Isolated, well-defined organovanadium(iii) on silica: single-site catalyst for hydrogenation of alkenes and alkynes.

A well-defined, isolated, single-site organovanadium(iii) catalyst on SiO2 [(SiO2)V(Mes)(THF)] was synthesized via surface organometallic chemistry, and fully characterized using a combination of analytical and spectroscopic techniques (EA, ICP, 1H NMR, TGA-MS, EPR, XPS, DR-UV/Vis, UV-Raman, DRIFTS, XAS). The catalyst exhibits unprecedented reactivity in liquid- and gas-phase alkene/alkyne hydrogenation. Kinetic poisoning experiments revealed that 100% of the V sites are active for hydrogenation.

A new oscillometric method for pulse wave analysis: comparison with a common tonometric method.

In the European Society of Cardiology-European Society of Hypertension guidelines of the year 2007, the consequences of arterial stiffness and wave reflection on cardiovascular mortality have a major role. But the investigators claimed the poor availability of devices/methods providing easy and widely suitable measuring of arterial wall stiffness or their surrogates like augmentation index (AIx) or aortic systolic blood pressure (aSBP). The aim of this study was the validation of a novel method determining AIx and aSBP based on an oscillometric method using a common cuff (ARCSolver) against a validated tonometric system (SphygmoCor). aSBP and AIx measured with the SphygmoCor and ARCSolver method were compared for 302 subjects. The mean age was 56 years with an s.d. of 20 years. At least two iterations were performed in each session. This resulted in 749 measurements. For aSBP the mean difference was -0.1 mm Hg with an s.d. of 3.1 mm Hg. The mean difference for AIx was 1.2% with an s.d. of 7.9%. There was no significant difference in reproducibility of AIx for both methods. The variation estimate of inter- and intraobserver measurements was 6.3% for ARCSolver and 7.5% for SphygmoCor. The ARCSolver method is a novel method determining AIx and aSBP based on an oscillometric system with a cuff. The results agree with common accepted tonometric measurements. Its application is easy and for widespread use.

[Transitional cell carcinoma of the bladder. Evaluation of plasma levels of cellular fibronectin as a stage-dependent marker]. / Das Transitionalzellkarzinom der Harnblase. Evaluation von zellulärem Fibronektin im Plasma als stadienabhängiger Marker.

Up to now markers for transitional cell carcinoma of the bladder (TCC) are missing. Fibronectin (FN) seems to play a key role in progression and invasion of malignant tumors. The aim of this study was to assess the value of cellular FN (cFN), a more specific subform of produced FN, in different stages of TCC.cFN was determined using a highly sensitive immunoassay which we developed. Blood samples were taken of 45 patients with the first diagnosis of TCC before undergoing TUR-B and 6 patients with metastatic TCC before chemotherapy; 70 patients with nonmalignant urological disorders served as a control group.Patients with TCC showed significantly elevated cFN plasma levels compared to controls (p<0.05). Patients with muscle-invasive disease (n=15) showed significantly higher cFN plasma levels compared to the group with superficial TCC. Patients with metastatic TCC showed the highest, but not significantly elevated cFN plasma levels compared to patients with muscle-invasive TCC.The elevated cFN plasma levels in TCC underline the important role of cFN for tumor progression and its potential role as a marker for TCC. Upcoming investigations are necessary to prove the value of the potential marker cFN during follow-up and its impact as a prognostic factor for recurrence and progression of TCC.

Evaluation of cellular fibronectin plasma levels as a useful staging tool in different stages of transitional cell carcinoma of the bladder and renal cell carcinoma.

