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Biomedical subjects

M Moll

Publications and source records attributed to M Moll.

At least 19 recordsLinked to original sources
PubMed1998

Chamber-specific alterations of norepinephrine uptake sites in cardiac hypertrophy.

The present study investigated local differences of sympathetic activation and sympathetic neuroeffector defects in nonhypertrophied right and hypertrophied left ventricles in a rat model with renin-induced pressure overload [TG(mREN2)27]. As judged from the depletion of myocardial norepinephrine stores, sympathetic activation was more pronounced in the left than in the right ventricles. In addition, norepinephrine uptake1 carrier sites were reduced in left but unchanged in right ventricles. Gene expression of the carrier was unchanged in stellate ganglia. An increase of Gialpha expression and a heterologous adenylyl cyclase desensitization occurred only in the left but not in the right ventricles, whereas a reduction of beta-adrenergic receptors was observed in both chambers. We concluded that general sympathetic activation can lead to beta-adrenoceptor downregulation but that pressure overload further increases sympathetic activation involving norepinephrine uptake mechanisms in the left ventricles, resulting in heterologous beta-adrenergic desensitization.

Adenylyl Cyclases↗
PubMed1995

Alterations of cardiac alpha- and beta-adrenoceptors and inotropic responsiveness in hypertensive transgenic rats harbouring the mouse renin gene (TGR(mREN2)27).

In the present study, we investigated the alpha- and beta-adrenoceptor-mediated effects on myocardial force of contraction (using phenylephrine in the presence of propranolol and isoprenaline) and receptor densities (binding studies using [3H]-prazosin and [125I]-iodocyanopindolol) in hypertensive transgenic rats (TGR(mREN2)27) and age-matched Sprague-Dawley rats (SP) as controls. In TGR(mREN2)27 the positive inotropic effects of isoprenaline and phenylephrine were reduced, while the effect of Ca2+ was unchanged. The EC50-values did not differ in both groups. A down-regulation of the beta-adrenoceptors was observed in the hypertrophied left ventricles of transgenic rats, which is postulated to be involved in the reduced beta-adrenoceptor-mediated positive inotropic effect. The alpha-adrenoceptor density was increased, which could represent a compensatory mechanism for the impaired effectiveness of the beta-adrenergic pathway. However, since the effect of alpha-adrenoceptor agonist is not enhanced but even reduced, an uncoupling of alpha-adrenoceptors from post receptor events could play a role in the observed effects.

Animals↗
PubMed1994

Retrograde ureteral intussusception.

A soft tissue mass causing ureteral obstruction should be considered malignant until proved otherwise. We report a case of retrograde ureteral intussusception that caused obstruction. To our knowledge, this condition has not been described in the recent literature.

Female↗
PubMed1994

CD7-negative helper T cells accumulate in inflammatory skin lesions.

Recently, we identified a particular T-cell subset in the peripheral blood of normal individuals that lack CD7 expression. In this study we determined the portion of CD7- T cells in the peripheral blood and skin of patients with various inflammatory skin diseases. We found that skin-infiltrating lymphocytes isolated from different benign and malignant skin lesions (n = 20) contain a high portion of CD7- helper T cells, whereas the number of CD7- T cells in the peripheral blood was not altered compared to healthy controls. Cell activation in vitro did not induce CD7 expression in negative T cells but increased CD7 expression in CD7-positive cells. Thus, lack of CD7 expression seems to be a stable characteristic in a major subset of skin-infiltrating lymphocytes. During long-term culture of CD7- helper T-cell clones derived from a psoriasis skin lesion, no phenotypic change in the CD7 phenotype could be monitored by sequential flow-cytometric analyses. No CD7 mRNA could be detected by Northern blot analysis, indicating transcriptional regulation of CD7 expression. The results show that CD7- T cells accumulate in certain inflammatory skin lesions without alteration of the circulating CD7- population. These cells may be identical to or derived from CD7- T cells of the peripheral blood.

Antigens, CD↗
PubMed1994

Beta-adrenergic neuroeffector mechanisms in cardiac hypertrophy of renin transgenic rats.

We studied neuroeffector defects in hypertrophied myocardium of hypertensive transgenic rats harboring the mouse Ren-2d gene. In transgenic rats, epinephrine and neuropeptide Y concentrations were reduced. A heterologous desensitization of adenylyl cyclase was observed, which was accompanied by a downregulation of beta 1-adrenergic receptors, an increase of inhibitory G protein alpha-subunits, and a mildly depressed catalyst activity of adenylyl cyclase, whereas the bioactivity of stimulatory G protein alpha-subunits and beta 2-adrenergic receptors was unchanged. Desensitization of adenylyl cyclase was accompanied by a reduced positive inotropic response to isoproterenol, whereas the effect of Ca2+ was unchanged. We conclude that sympathetic neuroeffector defects occur in transgenic rats similar to those observed in human failing myocardium. These alterations occur in the stage of hypertrophy and could contribute to contractile dysfunction in later stages.

