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Biomedical subjects

J Wagner

Publications and source records attributed to J Wagner.

At least 217 records · Page 12Linked to original sources
PubMed1994

Oncostatin M stimulates proliferation in B9 hybridoma cells: potential role of oncostatin M in plasmacytoma development.

Oncostatin M was found to stimulate the IL-6-addicted hybridoma line B9. Leukaemia inhibitory factor did not stimulate proliferation of this line. Both of these factors bind to the gp130 of the IL-6 receptor. In another cell line that is stimulated by LIF (DA.1), neither IL-6 nor oncostatin M stimulated proliferation. Previously it had been thought that the gp130 alone is sufficient to bind ligand and transduce signal and that oncostatin M could bind to and activate the LIF receptor, but these data show this is not always the case. Mice primed with Pristane were found to have IL-6 in their sera and peritoneal fluid only at a few time points following Pristane treatment; this was determined by IL-6-specific ELISA. When the same samples were analysed on IL-6-addicted B9 cells, stimulatory activity was found at all time points. When the Pristane-primed samples were assayed for oncostatin M activity in the A375 melanoma assay, there was oncostatin M activity at various time points. IL-6 did not have activity on the A375 cells. These data indicate that oncostatin M play a role in the generation of plasmacytoma in vivo.

Animals↗
PubMed1994

Effects of rapid buffers on Ca2+ diffusion and Ca2+ oscillations.

Based on realistic mechanisms of Ca2+ buffering that include both stationary and mobile buffers, we derive and investigate models of Ca2+ diffusion in the presence of rapid buffers. We obtain a single transport equation for Ca2+ that contains the effects caused by both stationary and mobile buffers. For stationary buffers alone, we obtain an expression for the effective diffusion constant of Ca2+ that depends on local Ca2+ concentrations. Mobile buffers, such as fura-2, BAPTA, or small endogenous proteins, give rise to a transport equation that is no longer strictly diffusive. Calculations are presented to show that these effects can modify greatly the manner and rate at which Ca2+ diffuses in cells, and we compare these results with recent measurements by Allbritton et al. (1992). As a prelude to work on Ca2+ waves, we use a simplified version of our model of the activation and inhibition of the IP3 receptor Ca2+ channel in the ER membrane to illustrate the way in which Ca2+ buffering can affect both the amplitude and existence of Ca2+ oscillations.

Animals↗
PubMed1994

PCR analysis of human renal biopsies--renin gene regulation in glomerulonephritis.

Animal studies show that the renin-angiotensin system contributes to hypertension, glomerulosclerosis and progressive chronic renal failure in renal disease. Direct data on the activity of the renal renin-angiotensin system (RAS) in human renal disease are scarce, however. The small amount of tissue in renal biopsies and insufficient sensitivity of analytical methods have precluded reliable measurements of the tissue components of the RAS in the past. Due to its highly sensitivity the quantitative polymerase chain reaction (QPCR) assay today allows the quantitation of gene transcription products in small tissue samples, for example, renal biopsies. The clinical applicability of the PCR has raised the interest in this methodology. We adopted quantitative PCR to study expression and regulation of the renin gene in patients with different forms of glomerulonephritis. For PCR a deletion mutant of the renin gene was used as an internal standard exhibiting the same primer binding sites as the human gene. The number of glomeruli per biopsy sample was counted by microscopic transillumination immediately after biopsy and was used as a reference base. Renin mRNA was expressed as fg per glomerulus. Compared to nonaffected tissue of tumor nephrectomy samples, renin gene expression was significantly lower in glomerulonephritic patients without converting enzyme inhibitor (CEI) treatment, that is, 63 +/- 20 (6) versus 250 +/- 50 (7) (P < 0.02), although plasma renin concentration was in the normal range. Significantly higher renin mRNA expression was found in patients with glomerulonephritis treated with CEI, that is, 210 +/- 50 (8) versus 63 +/- 20 (6) in patients not treated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Development of a geropsychiatric unit.

Acute services to older citizens often require health care professionals to manage problems that are difficult to assess and treat. Age-related complications such as physical decline and the presence of psychiatric and medical illness together can produce an array of confusing symptoms for the physician. This study examines the diagnostic outcomes of the first 100 patients admitted to an acute care-based geropsychiatric unit. Assessment protocols and treatment interventions are described and results of patient progress are discussed.

Aged↗
PubMed1994

Nuclear localization and cell cycle regulation of a murine protein tyrosine phosphatase.

MPTP is a murine homolog of the human T-cell protein tyrosine phosphatase (PTPase) and the rat PTP-S enzyme. Enzymatic activity of this ubiquitously expressed protein was demonstrated in immunoprecipitates from NIH 3T3 cells and in recombinant protein overexpressed in bacteria. Expression of beta-galactosidase-MPTP MPTP chimeric proteins in COS1 cells identified a nuclear localization signal at the carboxyl terminus of the MPTP that was sufficient to direct beta-galactosidase as well as a tagged version of the MPTP to the nucleus. Deletion analysis of amino acids within the nuclear targeting signal showed that this sequence does not conform to the bipartite type of nuclear localization signals. Furthermore, it was shown that the steady-state levels of MPTP RNA fluctuate in a cell cycle-specific manner. On the basis of these experiments, we discuss the possible function of MPTP in the cell cycle and other nuclear processes.

