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Biomedical subjects

M Neumann

Publications and source records attributed to M Neumann.

303 records · Page 17Linked to original sources
PubMedDate not supplied

Early shunting of 9 microns and 15 microns tracer microspheres from the acutely ischemic canine myocardium.

Recent reports have shown considerably differing results for myocardial shunting of 9 microns and 15 microns tracer microspheres (TMs) under various conditions. This could restrict the use of TMs for myocardial, especially collateral blood flow measurements. To determine the importance of coronary collateral blood flow and its early changes during the first 30 minutes after acute coronary artery occlusion (i.e. the 1st arrhythmic phase), we studied the shunting of 9 microns and 15 microns TMs from the ischemic myocardium during acute LAD ligation. In anesthetized dogs these TMs and subsequently Ringer solution were infused into the occluded coronary artery just distal to the ligation with constant low perfusion pressure. TM shunting (%S) into the lungs was then determined (%S = total lung radioactivity . 100/radioactivity infused). During a single LAD occlusion lasting 35 minutes (series I, n = 10) 9 microns TMs were infused immediately and 30 minutes after ligation, 15 microns TMs being infused after 15-20 minutes. In series II (n = 6) 9 microns TMs were infused immediately during the 1st, short (5 minutes) LAD occlusion. Following 90 minutes of reperfusion a 2nd LAD ligation (35 minutes) was performed with 9 microns TMs being infused immediately and 30 minutes after occlusion. During the first 30 minutes of acute coronary artery occlusion, TM shunting from the ischemic myocardium is negligible for 15 microns TMs (%S less than 0.5%; n = 5), whereas the mean 9 microns TM shunt of the early applied TM (i.e. A1, series I; n = 9; B2, series II; n = 6) amounts to a maximum of 1.21 +/- 0.2% (X +/- SEM). After 30 minutes of occlusion the mean 9 microns TM shunt amounts only to 0.71 +/- 0.15% (i.e. C1, series I; n = 4; C2, series II; n = 4). - In a coronary artery occlusion repeated once, 9 microns TM shunting, while increasing slightly due to the 90 minutes of reperfusion, still amounts to only 1.73 +/- 0.41% (n = 6). In three experiments 9 microns TMs were infused into the unoccluded, normally perfused LCX coronary artery during LAD occlusion. The mean LCX shunt value of 4% after a mean time of 25 minutes following TM infusion is in very good agreement with the 9 microns TM shunt values in the literature. These results clearly demonstrate that the TM technique with 9 microns microspheres is suitable for measuring changes in coronary collateral blood flow at least for a short time period after acute coronary artery occlusion.

Acute Disease↗
PubMedDate not supplied

Nonhomogeneous electrophysiological changes and the bimodal distribution of early ventricular arrhythmias during acute coronary artery occlusion.

There is experimental evidence that the bimodally distributed ventricular arrhythmias (phases Ia and Ib) during the first 30 min after coronary occlusion (CO) in dogs are not due to the same mechanism. In 39 dogs we related the incidence of phases Ia and Ib to the time courses of excitation thresholds (ET), refractoriness (REFR), conduction times (CT) and effective refractory periods (ERP) at 6-12 epicardial electrode sites within the ischemic zone. The regional collateral myocardial blood flow (RMBF-tracer microsphere technique) was determined in 14 out of the dogs. This measurement only served for rough grouping into dogs with low and higher RMBF at the electrode sites during ischemia. REFR was determined as temporal recovery of excitability at a constant current strength of 4-6 times preocclusion ET. ERP was intermittently measured at 2.0-8.0 mA. At low RMBF ET, REFR and CT increased very inhomogeneously (dispersion of ET increased from 0.06 to 2.42 mA) 2-8 min after CO, leading to Ia-arrhythmias (also depending on infarct size) which terminated as ET, REFR and CT partially recovered 10-30 min after CO, their dispersions being still markedly elevated. With further recovery of these electrophysiological parameters the phases Ib subsided. On the other hand, the ERP diminished for the most part within the first 10 min after CO with only minor further decrease. Remarkably the dispersion of ERP did not significantly increase within the ischemic zone (from mean = 15 +/- 5 ms to 22 +/- 8 ms at low RMBF and from 14 +/- 6 ms to 18 +/- 9 ms at higher RMBF, p = ns). As a consequence of the homogeneous and constant shortening of the ERP, the time course of REFR mainly was determined by the nonhomogeneous alterations of ET. At a higher RMBF there were only minor electrophysiological alterations, and Ia- or Ib-arrhythmias did not emerge. These results indicate a strong relation of the Ia- and Ib-arrhythmias to the ischemia-induced time courses and dispersions of ET, REFR and CT but not of ERP within the ischemic area. Although the phases Ia relate to a strong increase of ET, REFR and CT and the Ib-arrhythmias to a partial recovery of these parameters, both the Ia- and Ib-arrhythmias seem to depend on a "critical" extent of electrophysiological inhomogeneity within a "critical" mass of ischemic but excitable myocardium.

