Search PubMed⌕ Search

Biomedical subjects

C Johansson

Publications and source records attributed to C Johansson.

At least 217 records · Page 12Linked to original sources

Mitral regurgitation and diastolic flow profile in systemic sclerosis.

To evaluate the left ventricular filling characteristics in systemic sclerosis, we examined 30 consecutive patients, 15 men and 15 women, and related the findings to those from 48 age- and sex-matched controls. All patients were investigated by pulsed and continuous wave mitral Doppler, and M mode echocardiography. We found the A wave of the mitral flow velocity as recorded by pulsed wave Doppler to be higher in patients (0.74 +/- 0.07 vs 0.54 +/- 0.02 m/sec, P less than 0.002), while the E wave did not differ. The high A/E ratio indicating reduced distensibility, correlated to interventricular septal thickness (r = 0.53, P less than 0.001), and atrial emptying index (r = -0.55, P less than 0.001). Early filling was impaired, with a prolonged pressure half time (99 +/- 6 vs 84 +/- 4 msec, P less than 0.05), and a reduced first third filling fraction (0.41 +/- 0.02 vs 0.48 +/- 0.01, P less than 0.001). Mitral regurgitation was found in 67% of systemic sclerosis patients and in 15% of controls (P less than 0.001). Doppler measures of left ventricular filling properties were not related to the presence of mitral regurgitation or systolic blood pressure. We conclude that left ventricular distensibility and early filling properties are impaired in systemic sclerosis and not related to blood pressure, but rather to left ventricular wall thickness and therefore probably secondary to myocardial fibrosis. Mitral regurgitation is a common finding in systemic sclerosis.

Adult↗

Endogenous anabolic and catabolic steroid hormones in male and female athletes during off season.

Peripheral serum hormone levels during the off season were analysed in 10 male and 10 female athletes, all belonging to the Swedish national teams in skiing and orienteering and in age matched sedentary controls (15 males, 13 females). No clinical signs of overuse strain were observed in any of the athletes. No significant differences in hormone variables were found between male athletes and controls. The female athletes had significantly higher levels of cortisol and significantly lower ratios between total testosterone and cortisol, between non-SHBG-bound testosterone and cortisol and between 4-androstene-3, 17-dione and cortisol than the sedentary controls. The increased levels of cortisol found in the female athletes probably reflect an adaptation to several years of hard training. A decrease of the free T/cortisol ratio has earlier been shown to indicate an overuse distress. One may speculate that the low androgen/cortisol ratios found in the female athletes in contrast to the males could indicate that the female athletes might need longer time to recover from hard exercise than male athletes, or could suggest an insufficient dietary intake.

Adaptation, Physiological↗

Restoration of anabolic deficit and muscle glycogen consumption in competitive orienteering.

Consumption and restoration of muscle glycogen and changes in anabolic and catabolic steroid hormones were analyzed in five male elite orienteers during and after an orienteering competition. The magnitude of glycogen consumption and pronounced increase in serum-cortisol during the orienteering race reflect the great muscular output demands during forest running. The free testosterone/cortisol ratio was normalized to the initial level within four hours post-exercise. Synchronously, only 25% of the muscle glycogen loss was restored. Within 24 hours post-exercise all runners showed normalized levels of testosterone, cortisol and free testosterone/cortisol ratio. The glycogen content was also restored except in one of the runners. We conclude that daily orienteering competitions per se do not seem to create risks for developing a state of hormonal imbalance or significant decrease in glycogen when the carbohydrate supply is appropriate.

Adult↗

Role of VIP in local control of secretion.

Vasoactive intestinal peptide (VIP) is a potent stimulant of duodenal HCO3- secretion and may, like prostaglandins, have a stimulatory role in the local duodenal HCO3- response to luminal HCl. Using a proximal duodenal loop in conscious rats, we examined the local luminal release of HCO3-, VIP and prostaglandin (PG) E2 in response to increasing concentrations of HCl (0.01-150 mmol l-1), perfused for 5 min at 60-min intervals. HCO3- and PGE2 were detected in all basal saline perfusate effluents, and were increased in a concentration-dependent manner by all acid concentrations tested. VIP was increased in a concentration dependent manner from pH 3. Exogenous VIP did not affect the basal luminal output of PGE2, or vice versa. Inhibition of prostaglandin synthesis by indomethacin augmented the HCl-stimulated luminal release of VIP, as well as the HCO3- response to exogenous VIP. The results are in agreement with previous studies, demonstrating that PGE2 is an important regulator of the duodenal HCO3- response to HCl in the rat. In addition, prostaglandins may negatively modulate the release of VIP from local VIPergic neurones, as well as the HCO3- secretagogue effect of VIP. Released VIP may contribute to the HCO3- response at pH less than or equal to 3.

Acid-Base Equilibrium↗

Cholinergic mechanisms involved in release and effect of prostaglandin E2 in HCl-stimulated duodenal HCO-3 secretion in the conscious rat.

