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Biomedical subjects

J Meyer

Publications and source records attributed to J Meyer.

At least 361 records · Page 20Linked to original sources
PubMed1997

Effect of an encapsulated anti-elastase compound on experimental gingival inflammation in the rat.

An animal (rat) model of gingival injury ("impaction") induced a gingival inflammatory reaction, which was characterized by a breakdown of gingival collagen and the elastic network, as well as a significant increase of gingival elastase. The present study was conducted to investigate whether ceramides, sphingolipids composed of sphingosine N-acyl-linked to fatty acids, a chemical structure with antielastase properties, could counteract the development of such an inflammatory process. The ceramides used in these experimental series were extracted from wheat and characterized. The main fatty acids were 16:0, 18:1, 18:2, and the sphingoid moiety was phytosphingosine. Inhibition of elastase by ceramides was demonstrated in vitro and the concentration necessary to inhibit 50% of elastase activity was 41 mg/l using the synthetic substrate methoxysuccinyl-alanine-alanine-proline-valine-p-nitroanilide (MeOSuc-AlaAlaProValpNA). However, this anti-elastase activity was not observed in vivo in our animal model of gingival inflammation. A glycosaminoglycan (Heparin), recognized as a potent inhibitor of elastase, was entrapped in ceramides. A local treatment of impacted gingivae by encapsulated heparin led to a dose-related decrease of the elastase level in gingival extracts. Encapsulation in ceramides potentiated the effect exerted by heparin alone. This inhibitory effect of encapsulated heparin on elastase suggested a vector effect of these amphipathic molecules.

Animals↗
PubMed1997

Elevated plasma norepinephrine after in utero exposure to cocaine and marijuana.

OBJECTIVE: To compare plasma catecholamine concentrations between cocaine-exposed and unexposed term newborns and to determine the relationship between plasma catecholamines and newborn behavior. METHODS: Forty-six newborn infants participating in a prospective study of the neonatal and long-term effects of prenatal cocaine exposure were studied. Based on maternal self-report, maternal urine screening, and infant meconium analysis, 24 infants were classified as cocaine-exposed and 22 as unexposed. Between 24 and 72 hours postpartum, plasma samples for norepinephrine (NE), epinephrine, dopamine, and dihydroxyphenylalanine analysis were obtained. The Neonatal Behavioral Assessment Scale was administered at 1 to 3 days of age and at 2 weeks of age by examiners masked to the drug exposure status of the newborns. RESULTS: The cocaine-exposed newborns had increased plasma NE concentrations when compared to the unexposed infants (geometric mean, 923 pg/mL vs 667 pg/mL). There were no significant differences in plasma epinephrine, dopamine, or dihydroxyphenylalanine concentrations. Analysis for the effect of potential confounding variables revealed that maternal marijuana use was also associated with increased plasma NE, although birth weight, gender, and maternal use of alcohol or cigarettes were not. Geometric mean plasma NE was 1164 pg/mL in those infants with in utero exposure to both cocaine and marijuana compared to 812 pg/mL in those exposed to only cocaine and 667 pg/mL in those exposed to neither. Among the cocaine-exposed infants, plasma NE concentration correlated with an increased score for the depressed cluster (r = .53) and a decreased score for the orientation cluster (r = -.43) of the Neonatal Behavioral Assessment Scale administered at 1 to 3 days of age. Adjusting for marijuana exposure had no effect on these relationships between plasma NE and the depressed and orientation clusters. CONCLUSION: Plasma NE is increased in newborns exposed to cocaine and marijuana. Increased plasma NE is associated with selected neurobehavioral disturbances among cocaine exposed infants at 1 to 3 days of life but not at 2 weeks.

Cannabis↗
PubMed1997

Active and alpha-1 proteinase inhibitor complexed leukocyte elastase levels in crevicular fluid from patients with periodontal diseases.

