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P Wessels

Publications and source records attributed to P Wessels.

18 recordsLinked to original sources
PubMed2003

Rapidly tunable continuous-wave optical parametric oscillator pumped by a fiber laser.

We report on rapid, all-electronically controlled wavelength tuning of a continuous-wave (cw) optical parametric oscillator (OPO) pumped by an ytterbium fiber laser. The OPO is singly resonant for the signal wave and consists of a 40-mm-long periodically poled lithium niobate crystal in a four-mirror ring cavity. By tuning of the fiber-laser wavelength over 33 nm through an intracavity acousto-optic tunable filter, the OPO idler wavelength is tuned from 3160 to 3500 nm in 330 micros, corresponding to an idler frequency-tuning speed of 28 THz/ms. At a fiber-laser power of 6.6 W at 1074 nm, the singly resonant OPO generates 1.13-W cw idler radiation at 3200 nm.

Journal Article↗
PubMed2000

Intramedullary spinal cord metastasis as a first manifestation of a renal cell carcinoma: report of a case and review of the literature.

The authors report the case of a 70-year-old woman who developed a Brown-Sequard-syndrome within 6 weeks caused by an intramedullary spinal cord metastasis of an occult renal cell carcinoma. Intramedullary metastases are rare and represent only 4-8.5% of central nervous system metastases. An important feature of intramedullary metastases is the rapid progression of neurological deficits which necessitates rapid treatment. There are only eight earlier reports of intramedullary metastasis due to renal cell carcinoma (Schiff D, O'Neill BP. Intramedullary spinal cord metastases: clinical features and treatment outcome. Neurology 1996;47:906-12; Belz P. Ein Fall von intramedullaerer Grawitz-Metastase im Lumbalmark. Frankfurt Z Pathol 1912;10:431-44; Gaylor JB, Howie JW. Brown-Sequard-syndrome. A case of unusual aetiology. J Neurol Neurosurg Psychiatry 1938;1:301-5; Kawakami Y, Mair WGP. Haematomyelia due to secondary renal carcinoma. Acta Neuro Pathol 1973;26:85-92; Strang RR. Metastatic tumor of the cervical spinal cord. Med J Aust 1962;1:205-6; Von Pfungen. Uber einige Fälle von Haematomyelie nichttraumatischen Ursprungs. Wien Klin Rdsch 1906;20:44-50; Weitzner S. Coexistent intramedullary metastasis and syringomyelia of cervical spinal cord. Report of a case. Neurology 1960;674-8). To the best of our knowledge this is the first report on a patient in whom symptoms from the metastasis of a renal cell carcinoma preceded the detection of the primary tumor. This report presents the clinical, neuroradiological and histopathological findings of an intramedullary metastasis of a renal cell carcinoma and provides an overview of the literature on intramedullary spinal cord metastases.

Aged↗
PubMed1996

Biosynthesis of acylpeptidolactones of the daptomycin type. A comparative analysis of peptide synthetases forming A21978C and A54145.

A21978C and A54145 are antibacterial 13-residue peptides with a medium-chain-acylated amino terminus and a 10-residue lactone ring; they are produced by strains of Streptomyces roseosporus and Streptomyces fradiae, respectively. The structural differences in their peptide chains, which include amino acid replacements and modifications (L-Glu2-->L-Asn, L-Asn(OH)3-->L-Asp, Sar5-->Gly, L-Ala6-->L-Orn, L-Lys8-->D-Ala, L-Asp(OMe)9-->L-Asp, L-Asn11-->D-Ser, and L-lle13-->L-Kyn; Sar = sarcosine; L-Orn = L-ornithine, L-Kyn = L-kynurenine), reside in the multienzymatic templates directing their biosynthesis. We have examined the peptide synthetases employing immunodetection and substrate activation detected by the amino-acid-dependent ATP-PP1-exchange reaction. Two different antibodies specific for actinomycin synthetase 2 and a peptide sequence characteristic of acyl-CoA-synthetases/peptide synthetases were applied. For the A21978 system two peptide synthetases of 670 and 240 kDa were detected, together with two similar proteins of 630 and 440 kDa occurring in varying amounts. The latter are suggested to be degradation products of an unstable multienzyme. Activation of L-Asp, L-Thr, Gly, L-Orn, L-Ala and L-Ser were assigned to the high-molecular-mass components of 670, 630 and 440 kDa. The 240-kDa protein was purified to homogeneity and shown to catalyse activation of L-kynurenine. The A54145 system consisted of three peptide synthetases of 690, 590 and 250 kDa. Activations of L-Asn. L-Thr and Gly were found. The 250-kDa synthetase was capable of activating isoleucine and valine. Both systems thus show a comparable organisation; implications for the modular construction of their peptide synthetases are discussed.

