Biomedical subjects
Publications and source records attributed to L Berggren.
This paper discusses pictorial representations of diseases of the eye as well as images of visual perception phenomena. Realistic pictures are in general accurate and unambiguous. Pictures created by artists suffering from real or alleged visual troubles are more controversial and are often subjected to imaginative interpretations.
Gait analysis and dynamic foot pressure were used in a follow-up study of 42 children with idiopathic clubfeet. Mean age at follow-up was 9 years (range 4-15 years). Twenty-four of the 62 clubfeet were treated conservatively and 38 had at least one operative intervention. Gait analysis showed that the vertical and posterior ground forces were significantly lower from the clubfoot compared with the normal foot. Dynamic foot pressure demonstrated a significant shift of the center of pressure to the lateral side in the affected compared with the normal side. In bilateral clubfeet, a relationship between center of pressure and subjective complaints was observed.
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A boy with congenital glaucoma, mental retardation and dysmorphic features is described. Chromosome analyses revealed two different, apparently balanced translocations; between the long arms of chromosomes 2 and 10 as well as between the long arms of chromosomes 8 and 12; 46,XY t(2;10)(q33;q26)pat, t(8;12) (q24;q21). The healthy father of the patient had the same balanced translocation between the long arms of chromosomes 2 and 10; 46,XY, t(2;10)(q33;q26).
Streptococcal myositis (SM), is a very serious condition with a high mortality rate. The port of entry of the infection is often unknown. We present here a case report concerning a 68-year-old patient with fulminant SM preceded by symptoms of an upper respiratory tract infection. Haemolytic streptococci of group A were found in the blood, muscle tissue and throat. The patient survived after massive therapeutic interventions including intensive care with intravenous antibiotics, fasciotomy, plasma exchange, controlled respiratory ventilation and exarticulation through the shoulder. The patient's wife fell ill at the same time with a sore throat and the same type of streptococci (T-type 3) was found in both patients.
Of all patients attended to in a clinic during 1986, 441 had open angle glaucoma diagnosed during 1974-1986 on the basis of either a verified visual field defect, a glaucomatous disc, or a repeated intraocular pressure value of at least 35 mm Hg. At first presentation of recent cases 1984-1986 (N = 128) 65 per cent were more than 70 years old. Capsular glaucomas were twice as common as simple glaucomas (low tension cases included). 62 per cent of capsular but only 26 per cent of simple glaucomas had an initial pressure of 35 mm Hg or more (p < 0.001). One third of both capsular and simple glaucomas had an advanced visual field defect with breakthrough to the periphery in the worse eye already at first presentation. This was more common if the initial pressure was 35 mm Hg or more (p < 0.05). Almost half remained unilateral cases, and the rate of severely impaired visual function in the better eye did not exceed 15 per cent. While generally 30-50 per cent of glaucomatous field defects had progressed in five years, the progression in early detected cases was only three per cent (p < 0.05). Visual field defects with breakthrough to the periphery already at first presentation progressed more often than circumscribed scotomas (p < 0.02).
The aim of all treatment for glaucoma is to lower intra-ocular pressure. During the past decade, the short-action cholinergic agonists, eserine and pilocarpine, that have been used for over a hundred years have been replaced as the drugs of choice by beta-blockers, in particular the non-selective beta-blocker, timolol maleate. Of the series of drugs developed in recent years for the treatment of glaucoma, two types--carbonic anhydrase inhibitors and prostaglandin analogues--are undergoing phase III trials. The article provides an account of the pharmacological basis of glaucoma treatment today and in the immediate future.
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Immunoglobulin heavy-chain switching is effected by a DNA recombination event that replaces the C mu gene with one of the other heavy-chain constant-region (CH) genes located 3' to the C mu gene. How the specificity of this event is controlled is unknown. However, it has been shown that IgM+ cells capable of switching to specific isotypes have the corresponding unrearranged CH genes in an accessible or active chromatin state, as demonstrated by the fact that these specific CH genes are hypomethylated and are transcriptionally active. We now report that the RNAs transcribed from specific unrearranged CH genes are induced prior to switching under conditions that promote switching to these specific CH genes. For example, we find that bacterial lipopolysaccharide, which induces the IgM+ cell line I.29 mu to switch to IgA, induces transcripts from the germ-line C alpha gene(s) in I.29 mu cells prior to switch recombination. Two preparations of T-cell lymphokines (recombinant interleukin 4 and supernatant from the T-cell line 2.19, which contains interleukins 4 and 5) that promote switching to specific isotypes by lipopolysaccharide-treated spleen cells induce transcripts from the corresponding germ-line CH genes prior to expression of the new isotypes. For example, interleukin 4, which appears to be necessary for switching to IgE in vitro and in vivo, induces within 2 days large increases in germ-line C epsilon transcripts in lipopolysaccharide-treated spleen cells and in I.29 mu cells. The most straightforward interpretation of our data is that these lymphokines direct switching to specific isotypes by activating specific CH genes, making them accessible to the putative switch recombinase.
