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Biomedical subjects

A Andersson

Publications and source records attributed to A Andersson.

At least 181 records · Page 10Linked to original sources

Development of methods for registration of the force exerted by hand-fingers in industrial work.

In a manufacturing industry producing ground hard metal inserts, a small strain-gauge pressure transducer was built into the work prefix to measure the force exerted by the fingers. The procedure did not interfere with the work. The variation of force and of the time sequences between each force measurement were measured. The coefficient of variation (CV) was used as a measure of precision of the work.

Journal Article↗

Regulation of GAD expression in islets of Langerhans occurs both at the mRNA and protein level.

The expression of the autoantigen glutamate decarboxylase in islets of Langerhans was investigated under different culture conditions, which affect the functional activity of the beta-cell. Using immunoprecipitations and analyses of enzyme activity, an increase in glutamate decarboxylase was detected in rat islets cultured at a glucose concentration of 11 mmol/l compared with those cultured at 5.6 mmol/l glucose. To determine whether the change was induced at the level of mRNA expression, total RNA was extracted from rat islets cultured at 5.6 or 11 mmol/l glucose, reverse transcribed and amplified by the polymerase chain reaction. Comparative quantitation in a phosphor imager revealed a significantly higher (82%, P < 0.005) content of glutamate decarboxylase mRNA in islets cultured at 11 mmol/l glucose. In parallel, human recombinant interleukin-1 beta, and diazoxide were tested for their effects on the expression of glutamate decarboxylase. Islets cultured at 11 mmol/l glucose in the presence of 40 U/ml of interleukin-1 beta, showed a 63% decrease (P < 0.005) in enzyme activity compared with those cultured at 11 mmol/l glucose alone, and similar decreases were noted on analysis of glutamate decarboxylase biosynthesis and mRNA. Islets cultured at 11 mmol/l glucose in the presence of 22.5 mg/ml diazoxide exhibited a significant reduction in enzyme activity (59%; P < 0.001) compared with those cultured at 11 mmol/l glucose only. This reduction, however, was not accompanied by a decrease in the content of glutamate decarboxylase mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of preheating on potato texture.

Preheating potatoes at 50 to 80 degrees C has a firming effect on the cooked potato tissue. This effect is particularly pronounced at a preheating temperature of 60 to 70 degrees C followed by cooling. Several theories have been presented in the literature to explain this firming effect: retrogradation of starch, leaching of amylose, stabilization of the middle lamellae and cell walls by the activation of the pectin methylesterase (PME) enzyme, and by the release of calcium from gelatinized starch and the formation of calcium bridges between pectin molecules. Most probably, none of these theories alone can explain the phenomenon and more than one mechanism seems to be involved. Some of these mechanisms seem to be interdependent. As an example, calcium could be considered as a link all the way through release after starch gelatinization to cross-linking pectin substances in the cell wall and the middle lamellae, which has been demethylated by the PME enzyme. More research and "clear cut" experiments are needed in order to elucidate the role of each mechanism, especially which of them is the main contributor to the process of firming. Most probably, the calcium-pectin-PME mechanism plays a secondary role, that is, it only retards the collapse of the tissue structure that would otherwise occur during the final heating without preheating, and it is not the main factor of firmness.

Carboxylic Ester Hydrolases↗

Neonatal treatment with monoclonal natural antibodies restores a normal pattern of VH gene utilization in the non-obese diabetic mouse.

The utilization of individual VH7183 genes in the autoimmune non-obese diabetic (NOD) mouse and the normal C57BL/6 mouse, both carrying the IgHb haplotype, was investigated. Nucleotide sequence analyses of a large number of VHDJH rearrangements utilizing VH7183 gene segments allowed us to identify 10 individual members of this family in the IgHb haplotype. Eight of these members were isolated from both C57BL/6 and NOD mice, whereas two were found only in NOD mice. Analysis of polymerase chain reaction libraries derived from genomic DNA revealed that > 50% of the VH7183 rearrangements isolated from both neonatal and adult NOD mice were functional. In contrast, the frequency of functional rearrangements decreased from 61% in neonatal to 9% in adult splenic B cells of C57BL/6 origin. These observations suggested that adult NOD mice retained a neonatal pattern of VH7183 gene utilization. Most interestingly, the deviation from the normal pattern of VH7183 utilization observed in the adult NOD mouse could be 'normalized' by neonatal treatment with a natural mAb previously demonstrated to inhibit the development of diabetes in the NOD mouse. These data demonstrate that certain 'natural' mAbs can influence the development of T cell mediated autoimmunity in the NOD mouse and suggest that the B cell/Ig compartment may play an important role in this process.