Amino Acid Sequence↗
PubMed1994

Secondary metabolites by chemical screening, 26.1 7-O-beta-D-galactosyl-brefeldin A via transglycosylation with Penicillium brefeldianum.

A lactose-containing fermentation medium initiated the formation of 7-O-beta-D-galactosyl-brefeldin A [1] in the brefeldin A-producing organism, Penicillium brefeldianum. The detection, isolation, and physicochemical properties of 1, which has been produced by biological derivatization via transglycosylation, are described. Compound 1 is the first glycosylated brefeldin A derivative to have been prepared.

Animals↗
PubMed1990

A model to detect interactions between roxithromycin and oral contraceptives.

Twenty-two healthy women participated in a study to determine whether roxithromycin (a new macrolide antibiotic agent) obtunds the activity of a triphasic oral contraceptive. The duration of the study was four menstrual cycles. Medication was given as follows: (1) cycle 1, no medication to demonstrate ovulation; (2) cycle 2, triphasic oral contraceptive daily to suppress ovulation; (3) cycle 3, triphasic oral contraceptive daily plus roxithromycin, 150 mg b.i.d.; and (4) cycle 4, triphasic oral contraceptive daily plus rifampin, 300 mg daily. Sonography of the ovaries was performed on day 13, and serum progesterone was measured on day 21 of each cycle. Elevated progesterone indicated ovulation. The presence of a maturing follicle supported this finding. All volunteers ovulated in the first cycle and no volunteers ovulated in the second and third cycles. However, 11 women ovulated when rifampin and the triphasic oral contraceptive were given concomitantly. The findings suggest there is no reason to believe that roxithromycin interferes with the efficacy of oral contraceptives.

Adolescent↗
PubMed1988

A computer program in compiled BASIC for the IBM personal computer to calculate the mean platelet survival time with the multiple-hit and weighted mean methods.

We developed an easy-to-operate computer program for the IBM personal computer to calculate, display and store in a database platelet kinetic data determined by analysis of the rate of clearance of radiolabeled blood platelets from the circulation. This was done by curve fitting using the weighted mean method and multiple-hit model. These models are complementary and calculating the mean platelet survival time with both is recommended. Improvement of the weighted mean method was investigated. The optimized weighting and fitting the exponential function with the Marquardt non-linear least squares method improved the weighted mean method. The weighted mean and multiple-hit models fit the survival curve data equally well. The calculation of the mean platelet survival time with the weighted mean method was very fast. The duration of calculation with the multiple-hit model could take up to 2 minutes. Calculation of the mean platelet survival time using both models has the advantage that conditions when calculation of the mean platelet survival time would be invalid, can be detected. The computer program will promote the valid comparison of results obtained at different institutions.

Blood Platelets↗
PubMed1987

Kinetics and in vivo distribution of in-111-labelled platelets and platelet function in familial hypercholesterolaemia.

The kinetics, in vivo distribution and sites of sequestration of autologous In-111-labelled platelets and other platelet function parameters were studied in ten patients with type IIa or IIb familial hypercholesterolaemia and thrombotic complications of atherosclerosis. The in vitro platelet aggregation response to ADP (P = 0.50) and collagen (P = 0.46); binding of fibrinogen to platelets (P = 0.61); and plasma beta-thromboglobulin levels (P = 0.42) of the patients and normal reference subjects did not differ significantly. The in vivo distribution of In-111-labelled platelets at equilibrium was within normal limits, and at the end of platelet life-span the sequestration pattern of labelled platelets in the reticuloendothelial system was also normal (spleen P = 0.31; liver P = 0.54). There was minimal evidence of in vivo platelet activation: only mean platelet lifespan (MPLS), 195 +/- 57 hours (difference between mean MPLS of patients and controls was 25 hours, with a 95% confidence interval from 23 to 31 hours; P = 0.02); mean platelet platelet turnover, 2298 +/- 824 platelets/microliter/hour (P = 0.005); plasma platelet factor 4 (P = 0.02); and the mean circulating platelet aggregate ratio, 0.8 +/- 0.1 (P = 0.02); differed significantly from normal. These results suggest that abnormalities of platelet function and kinetics observed in type II hyperlipoproteinaemia cannot be ascribed wholly to the hyperlipidaemia, but may be induced by the associated atherosclerosis.

