytes (PMNs) release potent serine proteases, i.e. elastase, cathepsin G and proteinase 3, which contribute to the degradation of tissue and plasma components. Here, we describe the development of a plasma test to assess PMN-mediated fibrinogenolysis as a biochemical marker for actual PMN-derived proteolysis in vivo , useful for monitoring therapeutic efficacy, i.e. of elastase inhibitors. We generated a monoclonal antibody (MAb), designated 1-1/B3, with a high affinity for elastase-degraded fibrinogen (EDF). The epitope for 1-1/B3 becomes exposed in a time-dependent manner during digestion of fibrinogen with purified PMN-derived serine proteases and with isolated PMNs in vitro . However, 1-1/B3 does not react with plasma fibrinogen or with fibrin(ogen) degradation products generated by plasmin or by other active proteases that may occur locally, i.e. metalloproteases and lysosomal cathepsins. On the basis of MAb 1-1/B3, we developed a plasma test for the assessment of PMN-mediated fibrin(ogen) degradation products (PMN-FDP). In a panel of control plasmas, we observed concentrations of PMN-FDP of 8.2 ± 0.9 ng mL−1 ( n  = 18). These values were increased twofold in patients with α1-proteinase inhibitor deficiency (18.6 ± 3.3 ng mL−1; n  = 12;  P  < 0.0001) and even more in patients with sepsis (365.7 ± 97.7 ng mL−1; n  = 16;  P  < 0.0001). Furthermore, synovial tissue extracts from patients with rheumatoid arthritis contained increased levels of PMN-FDP, compared with synovial tissue extracts ( P  < 0.005) from patients with osteoarthritis.  相似文献   

10.
The authors investigated the production of interleukin-2 (IL-2) and interferon-gamma (IFN-γ) by phytohaemagglutinin (PHA)-stimulated T-lymphocytes from 21 untreated patients with acute brucellosis. PHA-stimulated T-lymphocytes from acute brucellosis patients showed normal IL-2 production but defective IFN-γ production (brucellosis patients 531 ± 103 pg mL−1 vs. healthy controls 1024 ± 212 pg mL−1) after 72 h of culture. This altered pattern of IL-2 and IFN-γ production by T-lymphocytes was observed in seven brucellosis patients whose T-lymphocytes exhibited a normal proliferative response to PHA (61 612 ± 18 422 cpm) as well as in the 14 patients with a defective T-lymphocyte proliferative response to the PHA after 5 days of culture (19 479 ± 4409 cpm). After antibiotic therapy, production of the two lymphokines by the PHA-stimulated T-lymphocytes from acute brucellosis patients was similar to that of T-lymphocytes from healthy control subjects. The authors conclude that PHA-stimulated T-lymphocytes from untreated patients with acute brucellosis have defective INF-γ production but normal IL-2 production.  相似文献   

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