Human leukocyte elastase is present in large amounts in the crevicular fluid of patients with periodontal disease and was considered as a putative biological marker of the evolution of such diseases. The aim of this work was to measure spectrophotometrically amounts of active elastase (AE) and elastase complexed to alpha 1 proteinase inhibitor (E-alpha 1-PI) in gingival crevicular fluid obtained, from patients suffering from rapidly progressive periodontitis (RPP group) or adult periodontitis (AP group) with different probing depths (3 to 5 mm and > 6 mm). AE and E-alpha 1-PI concentrations were negligible in healthy individuals. AE, but not E-alpha 1-PI, concentration appears to vary significantly with the probing depth in patients suffering either from rapidly progressive or adult periodontitis. No correlations were found between levels of AE and E-alpha 1-PI in the different groups of patients. AE concentration seems to be a marker of periodontal diseases in relation with probing depth.

Adult↗
PubMed1997

Vascular loops of the internal auditory canal: a diagnostic dilemma.

OBJECTIVE: To describe clinical and radiographic characteristics of vascular loops occupying the internal auditory canal. STUDY DESIGN AND SETTING: A retrospective review of patients with lesions initially suggestive of neoplasm, such as acoustic neuroma, who were subsequently found to have vascular compression of the facial and/or cochleovestibular nerves. The symptoms suggestive of this retrocochlear pathology, including vertigo, tinnitus, hearing loss, hemifacial spasm, and facial paralysis, were assessed. Subsequent evaluation with MRI revealed findings suggestive of intracannalicular neoplasm in three patients. MAIN OUTCOME MEASURES: Vascular loops with the cerebellopontine angle have been reported to approach the facial and cochleovestibular nerves at the level of the porus acousticus or within the internal auditory canal in approximately 65% of postmortem specimens. Although presumably the majority of individuals are asymptomatic, several cases are presented where vascular loop compression created symptoms and radiographic findings suggestive of neoplasm. RESULTS: Within this study, two patients underwent surgical exploration for expected neoplasm and were subsequently found to have pathology secondary to vascular loop compression. A third patient avoided surgical exploration due to radiographic confirmation with angiography. CONCLUSIONS: Although skepticism exists regarding true pathology occurring secondary to vascular loop compression, histologic confirmation of neural compression injury secondary to a vascular loop is presented. Further, diagnostic parameters and treatment are presented as well.

Aged↗
PubMed1997

Bone scintigraphy in the canine cruciate deficiency model of osteoarthritis. Comparison of the unstable and contralateral knee.

OBJECTIVE: To examine the effects on 99mTc medronate (MDP) bone scintigraphy of unilateral anterior cruciate ligament (ACL) transection in the unstable and contralateral knee of dogs. METHODS: Bone scintigraphy was performed in 5 dogs at baseline and 6 and 12 weeks after ligament transection, with images of both knees obtained 3-4 h after intravenous injection of the radionuclide. An image of the T4-T5 vertebral region was also acquired as an internal standard. In 3 additional dogs, scintigraphy was performed at baseline and 5 1/2 weeks after sham ACL transection. RESULTS: A marked increase in uptake of 99mTc MDP was seen in the unstable knee. In contrast, in all but one case uptake in the contralateral knee did not increase significantly. Sham ligament transection had no effect on uptake of the radionuclide. CONCLUSION: Changes occur in subchondral bone as well as in articular cartilage in the unstable knee in this model. The bony changes, which could be either primary or secondary to early changes in the biomechanical properties of the cartilage, may contribute to the pathogenesis of cartilage damage. No appreciable effects on bone turnover in the contralateral knee could be proved in this study.

Animals↗
PubMed1997

Radioiodine-labelled alpha-methyl-tyrosine in malignant melanoma: cell culture studies and results in patients.

Tyrosine is a precursor of melanin synthesis and might thus present a valuable marker for melanoma. The aim of this study was to evaluate the uptake of alpha-methyl-tyrosine (AMT) in melanoma cell cultures and to assess its usefulness as a radiopharmaceutical for staging melanoma patients with whole-body scintigraphy. Melanoma (M19-cell lines) and fibroblast (negative control) cell cultures were incubated with 125I-AMT and the radioactive uptake in the cell lines was measured in a gamma-counter over 24 h. For in vivo studies, planar whole-body scintigraphy and single photon emission computed tomography (SPECT) of the tumour region was performed following injection of 250-350 MBq 123I-AMT in six patients with known melanoma metastases. Findings were compared with results of whole-body positron emission tomography using 18F-fluorodeoxyglucose (FDG-PET) as a standard of reference. Fibroblasts showed an unchanged uptake of (mean +/- SD) 0.56 +/- 0.09% 15 min and 0.066 +/- 0.09% 24 h, respectively, after incubation of 125I-AMT, whereas there was an increased uptake in melanoma cell cultures over time from 0.9 +/- 0.05% to 7.5 +/- 1.6%. In staging melanoma patients, the sensitivity of whole-body AMT-scintigraphy compared with FDG-PET was 37% (10 of 27 metastases). AMT is transported and metabolized to a high extent in melanoma cells and 123I-AMT is accumulated in melanoma metastases. Owing to its low sensitivity, however, the clinical use of whole-body AMT scintigraphy cannot be recommended.