Adult↗
PubMed1986

Evidence that 111In-labelled platelets pool in the spleen, but not in the liver of normal humans and baboons.

The kinetics of pooling of platelets in the spleen may be used to measure spleen function. However, pooling of platelets in other organs, especially the liver, may affect these kinetic measurements. We have therefore compared, in man and baboon, the kinetics of 111In-labelled platelets and 111In-labelled red cells in the liver and spleen during the first 60 min after reinjection. This was determined in vivo with a scintillation camera and computer-assisted image analysis. Organ radioactivity was expressed as a percentage of that of the whole body. In both humans and baboons, the spleen accumulated many more platelets than red cells. Also, the red cells equilibrated more rapidly. The presence of a splenic platelet pool was thus confirmed. In contrast, the percentages of labelled platelets and labelled red cells in the liver were similar in both species. In both species, the sum total of labelled platelets in the circulation, i.e. recovery, and that quantified in the spleen at equilibrium, were equal to approximately 100%. These results confirm the presence of the exchangeable splenic platelet pool, and indicate that there are no significant exchangeable platelet pools in either the liver or any other organs.

Animals↗
PubMed1986

Evaluation of mathematic models to assess platelet kinetics.

Twelve mathematic methods used to calculate the mean platelet survival time were compared by determining the "goodness of fit" of the models to the platelet survival curves of 15 reference subjects and 54 patients. Platelets were labeled with [111In]oxine. The linear (LN), exponential, weighted mean, multiple hit (MH), Dornhorst (DH), Meuleman (ML), alpha order (AO), and polynomial (PO) mathematic models were investigated. The goodness of fit for the exponential model was determined by the nonlinear least squares method (EP), and also by the linear least squares method on logarithmically transformed data (EX) as is recommended. The modified weighted mean (MWM) and the usual weighted mean method (WM) obtained with these exponential models were tested. The Dornhorst (DH10) and Meuleman (ML10) models, where the potential age-dependent platelet survival times were kept constant at 10 days, were also evaluated. The goodness of fit results, expressed as % s.d. indicated that the LN (5.2%), EX (5.0%), EP (4.4%), WM (3.7%), DH10 (3.7%), and ML10 (3.7%) models all fitted the data significantly worse than the MWM, MH, DH, ML, AO, and PO models (range 3.2-3.3%). The mean platelet survival time determined with the MH model differed significantly from the results with the DH, ML, and AO models. The results of mean platelet survival time calculated with different mathematic models cannot, therefore, be compared directly. The models that fitted the platelet survival curve well varied slightly in sensitivity to noise as is indicated by the coefficient of variation of the mean platelet survival time estimates for the reference subjects (range 7.9-12.0%). Fitting data to at least two mathematic models has definite advantages. Data on which the calculations are based are probably invalid if the following are true: (a) if the mean platelet survival time estimated with the alpha order model is shorter than that estimated with the EP, MWM, or MH models, or (b) the mean platelet survival time estimated with either the DH, ML, AO, or PO models, is longer than the LN, MWM, or MH estimate of the mean platelet survival time. We conclude that the mean platelet survival time can be reliably estimated by fitting the data to either the MWM method (if limited computing facilities are available) or the MH model. Confidence in the result will be increased if considered in conjunction with the finding obtained with one other model; in those cases where the platelet survival time is very short, the alpha order model is recommended.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Platelets↗
PubMed1986

Platelet turnover and kinetics in immune thrombocytopenic purpura: results with autologous 111In-labeled platelets and homologous 51Cr-labeled platelets differ.

