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Biomedical subjects

R L Klein

Publications and source records attributed to R L Klein.

At least 73 records · Page 4Linked to original sources
PubMed1990

Childhood intussusception.

Intussusception of the intestine continues to be a significant surgical disease of childhood. The currently accepted therapy is to do a barium enema, followed by a laparotomy, if necessary. To evaluate our results in treating this disease, the charts of the last 169 patients admitted to the hospital, with the diagnosis of intussusception, were reviewed. Intussusception was confirmed in 157 patients, 92 of whom underwent successful reduction by barium enema (59 per cent). Sixty-four were treated with laparotomy (41 per cent). Of these 64, 34 were reduced manually (22 per cent) and 30 required resection (19 per cent). Two patients died (1.3 per cent). Our experience is in general agreement with that of other reported series, and we conclude that hydrostatic barium enema reduction is the treatment of choice for intussusception during childhood. Laparotomy should be reserved for those patients in whom the barium enema was unsuccessful.

Barium Sulfate↗
PubMed1989

Interaction of very-low-density lipoprotein isolated from type I (insulin-dependent) diabetic subjects with human monocyte-derived macrophages.

Very-low-density lipoproteins (VLDL) (density less than 1.006 g/mL) were isolated from type I (insulin-dependent) diabetic patients in good to fair glycemic control and from age-, sex-, and race-matched, nondiabetic, control subjects. VLDL were incubated with human, monocyte-derived macrophages obtained from nondiabetic donors, and the rates of cellular cholesteryl ester synthesis and cholesterol accumulation were determined. VLDL isolated from diabetic patients stimulated significantly more cholesteryl ester synthesis than did VLDL isolated from control subjects (4.04 +/- 1.01 v 1.99 +/- 0.39 nmol 14C-cholesteryl oleate synthesized/mg cell protein/20 h; mean +/- SEM, P less than .05). The stimulation of cholesteryl ester synthesis in macrophages incubated with VLDL isolated from diabetic patients was paralleled by a significant increase in intracellular cholesteryl ester accumulation (P less than .05). The increase in cholesteryl ester synthesis and accumulation in macrophages were mediated by a significant increase in the receptor mediated, high affinity degradation (2.55 +/- 0.23 v 2.12 +/- 0.20 micrograms degraded/mg cell protein/20 h) and accumulation (283 +/- 35 v 242 +/- 33 ng/mg cell protein/20 h) of 125I-VLDL isolated from diabetic patients compared with VLDL from control subjects. To determine if changes in VLDL apoprotein composition were responsible for the observed changes in cellular rates of cholesteryl ester synthesis and accumulation, we also examined the apoprotein composition of the VLDL from both groups. There were no significant differences between the apoproteins B, E, and C content of VLDL from both groups. We also determined the chemical composition of VLDL isolated from both groups of subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Apoproteins↗
PubMed1989

Differential distribution of neuropeptides and serotonin in pig adrenal glands.

A differential distribution of vasoactive neuropeptides and serotonin in chromaffin cells and nerve fibers within the adrenal glands of the pig (Sus scrofa) was found using immunohistochemical methods. Met- and leu-enkephalins, present at high levels in the medulla (measured by radioimmunoassay), occurred in adrenaline storing cells, some of which contained calcitonin gene-related peptide. Islets of chromaffin cells beneath the capsule also contained enkephalins and calcitonin gene-related peptide. Nerve fibers with enkephalin-like immunoreactivity were sparse, but many varicose fibers in the inner cortex and medulla showed calcitonin gene-related peptide immunofluorescence in a pattern similar to vasoactive intestinal polypeptide. Neuropeptide Y was mainly associated with perivascular fibers and neither neuropeptide Y nor vasoactive intestinal polypeptide immunoreactive chromaffin cells were detected. In contrast to the neuropeptides, most serotonin-like immunoreactivity coincided with noradrenaline histofluorescence. It is concluded that the distribution of nerve fibers with calcitonin gene-related peptide and vasoactive intestinal polypeptide would allow interactions between chromaffin and inner cortical cells. Stimuli activating noradrenaline chromaffin cells could release serotonin while stimulation of adrenaline storage cells would release enkephalin and, to a lesser extent, calcitonin gene-related peptide. Met-enkephalin, which occurs 3 4:1 over leu-enkephalin, is the most likely of the co-released peptides to reach distant receptors via the venous outflow.