Adult↗
PubMed1996

Coordination of the [2Fe-2S] cluster in wild type and molecular variants of Clostridium pasteurianum ferredoxin, investigated by ESEEM spectroscopy.

The [2Fe-2S] ferredoxin from Clostridium pasteurianum contains five cysteine residues in positions 11, 14, 24, 56, and 60. This pattern is unique, and a combination of site-directed mutagenesis and spectroscopy is therefore being implemented to identify the ligands of the [2Fe-2S] cluster. The possible involvement of ligands other than cysteine in some molecular variants of this ferredoxin has been considered, histidines being likely candidates. Therefore, the three histidine residues in positions 6, 7, and 90 of the amino acid sequence have been individually and collectively replaced by alanine or valine. The mutated ferredoxins have been purified and were all found to contain [2Fe-2S] clusters of which the UV-visible absorption spectra were identical to that of the wild-type protein. The H6A/H7A/ H90A triply mutated ferredoxin was further characterized by EPR and by ESEEM spectroscopy and was found to differ only marginally from the wild-type protein. The ESEEM spectra of wild-type ferredoxin displayed weak 14N hyperfine interactions at the three principal g-factors of the [2Fe-2S] center. The estimated 14N coupling constants (Aiso = 0.6 MHz; e2qQ approximately 3.3 MHz) indicate that the ESEEM effect is most likely due to 14N from the polypeptide backbone. 2H2O ESEEM spectra showed that the [2Fe-2S] cluster is accessible for exchange with solvent deuterons. ESEEM spectra of the previously characterized C24A and C14A/C24A variants have been recorded and were also found to be very similar to those of the wild-type protein. There was no evidence for coordination of the [2Fe-2S] cluster by [14N]histidine or other 14N nuclei, in either wild-type or mutant forms of the ferredoxin. By these criteria, the environment of the [2Fe-2S] center is not distinguishable from those in plant-type ferredoxins. Non-cysteinyl coordination most probably occurs only in the C14A/C24A variant, which contains no more than three cysteine residues. The data shown here indicate that the fourth ligand of the [2Fe-2S] cluster is neither a histidine residue nor another nitrogenous ligand. The possibility of oxygenic coordination for this molecular variant is discussed.

Clostridium↗
PubMed1996

Inhibition of retinoblastoma protein translation by UVB in human melanocytic cells and reduced cell cycle arrest following repeated irradiation.

In human melanocytes and a human melanoma cell line (MM96L), the level of the retinoblastoma gene product (pRB) detected by Western blotting transiently decreased to 55% and 70% of controls respectively 9-12 h after a noncytostatic exposure (75 Jm-2) to UVB (280-315 nm) and to 2% and 14% 48 h after a cytostatic exposure (300 Jm-2). The pRB levels in fibroblasts and HeLa showed minimal loss, and under some conditions increased compared with unirradiated cells. Equitoxic doses of gamma radiation, cisplatin or the antimetabolite deoxyinosine had little effect on pRB levels. UVC (254 nm) was less inhibitory compared with equitoxic UVB. No loss of pRB mRNA was found in MM96L after UVB, nor was pRB protein stability significantly affected. Synthesis of new pRB in MM96L 24 h after UVB was 16% of controls, suggesting that loss of pRB results from a UVB-specific inhibition of translation. Compared with HeLa cells and fibroblasts, MM96L cells exhibited reduced cycle arrest if irradiated when pRB was depleted by a previous UVB exposure. These results suggest a mechanism whereby down-regulation of pRB translation by UVB may play a role in genesis of melanoma.

