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Biomedical subjects

E Jennische

Publications and source records attributed to E Jennische.

At least 55 records · Page 3Linked to original sources
PubMed1990

Enterotoxins from Clostridium difficile; diarrhoeogenic potency and morphological effects in the rat intestine.

The action of toxins A, B, and C from Clostridium difficile was studied in the small intestine and colon of rats. All three caused fluid accumulation in the small intestine, maximal secretion being induced by 1 micrograms of toxin A, 20 micrograms of B, and 15 micrograms of C. Both toxins A and C caused shedding of epithelial cells from the villi without visible damage to crypt cells; toxin A caused further extensive necrosis and bleeding. Toxin B caused secretion without visible damage to the epithelial cells, though this activity was unstable and decreased significantly after one week of storage. In the colon, toxin A caused secretion and shedding of surface epithelial cells without damage to crypt cells, toxin C caused only a weak secretion, and toxin B had no effect at all. In terms of immunohistochemistry, it was found that toxin A bound to the enterocytes at the tips of the villi but not to goblet and crypt cells. The complex expression or interaction of the toxins produced by Cl difficile may explain the broad spectrum of disease (diarrhoea, colitis, and pseudomembranous colitis) associated with this micro-organism.

Animals↗
PubMed1990

Effects of testosterone on muscle insulin sensitivity and morphology in female rats.

Intact or oophorectomized (OVX) female rats were given moderate doses of testosterone for 12 wk. Insulin-stimulated glucose transport with submaximal insulin concentrations was studied with the euglycemic clamp technique. Glycogen synthesis and 2-deoxy-D-glucose uptake were measured during the clamp in the extensor digitorum longus, white and red portions of the gastrocnemius, and in the soleus muscles by tracer technique. Testosterone treatment resulted in elevations of circulating testosterone, increased plasma insulin concentrations, and a marked decrease in insulin-stimulated glucose transport. In control animals, glycogen synthesis and 2-deoxy-D-glucose transport increased with increasing concentrations of type 1 fibers. Testosterone inhibited glycogen synthesis and 2-deoxy-D-glucose transport to approximately 50% in all muscles except 2-deoxy-D-glucose transport in intact rats. Glycogen synthesis in the liver was not affected. Testosterone administration also resulted in changes in muscle morphology. The relative number of type 1 fibers decreased, whereas type 2 fibers increased. This was most pronounced in red muscles. There was also a decrease in capillary density after testosterone treatment. It was concluded that testosterone administered to female rats is followed by marked insulin resistance. This is correlated to alterations in muscle morphology with fewer type 1 fibers and a lower degree of capillarization, which are both known to be characteristics of insulin-insensitive muscles.

Animals↗
PubMed1989

Muscle regeneration. The effect of hypophysectomy on cell proliferation and expression of insulin-like growth factor-I.

Against the background of the importance of growth hormone (GH) for normal muscle growth, a study was performed to investigate whether lack of GH after hypophysectomy affects the cell proliferation and the local production of insulin-like growth factor-I (IGF-I) in the early stages of muscle regeneration in adult rats. The level of IGF-I in the serum of hypophysectomised rats was reduced to about 30% of that of controls. The incorporation of [methyl-3H]thymidine into the regenerating muscle showed a peak 6 days after the operation and then gradually declined to the end of the period of study 30 days after initiation of regeneration by ischemic necrosis. The DNA content rose to a maximum level after 6-8 days, and remained high after 30 days. There was no major difference in the incorporation of [3H]thymidine in regenerating muscle of hypophysectomised and control rats, but the DNA concentration in the regenerating muscles of hypophysectomised rats was significantly reduced after 30 days. There was a corresponding reduction in the number of nuclei per muscle fibre, indicating that hypophysectomy has a small effect on the cell proliferation during the early stages of muscle regeneration. Immunohistochemical demonstration of IGF-I in the regenerating muscle revealed the transient presence of immunoreactive material in satellite cells and myotubes after 6 to 8 days of regeneration but no immunoreactivity after 30 days. No obvious difference was observed between hypophysectomised and control rats, indicating that the endogenous production of IGF-I in regenerating skeletal muscle can occur independently of GH.

Animals↗
PubMed1989

Induction of insulin-like growth factor I messenger ribonucleic acid during regeneration of rat skeletal muscle.

