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Biomedical subjects

J Jakobsen

Publications and source records attributed to J Jakobsen.

At least 163 records · Page 9Linked to original sources
PubMed1982

Stenosis of the common bile duct in chronic pancreatitis.

The incidence of common bile duct stenosis in patients with chronic pancreatitis was studied in a consecutive series of patients admitted for endoscopic retrograde cholangiopancreatography (ERCP). Thirty-six out of 79 patients (46 per cent) with moderate or advanced chronic pancreatitis as defined by radiological criteria were found to have a stenosis of the intrapancreatic portion of the common bile duct. There were no age or sex differences between the patients with and without biliary stenosis, but significantly more patients with stenosis had advanced chronic pancreatitis. In about two-thirds of the patients the stenosis was smooth, symmetrical and tapering. In the remaining cases, a shorter stricture of the hour-glass type was found. A complete obstruction was never seen. About one-half of the patients with bile duct stenosis were icteric at the time of the investigation. The jaundice resolved spontaneously in all but 1 patient in 3-42 (median 14) days. Stenosis of the common bile duct is a frequent complication of chronic pancreatitis, but biliary-enteric bypass operation seems to be unnecessary in the great majority of the patients.

Adult↗
PubMed1982

Change in mast cell dimensions increases the profile number in sections of peripheral nerve of diabetic rats.

Mast cell proliferation has been reported in peripheral nerves of streptozotocin diabetic rats. We examined the question by light microscopy using morphometric techniques including estimation of shape and size. After 4 weeks of diabetes the mast cell area in transverse sections was 32.7 +/- 7.0 microns 2 vs. 22.5 +/- 5.4 microns 2 in controls (P less than 10(2)). Mast cell profiles approximated to ellipses in longitudinal sections, the long diameter being 11.4 +/- 1.2 microns vs. 14.0 +/- 1.0 microns in controls (P less than 10(4)). Correspondingly, the profile number was increased (30 +/- 6%) in longitudinal sections and decreased in transverse sections (11 +/- 16%). The present study does not provide evidence for mast cell proliferation in peripheral nerves in experimental diabetes, and, furthermore, underlines the need of evaluation of dimensions in studies of particle numbers.

Animals↗
PubMed1982

Hypnosis in dental education: a survey of U.S. dental schools, 1980.

This paper reports the results of a 1980 survey of the teaching of hypnosis in U.S. dental schools. Responses were received from 60 dental schools. Information was obtained on hypnosis education in both the predoctoral and postdoctoral curriculums, including what is being taught, how hypnosis education is structured in the curriculum, who is teaching hypnosis, the number of students receiving hypnosis education, and attitudes and policies about hypnosis education. Results of this survey were compared to previous surveys by Parrish (1973) and Scott (1977, for the United Kingdom). The survey reveals a gradual increase in the number of U.S. dental schools teaching hypnosis.

Curriculum↗
PubMed1981

Axonal transport of enzymes and labeled proteins in experimental axonopathy induced by p-bromophenylacetylurea.

Axonal transport was studied by several techniques in the sciatic nerves of adult male Sprague-Dawley rats with neuropathy induced by treatment with p-bromophenylacetylurea (BPAU) in dimethylsulfoxide solution. Control rats were treated with solvent alone. BPAU, 200 mg/kg, induced severe muscle weakness in the hindlimbs, beginning after a latent period of 1 week and progressing to near total paralysis by 2 weeks. Axonal transport of the endogenous transmitter enzymes, acetylcholinesterase, dopamine-beta-hydroxylase and choline acetyltransferase, was normal at both 2 and 15 days after administration of BPAU, as judged by the accumulation of enzyme activity above and below a set of double ligatures on the sciatic nerve. The velocity of fast anterograde transport of [35S] methionine labeled protein was also unaffected by BPAU. However, 4 abnormalities of transport were detected in BPAU- treated rats: (1) doubling of the time for initiation of fast anterograde transport after precursor injection in the dorsal root ganglion, (2) 25% fall in the velocity of slow axonal transport of [3H] leucine labeled protein, (3) 30% reduction in the proximal accumulation of fast transported labeled protein in ligated nerve, 8-30 h after injection of precursor, and (4) 50-60% reduction in distal accumulation of "early arriving" labeled protein, 8-14 h after precursor injection. The last abnormality, suggesting an impaired turnaround from anterograde to retrograde transport, was detected as soon as 2 days after BPAU administration. The turnaround abnormality was correlated with the severity of neuropathy as estimated by independent clinical scoring in the group of rats treated with 200 mg/kg of drug. However, further studies showed that turnaround was delayed even in rats treated with doses as low as 50 mg/kg, which never led to clinically evident neuropathy. Nevertheless it is proposed that the abnormalities of transport play a role, as yet undefined, in the distal axonopathy caused by BPAU.