1. In the present study possible relationships between cardiovascular and respiratory effects and plasma concentrations were investigated after administration of midazolam and diazepam. Eight healthy volunteers were given three injections at 20 min intervals of equipotent sedative doses of midazolam (0.05 mg kg-1) and diazepam (0.15 mg kg-1) in a randomized double-blind cross-over design. Blood pressure, blood-gases and respiration measured nonivasively, were monitored throughout the experimental session of 160 min, and frequent blood samples were collected during the session. 2. Correlations between the blood pressure reduction, the increase of PaCO2 in blood, and plasma concentrations were found for both drugs. A maximal reduction of blood pressure and PaCO2 was produced after sedative doses of midazolam and diazepam. 3. A possible acute tolerance development towards the blood pressure reduction was found after the repeated administration of diazepam but not after the midazolam administration. 4. The plasma concentrations producing half the maximal effects after administration of midazolam was 50-60 ng ml-1, indicating that the influence on blood pressure and PaCO2 after drug administration is evoked at lower plasma concentrations than sedation. 5. No correlation between the respiratory effects and plasma concentrations was found for either drug.
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The effects of repeated doses of benzodiazepines, diazepam and midazolam in combination with meperidine on arterial blood gases and transcutaneous PO2 were studied in eight healthy volunteers. The study was designed to mimic a clinical situation. Initially two doses of either midazolam 0.05 mg/kg or diazepam in fat emulsion 0.15 mg/kg were given in a randomized crossover fashion with a 20-min interval, followed by meperidine 0.5 mg/kg another 20 min later. The opioid effects were then antagonized by naloxone 0.4 mg. The initial doses of benzodiazepines caused an increase in PaCO2 and a decrease in PaO2. The changes in PaO2 were of short duration and recovered to baseline levels between injections. However, they came sooner and were more pronounced after midazolam. The changes in PtcO2 paralleled those in PaO2. The PtcO2 index as a measure of cardiac output and peripheral blood flow adequacy was increased immediately after the first injection of midazolam but was otherwise not different from control. There were no differences between the drugs concerning PtcO2 index. PaCO2 increased after the first benzodiazepine injection and remained so throughout the study. Addition of meperidine caused only small changes in PaO2 and PaCO2. These changes were reversed by naloxone. In spite of different elimination kinetics there was no difference in the duration of respiratory depression between the two benzodiazepines.
The effects of repeated sedative i.v. doses of midazolam and diazepam in combination with meperidine on breathing pattern and thoracoabdominal motion were studied in eight healthy male volunteers. At 20-min intervals in a randomized double-blind crossover design the subjects initially received two doses of midazolam 0.05 mg/kg or diazepam 0.15 mg/kg followed by meperidine 0.5 mg/kg and then naloxone 0.4 mg. Breathing pattern and thoracoabdominal motion were measured non-invasively, utilizing a computerized strain gauge technique. The initial injection of both benzodiazepines caused significant decreases in tidal volume, inspiratory time and expiratory time. There were no significant differences between the two drugs in any of these variables. Minute ventilation, mean inspiratory flow and respiratory timing were not significantly affected. The second injection of both benzodiazepines caused only insignificant additional changes. When meperidine was added, the effects on inspiratory time and tidal volume were small and not significant. However, expiratory time increased and was no longer significantly different from control. The injection of naloxone reversed the meperidine-induced changes only, and the breathing pattern was no longer different from that obtained during benzodiazepines alone. The decrease in tidal volume after the benzodiazepines was almost exclusively mediated by a decrease in the abdominal contribution. Additional doses of benzodiazepines did not enhance these changes. However, meperidine caused a further decrease in the abdominal contribution. This decrease was reversed by naloxone. This indicates that the combination of benzodiazepines and meperidine caused a profound decrease in diaphragmatic performance.
Changes in respiratory pattern and arterial PCO2 after three repeated intravenous sedative doses of midazolam 0.05 mg/kg or diazepam 0.15 mg/kg were studied in eight healthy male volunteers in a randomized double-blind crossover design. In order to reduce the influence of the measuring equipment, we utilized a noninvasive computerized technique to measure respiratory variables. Both drugs caused equal changes in breathing pattern with a decrease in tidal volume, an increase in respiratory rate and an unaltered minute ventilation. These alterations in breathing pattern were associated with CO2 retention. Respiratory changes were mainly induced by the first injection of either drug. Despite increased plasma drug concentrations, subsequent doses did not cause further changes in respiratory variables except for an increase in PCO2 after the second dose of midazolam. The clinical significance of these changes in PaCO2 in otherwise healthy individuals is probably limited. The duration of the subjective sensation of sedation was longer after diazepam than after midazolam.