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Biomedical subjects

A Nilsson

Publications and source records attributed to A Nilsson.

At least 217 records · Page 12Linked to original sources
PubMed1996

Renal function during intravenous infusion of urological irrigating fluids in the sheep.

BACKGROUND: Oliguria or anuria is an important sign of the transurethral resection syndrome, but the mechanism is not clear. METHODS: We gave an intravenous infusion of 40 ml/kg of glycine 1.5%, sorbitol 2%-mannitol 1%, and isotonic saline (control) in 6 conscious ewes and studied if irrigating fluids cause acute disturbances of kidney function. RESULTS: Both the electrolyte-free solutions induced an increase in urine flow and persistent hypo-osmolality. The renal clearances of p-aminohippuric acid and inulin as well as the unilateral renal blood flow, which was measured via ultrasonic flow probes, increased in response to infusion of glycine but not to sorbitol-mannitol. After the infusions, the renal clearances decreased transiently to below baseline levels. Hypertonic saline was given after half of the infusions of electrolyte-free irrigating fluid. This treatment redistributed water from the cells to the extracellular fluid, but had no effect on renal function. CONCLUSIONS: We conclude that 2500 ml of electrolyte-free irrigating fluid had no detrimental effects on kidney function in sheep. The changes we observed were essentially the same as after infusion of isotonic saline.

Animals↗
PubMed1996

Prevalence of diabetic retinopathy in relation to age at onset of the diabetes, treatment, duration and glycemic control.

To study the frequency of diabetic retinopathy in relation to age at diagnosis, treatment, duration of diabetes and glycemic control as measured by means of HbA1c levels, we performed a cross-sectional, registered-based study in the Helsingborg area of southern Sweden, comprising 2232 diabetic patients. Of the known diabetic population < 75 years old, approximately 70% were estimated to be included. We graded retinopathy according to the alternative classification of the Wisconsin study. With an age at diagnosis < 30 years (19% of patients) the prevalence of retinopathy was 64%, whereas with an age at diagnosis > or = 30 years the prevalence of retinopathy was 57% in insulin-treated, and 26% in non-insulin treated patients. Levels of glycated hemoglobin and duration of diabetes were associated with retinopathy in the group with younger onset. In the older-onset group, there was a relationship between retinopathy and duration of diabetes and insulin treatment; glycated hemoglobin had a relationship which was of borderline significance with any retinopathy, but clearly significant with the pooled group: severe non-proliferative, proliferative retinopathy and/or macular edema. Hyperglycemia and duration of diabetes were thus associated with retinopathy in both younger- and older-onset diabetes, but hyperglycemia less so in the older-onset group.

Adult↗
PubMed1996

Transient hypertriglyceridemia of infancy.

A premature boy who had suffered from IRDS, bronchopulmonary dysplasia and retinopathy of prematurity developed massive hypertriglyceridemia (48.1 mmol/L) together with moderate hypercholesterolemia (12.6 mmol/L) at 5 months of age. Lipoprotein electrophoresis revealed a marked elevation of the level of the very low density lipoprotein fraction. There was a moderate decrease in the activity of a lipolytic enzyme, lipoprotein lipase (LPL). The child had neither liver or renal disorder nor any inflammatory disease. The hyperlipidemia disappeared spontaneously at the age of 3 years. The cause of the decreased LPL activity could not be established. A partial genetic deficiency in lipoprotein lipase appears the most likely explanation, since no signs of secondary lowering of LPL activity could be found.

Child, Preschool↗
PubMed1996

Metabolism of orally fed [3H]-eicosapentaenoic and [14C]-arachidonic acid in essential fatty acid-deficient rats.