Animals↗
PubMedDate not supplied

Reflex sympathetic dystrophy syndrome in children.

We report 3 children with reflex sympathetic dystrophy syndrome, review the literature, and discuss current concepts of diagnosis and management. In this disorder, pain, tenderness, swelling, vasomotor instability, and dystrophic skin changes frequently develop after minor injury. The clinical diagnosis is supported by osteopenia detected on radiographs and either increased or decreased radionuclide uptake on bone scan of the affected extremity. Treatment with a graduated program of physical therapy and transcutaneous electrical nerve stimulation is beneficial in almost all patients. In contrast to adults, the prognosis of childhood reflex sympathetic dystrophy syndrome is favorable; most children recover completely after one episode.

Adolescent↗
PubMedDate not supplied

Restricted expression of HIV1 in human astrocytes: molecular basis for viral persistence in the CNS.

Besides macrophages and microglial cells, cells of astroglial origin are thought to be targets of HIV1 in the brain. HIV1 infection of astroglial cells results in restricted production of the virus. To analyse the molecular basis of this restricted infection phenotype, we established a chronically HIV1-infected low-producer astrocytoma cell line. These cells show only low levels of mRNA encoding structural proteins, due to a cell-determined blockage in the Rev/RRE regulatory axis. The low-producer state could not be overcome by treatment with known stimulators of virus expression such as phorbol ester, (12-O-tetradecanoylphorbol-13-acetate), tumour necrosis factor alpha or sodium butyrate. This indicates that the molecular mechanisms involved in restricting virus production in astroglial cells differ from those in latently infected T cells and monocytes.

Astrocytes↗
PubMedDate not supplied

[Bone density--reference values in German men. A study of the lumbar spine with the Lunar-DPX-densitometer].

UNLABELLED: The DXA-technique is a well established method to study bone mineral density (BMD). Until now there are no reliable reference data based on the male population of Germany. QUESTION: Are the data base, given by the manufacturer transferable to the male population in Germany? METHODS: So a cross sectional study based on 715 healthy males with German ethnic background (age 20-89) was carried out. Comparison was made to the ap spine reference data of northern Europe. RESULTS: The peak bone mass was 1,26 +/- 0,17 g/cm2 at the age of 20-24 years. After that the BMD decreases to the sixth decade (1,09 +/- 0,18 g/cm2), further on there is an increase to 1,18 +/- 0,21 g/cm2 in the ninth decade. CONCLUSION: Looking at a comparable Swedish study there are no significant differences, looking at a Finnish study there are statistically significant differences in the sixth decade (t = 3,246) and seventh decade (t = 2,413). The results of our study complete the data base until now, but one should be careful to transfer the data base provided by the manufacturer.

Absorptiometry, Photon↗
PubMedDate not supplied

Effects of vanadate on isolated vascular tissue: biochemical and functional investigations.

Vanadate is a potent inhibitor of Na+,K+-ATPase derived from bovine aorta. The Ca2+, Mg2+-ATPase of the same preparation was inhibited at 10 times higher concentrations. Compared with [3H]ouabain, 48V bound quickly to bovine aortic microsomes. Equilibrium binding experiments revealed one high-affinity, low-capacity and one low-affinity binding site for 48V, whereas [3H]ouabain possessed only one binding site of high affinity. A high NADH-vanadate reductase activity was measured in the same preparation, suggesting that, in this tissue, vanadate may be converted to vanadyl, a form to which the Na+,K+-ATPase is relatively insensitive. An increase in the contractile force of isolated rabbit aorta was measured with the following potency: phenylephrine greater than ouabain greater than vanadate. The order in intrinsic activity was as follows: phenylephrine congruent to ouabain greater than vanadate. The action of vanadate was rapid in onset and stable over several hours, while that of ouabain was slow and transitory. Vanadate increased tension in isolated rabbit veins to an extent similar to phenylephrine, but at concentrations two orders of magnitude higher. Vanadate action decreased with decreasing (Ca2+)0, but remained constant at a constant ratio of (Ca2+)0/(Na+)2(0). Vanadate-induced increases in tension were decreased by verapamil by about 43% and persisted in a solution in which Na+ was replaced by Li+. Vanadate increased electrically stimulated contractions. It is concluded that most of the effect of vanadate is due to an increase in calcium influx into the smooth muscle cell and that the effect of vanadate on Na+,Ca2+ exchange is of minor importance.

Animals↗
PubMedDate not supplied

Functional characteristics of optimized arterial tree models perfusing volumes of different thickness and shape.