Animals↗

Effects of treatment with oral isosorbide dinitrate on platelet function in vivo; a double-blind placebo-controlled study in patients with stable angina pectoris.

1. A randomised double-blind placebo-controlled cross-over study was performed to investigate the effects of oral isosorbide dinitrate (ISDN; 20 mg twice daily for 2 weeks) on various aspects of platelet function in vivo in 20 patients with stable angina pectoris. Measurements were performed at rest and after platelet activation by physical exercise (bicycle ergometry). 2. Compared with placebo, treatment with ISDN significantly decreased systolic blood pressure at rest by 7 (-14 to -1) mm Hg (mean and 95% CI) and tended to increase exercise capacity by 7 (-1 to 14) W and attenuate perceived chest pain during maximal work. The dosage was high, as judged by side-effects reported (mainly headache). Compliance was good, as assessed by electronic counter equipped tablet bottles (Medication Event Monitoring System); only one patient had a compliance rate below 60%. 3. Exercise significantly increased platelet aggregability as measured by filtragometry ex vivo; the time taken for platelet aggregates in whole blood drawn directly from an antecubital vein to occlude a microfilter was significantly decreased from 155 to 95 s (antilog of mean log values). Platelet secretion in vivo also increased, as indicated by significant elevations of beta-thromboglobulin in plasma; from 22 to 35 ng ml-1 (P = 0.006). 4. ISDN treatment did not inhibit platelet function. Relative to placebo, filtragometry readings (ISDN/placebo ratios; mean and 95% CI) were not altered either at rest (1.05 (0.83 to 1.32)) or immediately after exercise (0.98 (0.80 to 1.20)). Similarly, beta TG in plasma was unaltered by ISDN treatment; 1.09 (0.98 to 1.21) at rest, and 1.04 (0.82 to 1.30) immediately after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Plasma homocysteine in relation to serum cobalamin and blood folate in a psychogeriatric population.

Plasma homocysteine, serum cobalamin and blood folate were analysed in 296 consecutive patients referred to a psychogeriatric department for diagnosis of mental disease. Plasma homocysteine correlated with positive significance with age and serum creatinine, and with negative significance with serum cobalamin and blood folate. Approximately 35-40% of the patients with low serum cobalamin (< 150 pmol l-1) or low blood folates (< 150 nmol l-1) exhibited normal values of plasma homocysteine (< 19.9 mumol l-1). Possibly, these patients do not have a deficiency of the vitamins in the tissue. At least 7.5% of the patients with serum cobalamin levels (> 150 pmol l-1) showed an inexplicably increased level of plasma homocysteine. These patients might have a deficiency of tissue cobalamin despite the normal serum cobalamin levels. The effect of cobalamin supplementation for 7-10 days on plasma homocysteine was tested in 62 patients with different levels of serum cobalamins. We found the most pronounced decrease of plasma homocysteine in the patients with lowest serum cobalamin levels and in the patients with highest plasma homocysteine, indicating that the percentage decrease of the initial concentration of plasma homocysteine could reflect the degree of cobalamin deficiency. Folate supplementation for 7-10 days reduced plasma homocysteine not only in patients with folate deficiency but also in those with a normal folate status, and even in patients with cobalamin deficiency. The latter patients further reduced their plasma homocysteine after additional cobalamin treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Homocysteine and cysteine: determinants of plasma levels in middle-aged and elderly subjects.

