Inter-rater reliability of the Swedish modified version of the Postural Assessment Scale for Stroke Patients (SwePASS) in the acute phase after stroke

Background: Before implementation of the new scale, the Swedish modified version of the Postural Assessment Scale for Stroke Patients (SwePASS), to clinical practice, it is fundamental to analyze its measurement properties.Objective: To examine the inter-rater reliability of the SwePASS in the acute phase after stroke.

Methods: Day 3 to day 7 after admission to a stroke unit, 64 persons with stroke were assessed twice, using the SwePASS, by two physiotherapists. Inter-rater reliability was determined using percentage-agreement and the rank-invariant method: relative position, relative concentration, and relative rank variance.

Results: The raters showed a percentage agreement of ≥75% in the assessments using the SwePASS. For 9 of the 12 items, the percentage agreement was >80%. For 8 of the 12 items, there was a statistically significant change in position, revealed in relative position values between 0.08 and 0.15. Three items had statistically significant positive relative concentration values between ?0.11 and 0.10. Except for a statistically significant negligible relative variance value of 0.01 for the items 1 and 8, there was no relative variance.

Conclusions: The SwePASS shows an acceptable inter-rater reliability, albeit with potential for improvement. The reliability can be improved by a consensus how to interpret the scale between the raters prior to implementation in the clinic.     

Deep venous thrombosis and pulmonary embolism

All surgical patients are at risk for the development of deep venous thrombosis and subsequent pulmonary embolism or postphlebitic syndrome. The evolution of ultrasonographic imaging has increased the awareness of prevention, diagnosis, and treatment of deep venous thrombosis. Duplex imaging and Doppler color flow imaging have made the diagnosis of deep venous thrombosis relatively simple, painless, inexpensive, and definitive. These procedures have gained acceptance by both patients and physicians. Several risk factors have been identified that increase the chance of the development of deep venous thrombosis. These factors include a history of deep venous thrombosis, presence of a malignant process, increasing age, cigarette smoking, obesity, prolonged bed rest, and general anesthesia. The greater the number of risk factors, the more aggressive prophylaxis should be. Means of prophylaxis have improved, and surgeons now generally agree that some form of prophylaxis is required. Heparin and intermittent compression devices appear to be equally effective in preventing deep venous thrombosis. The addition of venous monitoring in high-risk patients permits immediate identification of the presence of deep venous thrombosis. During the last decade, the treatment of patients with deep venous thrombosis has changed little. Heparin followed by warfarin remains the treatment of choice. A small group of patients receive fibrinolytic therapy for deep venous thrombosis. Although the incidence of postoperative deep venous thrombosis has decreased during the last decade, it remains a significant complication.     

Sleep and recovery in physicians on night call: a longitudinal field study

Background  

It is well known that physicians' night-call duty may cause impaired performance and adverse effects on subjective health, but there is limited knowledge about effects on sleep duration and recovery time. In recent years occupational stress and impaired well-being among anaesthesiologists have been frequently reported for in the scientific literature. Given their main focus on handling patients with life-threatening conditions, when on call, one might expect sleep and recovery to be negatively affected by work, especially in this specialist group. The aim of the present study was to examine whether a 16-hour night-call schedule allowed for sufficient recovery in anaesthesiologists compared with other physician specialists handling less life-threatening conditions, when on call.     

Predictors of oral health quality of life in older adults

There is limited information regarding oral health status and other predictors of oral health‐related quality of life. An association between oral health status and perceived oral health‐related quality of life (OHQOL) might help clinicians motivate patients to prevent oral diseases and improve the outcome of some dental public health programs. This study evaluated the relationship between older persons' OHQOL and their functional dentition, caries, periodontal status, chronic diseases, and some demographic characteristics. A group of 733 low‐income elders (mean age 72.7 ISD=4.71, 55.6% women, 55.1% members of ethnic minority groups in the U.S. and Canada) enrolled in the TEETH clinical trial were interviewed and examined as part of their fifth annual visit for the trial. OHQOL was measured by the Geriatric Oral Health Assessment Index (GOHAI); oral health and occlusal status by clinical exams and the Eichner Index; and demographics via interviews. Elders who completed the four‐year assessment had an average of 21.5 teeth (SD=6.9). with 8.5 occluding pairs (SD=4.6), and 32% with occlusal contacts in all four occluding zones. Stepwise multiple regressions were conducted to predict total GOHAI and its subscores (Physical, Social, and Worry). Functional dentition was a less significant predictor than ethnicity and being foreign‐bom. These variables, together with gender, years since immigrating, number of carious roots, and periodontal status, could predict 32% of the variance in total GOHAI, 24% in Physical, 27% in Social, and 21 % in the Worry subscales. These findings suggest that functional dentition and caries influence older adults' OHQOL, but that ethnicity and immigrant status play a larger role.     