Expression of insulin-like growth factor I (IGF-I) was studied in regenerating skeletal muscle. Irreversible damage to muscle cells was induced in the extensor digitorum longus muscle of adult rats by ischemia, preceded by glycogen depletion. IGF-I mRNA levels during the regeneration process were studied for periods up to 10 days after injury using a solution hybridization assay. Increased IGF-I mRNA levels could be demonstrated within 24 h after injury; maximum levels were achieved in 3 days and decreased to approximately normal levels by 10 days. Changes in IGF-I mRNA levels could not be seen in undamaged contralateral extensor digitorum longus muscles during the experimental period. An increase in IGF-I mRNA was also evident in injured muscles of hypophysectomized animals. In situ hybridization at the time of maximum induction showed the presence of IGF-I mRNA in proliferating myoblasts and in satellite cells. IGF-I, thus, may act as a locally produced non-GH dependent trophic factor during regeneration of skeletal muscle after injury.

Animals↗
PubMed1989

Sequential immunohistochemical expression of IGF-I and the transferrin receptor in regenerating rat muscle in vivo.

The immunohistochemical expression of insulin-like growth factor I and the transferrin receptor was investigated in regenerating rat skeletal muscle. Muscle injury was induced in the extensor digitorum longus muscle in one hind limb by tourniquet ischemia. The regenerating muscles were investigated 3 to 7 days after the injury. Expression of IGF-I and the transferrin receptor was demonstrated in cryostat sections by a double-staining method. It was found that both markers were transiently expressed by the regenerating muscle cells. Expression of IGF-I immunoreactivity preceded that of the transferrin receptor and the staining for IGF-I disappeared 1 to 2 days before the staining for the transferrin receptor. The data are compatible with a regulatory role of IGF-I on the transferrin receptor.

Animals↗
PubMed1988

IGF-I immunoreactivity is expressed by regenerating renal tubular cells after ischaemic injury in the rat.

The immunohistochemical expression of the trophic peptide insulin-like growth factor I (IGF-I; somatomedin C) was investigated in the post-ischaemic regenerating rat kidney. The part of the nephron most severely injured by the ischaemic insult was the pars rectae or S3 region of the proximal tubules. In this part of the nephron no specific IGF-I immunoreactivity could be demonstrated under control conditions. Three days after injury, however, low regenerating tubular cells expressing IGF-I immunoreactivity could be demonstrated invading the damaged region. Five and 7 days post-ischaemia some of the regenerating cells showed IGF-I immunoreactivity while adjacent and similar-looking cells did not. In parallel with an increasing differentiation of the regenerating cells the IGF-I immunoreactivity vanished. Fourteen days after the injury the S3 cells had regained their normal morphology, and by this time the IGF-I immunoreactivity had returned to a normal undetectable level. It is concluded that there is a transient increase in the expression of IGF-I mainly confined to the early phase of post-ischaemic rat kidney regeneration. It is proposed that IGF-I exerts its trophic role by paracrine mechanisms.

Animals↗
PubMed1988

Immunocytochemical and biochemical localization of insulin-like growth factor I in the kidney of rats before and after uninephrectomy.

The localization of insulin-like growth factor I (IGF-I, somatomedin C) was investigated in the kidney of adult rats during normal conditions and after nephrectomy, using immunocytochemical and biochemical methods. In the normal kidney, IGF-I immunoreactivity could be demonstrated mainly in cells in the medullary collecting ducts and in those parts of the thin limb of Henle's loop located in the outer medulla. During compensatory growth all parts of the collecting ducts, including those in the cortex, showed IGF-I immunoreactivity, as did cells in the entire thin limb of Henle's loop. No IGF-I immunoreactivity could be demonstrated in the proximal or distal tubules, either in the control kidney or during compensatory growth. Biochemical measurements showed a significantly higher content of IGF-I in the inner medulla than in the cortex in the normal kidney. Uninephrectomy resulted in significantly increased IGF-I content in the cortex. It is suggested that IGF-I is produced mainly in the collecting ducts and in the thin limb of Henle's loop and exerts its effect on other parts of the nephron by paracrine mechanisms.

Animals↗
PubMed1987

Regenerating endothelial cells express insulin-like growth factor-I immunoreactivity after arterial injury.

In the present study the expression of insulin-like growth factor I (IGF-I; somatomedin C) immunoreactivity was examined in endothelial cells during repair after injury to the intima in the femoral artery of adult rats. Two types of injury were examined: (1) endothelial denudation induced by the use of a catheter, and (2) vessel compression by short-term ligation. In untreated rats, arterial endothelial cells showed no or, only infrequently, low IGF-I immunoreactivity in their cytoplasm. Endothelial cells at the border to the denuded area showed increased IGF-I immunoreactivity one day after injury to the intima of the femoral artery. Thrombocytes and fibrin deposits as well as vital endothelial cells, covered by clots, were immunonegative. The maximal intensity of IGF-I immunoreactivity was reached within 3 days after insult. The IGF-I immunoreactivity in the endothelial cells remained elevated for at least 4 weeks, compared to the controls. Intimal thickenings appeared within a week after injury and many cells in these thickenings showed intense IGF-I immunoreactivity as did the covering endothelial cells. Smooth muscle cells in the media were generally immunonegative during control conditions and after endothelial denudation. Spontaneously hypertensive rats (SHR) showed, similarly to their matched controls (WKY), approximately the same patterns of IGF-I immunoreactivity in their endothelial cells both under normal conditions and after injury. It is concluded that IGF-I is likely to be involved in the repair of the intima in injured arteries.

