Prevalence of paroxysmal atrial fibrillation depending on the regression of left ventricular hypertrophy in arterial hypertension.

Arterial hypertension (HTN) represents one of the major causes of atrial fibrillation, a cardiac arrhythmia with high prevalence and comorbidity. The aim of this study was to investigate whether paroxysmal atrial fibrillation can be treated by the regression of left ventricular hypertrophy achieved by antihypertensive therapy. Included in the present study were 104 patients who had had HTN for more than 1 year. None of them suffered from coronary heart disease. All patients were investigated by 24-h Holter ECG and echocardiography at baseline and after a mean of 24 months. Patients were divided into two groups: group A consisted of those (53.8%) who showed a regression of the left ventricular muscle mass index (LVMMI) during the follow-up (154.9+/-5.1 vs. 123.5+/-2.8 g/m(2)), and group B those (45.2%) who showed a progression of LVMMI (122.2+/-3.2 vs. 143.2+/-3.2 g/m(2)). In group A the prevalence of atrial fibrillation decreased from 12.5% to 1.8% (p<0.05), while it was increased in group B from 8.5% to 17.0%. The left atrial diameter was reduced following antihypertensive therapy in group A from 39.1+/-5.3 mm to 37.4+/-4.6 mm (p<0.01) and increased in group B from 37.0+/-0.7 mm to 39.0+/-0.9 mm (p<0.01). We conclude that a regression of the left ventricular muscle mass leads to a reduction of left atrial diameter and consecutively to a decrease in the prevalence of intermittent atrial fibrillation. This may be explained by a better left ventricular diastolic function following decreased vascular and extravascular resistance of the coronary arteries. This relation shows the benefits of causal antihypertensive therapy for the treatment of paroxysmal atrial fibrillation.     

Clinical symptoms and signs in sore throat patients with large colony variant β-haemolytic streptococci groups C or G versus group A

BACKGROUND: The role of large colony streptococci groups C or G as pathogen agents in sore throat has been questioned. AIM: To analyse clinical features of patients with large colony streptococci groups C or G compared with patients with group A streptococci (GAS) and with negative cultures. DESIGN OF STUDY: Prospective study of patients with sore throat. SETTING: Two Norwegian general practices in Stokke and Kongsberg communities with 6500 patients.METHOD: Frequency of clinical features in the three patient categories including the four Centor criteria (fever, anterior cervical lymphadenopathy, tonsillar exudates, and lack of cough), degree of pain on swallowing, pharyngeal rubor, C-reactive protein (CRP) values, patient age between 3 and 14 years, and duration of symptoms before seeing the doctor. A logistic regression analysis to find independent predictors was performed. RESULTS: Out of 306 patients with a sore throat, 244 were adults and 62 were children under 10 years old; 40% were men. One hundred and twenty-seven had GAS, 33 had streptococci groups C or G, and 146 had negative throat cultures. Forty-eight per cent of the GAS patients and 45% of the C or G patients met three or four of the Centor criteria. The logistic regression revealed that in patients with GAS considerable pain on swallowing, an age of 3-14 years and a duration of symptoms of < or =3 days or less were significantly associated with GAS infection in addition to the Centor criteria. The same results were found when all streptococci were analysed together, in addition elevated CRP was significant. In patients with streptococci group C or G an elevated CRP-value was significantly associated. CONCLUSION: Patients with tonsillitis caused by streptococcus groups C or G have, to a large extent, the same clinical picture as patients with GAS. Large colony streptococci groups C and G should be considered as throat pathogens in line with GAS.     

Adhesion of human platelets to albumin is synergistically increased by lysophosphatidic acid and adrenaline in a donor-dependent fashion.