Lectin-induced increase in clonogenic growth of haematopoietic progenitor cells

Abstract: The galactoside-specific plant lectin, Viscum album agglutinin (VAA-I) increases cellular parameters of natural host defence. It also binds to a variety of haematopoietic cells, including progenitors. We investigated whether VAA-I has a stimulatory effect on haematopoietic progenitor cells. Peripheral blood progenitor cells from 7 healthy volunteers were cultured in a colony assay with VAA-I plus erythropoietin (EPO) and stem cell factor (SCF). At 50 pg/ml VAA-I induced a significant increase in the cytokine-dependent clonogenic growth (52% in median, p<0.05). In another set of experiments purified CD34+ cells were isolated from the bone marrow aspirate of 4 patients with non-metastatic breast cancer using fluorescence-activated cell sorting. Binding to CD34+ cells was demonstrated by using directly fluorescence-conjugated VAA-I. Co-incubation with d -galactose significantly abrogated this effect. CD34+ cells were cultured in the presence of EPO, SCF, interleukin-3, granulocyte/monocyte colony-stimulating factor and granulocyte colony-stimulating factor. VAA-I alone had no measurable effect on the clonogenic growth of the isolated cells. However, at concentrations of 100 and 250 pg/ml VAA-I increased the cytokine-dependent proliferation and differentiation of CD34+ cells by a median of 75 and 85%, respectively. The results show that VAA-I binds to haematopoietic progenitor cells and has a co-stimulatory effect on their proliferation.     

Interleukin-1beta and TNF-alpha act in synergy to inhibit longitudinal growth in fetal rat metatarsal bones.

We hypothesized that pro-inflammatory cytokines can act locally in the growth plate to impair longitudinal growth. In a model of cultured fetal rat metatarsal bones, we found that IL-1beta and TNF-alpha act in synergy to inhibit longitudinal growth, an effect linked to decreased proliferation and increased apoptosis of growth plate chondrocytes. IGF-I could partially reverse all these effects. INTRODUCTION: Children with chronic inflammatory conditions, such as Crohn's disease or rheumatoid arthritis, experience impaired longitudinal growth. The inflammatory process itself, which includes upregulation of the pro-inflammatory cytokines interleukin (IL)-1beta, IL-6, and TNF-alpha, is believed to be at least partly responsible for the poor growth in these patients. This study aimed to clarify whether these cytokines can act locally in the growth plate to suppress longitudinal growth and whether any negative effects can be reversed by insulin-like growth factor-I (IGF-I). MATERIALS AND METHODS: The effects of cytokines on longitudinal bone growth were studied in fetal (day E20) rat metatarsal bones kept in culture. After a 7-day culture, the bones were sectioned, and chondrocyte proliferation was assessed by bromodeoxyuridine (BrdU) incorporation and apoptosis by TUNEL. RESULTS: When added separately, IL-1beta and TNF-alpha impaired longitudinal bone growth only at a high concentration (100 ng/ml each; p < 0.05 versus control). In contrast, when added in combination, IL-1beta and TNF-alpha potently inhibited growth at far lower concentrations (from 3 ng/ml each; p < 0.001 versus control) and also decreased chondrocyte proliferation and increased apoptosis. Growth failure induced by the combination of IL-1beta and TNF-alpha (10 ng/ml each) could be counteracted by anti-IL-1beta (100 ng/ml; p < 0.001), anti-TNF-alpha (100 ng/ml; p < 0.001), or IGF-I (100 ng/ml; p < 0.01). IL-6 did not affect longitudinal growth even when added in combination with IL-1beta or TNF-alpha (10 ng/ml each). CONCLUSIONS: We show that IL-1beta and TNF-alpha act in synergy to locally suppress longitudinal growth, an effect that can be partially reversed by IGF-I. Although growth hormone (GH)/IGF-I may improve longitudinal growth in children with chronic inflammatory diseases, our results suggest that the inflammatory process itself must be targeted to achieve normal growth.     