OBJECTIVES: Hyperhomocysteinaemia is an independent risk factor for cardiovascular disease. We explored possible determinants of plasma homocysteine and cysteine concentrations amongst middle-aged and elderly subjects. DESIGN AND SUBJECTS: Of 501 35-95-year-old randomly selected residents of Lund and Malmö, Sweden, 244 (49%; 131 men, 113 women) were investigated. RESULTS: Total plasma homocysteine concentrations were higher in men than in women (mean +/- SD: 13.9 +/- 4.1 and 12.3 +/- 4.1 mumol L-1; P < 0.001), increased markedly with age (Spearman's rho = 0.488; P < 0.001), and were correlated (P < 0.001) to concentrations of blood folate, serum vitamin B12, and serum creatine (rho = -0.366, -0.338, and 0.463). Users of multivitamins had lower homocysteine levels than nonusers [10.5 +/- 3.3 mumol L-1 (n = 31) and 13.5 +/- 4.2 mumol L-1 (n = 213), respectively; P < 0.001]. Total plasma cysteine concentrations also increased significantly with age and increasing serum creatinine, but were unrelated to gender, blood folate, serum vitamin B12 and use of multivitamins. CONCLUSIONS: Age, gender, folate, serum vitamin B12, serum creatinine and multivitamin usage are all important determinants of the plasma homocysteine concentration, whereas only age and serum creatinine are determinants of the plasma cysteine concentration. The age-related increase in homocysteine and cysteine may be linked to the age-related impairment of renal function, whereas the sex difference in plasma homocysteine may be because of the fact that more homocysteine is formed in men than in women in conjunction with creatine-creatinine synthesis.

Adult↗

Immunocytochemical detection of the carbohydrate antigen, Sialyl Lewis(x), in normal human skin and during irritant contact dermatitis.

Sialys Lewis(x) (SLex) is a ligand for the E-selectin and the interaction of E-selectin on the endothelium and SLex on T cells may be important for T-cell migration into the skin. We investigated the expression of SLex on Langerhans cells (LC) in normal skin and on LC repopulating epidermis deprived of LC due to a preceding irritant contact dermatitis. SLex was visualized by fluorescence and light microscopic immunocytochemistry using the monoclonal antibody, CSLEX-1. The results showed that about 40% of LC in normal epidermis express SLex. In the repopulation phase, most of the epidermal cells were CD1a+/SLex. We suggest that SLex is present on epidermal LC that have recently immigrated from the dermis.

Cell Movement↗

Polyamine requirements in nicotinamide-stimulated beta-cell differentiation in fetal porcine islet-like cell clusters.

The impact of nicotinamide on regulation of cell replication and hormone production by fetal porcine islet-like cell clusters (ICCs) containing a low fraction of beta-cells was investigated. For this purpose, ICCs were produced in tissue culture for 4 days in the presence or absence of nicotinamide (10 mM). ICCs formed in the presence of nicotinamide showed increased rates of (pro)insulin biosynthesis, contained more insulin, and displayed elevated contents of polyamines when compared with untreated ICCs. Immunocytochemical analyses of autoradiographed ICCs disclosed that nicotinamide expanded the relative size of the beta-cell population, and that the vitamin increased DNA synthesis of non-beta-cells only. The possibility that the effects of nicotinamide were conveyed by the increased polyamine content was explored by giving nicotinamide together with inhibitors of rate-limiting enzymes of polyamine biosynthesis, a maneuver that precluded the increases in polyamines of whole ICCs. Although this treatment prevented the increases in beta-cell population size, insulin production, and insulin content evoked by nicotinamide, the elevated cell replication nonetheless persisted. We conclude that the stimulatory effects of nicotinamide on insulin production and content by fetal porcine ICCs result from neoformation of beta-cells through differentiation. Since these effects were prevented by blocking the increased polyamine content, it is suggested that a stimulated synthesis of polyamines may be an important event in mediating the differentiating action of nicotinamide.

Animals↗

Plasma homocysteine and thiol compound fractions after oral administration of N-acetylcysteine.

