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Biomedical subjects

W Simon

Publications and source records attributed to W Simon.

At least 73 records · Page 4Linked to original sources
PubMed1981

Attenuation correction in gamma emission computed tomography.

A method of computing tomographic images from single photon radionuclide emission data is presented. The method takes into account attenuation of gamma rays inside the source and makes use of an iterative technique, based on the difference between the projection data obtained from the source and computed projections, called reprojections, from successive reconstructions of the sources. The method has been tested both by computer simulations and reconstruction of plastic phantoms imaged with 99mTc radionuclides. Substantial improvement in reconstruction accuracy over algorithms uncorrected for internal attenuation is demonstrated. Since the technique is iterative, it can be used with a variety of reconstruction algorithms or combined with other first approximation techniques of attenuation correction.

Gamma Rays↗
PubMed1981

[Is there good correlation between findings in lumbar myelography and surgery? (author's transl)].

Report on 1177 lumbar myelograms performed in 1977 - with comparison of the surgical findings (in 854 patients operated on for herniated disc) with those of myelography. The results are: 86% correct and 9.5% incorrect preoperative myelographic diagnosis; in 4.5% an evaluation was not possible because of scars from previous surgery. Additionally, our technique of lumbar myelography is being described.

Adolescent↗
PubMed1980

Avoiding megamouse experiments.

A method is described whereby large numbers of individually innocuous substances can be tested for combinations that are carcinogenic or otherwise toxic. The method substantially reduces the number of test animals required to a number far less than would be required for pairwise cross testing.

Animals↗
PubMed1979

Regulation of sodium and potassium transport in phytohemagglutinin-stimulated human blood lymphocytes.

Phytohemagglutinin (PHA) or concanavalin A treatment of lymphocytes causes an increase in membrane permeability so that the leak rates of Na and K increase 1.5- to 2-fold. Active Na and K transport increase proportionately in response to the increased membrane permeability. We have examined the role of lymphocyte Na concentration in sustaining the increased Na and K transport observed after PHA treatment. Cell Na concentration increases from 14.8 to 20.5 mmol/liter cell water in PHA-treated lymphocytes (P < 0.001). Four lines of evidence suggest that the 5-6 mmol/liter cell water increase in lymphocyte Na accounts for the increase in active Na and K transport in mitogen-treated lymphocytes. First, PHA does not increase directly the maximal Na, K-ATPase activity of isolated lymphocyte membrane vesicles. Second, when the Na concentration is increased by 6 mmol/liter cell water in unstimulated lymphocytes, Na and K transport increase nearly twofold. Third, the cell Na concentration (15 mmol/liter cell water) is near the K(m) for Na activation of the Na, K-ATPase in lymphocyte membranes. The ATPase activity thus, is capable of increasing as the cell Na rises above normal. Fourth, if lymphocytes are incubated in a medium containing a low Na concentration, K transport does not maintain the internal K concentration and the fall in cell K is accentuated in PHA-treated lymphocytes. These studies indicate that the adaptive acceleration of Na and K transport in mitogen-treated lymphocytes is mediated by a small increase in cell Na.

Biological Transport↗
PubMed1979

On-line continuous potentiometric measurement of potassium concentration in whole blood during open-heart surgery.

We describe a flow-through system with an ion-selective electrode for measurement of blood potassium ion concentration, continuously and on-line off the extracorporeal blood circulation in an operating theater during human open-heart surgery. Comparison measurements were made with the SMA flame photometer (blood plasma) and an Orion SS 30 sodium/potassium analyzer (whole blood). The potassium concentration values obtained with the flow-through system agree well with the ones determined with the flame photometer. The time delay of the measurement with the flow-through system was relatively long (2 min) but delays of only 10--20 s seem feasible. Short time delays can deepen insight and simplify rational treatment under surgery conditions.

Autoanalysis↗
PubMed1978

Parasinusoidal location of megakaryocytes in marrow: a determinant of platelet release.