Reliable markers for both renal cell carcinoma (RCC) and transitional cell carcinoma of the bladder (TCC) are lacking.During tumor progression and invasion components of extracellular matrix (ECM) are degraded and parts of these different components are detectable in plasma. Cellular fibronectin (cFN) represents a well characterized ECM protein. In contrast to fibronectin in plasma produced by hepatocytes (FN) cFN has a total extra domain sequence and occurs in much smaller amounts in the circulation. The aim of our study was to evaluate cFN as a marker and to determine its possible role in clinical staging of TCC and RCC.Blood samples were collected from 30 patients before they underwent transurethral resection of the bladder because of newly diagnosed TCC. Additionally samples were collected from 69 patients with RCC before therapy. Sixty patients with non-malignant urological disorders were recruited as control group. Determination of cFN in plasma was performed by using a highly sensitive time-resolved fluorescence immunoassay (TRFIA).The control group had median cFN plasma levels of 437 ng/ml. Patients suffering from TCC or RCC showed significantly higher cFN levels. In patients with muscle invasive TCC significant higher cFN levels (p < 0.05) could be demonstrated compared to non-muscle invasive TCC. Similar results were found in RCC with significant elevated cFN levels in metastatic RCC (p < 0.005) compared to localized stage of disease. No differences were found concerning tumor grading in both malignancies.In the face of significant elevated cFN levels in TCC and RCC our data underline the important role of cFN. For future investigations the elevated cFN levels in locally progressed and metastastic disease, indicating a clinically useful tool for preoperative staging and postoperative monitoring, are of high interest.

Alternative medicine. Achieving balance between herbal remedies and medical therapy.

The case patient was taking multiple herbal preparations as well as the prescription hypnotic zolpidem. The combination was probably increasing the patient's confusion, agitation, and aggression. The treatment team reached a compromise with the daughter after providing her with education and support. They continued the wheat germ oil and a multivitamin supplement, which appeared safe, even if of limited value. The patient continued taking valproate, 125 mg bid, which reduced her physical aggression and improved resistance to care. All other herbal remedies and zolpidem were discontinued. Balancing traditional therapies with requests for herbal remedies is a common challenge for physicians. The most successful intervention occurs when doctors familiarize themselves with herbal preparations and educate patients and families about the treatments.

Singlet oxygen ((1)O2) inactivates plasmatic free and complexed alpha2-macroglobulin.

alpha2-macroglobulin (alpha2M) is a broad-spectrum proteinase inhibitor and one of the major plasma proteins in humans. Activated phagocytes (especially granulocytes) generate large amounts of oxidants of the HOCI- and chloramine-type that release the mild nonradical, excited (light-emitting) oxidant singlet oxygen ((1)O2). These oxidants have been shown to inactivate several specific serine protease inhibitors in human blood [e.g., alpha1-antitrypsin or alpha2-antiplasmin (plasmin inhibitor)]. The studies reported here demonstrate that nonradical oxidants also inactivate plasmatic alpha2M. The effective dose for 50% inactivation (ED50) of plasmatic alpha2M is similar to that for plasmatic alpha2-antiplasmin. Chloramines are about 1,000-fold more effective than hydrogen peroxide (ED50)=0.75 micromol chloramine T/50 microl plasma). Serine protease-serine protease inhibitor complexes are resistant to oxidants. In contrast, here it is shown that alpha2-macroglobulin, even after binding to serine proteases is sensitive to oxidation, the captured protease is released from the protease/alpha2M complex. This is the first time that oxidative inactivation of a complexed (i.e., bound to a target protease) human protease inhibitor has be shown. The (1)O2 inhibitors methionine, cysteine, cystine, or ascorbate-in contrast to the oxy-radical scavengers mannitol, superoxide dismutase, or catalase-antagonize the chloramine/NaOCl-mediated inactivation of both uncomplexed and complexed alpha2M. Thus, the oxidant involved here is of nonradicalic nature and has reaction characteristics of (1)O2. For the inhibitory function, critical oxidizable methionines or the internal thiol-ester might be targets for (1)O2. Consequently, alpha2M can also be considered a carrier for proteases, since the alpha2M-complexed proteases regain full activity in an oxidative environment. In local areas of inflammation or thrombolysis, activated phagocytes could create microenvironments of uncontrolled protease activity by generation of (1)O2.