The total concentration of the atherogenic aminothiol acid homocysteine in plasma of healthy volunteers was decreased after oral administration of N-acetylcysteine (NAC), whereas the reduced and free (non-protein bound) fractions of homocysteine were increased. The decrease of the total fraction varied between 20 and 50% and was dose-related. Cysteinylglycine was also decreased after the administration of NAC, whereas cysteine did not change. Administration of high amounts of NAC probably displaces homocysteine and cysteinylglycine from their protein binding sites by disulfide interchange reactions. This leads to the formation of mixed low molecular-weight cysteine and NAC disulfides with high renal clearance and possibly also increased metabolic bio-availability, thereby eliminating homocysteine and cysteinylglycine from plasma. Since only a small amount of additional urinary homocysteine was recovered it is likely that this aminothiol acid is taken up by the tubular cells and further metabolized.

Acetylcysteine↗

Lack of association between plasma homocysteine levels and microangiopathy in type 1 diabetes mellitus.

The reactive vascular-injuring amino acid homocysteine was previously shown to be increased in plasma in diabetic patients with clinical signs of nephropathy. In this study, plasma homocysteine was measured in type 1 diabetic patients with normoalbuminuria (n = 22), microalbuminuria (n = 40) and proteinuria (n = 14) in order to investigate whether plasma homocysteine levels are increased already at the stage of incipient nephropathy, i.e. microalbuminuria. Furthermore, patients were characterized according to the degree of retinopathy. Plasma homocysteine in the whole population (n = 76) was related to B-Folate (r = 0.38, p < 0.01), S-Creatinine (r = 0.55, p < 0.001), S-Urea (r = 0.37, p < 0.01), U-Albumin (r = 0.46, p < 0.001), urinary N-acetyl-beta- glucosaminidase (r = 0.40, p < 0.001), systolic blood pressure (r = 0.36, p < 0.01) and diabetes duration (r = 0.44, p < 0.001). There were no differences in plasma homocysteine levels between patients with normoalbuminuria (8.0 +/- 1.7 mumol l-1; mean +/- SD) and those with microalbuminuria (9.1 +/- 3.4 mumol l-1). However, patients with clinical signs of nephropathy had higher plasma homocysteine levels (12.9 +/- 5.7 mumol l-1, p < 0.01) compared to the other two groups. There was no association between plasma homocysteine levels and different degrees of retinopathy. Thus, the present study does not show any relation between plasma homocysteine levels and early stages of diabetic nephropathy or retinopathy indicating that elevated concentrations of plasma homocysteine does not explain the increased risk for atherosclerosis observed in patients with microalbuminuria.

Adult↗

Effects of cyclosporin A on the blood flow of the native and transplanted rat pancreas and duodenum.

The aim of the present study was to evaluate the effects of cyclosporin A (CyA) on the blood perfusion of the transplanted pancreas. For this purpose syngeneic pancreaticoduodenal transplantations were performed in Wistar-Furth rats. After nephrectomy the graft was anastomosed using a nonsuturing cuff technique to the left renal vessels. Beginning 7 days after transplantation and then continuing for 2 weeks, CyA (15 mg/kg body weight) or vehicle was given p.o. once daily, 6 days a week. The serum CyA concentrations were greater than 600 ng/ml at all points in time tested. Intraperitoneal glucose tolerance tests were normal in CyA-treated animals after 12 days, but the pancreatic insulin concentration was decreased to the same extent in the native and transplanted pancreas. A microsphere technique was used to measure the blood perfusion of the pancreaticoduodenal graft, the native pancreas and duodenum, and remaining kidney 14 days after starting the CyA treatment. The renal blood flow was markedly decreased by CyA when compared with the control animals. In rats given vehicle alone, pancreatic, islet, and duodenal blood flows were higher in the graft than in the corresponding native organs. However, in rats given CyA, hyperperfusion of the graft was not observed. We conclude that the administration of CyA prevents the transplantation-induced blood flow increase seen in pancreaticoduodenal grafts of vehicle-treated rats. These observations may reflect graft denervation.

Animals↗