Search PubMed⌕ Search

Biomedical subjects

J Lang

Publications and source records attributed to J Lang.

At least 379 records · Page 21Linked to original sources
PubMed1986

Replacement of dog's aorta by autologous intestinal muscle in the infected retroperitoneum.

The free transplant of intestinal muscle lacking mucosa into an infected vascular bed has been shown to be a suitable replacement for the aorta in dogs. This type of transplant is incorporated into the infected area and shows a high tolerance against progressive infection. Therefore, an autologous transplant may be suitable to ensure continuous blood flow during the healing phase of a deep infection when a synthetic prosthesis is unsuccessful.

Animals↗
PubMed1986

Comparison of the inactivation of microsomal glucose-6-phosphatase by in situ lipid peroxidation-derived 4-hydroxynonenal and exogenous 4-hydroxynonenal.

1) The effect of 4-hydroxynonenal and lipid peroxidation on the activities of glucose-6-phosphatase and palmitoyl CoA hydrolase were studied. 2) 4-Hydroxynonenal inactivates glucose-6-phosphatase but has no effect on palmitoyl-CoA hydrolase. These effects are similar with those observed during lipid peroxidation of microsomes. 3) The inhibition of glucose-6-phosphatase by 4-hydroxynonenal can be prevented by glutathione but not by vitamin E. The inactivation of glucose-6-phosphatase during lipid peroxidation is prevented by glutathione and delayed by vitamin E. 4) The formation of 4-hydroxynonenal during lipid peroxidation was followed in relation to the inactivation of glucose-6-phosphatase. At 50% inactivation of glucose-6-phosphatase the 4-hydroxynonenal concentration was 1.5 microM. To obtain 50% inactivation of glucose-6-phosphatase by added 4-hydroxynonenal a concentration of 150 microM or 300 microM was needed with a preincubation time of 30 and 60 min, respectively. 5) It is concluded that the glucose-6-phosphatase inactivation during lipid peroxidation can be due to the formation of 4-hydroxynonenal. The formed 4-hydroxynonenal which inactivates glucose-6-phosphatase is located in the membrane. If this mechanism is valid it implies that a functional SH group of glucose-6-phosphatase is layered in the membrane. However, an inactivation of glucose-6-phosphatase by desintegration of the membrane by lipid peroxidation cannot be ruled out.

Aldehydes↗
PubMed1986

[Cartilage of the exterior nose].

The cartilages of the nose have been measured on 30 head-halves. The overlap-areas of the lateral nasal cartilages are also estimated. Some angles of the cartilages are included.

Cartilage↗
PubMed1986

[External laryngeal muscles--origin, insertion, length and potential force].

Measurements have been given of the mm. cricothyreoideus, thyreohyoideus and inferior pharyngeal constrictor muscle. Also measured were the circumferences of these muscles for estimating their potential force. The course of the superior laryngeal nerve, external branch to the thyreopharyngeal muscle and the twigs of the nerve were examined.

Female↗
PubMed1986

[Measurements of length and cross sections of the posterior and lateral cricoarytenoid and arytenoid muscles].

The inner muscles of the larynx have been dissected and its length values and circumferences were measured. The potential force of the posterior cricothyroid muscle was estimated with 26,65 N of the arytenoid muscles with 17,24 N, and for the lateral crico-arytenoid and thyreoarytenoid external muscles with 26,56 N. The development and the functions of the muscles are discussed.

Female↗
PubMed1986

[Medical findings on the trochlear nerve].

The exit-zone, the intracisternal course, the course in the sidewall of the cavernous sinus and inside the orbit were measured at 91 head-halves. Included are measurements of the length of the area nervosa, its nerve fibers and its distance to the total extracerebral length of the IVth nerve is estimated. The results are discussed with earlier investigations and some clinical approaches and neurophysiological methods are given.

Adult↗
PubMed1986

[Course and branches of the recurrent laryngeal nerve, inferior thyroid artery and inferior laryngeal artery].

Length, width, and thickness of the recurrent laryngeal nerve and its extra-laryngeal twigs were estimated. Included is the course of the nerve to the suspensory ligament of the thyroid gland, to the inferior horn of the thyroid cartilage and to trachea and esophagus. The origin of the inferior thyroid artery, its width and course to the twigs of the recurrent laryngeal nerve were studied. The origin zone of the inferior laryngeal artery is also described. The different terms and opinions about the twigs of the truncus thyreocervicalis and the thyroid axis are discussed.

