PubMed Health⌕ Search

Biomedical subjects

F Nilsson

Publications and source records attributed to F Nilsson.

At least 127 records · Page 7Linked to original sources
PubMed1975

Results of partial thyroidectomy for thyrotoxicosis.

In a retrospective study, two series of surgically treated patients with thyrotoxicosis were compared. The series differed with respect to preoperative treatment and operative techniquue. In one series a combined preoperative treatment with an antithyroid drug and 1-thyroxine was given and the recurrent nerves and parathyroid glands were routinely identified. In the other series no such operative routine was followed and iodine was given preoperatively. The complication rate was low in both series. There was no postoperative mortality. The existing differences, although subtle, in the frequency of recurrent nerve paralysis, postoperative hypoparathyroidism or hypothyroidism, as well as recurrent toxicosis, favoured the surgical approach with the combined preoperative treatment and a meticulous technique with identification of recurrent nerves and parathyroid glands.

Adult↗
PubMed1975

Analyses of small bowel propulsion, ileo-caecal passage and serum gastrin after truncal vagotomy. A methodological study in the rat with continuous intraduodenal infusion.

A test substance containing 51CrO--4 was administered to the duodenum of vagotomized or sham-operated, conscious rats for 5 hours at a rate of 3.3 mul/min. The distribution of 51Cr in the stomach, small bowel, caecum and colon was measured with a scintillation counter. Data reduction was made with automatic methods. The activity distribution in the small bowel was found to be irregular. A transit time of about 3 hours was observed between the duodenum and the caecum. The proximal 40% of the small bowel was passed in about 30 min at a constant rate. No differences between vaotomized animals and controls could be demonstrated. The passage from ileum to caecum in vagotomized animals indicated a process, with constant portions, each discharge containing about 11% of the total administered activity, implying two discharges per hour.

Animals↗
PubMedDate not supplied

A proteome analysis of livers from obese (ob/ob) mice treated with the peroxisome proliferator WY14,643.

The PPAR (peroxisome proliferator activated receptor) transcription factors are ligand-activated receptors which regulate genes involved in lipid metabolism and homeostasis. PPARalpha is preferentially expressed in the liver and PPARgamma preferentially in adipose tissue. Activation of PPARalpha leads to peroxisome proliferation in rodents and increased beta-oxidation of fatty acids. PPARgamma-activation leads to adipocyte differentiation and improved insulin signaling of mature adipocytes. Both of these PPAR receptors are potential targets for treatment of dyslipidemia in man. Studies by others using a proteomics approach have characterized the effects of PPARalpha agonists in livers from lean healthy mice. However, we wanted to map the effects of a therapeutic dose of a PPARalpha agonist in a disease model of insulin resistance and diabetes, the obese diabetic ob/ob mouse, by proteomics. Therefore, ob/ob mice, which have highly elevated levels of plasma triglycerides, glucose and insulin, were treated for one week with WY14,643 (180 micromol/kg/day), a well-characterized selective PPARalpha agonist. Plasma triglycerides, glucose and insulin levels were determined and we found significant therapeutic effects on triglycerides and glucose levels. The liver protein compositions were investigated by high-resolution two-dimensional gel electrophoresis which showed that WY14,643 produced up-regulation of at least 16 spots. These were identified by mass spectrometry and 14 spots were found to be components of the peroxisomal fatty acid metabolism. Thus, WY14,643 at a therapeutic dose, caused induction of peroxisomal fatty acid beta-oxidation in obese diabetic mice.

Animals↗
PubMedDate not supplied

Identification of the heme adduct and an active site peptide modified during mechanism-based inactivation of rat liver cytochrome P450 2B1 by secobarbital.

The olefinic barbiturate secobarbital (SB) is a sedative hypnotic known to be a relatively selective mechanism-based inactivator of rat liver cytochrome P450 2B1. Previous studies have demonstrated that such inactivation results in prosthetic heme destruction and irreversible drug-induced protein modification, events most likely triggered by P450 2B1-dependent oxidative activation of the olefinic pi-bond. However, the precise structure of the SB-modified heme and/or the protein site targeted for attack remained to be elucidated. We have now isolated the SB-heme adduct from P450 2B1 inactivated by [14C]SB in a functionally reconstituted system and structurally characterized it by electronic absorption spectroscopy and tandem collision-induced dissociation (CID), matrix-assisted laser desorption ionization on time of flight (MALDI-TOF), and liquid secondary ion mass spectrometry in the positive mode (+ LSIMS) as the N-(5-(2-hydroxypropyl)-5-(1-methylbutyl)barbituric acid)protoporphyrin IX adduct. The [14C]SB-modified 2B1 protein has also been isolated from similar inactivation systems and subjected to lysyl endopeptidase C (Lys-C) digestion and HPLC-peptide mapping. A [14C]SB-modified 2B1 peptide was thus isolated, purified, electrotransferred onto a poly-(vinylidene) membrane, and identified by micro Edman degradation of its first N-terminal 17 residues (S277NH(H)TEFH(H)ENLMISLL293) as the Lys-C peptide domain comprised of amino acids 277-323. This peptide thus includes the peptide domain corresponding to the distal helix I of P450 101, a region highly conserved through evolution, and which is known not only to flank the heme moiety but also to intimately contact the substrates. This finding thus suggests that SB-induced protein modification of P450 2B1 also occurs at the active site and, together with heme N-alkylation, contributes to the SB-induced mechanism-based inactivation of P450 2B1.

Amino Acid Sequence↗
PubMedDate not supplied

Glucose and insulin infusion directly after cardiac surgery: effects on systemic glucose uptake, catecholamine excretion, O2 consumption, and CO2 production.

Systemic glucose uptake was studied in 31 patients during 4 hr starting 1 hr after open heart surgery, using the hyperinsulinemic "clamp" technique at different plasma insulin levels and at a glucose concentration of 6 or 10 mmol/liter. Possible metabolic side effects related to the glucose uptake were studied by measurements of urinary catecholamine excretion, O2 consumption, CO2 production, and arterial PCO2. A peak systemic glucose uptake of 7.0 +/- 0.4 mg/kg body weight/min was found at a plasma insulin concentration of 3192 +/- 150 mU/liter and a blood glucose concentration of 10.2 +/- 0.1 mmol/liter. No significant difference was found in urinary catecholamine excretion compared to control patients. O2 consumption was unaltered while a 15% increase in CO2 production was observed.

Adult↗
PubMedDate not supplied

Splanchnic glucose balance and insulin resistance in the early postoperative phase of cardiac surgery.

The splanchnic balance of glucose was studied in the basal state and at three levels of "clamped" hyperinsulinemia (260 +/- 23, 510 +/- 59, 3875 +/- 367 mU/liter) in 24 patients (43-70 years of age), who had undergone coronary surgery about 1 hr previously. The splanchnic balance of glucose in the basal state was negative in all patients (-1.6 +/- 0.3 mg/kg/min) and was changed into a zero-balance within 30 min when 0.15 or 0.3 U/kg/hr of insulin was infused. At an insulin infusion rate of 1.0 U/kg/hr the net splanchnic glucose balance was turned into a significant positive balance of an average 0.9 +/- 0.3 mg/kg/min.

Adult↗