Animals↗
PubMed1987

Dynamic changes in insulin-like growth factor I immunoreactivity correlate to repair events in rat ear after freeze-thaw injury.

The distribution of the trophic peptide insulin-like growth factor I (IGF-I) in the rat ear was mapped after freeze-thaw injury. Immunocytochemical methods and antisera specific to human IGF-I were used. In the ear of normal adult rats scattered basal epidermal cells and a few cells in the underlying connective tissue and elastic cartilage expressed IGF-I immunoreactivity. Within 1 day after injury and reaching maximum in 3 days, all epidermal cells became stained as did invading macrophages and some of the other inflammatory cells. Concomitantly, there were hypertrophic changes. The staining leveled off after 1-2 weeks. Perichondrial cells became IGF-I immunoreactive in increasing frequency during the first week, reached maximal intensity and frequency in 2 weeks, and remained stained for at least 4 weeks. New cartilage was formed concomitantly on both sides of the old one. It is proposed that IGF-I is a substance of general importance for cell maintenance and tissue repair.

Animals↗
PubMed1987

Satellite cells express the trophic factor IGF-I in regenerating skeletal muscle.

The expression of insulin-like growth factor I (IGF-I, somatomedin C) was studied in regenerating skeletal muscle. Irreversible damage to skeletal muscle cells was induced in the extensor digitorum longus muscle (EDL) of adult rats by ischaemia, preceded by glycogen depletion, and the regeneration process was studied for periods up to 14 days after injury. The IGF-I was demonstrated by indirect immunofluorescence. Immunoreactivity against ribonucleotide reductase (RR) was used as a marker for DNA synthesis, that is, cell proliferation. Increased IGF-I immunoreactivity could be demonstrated within 24 h after injury in satellite cells, intramuscular nerves and in blood vessels. The IGF-I immunoreactivity remained virtually unchanged in the contralateral, undamaged EDL. An increasing number of satellite cells, expressing high IGF-I immunoreactivity, could be demonstrated in the injured EDL, and within 72 h myoblasts, expressing high IGF-I and RR immunoreactivity, were formed. Small immature muscle cells, displaying high IGF-I immunoreactivity, were observed 4 days after injury. Increased IGF-I immunoreactivity was still obvious in the regenerated muscle cells 14 days after injury while RR immunoreactivity was seen only in scattered satellite cells. It is concluded that IGF-I may act as a trophic factor during regeneration of skeletal muscle after injury.

Animals↗
PubMed1987

IGF-I expression in blood vessels varies with vascular load.

The present study was designed to investigate if the immunoreactivity of insulin-like growth factor I (IGF-I, somatomedin C) in blood vessels was changed in relation to the vascular load in adult rats. Occlusion of the right femoral artery resulted within 24 h in a strongly increased IGF-I immunoreactivity in the media of the contralateral, left, femoral artery and a significant decrease in the IGF-I expression in the right femoral artery distal to the occlusion. The increased labelling of the smooth muscle cells persisted for at least 21 days. Inactivity of the right hind limb, secondarily to an ischaemic insult, likewise induced a significant increase in IGF-I immunoreactivity, within 24 h, in the femoral vessels of the undamaged, contralateral left hind limb. It is concluded that IGF-I immunoreactivity varies with the dynamic load in the vascular walls. It is proposed that IGF-I may serve as a parahormone exerting its effect by paracrine and/or autocrine mechanisms, taking part in regulating the structural adaption of blood vessels in response to stress.

Animals↗
PubMed1987

Regenerating skeletal muscle cells express insulin-like growth factor I.

The expression of the trophic peptide insulin-like growth factor I (IGF-I; somatomedin C) was investigated in the regenerating soleus muscle of mice after injury by the snake venom taipoxin. No specific IGF-I immunoreactivity was observed in muscle cells during control conditions. Within 2 days after taipoxin injection, IGF-I immunoreactivity could be demonstrated in activated satellite cells. Myoblasts and myotubes expressed high IGF-I immunoreactivity. The IGF-I immunoreactivity was strictly cytoplasmatic and obviously associated with polyribosomes. No vesicular or membraneous IGF-I immunoreactivity could be demonstrated. It is concluded that IGF-I is synthesized in myogenic cells during skeletal muscle regeneration. It is suggested that IGF-I exerts its effects on skeletal muscle mainly by autocrine mechanisms.