Aged↗
PubMed1986

[Laryngeal nerves, branches in the interior of the larynx].

The recurrent laryngeal nerve divides in the most cases outside of the larynx into 2 twigs. The thicker ventral branch has a posterior and an anterior twig. From the posterior one, we counted 6.22 (1 to 12) branches to the posterior cricoarytenoid muscle and 1.48 (1 to 3) to the arytenoid muscle. From the anterior branch 3.54 (1 to 6) twigs run to the lateral cricoarytenoid muscle and 2.06 (1 to 5) to the thyreo-arytenoid muscle. An Ansa GALENI was found in 66%. Its diameter was cranial greater than caudal, its length was measured with 73.6 (56 to 96) mm. A single anastomose was found in 54%, and in 12% numerous variations. We found 8.5 (3 to 13) thicker twigs, which divided themselves in 17 thinner twigs. To the mucous membrane we found 78.5% and to muscles 21.5%. In cases without anastomoses, 3.5 (2 to 5) twigs were running to muscles and 13.4 (1 to 25) to the mucous membrane. The diameter and length of the twigs and their course to muscles and mucous membrane have been estimated. The results are discussed with those of earlier authors.

Humans↗
PubMed1985

Quantitative determination of the lipid peroxidation product 4-hydroxynonenal by high-performance liquid chromatography.

4-Hydroxynonenal is a product formed in tissue and tissue fractions from polyunsaturated membrane lipids through a free radical-induced lipid peroxidation process. The biological properties of this aldehyde have been studied in many respects. This article describes for the first time a sensitive and reproducible method for quantitative analysis of 4-hydroxynonenal in biological samples as well as in lipid-containing foodstuffs. The method involves extraction of the aldehyde by dichloromethane from cells or microsomes trapped on an Extrelut column. Oils and foodstuffs are extracted with excess water. After additional sample cleanup by solid-phase extraction on a disposable octadecyl silica gel (ODS) extraction column, the sample is analyzed by high-performance liquid chromatography using an ODS column and methanol/water 65/35 (v/v) or acetonitrile/water 40/60 (v/v) as eluant; the detection wavelength is 220 nm. The method developed has a high precision with coefficients of variation of 1.4% (microsomes) to 3.5% (olive oil). The recovery depends on the sample type and lies between 45% (control microsomes) and 96% (solution of hydroxynonenal in water). The method has been used for the determination of 4-hydroxynonenal in microsomes, platelets, and various foodstuffs.

Aldehydes↗
PubMed1985

Metabolism of the lipid peroxidation product 4-hydroxynonenal by isolated hepatocytes and by liver cytosolic fractions.

The metabolism of the lipid peroxidation product 4-hydroxynonenal and of several other related aldehydes by isolated hepatocytes and rat liver subcellular fractions has been investigated. Hepatocytes rapidly metabolize 4-hydroxynonenal in an oxygen-independent process with a maximum rate (depending on cell preparation) ranging from 130 to 230 nmol/min per 10(6) cells (average 193 +/- 50). The aldehyde is also rapidly utilized by whole rat liver homogenate and the cytosolic fraction (140 000 g supernatant) supplemented with NADH, whereas purified nuclei, mitochondria and microsomes supplemented with NADH show no noteworthy consumption of the aldehyde. In cytosol, the NADH-mediated metabolism of the aldehyde exhibits a 1:1 stoichiometry, i.e. 1 mol of NADH oxidized/mol of hydroxynonenal consumed, and the apparent Km value for the aldehyde is 0.1 mM. Addition of pyrazole (10 mM) or heat inactivation of the cytosol completely abolishes aldehyde metabolism. The various findings strongly suggest that hepatocytes and rat liver cytosol respectively convert 4-hydroxynonenal enzymically is the corresponding alcohol, non-2-ene-1,4-diol, according to the equation: CH3-[CH2]4-CH(OH)-CH = CH-CHO + NADH + H+----CH3-[CH2]4-CH(OH)-CH = CH-CH2OH + NAD+. The alcohol non-2-ene-1,4-diol has not yet been isolated from incubations with hepatocytes and liver cytosolic fractions, but was isolated in pure form from an incubation mixture containing 4-hydroxynonenal, isolated liver alcohol dehydrogenase and NADH and its chemical structure was confirmed by mass spectroscopy. Compared with liver, all other tissues possess only little ability to metabolize 4-hydroxynonenal, ranging from 0% (fat pads) to a maximal 10% (kidney) of the activity present in liver. The structure of the aldehyde has a strong influence on the rate and extent of its enzymic NADH-dependent reduction to the alcohol. The saturated analogue nonanal is a poor substrate and only a small proportion of it is converted to the alcohol. Similarly, nonenal is much less readily utilized as compared with 4-hydroxynonenal. The effective conversion of the cytotoxic 4-hydroxynonenal and other reactive aldehydes to alcohols, which are probably less toxic, could play a role in the general defence system of the liver against toxic products arising from radical-induced lipid peroxidation.