Using a proximal duodenal loop in conscious rats, we investigated interactions between prostaglandin E2 and nicotinic and muscarinic receptor mechanisms previously found to be involved in the duodenal HCO3- response to HCl. In previous studies using the same model, a 5-min perfusion of the duodenal loop with 150 mmol l-1 HCl produced a marked and sustained HCO3- response. In the present study, the identical challenge produced a rapid 20-fold increase in the luminal output of prostaglandin E2 during acid exposure, followed by a sustained more than twofold elevation above the basal level during the 45 min monitored. The prostaglandin synthesis inhibitor indomethacin (4 mg kg-1 i.p.) suppressed the output of prostaglandin E2 during the HCl challenge from 131 +/- 84 to 15.4 +/- 10.0 pmol cm-1 h-1, and in the post-stimulatory period from 17.3 +/- 9.1 to 4.4 +/- 2.2 pmol cm-1 h-1. The nicotinic receptor antagonist hexamethonium (20 mg kg-1 i.v.) had no effect on the output of prostaglandin E2. The muscarinic receptor antagonist atropine (0.5 mg kg-1 s.c.) had no effect on the output of prostaglandin E2 during HCl challenge, but reduced the post-stimulatory output to 7.7 +/- 4.1 pmol cm-1 h-1. Perfusion of the duodenal loop with 0.1 mmol l-1 prostaglandin E2 produced a HCO3- response that was abolished by hexamethonium (20 mg kg-1 i.v.), but not affected by atropine (0.5 mg kg-1 s.c.).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Interactions between antral peptides and prostaglandin biosynthesis in gastric acid regulation in man.

UNLABELLED: The role of endogenous prostaglandins as modulators of antral hormone release and gastric acid secretion was studied in the intact human stomach. The subjects (n = 9) received indomethacin prior to gastric perfusion at pH greater than 7 or less than 2 and subsequent vagal stimulation. Indomethacin was also tested against parenteral somatostatin (n = 10) and pentagastrin (n = 8). The release of somatostatin into the circulation was biphasic after vagal stimulation, and the plasma levels were inversely proportional to those of plasma gastrin. Acidification of the gastric antrum from pH greater than 7 to less than 2 increased twofold the basal plasma levels of somatostatin (p less than 0.05) and suppressed basal and vagally stimulated gastrin release (p less than 0.05) and gastric acid secretion (p less than 0.05). Indomethacin prior to acidification had little effect in the basal state. Following stimulation the release of somatostatin increased, as indicated by a twofold elevation of somatostatinlike immunoreactivity in the gastric lumen (p less than 0.05), but there was less inhibition of plasma gastrin (p less than 0.05) and gastric acid secretion (p less than 0.05) as compared to acidification alone. During alkaline gastric perfusion, indomethacin increased circulating somatostatin (p less than 0.05) levels without affecting plasma gastrin or gastric acid. Indomethacin given against intravenously infused somatostatin (0.1 microgram.kg-1.h-1) partially reversed the inhibited gastrin response to vagal stimulation without affecting somatostatin-suppressed gastric acid secretion. The effects of indomethacin against pentagastrin were marginal. IN CONCLUSION: Gastric acidification in man stimulates plasma release of somatostatin in parallel to suppressing gastrin release and gastric acid secretion. Endogenous prostanoids participate to regulate antral hormone interactions and may have dual actions on antral somatostatin, as negative modulators of release and as mediators of somatostatin effects on the gastrin cell. It is suggested that an unrestricted release of antral somatostatin is reflected in the gastric lumen rather than in the circulation.

Adult↗

Histologic comparison of ceramic and titanium implants in cats.

This study compared the reparative processes around cylindrical glass-ceramic-coated and pure titanium implants placed in feline femurs. Six weeks after implant placement, bone specimens with inserted implants were prepared for histologic examination including histomorphometric quantification of the relative implant surface areas that were in contact with bone. The glass-ceramic implants were surrounded by a 0.2- to 0.5-mm envelope of fibrous connective tissue [corrected]. By contrast, the major part of the titanium implants (81% +/- 5%) was in direct contact with living lamellar or woven bone. Thus, titanium and glass ceramic evoked different reparative processes when implanted in bone, and only the titanium implants appeared to become osseointegrated.

Animals↗

Extracolonic diagnoses in ulcerative colitis: an epidemiological study.

In a population-based study of 1274 patients with ulcerative colitis (UC), the overall prevalence of extracolonic diagnoses was 21%. Seventy percent of patients with extracolonic diagnoses had extensive colitis. Patients without extracolonic diagnoses had only 28% extensive colitis (p less than 0.001), compared with 37% in the entire test population. The prevalence was higher in familial UC (p less than 0.05). The extracolonic diagnoses could be classified into two major groups, activity related and autoimmune, with regard to the extent and activity of UC and to the effects of medical and surgical treatment. Three hundred sixty-four diagnoses were distributed in 271 UC patients. It is concluded that extracolonic diagnoses are less frequent in an unselected patient group. However, extracolonic diagnoses are associated with the extent of UC at the time of diagnosis and with familial UC, and they can be classified as either activity related or autoimmune, with characteristic combinations of several extracolonic diagnoses occurring in 25% of the 271 patients.

Autoimmune Diseases↗

Induction of mRNA for HLA-DR beta in human keratinocytes cocultured with interferon-gamma.