Adenylyl Cyclases↗
PubMed1993

CD7- T cells represent a subset of normal human blood lymphocytes.

In the peripheral blood of normal adults we identified a subpopulation of mature human T cells that lacks expression of CD7. These CD3+CD7- T cells represent 9% +/- 3.4 SD of PBMC as estimated by analyses of 38 different normal donors. The majority of CD7- T cells express TCR alpha/beta, and are of CD4 helper and CD45RO+CD45RA- "memory" phenotype as determined by three-color fluorescence analysis. We established seven CD4+CD7- T cell clones in vitro from purified CD7- blood T cells and compared these cells to CD4+CD7+ clones. Nonexpression and expression, respectively, of CD7 was a stable feature of all clones during long term culture for more than 6 mo. No CD7 mRNA could be detected by dot blot and Northern blot analysis of purified CD7- T cells and of expanded T cell clones implicating a transcriptional regulation of CD7 Ag expression. Ionomycin/TPA and PHA stimulation were not capable to induce CD7 expression in CD7- cells but up-regulated CD7 expression in CD7+ cells. Whereas CD7- cells of cutaneous T cell lymphoma exhibit a cerebriform nucleus (Sézary cells), no evidence was obtained for cerebriform nuclear morphology in normal CD7- T cells from peripheral blood. We suggest that these CD7- T cells represent a physiologic subset of mature T cells and may be the circulating counterpart of those lymphocytes that are found to be enriched in normal skin and in a variety of benign and malignant skin diseases.

Antigens, CD↗
PubMed1991

Congenital earpits or auricular sinuses.

Congenital earpits or auricular sinuses are defects in the development of the outer ear from the 1st and 2nd branchial arch. They are most often located in front of the ear. Six cases are described. Early surgery is recommended because of a tendency towards infection with scarring. They can be associated with serious internal abnormalities, especially deafness and kidney malformations.

Adolescent↗
PubMed1988

Metabolic and cutaneous events associated with hypoglycemia detected by sleep sentry.

Eighteen insulin-dependent diabetic subjects [age (mean +/- SD) 33.2 +/- 10.6 yr] participated in a study designed to determine the metabolic and cutaneous parameters associated with activation of the nocturnal hypoglycemia monitor Sleep Sentry. Plasma glucose, glucagon, epinephrine, norepinephrine, and pancreatic polypeptide concentrations were determined every 10 min during a 2-h constant intravenous insulin infusion (40 mU.kg-1.h-1). In addition, skin temperature and electrical conductance were monitored at the same time intervals, and subjects were asked to rate the degree to which they felt cold and/or sweaty. Ten of the subjects (alarmers) activated the device with a mean plasma glucose nadir of 52.8 +/- 13.8 mg/dl, whereas eight (nonalarmers) failed to do so despite a mean plasma glucose nadir of 50.5 +/- 8.2 mg/dl. There were no significant differences between alarmers and nonalarmers with respect to initial or nadir plasma glucose levels, rate of fall of plasma glucose, or changes in plasma epinephrine, norepinephrine, or pancreatic polypeptide concentrations. In addition, changes in skin temperature and conductance were similar in both groups as were descriptive variables including age, disease duration, gender, and level of glucose control. No subject reported an increase in coldness, whereas 80% of both groups reported an increase in sweatiness. Three subjects studied on more than one occasion over a year failed to exhibit consistent activation of the alarm. This study suggests that it may not be possible to identify patients for whom the Sleep Sentry would be a reliable addition to their self-management regimen and that physicians should exercise caution in recommending its use.

Adult↗
PubMed1987

New aspects of the kinetics of isoenzyme CK-MB during myocardial infarction: discontinuous release?

Intermittent liberation of the serum marker myoglobin is found in acute myocardial infarction, and the ST segment of the electrocardiogram also shows a phasic rise and fall. We therefore measured the serum marker CK-MB at close intervals of time and recorded an oscillation in the serum level. The peaks are not as high as in the serum myoglobin time curve, and it is not easy to decide if they represent the intermittent liberation of the serum marker. It was possible to distinguish between a "high release" and a "low release" group of patients: the former having a maximum CK-MB value of greater than 100 U/l and the latter of less than 100 U/l. Most patients showed 2-3 "initial peaks" within the first 8 h. The highest of these immediately preceded the climb to the definitive maximum value. We conclude that the small size of the peaks in the CK-MB time curve is due to a different mechanism of enzyme release.

Adult↗
PubMed1986

New perspectives on the function of coronary artery spasm in acute myocardial infarction: the thromboischemic reentry mechanism. A review of 10 years research on the pathophysiology of AMI.

Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.

Animals↗