The metabolism of individual polyunsaturated fatty acids (PUFA) may be influenced differently by nutritional status and nutritional intake. In normal rats, radioactive arachidonic acid (20:4(n-6), is preferentially retained in tissue phospholipids compared to linoleic (18:2(n-6), or eicosapentaenoic acid (20:5(n-3). This study compares the fate of 20:4(n-6) and 20:5(n-3) acids in essential fatty acid-deficient (EFAD) rats. [3H]-20:5 and [14C]-20:4 were fed in a fish oil emulsion to EFAD rats. Tissue lipids were analysed for radioactivity at 1, 2 and 4 h. The conversion of [3H]-20:5 to docosapentaenoic acid (22:5) and docosahexaenoic acid (22:6) was examined using high performance liquid chromatography (HPLC). The recovery of 3H in small intestine was lower than that of 14C (26 vs. 36% after 4 h, p < 0.001), but was higher in the liver (26 of 3H vs. 22% of 14C, p < 0.01), kidneys (1.5 vs. 1.2%, p < 0.001) and colon (0.3 vs. 0.2%, p = 0.01). The percentages of 3H and 14C in phospholipids were investigated in intestine and liver, and were higher in EFAD rats than in normal rats, particularly for phosphatidylethanolamine (PE). The proportions of [3H]-20:5 transformed to 22:5 and 22:6 did not exceed 7% in the intestine and 10% in the liver. In conclusion, the metabolism of dietary fatty acids 20:4 and 20:5 differed less than in normal rats, mainly due to the preferential retention of both fatty acids in phospholipids.

Animals↗
PubMed1996

Severe varicella pneumonia in adults in Stockholm County 1980-1989.

Varicella pneumonia in adults is considered to be a serious complication, with mortality rates of 9-50%, but the true incidence and clinical course is not known. We therefore studied all adult patients in Stockholm County hospitalized during the period 1980-1989 with varicella. 36/305 (12%) varicella patients admitted to hospital were diagnosed as having pneumonia, corresponding to a mean incidence of 0.32/100,000 inhabitants per year. In most patients the pneumonia had a mild to moderate clinical course and no deaths occurred (mortality rate 0%, CI95 [0, 9.7]). However, 13 patients had a severe tachypnoea (> or = 30 breaths/min) and 4 of these required intensive-care treatment. Ten patients were treated with acyclovir, in most cases combined with corticosteroids. We conclude that the incidence of severe varicella pneumonia is low in the adult population, and that the mortality rate of this complication is probably lower than previously described.

Acyclovir↗
PubMed1996

In vitro effects of ethanol on human gastric and pancreatic lipolytic activities/enzymes.

BACKGROUND: Ethanol ingestion may disturb fat digestion and absorption by affecting gastric, intestinal, hepatic, and pancreatic functions. Involved mechanisms are not well understood. We examined in vitro ethanol effects on gastric and pancreatic lipolytic activity. METHODS: Human gastric juice, pure gastric lipase, pancreatic lipase, colipase, carboxyl ester lipase, phospholipase A2, and duodenal contents were a) preincubated at 37 degrees C with ethanol (0-30%) and then assayed under normal conditions (pH-stat titration), or b) assayed in the presence of various ethanol concentrations (0-30%). RESULTS: Ethanol reduced gastric and pancreatic lipolytic activities in a dose-dependent manner. The effect was more pronounced with alcohol present in the assay medium, with 5% ethanol reducing carboxyl ester lipase activity by 10%, gastric lipase activity by 20%, and pancreatic lipase activity by 46%. Colipase and phospholipase A2 activities were only slightly affected by ethanol. CONCLUSIONS: Observed effects of ethanol on gastric and pancreatic lipase may be important when fat digestion is already impaired due to gastric, intestinal hepatic, and/or pancreatic diseases.

Carboxylesterase↗
PubMed1995

Protein conformational changes during the bacteriorhodopsin photocycle. A Fourier transform infrared/resonance Raman study of the alkaline form of the mutant Asp-85-->Asn.