The relationship between the 'shape of an organ' and the 'cost of blood transport' to perfuse its tissue was evaluated on the basis of optimized arterial model trees simulated to perfuse square-based 100-cm(3) volumes of different shape ('flat' versus 'thick' as defined by the ratio of thickness to side-length h/s < or =1). Specifically, the effects of 'shape' on tree structure, blood transport, and on hemodynamic characteristics were investigated. Branching models of arterial trees were generated by constrained constructive optimization (CCO), based on an identical set of model parameters. All model trees were geometrically and topologically optimized for intravascular volume. Tree structures achieved tremendous savings of blood (transport medium) in comparison to a system of separate tubes. Thickening the perfusion volume (increasing h/s) resulted in a significant decrease of mean transport length, deposition time, and intravascular total volume in the tree. 'Thick' perfusion volumes induced CCO trees to branch more symmetrically into a number of equivalent subtrees repetitiously splitting into smaller ones; 'flat' structures were dominated throughout by a few asymmetrically branching major vessels. In summary, we conclude from systematic variation of shape that thicker perfusion volumes (h/s >0.1) facilitate efficient delivery of blood in comparison to large amounts of 'dead volume' to be carried over long distances in very thin pieces of tissue.

Arteries↗
PubMedDate not supplied

MDR hamster cells exhibiting multiple altered gene expression: effects of dexniguldipine-HCl (B859-35), cyclosporin A and buthionine sulfoximine.

An actinomycin D selected, multidrug-resistant (MDR) hamster CHO subline showed strong expression of the P-glycoprotein and sorcin genes together with several other alterations such as a: (i) reduced growth rate, (ii) lowered topoisomerase II, (iii) lowered glutathione-S-transferase-P gene expression, and (iv) the emergence of a 15.5 kDa protein. Besides high resistances to adriamycin, actinomycin D, and vincristine, we observed a lowered sensitivity towards bleomycin, a rather hydrophilic drug usually not involved in P-glycoprotein associated MDR. Moreover, the MDR subline showed a pronounced collateral (enhanced) sensitivity towards the sterically pure dihydropyridine anticancer drug dexniguldipine-HCl (B859-35) preventing its characterization for MDR modulation here. At a non-cytotoxic dose (10 microM) the immunosuppressive cyclic peptide cyclosporin A completely abolished the resistance to vincristine, partially reversed the resistance to teniposide and strongly enhanced the sensitivity towards bleomycin, while not influencing the drug sensitivities of the parental cell line. Buthionine sulfoximine (BSO), an agent depleting cellular glutathione levels, distinctly increased the sensitivity towards teniposide at nontoxic doses (50 microM) exclusively in the MDR subline, while it did not alter vincristine or bleomycin cytotoxicity.

Adenine Phosphoribosyltransferase↗
PubMedDate not supplied

[The treatment of acute fatty liver of pregnancy using plasma exchange].

A 33-year-old gravida 6, para 5, developed acute fatty liver of pregnancy at 35 weeks' gestation. This clinical picture was seen after caesarean section and delivery of a healthy infant. Post partum hepatic dystrophy associated with coma hepatica, acute renal failure and disseminated, intravascular coagulation was successfully treated with three large-volume plasmaphereses using FFP exchange plasma in combination with haemodialysis. The patient survived and her liver function was restored to normal.

Acute Kidney Injury↗
PubMedDate not supplied

Deafferentation pain exacerbated by subarachnoid lidocaine and relieved by subarachnoid morphine. Case report.

BACKGROUND AND OBJECTIVES: Neuropathic pain syndromes are often resistant to traditional pharmacologic treatment. The authors describe a patient with chronic deafferentation pain of the legs associated with peripheral neuropathy that was refractory to multidisciplinary pain clinic management. METHODS: Numerous medications had been tried, including nortriptyline, mexiletine, and oral and parenteral opioids. Spinal cord stimulation was also ineffective, despite a satisfactory pattern of stimulation-induced paresthesias. For diagnostic purposes, differential spinal anesthesia with lidocaine and morphine was performed, with evoked potential monitoring used to evaluate the intensity of spinal anesthetic block. RESULTS: Paradoxically, lidocaine spinal anesthesia exacerbated pain, whereas subarachnoid morphine provided rapid pain relief. Long-term pain control has been maintained with an implanted spinal infusion pump. CONCLUSIONS: Evoked potential data acquired during lidocaine spinal anesthesia and the rapid pain relief provided by subarachnoid morphine suggest that deafferentation pain may involve segmental, opioid-sensitive dorsal horn pain generators. The long-term pain relief afforded the patient demonstrates that subarachnoid opioids may be efficacious for some forms of neuropathic pain.

Adult↗
PubMedDate not supplied

BCR/ABL modulates the cytokine and retinoic acid response of c-Rel in human myeloid cells.

A human myeloid cell line, Mo7, and a daughter cell line expressing the bcr/abl oncogene, Mo7-P210, were used in a comparative study analyzing the effects of p210BCR/ABL expression on tyrosine phosphorylation, specific DNA binding and expression of the proto-oncoprotein c-Rel. The steady state expression of c-Rel was indistinguishable in both cell lines. Tyrosine phosphorylation and DNA binding of c-Rel were slightly elevated in Mo7-P210 cells. Further, Mo7 and Mo7-P210 cells showed different responses concerning c-Rel after stimulation with cytokines and retinoic acid. The results presented here demonstrate that c-Rel can be modulated by hematopoietic cytokines and suggest that bcr/abl expression has an impact on these responses and that c-Rel may be a downstream effector for p210BCR/ABL.

Base Sequence↗