Cell Cycle↗
PubMed1996

Zinc- and iron-rubredoxins from Clostridium pasteurianum at atomic resolution: a high-precision model of a ZnS4 coordination unit in a protein.

The Zn(Scys)4 unit is present in numerous proteins, where it assumes structural, regulatory, or catalytic roles. The same coordination is found naturally around iron in rubredoxins, several structures of which have been refined at resolutions of, or near to, 1 A. The fold of the small protein rubredoxin around its metal ion is an excellent model for many zinc finger proteins. Zn-substituted rubredoxin and its Fe-containing counterpart were both obtained as the products of the expression in Escherichia coli of the rubredoxin-encoding gene from Clostridium pasteurianum. The structures of both proteins have been refined with an anisotropic model at atomic resolution (1.1 A, R = 8.3% for Fe-rubredoxin, and 1.2 A, R = 9.6% for Zn-rubredoxin) and are very similar. The most significant differences are increased lengths of the M-S bonds in Zn-rubredoxin (average length, 2.345 A) as compared with Fe-rubredoxin (average length, 2.262 A). An increase of the CA-CB-SG-M dihedral angles involving Cys-6 and Cys-39, the first cysteines of each of the Cys-Xaa-Xaa-Cys metal binding motifs, has been observed. Another consequence of the replacement of iron by zinc is that the region around residues 36-46 undergoes larger displacements than the remainder of the polypeptide chain. Despite these changes, the main features of the FeS4 site, namely a local 2-fold symmetry and the characteristic network of N-H...S hydrogen bonds, are conserved in the ZnS4 site. The Zn-substituted rubredoxin provides the first precise structure of a Zn(Scys)4 unit in a protein. The nearly identical fold of rubredoxin around iron or zinc suggests that at least in some of the sites where the metal has mainly a structural role-e.g., zinc fingers-the choice of the relevant metal may be directed by its cellular availability and mobilization processes rather than by its chemical nature.

Bacterial Proteins↗
PubMed1996

Comparison of myocardial perfusion reserve before and after coronary balloon predilatation and after stent implantation in patients with postangioplasty restenosis.

BACKGROUND: Stents provide a scaffold for coronary arteries after angioplasty and inhibit elastic recoil. METHODS AND RESULTS: In 25 patients with postangioplasty restenosis of the left anterior descending artery, ECG-gated digital subtraction coronary angiograms were recorded at baseline and during hyperemia (12 mg papaverine IC) before and after balloon predilatation (PTCA), after implantation of a Palmaz-Schatz stent, and after 6 months. Densitometric evaluation revealed different time and density parameters to calculate two definitions of myocardial perfusion reserve (MPR1 and MPR2) and maximum flow ratio (MaxFR). Poststenotic MPR1 increased from 1.57 +/- 0.14 to 2.59 +/- 0.86 after PTCA and to 3.10 +/- 0.41 after stenting, with 2.90 +/- 0.65 at follow-up (ANOVA, P < .05), while reference MPR1 remained unchanged at 3.10 +/- 0.40. Poststenotic MPR2 increased from 1.36 +/- 0.28 to 2.50 +/- 1.20 and to 3.40 +/- 0.58, respectively, with 3.20 +/- 0.92 at follow-up (ANOVA, P < .05), while reference MPR2 remained unchanged at 3.40 +/- 0.60. MaxFR was 2.13 +/- 0.53 after PTCA, elasticity 2.83 +/- 0.35 after stenting, and 2.73 +/- 0.58 at follow-up (ANOVA, P < .05). A good correlation was found between minimal stenotic luminal diameter and MPR1 or MPR2 (r = .87 and r = .94) and between luminal gain and MaxFR (r = .75). A negative correlation was measured between recoil and MPR1, MPR2, and MaxFR (r = -.80, r = -.86, and r = -.83). At follow-up, a steeper correlation was found between MPR and minimal stenosis diameter (MPR1: slope, 0.52 versus 0.91; MPR2: slope, 1.48 versus 1.95) and between MaxFR and net lumen gain (slope, 0.78 versus 1.27). CONCLUSIONS: Coronary stent implantation in patients with postangioplasty restenosis normalized poststenotic myocardial perfusion immediately as a result of a larger postprocedural lumen and a more pronounced inhibition of elastic recoil. After 6 months this benefit was sustained despite progressive lumen loss.