Bacteriorhodopsin is a light-driven proton pump, which undergoes a photocycle consisting of several distinct intermediates. Previous studies have established that the M-->N step of this photocycle involves a major conformational change of membrane embedded alpha-helices. In order to further investigate this conformational change, we have studied the photocycle of the high pH form of the mutant Asp-85-->Asn (D85Nalk). In contrast to wild type bacteriorhodopsin, D85Nalk has a deprotonated Schiff base and a blue-shifted absorption near 410 nm, yet it still transports protons in the same direction as wild type bacteriorhodopsin (Tittor, J., Schweiger, U., Oesterhelt, D. and Bamberg, E. (1994) Biophys. J., 67, 1682-1690). Resonance Raman spectroscopy of D85Nalk and D85Nalk regenerated with retinal labeled at the C-15 position with deuterium reveals the existence of an all-trans configuration of the chromophore. Fourier transform infrared difference spectroscopy shows that the photocycle of this light-adapted form involves similar events as the wild type bacteriorhodopsin photocycle including the M-->N protein conformational change. These results help to explain the ability of D85Nalk to transport protons and demonstrate that the M-->N conformational change can occur even in the photocycle of an unprotonated Schiff base form of bacteriorhodopsin.

Asparagine↗
PubMed1995

Asp 46 can substitute Asp 96 as the Schiff base proton donor in bacteriorhodopsin.

Bacteriorhodopsin functions as a light-driven proton pump in the purple membrane of Halobacterium salinarium. A variety of studies have established that a proton is transferred over an approximately 10 A distance from Asp 96 to the retinylidene Schiff base during the M --> N transition of the bR photocycle. In order to further explore the mechanism of this Schiff base reprotonation, we compared the properties of the double mutant Thr 46 --> Asp/Asp 96 --> Asn (T46D/D96N), the single mutants Asp 96 --> Asn (D96N) and Thr 46 --> Asp (T46D), and wild-type bR. In contrast to D96N, which exhibits a very slow M decay, T46D/D96N has an M decay close to that of wild-type bR. FTIR difference spectroscopy detects bands in the carboxyl and carboxylate stretch region of T46D/D96N consistent with the deprotonation of Asp 46 during the M --> N transition. In addition, bands associated with structural changes of Asn 96 in the mutant D96N are absent in T46D/D96N. Resonance Raman spectroscopy provides evidence that both T46D/D96N and T46D have a long-lived N-like species in their photocycles. These data demonstrate that Asp 46 can substitute for Asp 96 as the proton donor group in the reprotonation pathway of the Schiff base during the M --> N transition. However, N decay is delayed in comparison to wild-type bR. This may be due to a partial block in the proton pathway leading from the cytoplasmic medium to Asp 46.

Asparagine↗
PubMed1995

Alkaline sphingomyelinase activity in rat gastrointestinal tract: distribution and characteristics.

Previous studies indicated that there was an alkaline sphingomyelinase (SMase) activity in small intestine, but its properties have not been studied in detail. In the present work, we studied the distribution of this enzyme activity in rat gastrointestinal tract and characterized it in intestinal mucosal homogenates. Little alkaline SMase activity was detected in the stomach and the duodenum. The activity in both mucosa and intestinal content increased in the small intestine and reached the maximum at the distal jejunum, then declined in the ileum and slightly increased again in the colon. The activity distribution pattern differed markedly from those of acid SMase and alkaline phosphatase. Little alkaline SMase activity could be found in bile, liver and pancreas before or after treatment with trypsin. The optimum pH of the alkaline SMase was 9. It specifically hydrolyzed sphingomyelin (SM), not phosphatidylcholine, to ceramide and phosphocholine. The alkaline SMase was bile salt dependent and was optionally activated by 3 mM bile salts. Triton X-100 could not mimic the effect of bile salt, rather dose-dependently inhibited the enzyme activity. Ca2+, Mg2+ did not change the alkaline SMase activity in the presence of bile salts, and reduced the activity in the absence of bile salt. Trypsin inactivated acid SMase in pancreas, liver and duodenum but had no influence on intestinal alkaline SMase activity. In conclusion, the intestinal alkaline SMase has a specific distribution pattern and the characters of it differ in several respects from the known acid and neutral SMases.

Alkaline Phosphatase↗
PubMed1995

Binding of prothrombin to chyle chylomicrons: effects of temperature and calcium ions, and role of surface phospholipids.