Adrenal Glands↗
PubMed1988

Subarachnoid haemorrhage produces differential effects on transmitter kinetics at cerebral periarterial noradrenergic terminals.

The functional states of cerebral perivascular noradrenergic terminals were investigated following experimental 'closed-space' subarachnoid haemorrhage (SAH) in cat. The left middle cerebral artery (L-MCA) was compared to the ruptured right (R-MCA) one. Permeability kinetics of 3H-NA (noradrenaline) were measured simultaneously in isolated segments of paired R- and L-MCAs, testing responses to electrical field stimulation and the presence of the alpha-adrenoceptor antagonist, phentolamine, at different concentrations and times post-SAH. Fractional 3H-NA efflux from ruptured R-MCAs was reduced to undetectable levels at 18 h to at least 3 d post-SAH. Response to electrical stimulation partially recovered at 10 d and approached the controls by 16 to 30 d. In the L-MCAs, 3H-NA efflux was decreased up to 90% at 18 h, but recovered to control level by 3 d, unless it too became involved by encroachment of blood from the SAH side. The fractional 3H-NA efflux in the controls was typically augmented by phentolamine, reaching a peak at 0.3 microM of the drug. This overflow response was completely lost between 0.03 and 3.0 microM phentolamine in the R-MCAs for at least 30 d post-SAH, whereas uninvolved L-MCAs regained drug-induced overflow at 10 to 16 d post-SAH. Uptake of 3H-NA after SAH was also decreased 30 to 50% for both MCAs at 18 h and 3 d post-SAH. Control 3H-NA uptake was regained by 10 d post-SAH in the L-MCA but not until 16 d in the R-MCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Alimentary tract duplications in children: case and literature review.

This report reviews 11 alimentary tract duplications over a 25-year experience at Children's Hospital Medical Center of Akron, Ohio. The cases are compared and contrasted to the literature with respect to lesion, location, and patient presentation. There were no multiple duplications in this series. Clinical presentations were related to obstruction, abdominal pain, and/or hemorrhage. There were four foregut duplications, five midgut duplications, and two hindgut lesions. All patients were treated by surgical removal and all survived. One case was an incidental finding at appendectomy. Pooled data from five large series of duplications revealed the ileal region to be involved in 41 percent of all duplications, followed by esophageal (21%), gastroduodenal (12%), and jejunal (8%). Diverticular, recanalization, and split notochord theories of pathogenesis are discussed. The curious association between duplications and gastric mucosa is explored.

Adolescent↗
PubMed1988

Enhancement of platelet aggregation by low-density lipoproteins from IDDM patients.

Low-density lipoprotein (LDL) is known to enhance platelet sensitivity to some aggregating agents. In this study, we observed that LDL isolated from patients with insulin-dependent diabetes mellitus (IDDM) enhanced thrombin-induced platelet aggregation to a greater extent than LDL isolated from matched controls (P less than .01). Thromboxane B2 production during aggregation was also significantly more enhanced by LDL isolated from IDDM than by control LDL (P less than .01). There was no difference in the lipid composition (free and esterified cholesterol, total phospholipids, and triglycerides) of LDL isolated from diabetic and control subjects. In contrast, the extent of glycosylation of LDL isolated from diabetic patients was significantly greater than that observed in LDL from normal subjects (P less than .01), and a positive correlation (r = .605, P less than .01) between the degree of LDL glycosylation and the rate of platelet aggregation was observed. LDL glycosylated in vitro enhanced thrombin-, collagen-, and adenosine 5'-diphosphate-induced platelet aggregation to a greater extent than control LDL (P less than .01). Although LDL glycosylated in vitro was taken up by platelets to a greater extent than control LDL (P less than .05), the lipid composition (free cholesterol and phospholipid) of platelets was not significantly changed. We postulate that an increased degree of glycosylation of LDL may enhance its uptake by platelets and lead to increased platelet reactivity to aggregating agents, probably by altering the structure of the platelet membrane. The enhancement of platelet aggregation by LDL may contribute to the accelerated development of atherosclerosis in diabetes mellitus.