Amino Acid Sequence↗
PubMed1994

Differential effects of insulin-like growth factor I and growth hormone on developmental stages of rat growth plate chondrocytes in vivo.

Skeletal growth depends upon enchondral ossification in growth plate cartilage, within which chondrocytes undergo well defined stages of maturation. We infused IGF-I or growth hormone (GH), two key regulators of skeletal growth, into hypophysectomized rats and compared their effects on growth plate chondrocyte differentiation using qualitative and quantitative autoradiography, stereology, and incident light fluorescence microscopy. Stem cell cycle time was shortened from 50 to 15 and 8 d after treatment with IGF-I and GH, respectively. Proliferating cell cycle time decreased from 11 to 4.5 and 3 d, and duration of the hypertrophic phase decreased from 6 to 4 and 2.8 d. Average matrix volume per cell at each differentiation stage was similar for normal, hormone-treated, and untreated hypophysectomized groups. Mean cell volume and cell height were significantly reduced by hypophysectomy at the proliferative and hypertrophic stages, but were restored to physiological values by IGF-I and GH. In contrast, cell productivity, i.e., increases in cell volume, height, and matrix production per unit of time, did not reach normal values with either IGF-I or GH, and this parameter was inversely proportional to cell cycle time or phase duration. IGF-I and GH are thus capable of stimulating growth plate chondrocytes at all stages of differentiation, albeit to variable degrees with respect to individual cell activities. Although it is generally accepted that GH acts at both the stem and proliferating phases of chondrocyte differentiation, our data represent the first evidence in vivo that IGF-I is also capable of stimulating stem cells.

Animals↗
PubMed1994

The cAMP-dependent protein kinase regulates transcription of the dopamine beta-hydroxylase gene.

Dopamine beta-hydroxylase (DBH) catalyzes the conversion of dopamine to norepinephrine, and is expressed specifically in neurons and neuroendocrine cells that release norepinephrine and epinephrine. In the present study, we used DBH-expressing human neuroblastoma SK-N-BE(2)C and rat pheochromocytoma (PC12) cell lines to investigate the role of cAMP-dependent protein kinase (PKA) in transcriptional regulation of the DBH gene. Coexpression of the catalytic subunit of PKA (PKAc) robustly stimulated the transcriptional activity of the DBH gene in a dose-dependent manner. Conversely, coexpression of a specific inhibitor of PKA abrogated forskolin- and cAMP-mediated but not phorbol ester-mediated transcriptional induction of DBH. Deletion of the cAMP response element (CRE) dramatically reduced the stimulatory effect of PKA, indicating that the CRE mediates the induction of DBH by PKA. In DBH-nonexpressing HeLa and C6 glioma cell lines, coexpression of PKAc changed the transcriptional activity of the DBH promoter to a minimal degree, indicating that basal and PKA-mediated transcription of the DBH gene occur in a cell type-specific manner. Finally, both basal and cAMP-stimulated transcription of the DBH gene are diminished in three PKA-deficient PC12 cell lines, compared to wild-type cells. Based on these data, we conclude that PKA, via the CRE, plays an important role in basal and cAMP-inducible transcription, but is not required for phorbol ester-mediated induction, of the DBH gene in noradrenergic cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Arthroscopic arthroplasty of the ankle joint.

Anterior ankle impingement syndrome is characterized by pain, edema, and limited ankle dorsiflexion. The article examines this syndrome in detail from a variety of perspectives, including indications and contraindications, physical examination, various diagnostic modalities, surgical anatomy, surgical approach, procedures for arthroscopy, and complications.

Ankle Injuries↗
PubMed1994

[Electrocardiographic and hemodynamic adverse effects of contrast media in coronary angiography].

In a randomized double-blind study in 50 patients (38 men, 12 women of medium age 52.2 +/- 8 years) the new non-ionic low-osmolal x-ray contrast agent Iomeprol 400 is compared with the high-osmolal contrast medium natrium-meglumine-diatrizoate (Urografin 76). Electrocardiographic, hemodynamic as well as general effects and side-effects such as bradycardias, tachyarrhythmias, allergic reactions, attacks of hyperhidrosis, nausea, vertigo, thoracal pain, cephalgies after selective coronary angiography and levocardiography were registered. Between the two groups of patients there were no major differences concerning age, sex, weight, and coronary status. After coronary angiography in the two groups the following parameters were statistically significant: Iomeprol 400 led to a smaller reaction of heart rate (P = 0.001 during left coronary injection or P = 0.003 during right coronary injection), to a lower rise of the QT-time (P = 0.0005 for right coronary injection or P = 0.0001 for left coronary injection) as well as to a mild change of the T-vector (P = 0.0002 in right coronary injection or P = 0.0001 in left coronary injection). After levocardiography using natrium-meglumine-diatrizoate versus Iomeprol 400 a significantly stronger decrease in systolic (P = 0.0001) and diastolic (P = 0.0001) aortic pressure was registered. The increase of heart rate was less frequent with Iomeprol 400 than using the ionic contrast medium, which was compared to it (P = 0.048). In the general effects with Iomeprol 400 a statistically significantly less frequent appearance of bradycardias was registered (P = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Extra-hepatic transcription of plasma prekallikrein gene in human and rat tissues.