Mean platelet survival and turnover were simultaneously determined with autologous 111In-labeled platelets (111In-AP) and homologous 51Cr-labeled platelets (51Cr-HP) in ten patients with chronic immune thrombocytopenic purpura (ITP). In vivo redistribution of the 111In-AP was quantitated with a scintillation camera and computer-assisted image analysis. The patients were divided into two groups: those with splenic platelet sequestration (spleen-liver 111In activity ratio greater than 1.4), and those with diffuse sequestration in the reticuloendothelial system. The latter patients had more severe ITP reflected by pronounced thrombocytopenia, decreased platelet turnover, and prominent early hepatic platelet sequestration. Mean platelet life span estimated with 51Cr-HP was consistently shorter than that of 111In-AP. Platelet turnover determined with 51Cr-HP was thus over-estimated. The difference in results with the two isotope labels was apparently due to greater in vivo elution of 51Cr. Although the limitations of the techniques should be taken into account, these findings indicate that platelet turnover is not always normal or increased in ITP, but is low in severe disease. We suggest that this may be ascribed to damage to megakaryocytes by antiplatelet antibody. The physical characteristics in 111In clearly make this radionuclide superior to 51Cr for the study of platelet kinetics in ITP.

Adolescent↗
PubMed1985

An improved method for the quantification of the in vivo kinetics of a representative population of 111In-labelled human platelets.

The recommended and commonly used methods for the isolation of platelets from whole blood do not harvest a representative platelet population. There is evidence that these methods may result in the loss of a functionally more active platelet subpopulation. We describe a method whereby a completely representative population of platelets was isolated from the whole blood of 28 normal human volunteers by repeated washing of platelets from the red-cell layer. The harvesting efficiency was 98.3% +/- 2.8%. The platelets were labelled with 111In-oxine in a saline milieu with a labelling efficiency of 86.4% +/- 6.8%. The disappearance of reinjected labelled autologous platelets from the circulation was almost linear, and the mean platelet survival was estimated to be 224 +/- 23 h. At equilibrium, 61% +/- 12% of the labelled platelets were recovered from the circulation. The in vivo distribution at equilibrium and the sites of sequestration of the senescent labelled platelets were determined by geometric-mean whole-body quantification in six of the volunteers. This improved method permits accurate quantification of organ 111In radioactivity. Following reinjection, the labelled platelets pooled in the spleen and the accumulated activity can be presented by a single exponential function. At equilibrium, 31.1% +/- 6.1% and 9.6% +/- 1.2% of the platelets were in the spleen and liver, respectively. Splenic and hepatic radioactivity increased significantly with time, and at the end of the platelet life span, 35.6% +/- 9.7% and 28.7% +/- 8.3% of the labelled platelets were sequestrated in these organs, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Kinetics, in vivo redistribution and sites of sequestration of indium-111-labelled platelets in giant platelet syndromes.

Six patients with giant platelet syndrome were examined: four with Bernard-Soulier syndrome (two were asplenic); one with hereditary thrombopathic thrombocytopenia; and one with May-Hegglin anomaly. Autologous platelets were labelled with In-111-oxine and in vivo redistribution and sites of sequestration measured with quantitative imaging. In Bernard-Soulier syndrome platelet survival was normal or moderately shortened; platelet turnover was decreased only in the two patients with thrombocytopenia. In the patients with thrombopathia or May-Hegglin anomaly, platelet survival and turnover was moderately decreased. In those patients with normal-sized spleens, the mean splenic platelet pool consisted of 35.5% of the platelet mass, i.e. normal. The intrasplenic transmit time of the megathrombocytes was prolonged. Splenic blood flow was within normal limits. There was a marked accumulation of platelets in the liver at equilibrium: 15.5-58.8% of whole body radioactivity (normal 9.6 +/- 1.2%). This finding is unexplained. The final sites of sequestration of platelets were mainly in the liver and spleen, similar to that seen in normal subjects. We conclude that there is no inverse relationship between cell size and splenic platelet transit time. Platelet size therefore does not determine the size of the splenic platelet pool. The size of the platelets also does not seem to affect the sites of sequestration at the end of their life span.

Adult↗
PubMed1985

Kinetics, distribution, and sites of destruction of indium-111 oxine labelled red cells in haemolytic anaemia.

The survival of red cells labelled with indium-111 oxine in the circulation was determined. In vivo distribution at equilibrium and sites of deposition at the T50In--that is, the half life of labelled red cells--were quantitated with a scintillation camera and computer assisted image analysis. Although the rate of elution. Of 111In from the red cells was higher than that of chromium-51-disodium chromate, estimates of T50In and T50Cr corresponded reasonably well and were shortened in haemolytic anaemia. In normal subjects red cells were sequestered mainly in the liver and spleen. In five patients with different types of haemolytic anaemia two distinct patterns of red cell sequestration could be recognised: mainly splenic sequestration, and destruction of red cells in the liver, spleen, and the bone marrow. These patterns were expected for the particular disease studied.