Adolescent↗
PubMed1988

Glycosylation of low-density lipoprotein enhances cholesteryl ester synthesis in human monocyte-derived macrophages.

Glucose can react with the lysine residues of low-density lipoproteins (LDLs) and convert the lipoprotein to a form with a receptor-mediated uptake by cultured cells that is impaired. However, in contrast to other modified lipoproteins taken up by both murine and human macrophages via the scavenger-receptor pathway that may induce the formation of foam cells, glycosylated LDL is not recognized by murine macrophages, and thus far, it has not been shown to lead to marked intracellular accumulation of cholesterol in human macrophages. This study illustrates that glycosylated LDL incubated with human monocyte-derived macrophages, at a concentration of 100 micrograms LDL/ml medium, stimulates significantly more cholesteryl ester (CE) synthesis than does control LDL (10.65 +/- 1.5 vs. 4.8 +/- 0.13 nmol.mg-1 cell protein.20 h-1; P less than .05). At LDL concentrations similar to those of plasma, the rate of CE synthesis in macrophages incubated with glycosylated LDL is more markedly enhanced than that observed in cells incubated with control LDL (3-fold increase). The marked stimulation of CE synthesis in human macrophages exposed to glycosylated LDL is paralleled by a significant increase in CE accumulation in these cells (P less than .001). The increase in CE synthesis and accumulation seem to be mediated by an increase in the degradation of glycosylated LDL by human macrophages. Glycosylated LDL enters the macrophages and is degraded by the classic LDL-receptor pathway in slightly smaller amounts than control LDL, but its degradation by pathways other than the classic LDL receptor or scavenger receptor is markedly enhanced.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholesterol Esters↗
PubMed1987

Stimulation of cholesteryl ester synthesis in human monocyte-derived macrophages by low-density lipoproteins from type 1 (insulin-dependent) diabetic patients: the influence of non-enzymatic glycosylation of low-density lipoproteins.

Diabetes mellitus is an independent risk factor in the development of atherosclerosis. In this study we aimed to demonstrate whether there is an abnormal interaction between low-density lipoproteins from diabetic patients and human macrophages. We measured cholesteryl ester synthesis and cholesteryl ester accumulation in human monocyte-derived macrophages (obtained from non-diabetic donors) incubated with low density lipoproteins from Type 1 (insulin-dependent) diabetic patients in good or fair glycaemic control. Low density lipoproteins from the diabetic patients stimulated more cholesteryl ester synthesis than low density lipoproteins from non-diabetic control subjects (7.19 +/- 1.19 vs 6.11 +/- 0.94 nmol/mg cell protein/20 h, mean +/- SEM, p less than 0.05). The stimulation of cholesteryl ester synthesis by low density lipoproteins isolated from diabetic patients was paralleled by a significant increase in intracellular cholesteryl ester accumulation (p less than 0.02). There were no significant differences in the lipid composition of low density lipoproteins between the diabetic and control groups. Non-enzymatic glycosylation of low density lipoproteins was higher in the diabetic group (p less than 0.01) and correlated significantly with cholesteryl ester synthesis (r = 0.58). Similarly, low-density lipoproteins obtained from non-diabetic subjects and glycosylated in vitro stimulated more cholesteryl ester synthesis in macrophages than control low density lipoproteins. The increase in cholesteryl ester synthesis and accumulation by cells exposed to low density lipoproteins from diabetic patients seems to be mediated by an increased uptake of these lipoproteins by macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Complex carbohydrate composition of large dense-cored vesicles from sympathetic nerve.