Alcohol Dehydrogenase↗
PubMed1985

Separation and characterization of the aldehydic products of lipid peroxidation stimulated by carbon tetrachloride or ADP-iron in isolated rat hepatocytes and rat liver microsomal suspensions.

Carbonyl products were separated and identified in suspensions of rat liver microsomal fractions and in isolated hepatocytes, after stimulation of lipid peroxidation by incubation with the pro-oxidants CCl4 and ADP-iron. The carbonyl products were allowed to react with 2,4-dinitrophenylhydrazine, and the derivatives were extracted and separated by t.l.c. into three zones of non-polar materials, and one fraction of polar derivatives that remained at the origin. Separation of the individual non-polar hydrazones in each zone by h.p.l.c. demonstrated that zone I prepared from microsomal fraction or hepatocytes incubated with CCl4 or ADP-iron contained mainly 4-hydroxyhex-2-enal, 4-hydroxynon-2-enal and 4-hydroxynona-2,5-dienal. Zone III consisted mainly of the alkanals propanal, pentanal and hexanal, the 2-alkenals propenal, pent-2-enal, hex-2-enal, hept-2-enal, oct-2-enal and non-2-enal, the ketones butanone, pentan-2-one and pentan-3-one, and deca-2,4-dienal. Incubation of a microsomal fraction with ADP-iron was much more effective in producing malonaldehyde and other carbonyl products than an incubation with CCl4. Despite such quantitative differences, there were no obvious qualitative differences in the h.p.l.c. spectra obtained from zones I and III. However, the stoichiometric evaluation of fatty acid loss and the production of malonaldehyde and other carbonyls suggests that the pathways of lipid peroxidation triggered by CCl4 and ADP-iron are different. The accumulation of carbonyl products of lipid peroxidation in isolated hepatocytes is strongly affected by their metabolism; in particular, 4-hydroxyalkenals were found to be metabolized very rapidly. Nonetheless, both CCl4 and ADP-iron produced stimulation in the production of malonaldehyde and non-polar carbonyl production. After incubation of rat hepatocytes with CCl4 or ADP-iron it was found that approx. 50% of the total amount of non-polar carbonyls produced during incubation escaped into the external medium. This was not leakage from dead cells, as 90-95% of the hepatocytes had retained their integrity at the end of the incubation. Release of carbonyl products from cells stimulated to undergo lipid peroxidation may be a mechanism for spreading an initial intracellular disturbance to affect critical targets outside the parent cell.

Adenosine Diphosphate↗
PubMed1985

Anatomy of the midline.

Described are the anatomy and topography of the midline structures particularly in relation to the surgical approaches. Furthermore measurements of the third ventricle and the various distances between surface areas of the brain and skull and different landmarks of the cerebral midline are presented.

Brain↗
PubMed1985

Biphasic effect of a gradual rise in plasma calcium concentration on vulnerability to fibrillation.

The possible potentiation by a rise in plasma calcium concentration of the effects of acetylcholine (ACh) on the atrial myocardium was investigated, mainly with a view to define the increase in vulnerability to fibrillation by hypercalcaemia. The effective refractory period (ERP) of the atrial myocardium, the atrial fibrillation threshold (AFT) and the atrial fibrillation rate (AFR) were measured repeatedly before and during the intravenous infusion of calcium at the rates of 0.025, 0.050 and 0.100 mmol . kg-1 . min-1 in dogs whose heart was, in addition, submitted to a cholinergic influence. 1. As long as the rise in plasma calcium concentration did not reach 100% approximately, this influence was enhanced considerably: in particular, ACh shortened ERP and raised AFR to a much larger extent, so that it resulted in fibrillation with a minor electrical stimulation. 2. When the rise in plasma calcium concentration exceeded 100%, hypercalcaemia became inhibitory of the effects of ACh, with a reversal in the modification of all the parameters, AFT especially, and, finally, prevention or even conversion to sinus rhythm of fibrillation.

Acetylcholine↗