The expression of plasma prekallikrein (PPK) mRNA has been investigated applying reverse transcription, followed by polymerase chain reaction, of mRNA (RT-PCR) in various human and rat tissues. PPK gene transcripts were detected in liver and kidney in both species and, in addition, in human adrenal gland and placenta. No PPK mRNA was identified in rat adrenal gland, heart, aorta, lung, brain cortex and medulla, hypothalamus, and uterus. These results show that PPK gene expression is not restricted to the liver.

Adrenal Glands↗
PubMed1993

Prehospital thrombolysis: beneficial effects of very early treatment on infarct size and left ventricular function.

OBJECTIVES: The purpose of this study was to compare the effects of very early (< or = 1.5 h after symptom onset) and later (> 1.5 up to 4 h) thrombolytic therapy on infarct size, left ventricular function and early mortality in patients with acute myocardial infarction. To start thrombolysis at the earliest possible moment, it was performed in the prehospital setting. A cutoff time of 1.5 h was prospectively stipulated. BACKGROUND: Shortening of ischemic time is crucial within the 1st 2 h. Prehospital thrombolysis can reduce time to treatment and enables very early initiation of therapy for many patients. METHODS: One hundred seventy patients received 30 mg of anistreplase up to 4 h from symptom onset by a mobile intensive care unit physician. Infarct size was measured from cumulative release of alpha-hydroxybutyrate dehydrogenase, and left ventricular function was assessed by contrast angiograms 10 days after the infarction. RESULTS: The decision to treat on scene was correct in 98% of patients. There were no bleeding complications or deaths outside the hospital setting. In 28 patients (17%) the ischemic process was interrupted. Findings with thrombolytic therapy initiated < or = 1.5 (96 patients) versus > 1.5 h (74 patients) were the following: initial extent of epicardial injury, 1.6 +/- 0.9 versus 1.4 +/- 0.7 mV, p = NS; infarct size by cardiac enzyme release 646 +/- 634 versus 886 +/- 712 IU/liter, p < 0.05; ejection fraction 57 +/- 14% versus 51 +/- 13%, p < 0.05; regional dyssynergic area 24 +/- 22 versus 33 +/- 24 U, p < 0.05; 21-day mortality 1 of 96 versus 5 of 74 patients (1% vs. 7%, p < 0.05). CONCLUSIONS: The data suggest that in evolving myocardial infarction up to 4 h in duration, the start of thrombolytic therapy at < or = 1.5 h compared with > 1.5 h limits infarct size, preserves left ventricular function and may save lives.

Aged↗
PubMed1993

Open, noncontrolled dose-finding study with a novel recombinant plasminogen activator (BM 06.022) given as a double bolus in patients with acute myocardial infarction.

The novel recombinant plasminogen activator (r-PA) (BM 06.022) is a mutant of tissue-type plasminogen activator expressed in escherichia coli which can be given as a bolus because of a prolonged half-life. The primary objective of this trial was to determine the efficacy of an intravenous r-PA double bolus (first bolus of 10 MU followed by 5 MU after 30 minutes) in patients with acute myocardial infarction. All patients received heparin intravenously and acetylsalicylic acid orally. Efficacy was assessed from infarct artery patency by coronary angiography (Thrombolysis in Myocardial Infarction trial perfusion grades 2 or 3) in 50 patients. Ninety minutes after administration of the first r-PA bolus, the infarct-related coronary artery was patent in 39 of 50 patients (78%; 95% confidence interval 64 to 88%). An angiographically confirmed reocclusion occurred in 1 patient between 90 minutes and 24 to 48 hours. The reocclusion rate was influenced by 8 interventions and 1 angiogram missing at 24 to 48 hours. Measurements of hemostatic parameters showed a decrease in fibrinogen to 37% of baseline value. There were 3 clinical reinfarctions before discharge and 2 major puncture site hemorrhages. No further serious bleeding and no serious adverse event with lethal outcome occurred. The 10 + 5 MU r-PA double bolus regimen appears to be effective with regard to patency and the success of thrombolysis. The incidence of reocclusion is very low. From the limited number of patients treated in this study, one need not be concerned about the safety profile of r-PA.

Clinical Enzyme Tests↗