Investigation by isoelectric focusing of the initial carbohydrate-deficient transferrin (CDT) and non-CDT transferrin isoform fractionation step involved in determination of CDT by the ChronAlcoI.D. assay.

BACKGROUND: The introduction of a new set of reagents for the determination of carbohydrate-deficient transferrin (CDT) as a marker of chronic alcohol abuse requires an independent evaluation of the analytic specificity of the test. This information is needed for correct interpretation and classification of test results. METHODS: Isoelectric focusing on the PhastSystem(TM) followed by immunofixation, silver staining, and densitometry was used to validate the initial transferrin isoform fractionation step on anion-exchange microcolumns involved in the ChronAlcoI.D. assay. RESULTS: The in vitro transferrin iron load was complete and stable. The CDT and non-CDT transferrin fractionation on anion-exchange microcolumns was reliable and reproducible (CV < or = 10%). Except for quantitatively unimportant traces of trisialo-Fe(2)-transferrin (<5% of total CDT), only asialo-, mono-, and disialo-Fe(2)-transferrin were detected in the microcolumn eluates (n = 170). There was a loss of proportionally similar amounts of asialo-Fe(2)-transferrin (during column rinsing) and disialo-Fe(2)-transferrin (on the anion exchanger). Thus, the peak height ratios for disialo- and asialo-Fe(2)-transferrin did not change from >1 (serum) to <1 (eluates) as described for the CDTect assays. The transferrin patterns in the ChronAlcoI.D. eluates were representative of those in serum. Transferrin D variants with isoelectric points close to that of trisialo-Fe(2)-transferrin C1 did not cause overdetermination of CDT by the ChronAlcoI.D. test. CONCLUSIONS: The initial CDT and non-CDT fractionation step involved in determination of CDT by the ChronAlcoI.D. assay is efficient for eliminating non-CDT transferrins from serum before quantification of CDT in the final turbidimetric immunoassay. We recommend IEF for validation of other (commercial) CDT analysis methods and of odd CDT results.

Systemic inflammatory parameters in patients with atherosclerosis of the coronary and peripheral arteries.

Plasma concentration of markers of inflammation are increased in patients with atherosclerosis. However, it is unclear whether the pattern and magnitude of this increase vary with the site and extent of disease. In 147 patients undergoing semiquantitative coronary angiography, we measured the acute-phase reactants C-reactive protein (CRP) or serum amyloid A (SAA); the proinflammatory cytokine interleukin 6 (IL-6); the active and total fractions of the anti-inflammatory cytokine transforming growth factor-beta (TGF-beta); the macrophage activation marker neopterin; and the infection marker procalcitonin. Compared with 62 patients without either coronary artery disease (CAD) or peripheral artery disease (PAD), 57 patients with CAD but no PAD showed greater median CRP (0. 4 versus 0.2 mg/dL, P=0.004) and IL-6 (3.8 versus 1.6 pg/mL, P=0. 007) levels and a lower level of active-TGF-beta (57 versus 100 ng/mL, P=0.038). Moreover, CRP, IL-6, and neopterin levels showed a positive and the active TGF-beta level a negative correlation with the extent of coronary atherosclerosis. Compared with these 57 patients with CAD alone, 15 patients with PAD and CAD had higher median levels of SAA (17 versus 7 mg/mL, P=0.008), IL-6 (12 versus 4 pg/mL, P=0.002), neopterin (14 versus 11 mg/dL, P=0.006), and total TGF-beta (11834 versus 6417 ng/L, P=0.001). However, these strong univariate associations of markers of inflammation and atherosclerosis were lost in multivariate analysis once age, sex, and high density lipoprotein cholesterol or fibrinogen were taken into account. Increased plasma levels of CRP, SAA, IL-6, TGF-beta, neopterin, and procalcitonin constitute an inflammatory signature of advanced atherosclerosis and are correlated with the extent of disease but do not provide discriminatory diagnostic power over and above established risk factors.