Highly purified noradrenergic, large, dense-cored vesicles were isolated from bovine sympathetic nerve endings by sucrose-D2O density gradient centrifugation. Their concentration of glycoprotein hexosamine and sialic acid was 6.6 and 3.9 mumol/100 mg lipid-free dry weight, respectively, values which are similar to those previously found in bovine chromaffin granules. However, whereas chromaffin granule glycoproteins are characterized by their high proportion of N-acetylgalactosamine-containing O-glycosidically-linked oligosaccharides (present in the chromogranins), such oligosaccharides accounted for only 17% of those in noradrenergic synaptic vesicle glycoproteins. Fractionation of N-3H-acetylated glycopeptides by sequential lectin affinity chromatography demonstrated that approximately two-thirds of the oligosaccharides were of the tri- and tetraantennary complex type, accompanied by 14% biantennary oligosaccharides and 3% high-mannose oligosaccharides. The vesicles had a relatively low concentration of chondroitin sulfate (less than 5% of that in chromaffin granules) but significant amounts of heparan sulfate (0.4 mumol N-acetylglucosamine/100 mg lipid-free dry weight). No hyaluronic acid was detected. The concentration of ganglioside sialic acid in the noradrenergic vesicles was approximately 1 mumol/100 mg lipid-free dry weight, which is significantly higher than that of a crude membrane mixture from which the vesicles were prepared; the ratio of N-acetyl- to N-glycolylneuraminic acid was 0.8. Several molecular species of gangliosides were detected by thin-layer chromatography, but most of these did not exactly comigrate with bovine brain gangliosides. Cholera toxin binding indicated that approximately half or less of the gangliosides belong to the gangliotetraose series.

Animals↗
PubMed1986

An immunological characterization of five common antigens of chromaffin granules and of large dense-cored vesicles of sympathetic nerve.

Bovine chromaffin granules and large dense-cored vesicles of bovine splenic nerve were compared by one- and two-dimensional immunoblotting. Both types of vesicles contain chromogranin A, B and C. However, the proteolytic processing of these chromogranins within these vesicles is apparently different. Chromogranin B in chromaffin granules is processed by more than 80% whereas in nerve vesicles only 15% has been broken down to smaller proteins. In addition both types of vesicles contain dopamine beta-hydroxylase and cytochrome b-561.

Animals↗
PubMed1986

T-cryptantigen exposure in neonatal necrotizing enterocolitis.

Sixty-two infants with necrotizing enterocolitis were prospectively evaluated for evidence of the Thomson-Friedenreich cryptantigen (TCA) on their red cell surfaces. The TCA is exposed when bacterially derived neuraminidase acts on the surface of the red cells, cleaving off the N-acetylneuraminic acid, which hides the antigen. Seventeen patients (27%) had red cell TCA exposure as demonstrated by agglutination of their red cells by peanut lectin. This test is a simple agglutination procedure, which can be easily performed and yields results in a matter of minutes. Patients with TCA exposure require surgery 76% of the time compared with 18% of the time of those who did not demonstrate this phenomenon, a highly significant difference (P less than .01). All patients strongly positive for TCA exposure had intestinal perforations found at laparotomy. Patients with TCA exposure had clostridia cultured from blood, peritoneal fluid, or stool in 88% of the cases. Isolation of Clostridium perfringens was highly associated with strong TCA exposure and advanced disease. Since naturally occurring anti-TCA is found in normal adult plasma, hemolysis was observed in TCA-exposed patients who received plasma-containing blood products. The presence of TCA exposure in babies with necrotizing enterocolitis had prognostic and therapeutic implications. It indicates the need for antibiotic coverage against anaerobic organisms, strict avoidance of plasma-containing blood products, and the use of washed blood products if the patient is to be transfused. It also alerts the surgeon to the possibility of early operative intervention.

Agglutination Tests↗
PubMed1986

Enkephalin contents reflect noradrenergic large dense cored vesicle populations in vasa deferentia.