Adolescent↗
PubMed1984

Indium-111-labelled human platelets: a method for use in severe thrombocytopenia.

We describe and evaluate a simple method for labelling autologous human platelets with Indium-111-oxine in patients with severe thrombocytopenia. Twenty patients with immune thrombocytopenia and platelet counts ranging from 5 to 119 X 10(9)/1 were investigated. Platelets were isolated from blood by differential centrifugation, residual platelets were repeatedly washed from the red cell layer and buffy coat and labelled with In 111 in saline. A mean of 55% +/- 21 of platelets were harvested from the blood, labelled with 49% +/- 24 efficiency and 15.8 X 10(8) labelled platelets reinjected to the patients. Contamination of the platelets with red cells and plasma was low. The labelled platelets were viable as assessed by in vitro aggregation, recovery in the circulation and mean survival time. This method permits quantitative platelet imaging with autologous labelled platelets in patients with severe thrombocytopenia.

Blood Platelets↗
PubMed1982

A quantitative study of indium-111-oxine platelet kinetics in acute and chronic renal transplant rejection.

Thirteen patients were investigated on 22 occasions at times varying from 1 day to 10 years after living family donor or cadaver renal transplantation. Platelet survival in the circulation, and in vivo platelet distribution and sites of deposition and sequestration was quantitatively determined with Indium-111-oxine (In-111-oxine) labelled platelets and a scintillation camera interfaced with a computer assisted imaging system. In all patients platelet survival was shortened and the platelet survival curve exponential. In patients with no evidence of transplant rejection and those with chronic rejection, there was no measurable or visible accumulation of labelled platelets in the kidney. The sequestration pattern of In-111 labelled platelets at the end of platelet life span was within normal limits and located in the reticuloendothelial system. In those patients with acute transplant rejection, platelet survival was shortened. Labelled platelets accumulated in the kidney: this was clearly visualized on scintigraphy and reflected by a significant increase in the radioactivity count density of the kidney. Platelets not deposited in the transplant were sequestrated in the reticuloendothelial system. This study demonstrates the diagnostic value of In-111 labelled platelet kinetics in the investigation of acute renal failure after renal transplantation. This investigation appears of limited clinical value in chronic rejection.

Adult↗
PubMedDate not supplied

Kinetics and mobilization from the spleen of indium-111-labeled platelets during platelet apheresis.

The rate and extent of platelet mobilization from the spleen were measured, and their relationship to the removal of platelets from the peripheral blood during discontinuous flow platelet apheresis was determined in four normal volunteers. Autologous platelets were labeled with Indium-111-oxine and in vivo whole body and organ In-111 radioactivity quantitated with a scintillation camera and a computer-assisted imaging system. Dynamic changes in splenic radioactivity were monitored during 12 cycles of platelet apheresis. The number of platelets harvested and changes in whole body and blood In-111 activity were determined during the procedure. The platelet life-span was estimated, and the sites of sequestration of labeled platelets was measured. Platelet apheresis removed a mean of 64 percent of platelets in the circulation; i.e., 48 percent of all platelets in the body. During the procedures, 28.0 +/- 9.4 percent In-111-labeled platelets in the body were removed, splenic radioactivity decreased by 36.5 +/- 13.2 percent, and whole body activity decreased by 34.5 +/- 9.7 percent. In-111 activity in the spleen and whole body decreased in parallel, indicating a dynamic equilibrium between these pools. The life-span of the labeled platelets was 226 +/- 25 hours, similar to that of normal subjects. The major sites of sequestration of senescent platelets were the spleen (37.9 +/- 20%) and liver (30.3 +/- 5.6%); this is similar to that found in normal subjects. We conclude that as platelets are removed from the peripheral blood, the blood pool is rapidly and effectively replenished from the splenic platelet pool. These two pools are in dynamic equilibrium and permit removal of large numbers of platelets without resultant thrombocytopenia. Platelet apheresis does not adversely effect platelet life-span, and the sequestration pattern in the reticuloendothelial system is normal.

Adult↗