CDTect-RIA and CDTect-EIA for determination of serum carbohydrate-deficient transferrin compared.

CDTect-RIA and CDTect-EIA for determination of serum carbohydrate-deficient transferrin (CDT) by radioimmunoassay and enzyme immunoassay respectively were tested for equality and precision in four European laboratories. For correlational studies, serum samples with CDT concentrations up to 130 U/l were analysed in accordance with a uniform trial schedule. The regression of CDT values obtained by the two procedures was computed for each laboratory using the method of Passing and Bablok. Slopes and intercepts of the regression functions did not differ significantly from the values 1 or 0, as proved by the corresponding 95% confidence intervals. Precision studies were computed using analysis of variance. For CDT concentrations at the upper reference limit for men, the within-day coefficients of variation (CVs) ranged between 0.7 and 6.4% (median 5.2%) for CDTect-RIA and from 4.3 to 9.2% (median 6.2%) for CDTect-EIA. The corresponding pure between-day CVs were 5.0-18.5% (median 9.8%) and 3.5-14.5% (median 10.9%). The study demonstrates the equality of CDT values obtained by CDTect-RIA and CDTect-EIA. According to this study, the two methods can be used interchangeably without getting fluctuating CDT values, e.g. in longitudinal studies.

Immunological measurement of transforming growth factor-beta 1 (TGF-beta1) in blood; assay development and comparison.

Development of a new, sensitive immunoassay for measuring transforming growth factor beta 1 (TGF-beta1) is described and compared with four commercially available TGF-beta1 immunoassays. Preanalytical conditions were evaluated. The nonlinearity found in serum or plasma is due to masking of TGF-beta1 by binding proteins in blood. Mixing TGF-beta1 with latency-associated peptide or alpha2-macroglobulin at physiological concentrations suppressed most of the TGF-beta1 signal. Plasma fibronectin showed no effect, even at concentrations exceeding its physiological range. Equilibrium concentrations computed from a model system confirmed the experimental results. Dilutional nonlinearity could be markedly reduced by an appropriately designed activation procedure that minimized the effects of reassociation between TGF-beta1 and its binding partners during restoration of a neutral pH. Plasma should be used for measuring TGF-beta1 in blood. Because serum TGF-beta1 is highly significantly correlated with the platelet count, probably most of the TGF-beta1 is released by platelet degranulation.

Serum laminin and hyaluronan in liver cirrhosis: markers of progression with high prognostic value.

BACKGROUND/AIMS: In a prospective study with a mean follow-up period of 12.5 +/- 3.5 months, we investigated the extracellular matrix components laminin and hyaluronan in serum for their diagnostic value in portal hypertension and in clinically severe complications of progressive liver cirrhosis. METHODS: In 38 patients with liver fibrosis (n = 4) and cirrhosis (Child A: n = 17, B: n = 7, C: n = 10), the serum concentrations of laminin and hyaluronan were determined. Portal hypertension was assessed by endoscopic control of the esophageal varices and by Doppler sonography of the portal blood flow. RESULTS: Neither laminin nor hyaluronan correlated with portal hypertension, but highly significantly increased (p < 0.001) concentrations of 3.25 +/- 0.2 U/ml (laminin) and 493 +/- 248 ng/ml (hyaluronan) were found in patients with complications of liver cirrhosis when compared to those without complications (Ln: 2.13 +/- 0.26 U/ml, HA: 206 +/- 184 ng/ml). At cut-off levels of 2.6 U/ml (laminin) and 200 ng/ ml (hyaluronan), the diagnostic sensitivity and specificity for severe complications of liver cirrhosis was 0.71 and 0.86 (Ln) and 0.90 and 0.67 (HA), respectively. The positive predictive values were of 0.8 (laminin) and 0.6 (hyaluronan). The relative risk of patients presenting elevated concentrations of laminin or hyaluronan at the start of the study for later development of severe complications was 2.7. CONCLUSIONS: Both parameters, especially serum laminin, can be used as prognostic markers in addition to the Child criteria in liver cirrhosis.