Lysophosphatidic acid (LPA) and adrenaline are weak platelet activators considered important for thrombus formation, and were previously shown to synergistically increase platelet aggregation. Here we investigate synergistic activation by LPA and adrenaline when measuring platelet adhesion. Platelet-rich plasma from healthy blood donors together with adrenaline and/or LPA were added to protein-coated microplates. Platelets were allowed to adhere and the amount of adhesion detected enzymatically. The LPA and adrenaline combination induced a synergistic increase of platelet adhesion to a normally non-adhesive albumin surface. The degree of synergy varied markedly between individuals; these variations could not be explained by age, gender, blood type or different amounts of platelets, oxidized low-density lipoprotein, insulin or glucose in plasma. There was a trend indicating increased synergistic effect for platelets sensitive to adrenaline stimulation. The synergistic effect was blocked by the alpha2-adrenoceptor antagonist yohimbine and inhibited by the ADP scavenger system creatine phosphate/creatine phosphokinase and antibodies against alphaIIbbeta3. Furthermore, platelets adhering to albumin after adrenaline and LPA treatment expressed P-selectin. In conclusion, LPA and adrenaline act synergistically to increase alphaIIbbeta3-mediated platelet adhesion to albumin, dependent on alpha2-adrenoceptor signalling and platelet secretion. We also confirm that synergistic platelet activation achieved with LPA and adrenaline is highly donor dependent.     

Neonatal Exposure to a Combination of N-Methyl-d-aspartate and γ-Aminobutyric Acid Type A Receptor Anesthetic Agents Potentiates Apoptotic Neurodegeneration and Persistent Behavioral Deficits

Background: During the brain growth spurt, the brain develops and modifies rapidly. In rodents this period is neonatal, spanning the first weeks of life, whereas in humans it begins during the third trimester and continues 2 yr. This study examined whether different anesthetic agents, alone and in combination, administered to neonate mice, can trigger apoptosis and whether behavioral deficits occur later in adulthood.

Methods: Ten-day-old mice were injected subcutaneously with ketamine (25 mg/kg), thiopental (5 mg/kg or 25 mg/kg), propofol (10 mg/kg or 60 mg/kg), a combination of ketamine (25 mg/kg) and thiopental (5 mg/kg), a combination of ketamine (25 mg/kg) and propofol (10 mg/kg), or control (saline). Fluoro-Jade staining revealed neurodegeneration 24 h after treatment. The behavioral tests-spontaneous behavior, radial arm maze, and elevated plus maze (before and after anxiolytic)-were conducted on mice aged 55-70 days.

Results: Coadministration of ketamine plus propofol or ketamine plus thiopental or a high dose of propofol alone significantly triggered apoptosis. Mice exposed to a combination of anesthetic agents or ketamine alone displayed disrupted spontaneous activity and learning. The anxiolytic action of diazepam was less effective when given to adult mice that were neonatally exposed to propofol.     

An innovative examination ending the medical curriculum

There has been increasing interest in curriculum innovation in many medical schools. The pedagogic principles for learning and for assessment should be congruent. Changing the curriculum and pedagogic principles for medical education implies that the examinations should also be adapted to the new principles. At the Faculty of Health Sciences, Linköping University, we use a student-oriented programme with problem-based learning, early patient contact, multiprofessional integrated education, and integration between basic science and clinical medicine and between traditional medical subjects. We also encourage the students to adopt a scientific attitude from the very beginning. To assess the students at the conclusion of the medical curriculum, we have developed a new form for the final examination containing measurements of clinical ability based on a videotaped patient consultation, an assessment of the student's performance and presentation of a scientific project, the student's analysis of a published scientific paper and an extensive oral examination based on the students' own scientific papers. Our experience, including results from questionnaires to students and teachers, is that the method is suitable for a final examination and assesses qualities that we previously were not able to assess.     