Opioid peptides including met- and leu-enkephalins are co-stored with catecholamines at similar concentrations in highly purified chromaffin granule fractions from bovine adrenal medulla and large dense cored vesicle (LDV) fractions from bovine splenic nerve. An initial attempt was made to test the universality of the co-storage of enkephalins in LDVs of sympathetic nerves. Based on a number of practical considerations, vasa deferentia were chosen from seven species. Leu-and met-enkephalin contents were quantitated by radio-immunoassays and norepinephrine by HPLC with electrochemical detection. Norepinephrine contents varied 11-fold and generally paralleled the density of sympathetic innervation among the species as reported in the literature. Leu-enkephalin contents varied 26-fold, generally paralleling the percentage composition of LDVs in the respective terminal varicosities among the species and animal size (axonal length). Met-enkephalin contents varied 20-fold, generally paralleling the density of sympathetic innervation, but not the percentage LDVs. Various amounts of met-enkephalin were also likely stored in cells other than sympathetic nerves, including chromaffin-like cells, the incidence of which varied according to species. Thus, the met- to leu-enkephalin ratios varied from 1.2:1 in dog; 1.7-1.9:1 in rabbit, cat and bull; 2.9:1 in man; 8.2:1 in rat; and essentially only met-enkephalin in guinea pig. The data imply differences in the processing of preproenkephalins in the same tissue of different species as well as in different cells of that tissue.

Animals↗
PubMed1986

Exocytosis from large dense cored vesicles outside the active synaptic zones of terminals within the trigeminal subnucleus caudalis: a possible mechanism for neuropeptide release.

It has been hypothesized that chemical interactions between neurons in the central nervous system can occur in the absence of well defined synaptic complexes, but morphological correlates have been difficult to find. The present study demonstrates exocytotic release from large (70-130 nm) dense cored vesicles at structurally nonspecialized areas along the plasmalemma of structurally different categories of terminals and occasionally from dendrites and axons within the neuropil of the trigeminal subnucleus caudalis. In rats, the marginal (lamina I) and substantia gelatinosa (lamina II) layers contain the central terminals of primary afferent fibers from the infraorbital nerve that supply the skin and whiskers (vibrissae). Different types of interneurons are also present and may modify the input being relayed to higher centers. While exocytotic profiles were present in control animals, they increased significantly (P less than 0.01) on the ipsilateral side 1-24 h after a unilateral skin lesion in the vibrissae area. A second increase (P less than 0.001) occurred 14-15 days after the lesion. Virtually all examples of large vesicle exocytosis were observed at structurally nonspecialized sites while those at the active synaptic zones involved small clear vesicles. Substance P-like immunofluorescence, present in controls and on the ipsilateral side during the first 6 days, subsequently declined until 4 weeks after surgery when some recovery was noted. The increase in large vesicle exocytosis and the decrease in substance P are interpreted to reflect functional adjustments of different neurons in response to the lesion. The exocytosis involving large dense cored vesicles may serve to deliver transmitters and/or neuropeptide modulators to appropriate receptors in a wider area than release into a specialized synaptic cleft would allow.

Animals↗
PubMed1986

Exocytosis from large dense cored vesicles as a mechanism for neuropeptide release in the peripheral and central nervous system.

Nerve terminals often contain morphologically distinct populations of large (75-110 nm) and small (45-55 nm) vesicles. The small vesicles are speculated to account for release of transmitter quanta as they accumulate at presynaptic membranes. Large vesicles can co-store neuropeptides and classical transmitters but their function in neurotransmission has been disputed because they do not appear to accumulate at chemical synapses. However, there is now evidence that the large vesicles play a role in neurotransmission or its modulation even though they may not be eminently involved in synaptic release. Thus, exocytosis occurs along the synapse-lacking membranes of peripheral noradrenergic varicosities. Large vesicles may continue to function in peptide release even after the classical transmitter has been depleted as demonstrated in the pig vas deferens. Three days of reserpine administration causes a parallel loss of noradrenaline and small vesicle contents but does not decrease enkephalin-like immunoreactivity or large vesicle electron density. In the central nervous system of the rat, where substance P and enkephalin have been localized to large vesicles, exocytosis occurs from several types of terminals. The large vesicles appear preferentially to release their contents at morphologically non-specialized sites even when characteristic synapses are present. Thus different mechanisms of transmitter and neuropeptide release may coexist. The nonsynaptic discharge may allow substances to diffuse over a wider distance whereas release into a synaptic cleft could restrict receptor interaction.

Animals↗