[The clinical value of laminin determination in advanced liver cirrhosis]. / Klinischer Wert der Lamininbestimmung bei fortgeschrittener Leberzirrhose.

OBJECTIVE: To test prospectively whether serum laminin levels, which is taken to indicate portal hypertension, can predict the occurrence of severe complications in advanced cirrhosis of the liver. PATIENTS AND METHODS: In 38 patients (21 men, 17 women; mean age 55.6 +/- 13.4 years) with liver fibrosis (n = 4) or liver cirrhosis (n = 34) serum laminin was measured by a commercially available radioimmunoassay (Behring, Marburg). The severity of liver cirrhosis was graded according to the Child-Pugh-Christensen criteria. Portal hypertension was assessed by standard endoscopic methods and portal-vein duplex sonography. Within a mean observation period of 12.5 +/- 3.5 months, the following were used as signs of severe clinical complications of liver cirrhosis: stages III and IV of hepatic coma, treatment-refractory ascites, portal vein thrombosis and death due to multi-organ failure. Acute bleeding from oesophageal varices was confirmed by emergency endoscopy. RESULTS: At laminin concentrations of 3.25 +/- 0.20 U/ml there was a highly significant correlation (P < 0.001) with complications of liver cirrhosis. Using 2.6 U/ml as the critical level, the occurrence of severe complications had a positive predictive value of 0.80 with a sensitivity and specificity of 0.71 and 0.86 respectively. This means that a patient who, at the beginning of the study period, had a raised laminin concentration, had a relative risk of 2.65 (1.41-4.97) for later severe complications. CONCLUSION: Serum laminin concentration has a diagnostic efficiency of 0.79 as a prognostic indicator and can thus serve as a valuable addition to the Child-Pugh-Christensen classification of liver cirrhosis.

Fibronectin in human bile fluid for diagnosis of malignant biliary diseases.

In a preliminary study, we demonstrated a strong association between the concentration of the glycoprotein fibronectin (FN) in human bile fluid and the presence of malignant biliary diseases. We now present the results of measurements of total FN (tFN) and cellular FN (cFN) within a larger group of 71 patients. Bile fluid was collected during routine endoscopic retrograde cholangiography or by transhepatic puncture, respectively, from patients admitted for examination/treatment of biliary obstruction. Determination of tFN in bile was performed using a previously described time-resolved fluorescence immunoassay (TRFIA). For cFN, a newly developed TRFIA, using a specific monoclonal antibody for the EDA epitope of cFN, was applied. Within the noncarcinoma group of patients (n=50), consistently low concentrations of tFN (median = 5 ng/mL) were found. In most of these cases, the corresponding concentrations of cFN were below the detection limit (2.6 ng/mL) of this assay. Highly significantly elevated concentrations were found for both tFN (median = 1,220 ng/mL) and cFN (median = 243 ng/mL) in the carcinoma group (n = 21) in comparison with the noncarcinoma group (P < or = .01). By adopting cutoff values of 60 ng/mL for tFN and >0 ng/mL for cFN, diagnostic sensitivities for carcinoma of the biliary tract of 0.89 and 0.92, and specificities of 0.96 and 0.98, respectively, were computed. FN in bile fluid is suggested as a sensitive, specific, and easily determined marker for differential diagnosis of malignant and benign diseases of the biliary tract.

Two sensitive time-resolved fluoroimmunoassays for cellular fibronectin.