Acetylcholinesterase↗
PubMed1981

Retrograde axonal transport. A possible role in the development of neuropathy.

The accumulation of 3H-fucose labelled glycoprotein and 35S-methionine labelled protein carried by the retrograde axonal transport in the sensory fibres of the sciatic nerve was examined on the day after injection of streptozotocin in rats. The accumulation of fucose-label was reduced (2.8 +/- 0.4 (SD) versus 2.1 +/- 0.5 (arbitrary units), 2p = 0.0044) indicating a decreased retrograde flux of glycoproteins. This early transport abnormality could have a key role in the development of peripheral neuropathy in diabetes.

Animals↗
PubMed1980

Impaired retrograde axonal transport from a nerve crush in streptozotocin diabetic rats.

The axonal transport of proteins in crushed nerves of streptozotocin (40 mg/kg) diabetic rats was investigated 4 weeks after induction of diabetes. 35S-methionine was used as a marker for protein and 3H-fucose as a marker for glycoprotein. The precursors were injected into the fifth lumbar spinal ganglion and the accumulation of TCA-insoluble activity proximal and distal to a sciatic nerve ligature was measured at different time intervals after application of a crush. The start of accumulation distal to the ligature was delayed by 1 hour for proteins as well as for glycoproteins. Furthermore, the total amount of accumulated protein after 19 h was decreased by 18% while the decrease was 21% for glycoprotein. By insulin treatment the differences could both be prevented and reversed after 3 days of normoglycaemia. These findings demonstrate an impaired response to a nerve crush and might be the explanation for the regenerative abnormalities of peripheral nerves in diabetes.

Animals↗
PubMed1980

Axonal transport in rats after galactose feeding.

Axonal transport was studied in galactose-fed rats. Precursors for proteins and glycoproteins were injected into the fifth lumbar spinal ganglion and retrograde axonal transport as well as slow axonal transport were estimated at different time intervals during the following 4 weeks. Galactose-feeding was found to produce a progressive reduction of the retrograde axonal transport of glycoproteins in intact nerve (2.9 +/- 0.2 (arbitrary units) after five days of galactose-feeding as compared to 1.9 +/- 0.7 after 28 days, 2p = 0.025). The slow axonal transport velocity of structural proteins was reduced from 0.97 +/- 0.09 mm/day to 0.84 +/- 0.04 mm/day, 2p = 0.0030. The present findings as well as structural and electrophysiological abnormalities of the nerves of galactose-fed rats are similar to the changes found in diabetic rats. The similarities point to a decisive role for glucose or its metabolites in the development of diabetic neuropathy.

Animals↗
PubMed1980

Decreased axonal transport of structural proteins in streptozotocin diabetic rats.

We have examined the various axonal transport rates in sciatic nerve of streptozotocin diabetic rats 3 h and 10,25, and 50 d after the injection of tritiated proline into the fifth lumbar dorsal root ganglion. Proline-labeled proteins conveyed by the slow transport system were advanced more slowly in diabetic rats. No compensation for this delay took place in terms of protein synthesis, half-life, or transported amount. The decreased deliverance of slowly transported proteins (structural proteins) to the axons may well account for the reduced axon calibre shown in earlier reports. A hypothesis is proposed suggesting that the primary event in the development of neurological abnormalities in diabetes is an impairment of the retrograde axonal transport, secondarily leading to the abnormality of the anterograde transport of structural proteins.

Animals↗
PubMed1980

Reduced perikaryal volume of lower motor and primary sensory neurons in early experimental diabetes.

The volume of nerve cell bodies of the anterior horn of the fifth lumbar segment and of the fifth lumbar dorsal root ganglion were measured by stereological methods in rats with 4-wk duration of streptozotocin diabetes and in age-matched controls. The perikaryal volume of motor and sensory neurons was reduced by 18% in diabetic rats and a shift between the number of A- and B-cells was observed in the dorsal root ganglion. The findings are in accordance with our earlier observation of reduced axonal size of myelinated fibers in the common peroneal nerve. Furthermore, the data lead us to suppose that the nervous system abnormalities in early diabetes are not exclusively restricted to the peripheral nerves.

Animals↗
PubMed1980

Nervous system abnormality and nervous disease in diabetes.

Symptomatic diabetic neuropathy is present only in a few percent of the total diabetic population. In contrast abnormalities of the various parts of the nervous system can be demonstrated very early using neurophysiological techniques. These abnormalities are reversible at first, but progressive with duration of diabetes. Similar nervous abnormalities are present in experimental diabetes in the rat. The earliest structural changes have been demonstrated to be a decreased calibre of the myelinated axons. An abnormality in the axonal transport of proteins is possibly the very first change to appear. These recent results have enabled us to propose a hypothesis concerning the sequence of events in the development of the peripheral nerve abnormalities.

Animals↗