Sex-specific effects for body mass index in the new Norwegian twin panel

Sex-specific effects for body mass index (BMI) were explored in a newly established, population-based Norwegian twin panel. The sample includes 5,864 individuals, aged 18–25 years, who responded to a questionnaire containing items for zygosity classification, height, weight, health, health-related behaviors, well-being, and demographic information. Among the 2,570 intact pairs who returned the questionnaire there were 416 identical (MZ) male pairs, 387 fraternal (DZ) male pairs, 528 MZ female pairs, 443 DZ female pairs, and 796 unlike-sexed pairs. Alternate sets of models testing for either sex-specific genetic or environmental parameters were evaluated using structural equation analysis. Results from the most parsimonious model indicated that the genes contributing to variation in BMI are not identical for men and women; rather, some genetic effects were shared by the sexes and some were unique to each sex. Total variation in BMI could be explained by sex-specific additive genetic effects, as well as genetic and non-shared environmental effects common to men and women. Estimates of heritability were .708 for men and .789 for women, and the male-female genetic correlation was 0.622. The series of models specifying sex-specific shared environment also fit the data and suggests that shared environmental factors may be important for males but not for females. The findings raise questions concerning the relationship between sex-specific effects for BMI and sex differences in health outcomes. ©1995 Wiley-Liss, Inc.     

Supersensitivity to the Antinociceptive Effect of a 5-HT1 Receptor Agonist after Lesion of Raphe-Spinal Serotonergic Neurones

Abstract: The actions of the 5-hydroxytryptamine type-1B (5-HT₁) receptor agonist 1(m-chlorophenyl)piperazine (mCPP) on response latencies in the tail-flick test and tail skin temperature were examined in mice after pretreatment with the 5-HT neurotoxin, 5,6-dihydroxytryptamine (5,6-DHT). All the compounds were given intrathecally. The level of 5-HT in spinal cord was reduced by 79% 4 days after intrathecal injection of 5,6-DHT (10 μg). There was a significant relationship between the tail-flick latency and tail skin temperature, and the reduced baseline tail-flick latencies induced by 5,6-DHT were non-significant after the change in skin temperature was taken into account. Intrathecal mCPP (5 μg) significantly increased the tail-flick latency and significantly reduced the tail skin temperature in 5,6-DHT pretreated animals when compared to control animals. These differences in tail-flick latencies could not be explained by alterations in skin temperature. The results provide evidence that neurotoxic lesion of descending 5-HT pathways induces supersensitivity to the antinociceptive effect of 5-HT₁ receptor stimulation.     

The effect of supervised rehabilitation on strength, postural sway, position sense and re-injury risk after acute ankle ligament sprain

The effect of an early rehabilitation program, including postural training, on ankle joint function after an ankle ligament sprain was investigated prospectively. Ninety-two subjects, matched for age, sex, and level of sports activity, were randomized to a control or training group. All subject received the same standard information regarding early ankle mobilization. In addition, the training group participated in supervised physical therapy rehabilitation (1 h, twice weekly) with emphasis on balance training. Postural sway, position sense and isometric ankle strength were measured 6 weeks and 4 months after the injury, and at 12 months re-injury data were obtained. In the training group, there was a significant difference between the injured and uninjured side for plantar flexion (P < 0.01), eversion (P < 0.01) and inversion (P < 0.05), but not for dorsiflexion at 6 weeks. In the control group, there was a significant difference between the injured and uninjured side for plantar flexion (P < 0.01), eversion (P < 0.01), inversion (P < 0.01), and dorsiflexion (P < 0.05) at 6 weeks. Postural sway, but not position sense, differed between the injured and uninjured side in both groups (P < 0.01) at 6 weeks. The side-to-side percent differences were similar in both groups for all variables (P > 0.05) at 6 weeks, and there were no side-to-side differences at 4 months in either group. In the control group, 11/38 (29%) suffered a re-injury, while this number was only 2/29 (7%) in the training group (P < 0.05). These data showed that an ankle injury resulted in reduced ankle strength and postural control at 6 weeks, but that these variables had normalized at 4 months, independent of the supervised rehabilitation. However, the findings also demonstrated that supervised rehabilitation may reduce the number of re-injuries, and therefore may play a role in injury prevention.