Two sensitive sandwich-type immunoassays for determination of cellular fibronectin (cFN) in cell culture supernatants and in human plasma were developed. Both assays used a monoclonal antibody with specificity against the EDA sequence, which is characteristic for the cellular form of human and rat FN. Assay 1 involves binding of FN on gelatin-coated microwells followed by reaction with the anti-cFN antibody, whereas in assay 2 the anti-cFN antibody was immobilized first and detection was with an anti-FN antiserum. Time-resolved fluorescence spectrophotometry with measurement of an Eu3+ chelator after dissociation of the solid-phase complexes with urea/sodium dodecyl sulfate in the presence of excess Eu3+ was the detection method. The detection limit of the new assays was between 2.6 and 4.0 micrograms/L cFN. In serial dilution of human plasma samples, parallelism with the calibration curve was obtained over the whole measuring range (12-1000 micrograms/L) with assay 2, whereas assay 1 had deviations of the dilution curves at concentrations > or = 100 micrograms/L. The between-run CVs for assays 1 and 2 were 11.4% and 7.2%, respectively, at a concentration of 200 micrograms/L (median value of 18 experiments). Respective within-series CVs of 4.3% and 4.7% were obtained at the same concentration. The recovery of added cFN from human plasma was between 90% and 96%.

[Fibronectin in human bile--a new parameter for diagnosis of malignant bile duct processes?--A pilot study]. / Fibronectin in menschlicher Galle--ein neuer Parameter zur Diagnostik maligner Gallengangsprozesse?--Eine Pilotstudie.

In a pilot study it was investigated whether concentration of the glycoprotein fibronectin in the bile fluid can assist in differentiating between malignant and benign biliary tract obstructions. During endoscopic-retrograde cholangiography (ERC) and percutaneous transhepatic cholangiography (n = 3) native bile was aspirated in 29 patients. The concentration of fibronectin was determined by time resolved fluorescence immuno-assay. In 19 patients no biliary malignoma was present (choledocholithiasis: n = 9, normal finding: n = 10). Ten patients suffered from biliary or pancreatic cancer (infiltrating pancreatic cancer: n = 6; primary biliary tract cancer: n = 3, Klatskin tumor: n = 1). In the non malignant group a median fibronectin concentration of 12.0 ng/ml (lower-upper quartile 5-30 ng/ml) was found. A highly significantly elevated (p < 0.001, non parametric Kruskal-Wallis-test) median fibronectin concentration of 1675 ng/ml (lower-upper quartile 155-3430 ng/ml) could be determined in the malignant group. Our results show that in analogy to ascites, the concentration of biliary fibronectin is an important and easily determinable parameter in the differential diagnosis of benign und malignant diseases of the biliary tract.

Synergism between hepatocytes and Kupffer cells in the activation of fat storing cells (perisinusoidal lipocytes).