Megakaryocytopoiesis occurs in the hematopoietic (extravascular) compartment of marrow. Thus, platelets must traverse the wall of the vascular sinuses of marrow to enter the circulation. We have examined mouse and rat marrow, fixed by rapid immersion so as to maintain anatomical relationships as close to the natural state as possible. Quantitative transmission electron microscopy (TEM) of random transections of femurs established that megakaryocytes reside less than 1 mu from a marrow sinus wall with a probability unlikely to be the result of chance (P less than 0.001). An intimate relationship exists between the megakaryocyte periphery and the abluminal surface of the endothelial lining cell. At the time of platelet release megakaryocyte cytoplasm invaginates and penetrates the endothelial lining cell. The penetrating cytoplasm is detached and enters the marrow circulation. From their dimensions in comparison to circulating platelets, the released cytoplasm represents a packet of platelets that undergoes further fragmentation in the circulation. The parasinusoidal location of megakaryocytes and the process of sinus-wall penetration and platelet delivery was observed by TEM and scanning electron microscopy. These studies provided quantitative support for a specific anatomical arrangement of megakaryocytes in marrow. Moreover, the process of platelet release appears to be a physiological form of metastasis with invasion of vascular walls and vascular spread of cells, that are in this case amitotic.

Animals↗
PubMed1978

In vivo enzyme activity of purified human brain renin.

Cerebrospinal fluid (CSF) of rats contains high angiotensinogen concentrations. When 3500-fold purified renin from human brain was injected into the brain ventricles of rats, angiotensin I concentrations increased from undetectable levels to 147.9 +/- 18.8 fMol per ml CSF. In parallel, mean arterial blood pressure increased from 93 +/- 2.4 mm Hg to 107 +/- 3.7 mm Hg. The increase in blood pressure could be abolished by intraventricular administration of saralasin, a blocker of angiotensin II receptors. Intraventricular injection of cathepsin D had no effect on arterial blood pressure and the agiotensin I concentration in CSF remained below detection limits of the radioimmunoassay. We conclude that brain renin acts on endogenous brain angiotensinogen under physioloical in vivo conditions to form angiotensin I. The latter is converted to angiotensin II and leads to biological effects, i.e. increase of blood pressure.

Angiotensin I↗
PubMed1978

Increased blood pressure responses to central angiotensin II in spontaneously hypertensive rats.

The blood pressure responses following infusions of angiotensin II (ANG II) into the brain ventricles (i.v.t.) have been tested in spontaneously hypertensive (SH) rats and in normotensive Wistar Kyoto (WK) rats. The mean arterial blood pressure increases were significantly higher in SH rats than in WK rats. Propranolol treatment reduced blood pressure increases to i.v.t. ANG II in WK, but not in SH rats. The higher sensitivity to i.v.t. ANG II in SH rats supports a role of central ANG II in the maintenance of high blood pressure in SH rats.

Angiotensin II↗
PubMed1978

Effects of enkephalins on arterial blood pressure are reduced by propranolol.

1. The cardiovascular effects of enkephalins have been tested in normotensive Wistar-Kyoto rats. Methionine-enkephalin and leucine-enkephalin increased blood pressure and heart rate after infusion into the brain ventricles. 2. After intravenous injection, blood pressure was increased by methionine-enkephalin and leucine-enkephalin, but heart rate was increased by methionine-enkephalin only. 3. Propranolol treatment reduced the increases in blood pressure following intraventricular methionine-enkephalin and leucine-enkephalin, while only the methionine-enkephalin-induced increases in heart rate were reduced by propranolol. 4. Heart rate and blood pressure responses after intravenous administration of methionine-enkephalins and leucine-enkephalin were not affected by propranolol. 5. Since opioid peptides occur in the blood and in regions of the brain involved in blood pressure regulation, the demonstrated cardiovascular effects to intraventricular and intravenous enkephalins support a role of these peptides in central and peripheral mechanisms of blood pressure control.

Animals↗