Explanted human keratinocytes exposed in vitro to recombinant interferon-gamma (IFN-gamma) were investigated for the appearance of mRNA for HLA-DR. Using in situ hybridization with a (35S)UTP-labelled HLA-DR beta cRNA probe, mRNA-positive cells were detected already within 6 h with maximal numbers of positive cells as well as the amount of mRNA per cell after 48 h. The corresponding protein HLA-DR, as analysed by immunoperoxidase staining, was detected on 20%-40% of the cells after 24 h and on almost all cells within 48 h. The expression of HLA-DQ and -DP antigens were always exceeded by that of HLA-DR. Whereas an increase in the concentration of IFN-gamma above 50 U/ml did not affect the maximal level of HLA-DR reactive cells, there was a fourfold increase in the frequency of cells reactive with HLA-DQ and a twofold increase for HLA-DP when the IFN-gamma concentration was raised from 50 to 500 U/ml. When IFN-gamma was withdrawn from the cultures, HLA-DR mRNA and protein synthesis ceased--indicating the continuous need for IFN-gamma to maintain the HLA-DR synthesis in keratinocytes.

DNA↗

Ultrastructural differences of the interface zone between bone and Ti 6Al 4V or commercially pure titanium.

Commercially pure (CP) titanium and Ti 6Al 4V alloy were sputtered onto polycarbonate plastic implants to analyse hard tissue reactions to the two metals. The implants were inserted in the tibial metaphyses of five rabbits. Three months later they were removed and processed for light microscopy (LM) and transmission electron microscopy (TEM) investigations. At the LM level, disordered woven bone was seen in the interface zone of Ti 6Al 4V, whereas organized bone was observed in direct contact with the CP titanium implants. TEM examination of Ti 6Al 4V sections revealed a 500-1000 A thick collagen-free proteoglycan layer compared to 200-400 A for CP titanium. A surface analysis test was performed to compare the magnetron sputtered film with bulk Ti 6Al 4V alloy. This test revealed no major differences between the experimental implant and the bulk alloy. More natural-like tissue reactions were observed to CP titanium than to Ti 6Al 4V alloy.

Alloys↗

Oral E2 prostaglandins affect endocrine cell populations in the gastric antrum of the rat.

The aim of the present study was to investigate antral endocrine cell populations and tissue and circulating hormone levels following a 4-week oral regimen with prostaglandin E2 (25, 250 and 5000 micrograms/kg-1 b.i.d.) or a stable methyl analogue (5 and 50 micrograms kg-1 b.i.d.). Epithelial hyperplasia of the gastric antrum was observed with the highest dose of prostaglandin E2 and both doses of the analogue, as evaluated by stereological methods and conventional cell count. The treatments significantly affected the endocrine cell population. Somatostatin-immunoreactive cells were increased in proportion to the increased epithelial cellularity and plasma levels of somatostatin were increased in parallel. The tissue content of somatostatin-like immunoreactivity differed according to the extraction procedure used, and was significantly higher than controls in specimens extracted in neutral water. In the neutral extracts an immunoreactive somatostatin of unidentified molecular structure dominated quantitatively over somatostatin 14 and 28, which were the major components in acetic acid extracts. The serotonin-immunoreactive cell population was also significantly increased by natural prostaglandin E2 and the analogue but the gastrin cell population was not significantly affected by treatments. Accordingly, no significant changes were observed in tissue or plasma gastrin levels. It is concluded that the epithelial hyperplasia of the antral epithelia produced by E2 prostaglandins is associated with selective changes of endocrine cell populations. The changes were proportional to the increases of epithelial cellularity and required quantitative determination of the total antral volume to be detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Evidence for a major additive gene in ulcerative colitis.

Complex segregation analysis of 124 families with ulcerative colitis with two or more affected individuals suggests a rare additive major gene causing the disease with about 20% affected among the heterozygotes for the gene. There was no evidence for multifactorial inheritance.

Colitis, Ulcerative↗

Knee extensor muscle function before and after reconstruction of anterior cruciate ligament tear.

Knee extensor performance, in 17 subjects with chronic anterior cruciate ligament (ACL) tear, was investigated preoperatively and on four different occasions postoperatively, using isokinetic measurements and electromyography of single maximum and repetitive manoeuvres. Preoperatively maximum mechanical output was comparatively low (injured leg), deteriorating further by 50% at fourteen weeks postoperatively. Endurance also falls markedly. Thereafter knee-extensor performance improved successively, mostly during intensive training (14-20 weeks postoperatively) irrespective of the training programme used. After one year, maximum performance was still unequal but the injured leg had achieved the "normal" preoperative noninjured value. Fatiguability/endurance level improved over preoperative values. Muscular work/integrated EMG was stable while EMG/t increased. Twenty weeks postoperatively quadriceps area was decreased to 69%, cf. noninjured control. The early postoperative loss of performance was evidently caused by loss of muscle mass. Neuromuscular relearning appears to be a sizable factor in later recovery. Isokinetic training does not offer any specific advantage in the early muscular rehabilitation after ACL reconstruction.

Adolescent↗