Animals↗
PubMed1987

Lack of casual relationship between medullary blood congestion and tubular necrosis in postischaemic kidney damage.

The effect of haemodilution on medullary blood congestion and tubular necrosis was investigated in the rat kidney. Male Sprague-Dawley rats were subjected to 60 min of unilateral, kidney ischaemia and 24 h of reperfusion. Haemodilution was performed by replacing blood by homologous serum and was done either before induction of ischaemia or during the ischaemic period. Cellular necrosis was evaluated morphologically by a histochemical staining for calcium and a dye-exclusion test. Trapped erythrocytes were visualized by the DAB reaction. It was found that haemodilution could totally prevent medullary congestion. In spite of this, the extent and distribution of necrotic tubular cells in the outer stripe of the outer medulla were the same whether the animal was subjected to haemodilution or not. Our results strongly suggest that the cellular necrosis and the medullary congestion are two separate phenomena occurring at the same time, but without a causal relationship to each other.

Acute Kidney Injury↗
PubMed1987

Transient expression of insulin-like growth factor I immunoreactivity in skeletal muscle cells during postnatal development in the rat.

The immunohistochemical expression of insulin-like growth factor I (IGF-I; somatomedin C) was investigated in hindlimb skeletal muscle of rats during postnatal development. IGF-I immunoreactivity could be demonstrated in satellite fibres and myotubes 1, 2 and 3 days after birth, while no IGF-I immunoreactivity could be demonstrated in the more mature primary fibres. Five days after birth only scattered cells showed IGF-I immunoreactivity and 10 days after birth no specific IGF-I immunoreactivity could be demonstrated in muscle cells, i.e. the adult pattern was established. It is concluded that IGF-I immunoreactivity is expressed during a limited period of postnatal skeletal muscle maturation in rats. IGF-I is probably synthesized by IGF-I immunoreactive muscle cells and contributes to the differentiation/maturation process by autocrine and/or paracrine mechanisms.

Age Factors↗
PubMed1986

Postischemic skeletal muscle injury: patterns of injury in relation to adequacy of reperfusion.

Ischemia-induced skeletal muscle injury was studied in rats subjected to tourniquet hindlimb ischemia for 3, 4, or 5 hr. The extent of injury was evaluated morphologically after 5 or 20 hr of reperfusion by a dye exclusion test using Evans blue/albumin (EBA) and a histochemical stain for calcium, Alizarin red S (ARS). In addition, the distribution of Evans blue in the postischemic muscle served as a means for detecting areas of defect reperfusion--no reflow. The combination of EBA and ARS allowed easy and reproducible quantification of induced injury in adequately reperfused areas. In areas of no reflow none of the markers used were useful. Muscle cells in these areas appeared structurally well preserved even 20 hr after release of the tourniquet and no cytoplasmic calcium accumulation could be demonstrated in muscle cells by staining with ARS. In many of these areas, however, ARS-positive structures were found between muscle cells, distributed in a pattern corresponding to the capillary network. The nature of these structures, constituting a morphological correlate to the no-reflow phenomenon, is unclear. It is concluded that for the proper evaluation of postischemic skeletal muscle injury, a suitable marker allowing estimation of the adequacy of the reperfusion must be used.

Animals↗
PubMed1986

Relation between alloxan-induced plasma membrane dysfunction and inhibition of insulin secretion in pancreatic B-cells in vivo.

The acute effects of alloxan on plasma membrane function and insulin content of pancreatic B-cells were investigated in vivo. Rats received a single injection of alloxan, 75 mg/kg b.w. intravenously. The animals were sacrificed up to 24 h after treatment. The membrane damage was evaluated by a dye-exclusion test, demonstrating cells unable to exclude Evans blue/albumin (EBA) complexes. The insulin content was demonstrated by immunofluorescence. The alloxan injection resulted in a transient decrease in insulin content, later followed by a sustained increase, indicating inhibition of secretion. Increased levels of insulin were evident 50 min after alloxan treatment, and concomitantly an increasing number of injured, i.e. EBA-positive, cells could be demonstrated in the islets. Inhibition of insulin secretion appeared to precede inhibition of insulin synthesis as well as development of membrane dysfunction. It is suggested that the early inhibition of insulin secretion, induced by alloxan, is due to interference with cytoplasmic sulfhydryl and disulfide containing proteins.

Alloxan↗