This study concerns the cooperation of hepatocytes (PC) and Kupffer cells (KC) in the activation of rat liver fat storing cells (FSC) in culture. Various dilutions of conditioned media collected from early, serum-free cultures of both cell types were added separately and in combination, either simultaneously or sequentially, to early, non-confluent, primary cultures of FSC maintained under serum-reduced (0.5% fetal calf serum) conditions to determine the effects on proliferation (incorporations of [3H]thymidine and bromodeoxyuridine [BrdUrd], DNA-content, cell number), transformation and morphology (phase contrast microscopy, immunostainings of desmin and smooth muscle-alpha-actin), on the deposition of fibronectin and laminin and on the formation of 35S sulfated medium proteoglycans. Media of both cell types stimulated cell proliferation in a dose-dependent manner but combined PC- and KC-conditioned media was most potent and increased the incorporation of [3H]thymidine to 4-times above control values. The multiplication stimulatory effects visualized by labeling cell nuclei with BrdUrd and the increase of cell number per culture well were additive. The sequential addition of KC-conditioned medium to FSC preexposed to PC-conditioned medium increased the multiplication of FSC further and in an additive manner. The mitogenic activity of the PC-medium and the enhancing effect of KC-induced FSC proliferation was measured also when PC were damaged by incubation under anoxic conditions during generation of the conditioned medium. This observation indicates the release of the mitogen by membrane damage presumably from a cytoplasmic pool. The PC-medium did not induce either significant morphological changes or transformation of FSC towards myofibroblast-like cells. KC, however, generated transformation of FSC as indicated by more elongated cells with spindle-like cellular extensions and a reduction of retinoid droplets. Both these morphological effects were visible when PC and KC media were added simultaneously. Both media act synergistically on the deposition of fibronectin and laminin in FSC cultures and these components were found to be elevated 2.3 and 2.8-fold, respectively, if the cells were exposed to the combined media. Proteoglycan synthesis was also maximally enhanced if FSC were exposed to PC- and KC-media simultaneously. These findings suggest the involvement of (damaged) hepatocytes in the process of FSC activation. A model of sequential, spatial and time-dependent activation of FSC is suggested where cells in the immediate proximity of hepatocytes are primed to proliferate by a mitogenic signal released by membrane damage presumably from a cytoplasmic pool of injured hepatocytes into the pericellular environment. This non-inflammatory stimulation is followed by secretions of activated Kupffer cells and other inflammatory cell types which further enhance the activation of FSC.(ABSTRACT TRUNCATED AT 400 WORDS)

Laminin and aminoterminal propeptide of type III procollagen in seminal plasma from fertile and vasectomized men.

The components of the extracellular matrix, laminin and aminoterminal propeptide of type III procollagen (PIIINP) were determined in seminal plasma of 50 patients with vasectomy and of 50 age-matched fertile patients. The concentration of laminin was highly significantly (P < 0.001) elevated in the fertile group as compared to the vasectomy group, whereas the concentrations of PIIINP were not significantly different between these two groups. Only weak correlations were observed between the concentrations of laminin and PIIINP. It is suggested that part of the laminin found in seminal plasma is derived from the ductus deferens, while the source of PIIINP is probably located at an upper part of the urogenital tract.

PIP: The aim was to examine the effect of the resection of the ductus deferens on the pattern of extracellular matrix components in seminal plasma. The components laminin and aminoterminal propeptide of type III procollagen (PIIINP) were determined in seminal plasma of 50 patients with vasectomy and of 50 age-matched fertile patients. Fifty ejaculates from normal fertile men and 50 ejaculates from patients with vasectomy were randomly selected from a pool of clinical specimens at the Kantonsspital Aarau, Switzerland. Age ranges were between 19 and 43 years. Laminin was measured with a competitive radio immunoassay using a rabbit antiserum against the pepsin-resistant fragment P1 of human laminin. PIIINP was measured with a new radioimmunoassay using monoclonal antibodies against the aminoterminal propeptide in a 2-stage sandwich assay. Laminin and PIIINP could be detected in all seminal plasma of the fertile group and the vasectomy group, respectively. The median concentration of laminin in seminal plasma was 1.98 kU per liter in the fertile group and 1.25 kU per liter in the vasectomy group. The median concentration of PIIINP in the seminal plasma of the fertile group was 0.59 kU per liter and 0/52 kU per liter in the vasectomy group. For laminin the concentration levels in the fertile and the vasectomy group were significantly different (P or= 10 -7). No significant differences were obtained for PIIINP (P 0.05). The concentration of laminin was very significantly (P 0.001) elevated in the fertile group as compared to the vasectomy group, whereas the concentration of PIIINP were not significantly different. In the combined groups, a weak correlation between laminin an PIIINP was observed (P 0.05). This correlation was even lower in the fertile group (P 0.05), whereas within the vasectomy group it was slightly higher. If results can be verified in larger groups of patients with aspermia caused by testicle disorders and by a block of the ductus deferens, the determination of laminin in seminal plasma might prove useful as an adjuvant diagnostic measure.