The ability of chyle chylomicrons to bind prothrombin has been studied. Rat chyle chylomicrons were incubated with human 125I-prothrombin and binding was examined by separating the chylomicrons from free 125-I-prothrombin by density-gradient ultracentrifugation, and by gel filtration on Sepharose CL-2B. A significant binding of prothrombin to chyle chylomicrons occurred. The complex formation was calcium dependent, and decreased markedly when the temperature was lowered from 37 degrees C to 20 degrees C and when PH was raised above 8. The time course for the binding at 37 degrees C in presence of 2 mmol/L CaCl2 exhibited an initial lag phase at about 10 minutes. Thereafter most of the binding occurred within 30 minutes. Bound prothrombin could not be removed from chyle chylomicrons by treatment with EDTA, suggesting that this binding is not a simple Ca2+ dependent association between prothrombin and chyle chylomicrons. Inclusion of 1% purified human serum albumin caused a 50% decrease in binding, half of which was reversed by increasing the Ca2+ ion concentration. Addition of pancreatic phospholipase A2 (PLA2) in doses sufficient to hydrolyze more than 95% of the phosphatidylethanolamine (PE) and 37% of the phosphatidylcholine (PC) decreased the binding by 50%. Doses of PLA2 that hydrolyze more than 95% of the phosphatidylethanolamine (PE) and 37% of the phosphatidylcholine (PC) decreased the binding by 50%. Doses of PLA2 that hydrolyzed 60-80% of (PE and 4-10% of the PC decreased the binding by only 7-15%. It is suggested that the binding of prothrombin to chyle chylomicrons is in part mediated by negatively charged phospholipids of the chylomicron surface, although a specific role of the PE could not be demonstrated.

Animals↗
PubMed1995

Phosphorylation of eukaryotic elongation factor 2 in differentiating and proliferating HL-60 cells.

Ca(2+)-and calmodulin-dependent protein kinase III (CaM PKIII) phosphorylates eukaryotic elongation factor 2 (eEF-2) in HL-60 cells. Dephosphorylation of the factor in these cells is catalyzed by phosphoprotein phosphatase 2A alone. Differentiation of the HL-60 cells by all-trans retinoic acid resulted in a reduced growth rate and a marked decrease in the intracellular concentration of eEF-2. During differentiation the activity of the eEF-2 kinase is gradually reduced and reaches 10% of that found in undifferentiated cells 5 days after the onset of differentiation. The capacity to dephosphorylate phospho-eEF-2 remained unaltered in the growth-arrested cells. Differentiation without reduced proliferation was induced in the HL-60 cells by interferon-gamma. Under these conditions, differentiation had no effect on the cellular content of eEF-2 or the ability to dephosphorylate phospho-eEF-2. However, the differentiated cells showed a dramatic decrease in the specific activity of the eEF-2 kinase. The results show that the cellular content of eEF-2 varies with the rate of proliferation and that the activity of the eEF-2 kinase is high in undifferentiated proliferating cells and decreases upon differentiation even under conditions of an unaltered growth rate.

Animals↗
PubMed1995

Role of platelet factor Xa in chylomicron-prothrombin complexes induced platelet activation.

The effects of chylomicron-prothrombin complexes on platelet activation, including platelet aggregation, serotonin release, arachidonic acid release and increases of platelet cytosolic [Ca2+]i were examined. Furthermore the role of platelet factor Xa on the conversion of chylomicron bound prothrombin to thrombin was studied by using a synthetic inhibitor of factor Xa, TenStop. The chylomicron-prothrombin complexes could induce platelet aggregation and enhance the platelet serotonin release and arachidonic acid release in contrast to native chyle chylomicrons. An increase of platelet [Ca2+]i was observed during incubation with chylomicron-prothrombin complexes. TenStop inhibited platelet aggregation and serotonin release that were induced by chylomicron-prothrombin complexes in a dose-dependent manner, whereas the TenStop itself did not inhibit the platelet aggregation induced by thrombin and collagen. It is concluded that platelet activation induced by chylomicron-prothrombin complexes is related to the platelet factor Xa that could be the key factor in the conversion of chylomicron bound prothrombin to thrombin.

Animals↗