Brain tissue microarrays in dementia research: White matter microvascular pathology in Alzheimer's disease

Tissue microarrays (TMA) consist of up to 1000 cylindrical tissue cores from different donor paraffin blocks relocated into one recipient block, allowing for efficient histopathological studies by fluorescence in situ hybridization, RNA in situ hybridization or immunohistochemistry. On the background of the increasing interest of the TMA technique in cancer research and the suggestion of its application also in studies of non‐neoplastic intracranial disorders, the technique was applied to pathologic white matter in AD brains. Eight cases with AD and concomitant white matter pathology were neuropathologically diagnosed on whole brain coronal slides. The TMA technique was used to grade severity of white matter pathology and to quantify small vessels with traditional staining and immunohistochemical markers. These measurements were compared with the whole brain neuropathological assessment. The technique produced good results with preserved tissue structures as confirmed by the whole brain evaluation. Severity of white matter pathology evaluated on the TMA cores correlated negatively with small vessel quantities, and statistically significant differences in vessel quantities paralleled different grades of white matter pathology. It is concluded that the TMA technique could be further utilized in studies of dementing disorders, and may have its advantages in large, clinically well‐characterized materials (e.g. in quantitative mapping of white matter changes).     

Mechanisms of nasal hyper-reactivity

Hyper-reactivity to non-specific challenges has been considered a hallmark of asthma and is defined as an abnormal responsiveness of the bronchial airways to a variety of provocative agents. The mechanisms underlying hyper-reactivity in the upper and lower airways are not known. By using the nose to study the inflammatory response possible abnormalities can be investigated carefully and pathophysiology of specific airway hyper-reactivities can be better understood. Other factors than merely constriction of the bronchial smooth muscles can cause narrowing of the free lumen to airflow. Functionally different and very distinct mucosal end-organ reactivities may also be increased. If these reactivities can be well assessed, specific airway hyper-reactivity can be defined. In the present report, specific mucosal end-organ hyper-reactivites in the allergic nasal mucosa are presented. Certain widespread hypotheses, such as the role of the eosinophil and the “increased absorption permeability theory”, are disputed.     

Retrospective versus original information on diet: implications for epidemiological studies

The aim of this study was to evaluate the use of retrospective information on diet in relation to the information originally reported. Hospital controls (n = 131) who participated in a case-control study on diet and pancreatic cancer in Stockholm, Sweden, answered a second postal questionnaire four years later about their current and previous food consumption. The food consumption was dichotomized for the purpose of the analysis. In relation to the original information, the use of retrospective information overestimated previous food consumption among subjects with increased intake, while retrospective information underestimated previous food consumption among subjects with decreased intake. These tendencies were slightly more pronounced in the age group 60-79 years than in the age group 40-59 years. For subjects with unchanged food consumption, there was a high agreement between original and retrospective information. Considerable differential misclassification could be introduced in an epidemiological study if cases and non-cases differ with regard to changes in food consumption.     

No persistent effect of angiotensin converting enzyme inhibitor treatment in Milan hypertensive rats despite regression of vascular structure.

Milan hypertensive rats were treated, from ages 4 to 24 weeks, with the angiotensin converting enzyme (ACE) inhibitor, perindopril, in doses of 1.5 mg/kg per day or 0.4 mg/kg per day. Controls were untreated Milan hypertensive rats. At age 24 weeks, a mesenteric biopsy was taken, from which two resistance vessels were taken out and mounted on a myograph for structural and functional analysis. Thereafter, treatment was withdrawn and the blood pressure of the rats was followed until age 36 weeks. Perindopril treatment had a dose-dependent effect on blood pressure as well as on both structural (media thickness, media: lumen ratio) and functional (estimated pressure against which vessels could contract) parameters of the resistance vessels. However, when treatment was withdrawn, blood pressure rose to (low-dose perindopril group) or above (high-dose perindopril group) control levels. The results contrast with previous studies using spontaneous hypertensive rats (SHR) where, using the same protocol, blood pressure remains low after withdrawal of treatment with ACE inhibitors, including perindopril, although the effect on resistance vessel parameters is similar. The results show that the persistent effect of ACE inhibitor therapy which has been seen in SHR is not a general feature of genetic hypertension. Furthermore, these results raise doubts as to whether the persistent effect seen in SHR is due to a general effect of ACE inhibitor treatment on vascular structure.