Absorptiometry, Photon↗
PubMed1996

Cysteine ligand swapping on a deletable loop of the [2Fe-2S] ferredoxin from Clostridium pasteurianum.

The [2Fe-2S] ferredoxin from Clostridium pasteurianum is unique among ferredoxins, both by its sequence and by the distribution of its cysteine residues (in positions 11, 14, 24, 56, and 60). In previous investigations, a combination of site-directed mutagenesis and of spectroscopic techniques showed that cysteines 11, 56, and 60 are ligands of the [2Fe-2S] cluster in the wild type protein and that cysteine 14 is not, but the status of cysteine 24 remained unclear. New mutated forms of this ferredoxin have been obtained and characterized. The data show that cysteine 24 is a ligand of the cluster in the wild type protein. When cysteine 24 is mutated into alanine, it is replaced as a cluster ligand by cysteine 14. The fourth ligand of the cluster can also be a cysteine residue newly introduced in position 16 when both cysteines 14 and 24 are replaced by alanine. These results suggest that the region encompassing cysteines 14 and 24 is a solvent-exposed flexible loop, in agreement with structure predictions. A number of nondeleterious deletions of variable length (3-14 residues) have been performed in the region of residues 17-32. The deletions were found to modify only marginally the spectroscopic properties of the [2Fe-2S] cluster but resulted in variations of its redox potential over a range of nearly 100 mV. This is the first instance of ligand swapping in a [2Fe-2S] protein, and the first time in any ferredoxin that a large loop has been excised from the structure without preventing the assembly of the iron-sulfur chromophore. Some of the molecular variants described here also highlight the similarities between the C. pasteurianum [2Fe-2S] ferredoxin and the 25 kDa subunit of the proton-translocating NADH: ubiquinone oxidoreductase of Paracoccus denitrificans.

Amino Acid Sequence↗
PubMed1996

[Diagnostic and differential diagnostic value of troponins].

PATIENTS AND METHOD: In consideration of own investigations and analysis of the most important publications of other authors, a critical interpretation of the concentrations of Troponin T (cut off: < 1 microgram/l) and Troponin I (cut off: < 0.4 microgram/l) was done in patients with acute and chronic muscle diseases, with chronic renal failure, with acute myocardial infarction, and stable and unstable angina pectoris, after coronary angioplasty, following cardiac surgery and critical care patients. RESULTS: In all cases with acute damage of the skeletal muscles (post operationem) the concentrations of TnT and TnI were in normal ranges. - In patients with chronic muscle diseases (M. Duchenne, Dermatomyositis) in 75% the TnT concentrations increased, while TnI concentrations were < 0.4 microgram/l. - In end stage renal disease patients undergoing chronic maintenance hemodialysis we found in 39% constantly elevated concentrations of TnT. TnI in all cases were in normal range. - In acute myocardial infarction in 97% of all patients both Troponins were increased, beginning 2 to 4 hours after onset. A normalization was observed between the 5th and 9th day. Very important is the differentiation between stable, and instable angina pectoris. In stable angina the concentration of both Troponins were in normal range, in contrast in 33 to 41% of all patients with unstable angina TnT and TnI were increased, in 9 to 16% even if the ECG showed no alteration. Elevated TnT or TnI concentrations predicted a significantly increased mortality. After coronary angioplasty and heparin treatment all patients had once more an elevation of TnT and TnI 8 and 27 hours after the invasive therapy. One of these substantial reasons for these minor myocardial cell necrosis is beside the endothelial injury the activation of the platelets and the coagulation system. - During the therapy with hirudin increases of TnT and TnI was not observed. Following cardiac surgery (ACVB) 6 to 48 hours after aortic unclamping 76 patients with TnI < 1 microgram/l had no perioperative myocardial infarction, while 14 patients with TnI concentrations > 1 microgram/l in 71.4% (n = 10) developed an acute infarction. - In patients in critical care units we observed only increased TnI concentrations in shock, especially in septic shock with multiple organ failures.

Adolescent↗