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Context: Athletes participating in sport are exposed to a high injury risk. Previous research has found a great number of risk factors (both physiological and psychological) that could increase injury risk. One limitation in previous studies is that few have considered the complex interaction between psychological factors in their research design., Objective: To study whether personality, stress, and coping predicted injury occurrence in an elite soccer population based on a hypothesized model., Design: Prospective., Participants: 56 (n = 38 male, n = 18 female) Swedish Premiere League soccer players were selected based on convenience sampling., Intervention: Participants completed 4 questionnaires including the Swedish Universities Scales of Personality, Life Events Survey for Collegiate Athletes, and Brief COPE during the initial questionnaire administration. Subsequent to the first meeting, participants also completed the Hassle and Uplift Scale5 once per wk for a 13-wk period throughout the competitive season., Main Outcome Measures: A path analysis was conducted examining the influence of personality traits (ie, trait anxiety), state-level stressors (ie, negative-life-event stress and daily hassles), and coping on injury frequency., Results: Results of the path analysis indicated that trait anxiety, negative-life-event stress, and daily hassle were significant predictors of injury among professional soccer players, accounting for 24% of the variance., Conclusion: The findings highlight the need for athletes, coaches, and medical practitioners to attempt to reduce state-level stressors, especially daily hassles, in minimizing injury risk. Educating and training athletes and coaches in proactive stress-management techniques appears warranted.

Athletes participating in sport are exposed to a relatively high injury risk. Previous research has suggested that it could be possible to reduce sports injuries through psychological skills training. The purpose of this study was to examine the extent to which a cognitive behavioural biofeedback intervention could reduce the number of sports injuries in a sample of players in Swedish elite football high schools. Participants from four elite football high schools (16-19 years old) were divided into one experiment (n = 13) and one control group (n = 14). Participants were asked to complete three questionnaires to assess anxiety level (Sport Anxiety Scale), history of stressors (Life Event Scale for Collegiate Athletes) and coping skills (Athletic Coping Skills Inventory - 28) in a baseline measure. Mann-Whitney U-tests showed no significant differences in pre-intervention scores based on the questionnaires. The experimental group participated in a nine-week intervention period consisting of seven sessions, including: somatic relaxation, thought stopping, emotions/problem focused coping, goal setting, biofeedback training as well as keeping a critical incident diary. A Mann-Whitney U test showed no significant difference between the control and experimental group U (n1 = 13, n2 = 14) = 51.00, p = 0.054. However, considering the small sample, the statistical power (0.05 for present study), to detect effects was low. The results of the study are discussed from a psychological perspective and proposals for future research are given. Key pointsCognitive-behavioral training together with biofeedback training seems to be an effective strategy to decrease the occurrence of injuries.More intervention studies should be conducted applying existing biofeedback methodology, especially in the injury preventive area.Future research should develop a bio-psychological injury model aimed at predicting injury occurrence which describes the physiological stress responses and how they can be measured in more detail.

Background: Cerebral pressure autoregulation (CPA) is defined as the ability of the brain vasculature to maintain a constant blood flow over a range of different systemic blood pressures by means of contraction and dilatation., Objective: To study CPA in relation to physiological parameters, treatment, and outcome in a series of traumatic brain injury patients., Methods: In this prospective observational study, 44 male and 14 female patients (age, 15-72 years; mean, 38.7 years; Glasgow Coma Scale score, 4-13; median, 7) were analyzed. Patients were divided into groups on the basis of status of CPA (more pressure active vs more pressure passive) and level of cerebral perfusion pressure (CPP; low vs high CPP). The proportions of favorable outcome in the groups were assessed. Differences in physiological variables in the different groups were analyzed., Results: Patients with more impaired CPA treated at CPP levels below median had a significantly higher proportion of favorable outcome compared with patients with more impaired CPA treated at CPP levels above median. No significant difference in outcome was seen between patients with more intact CPA when divided by level of CPP. In patients with more impaired CPA, CPP<50 mm Hg and CPP<60 mm Hg were associated with favorable outcome, whereas CPP>70 mm Hg and CPP>80 mm Hg were associated with unfavorable outcome. In patients with more intact CPA, no difference in physiological variables was seen between patients with favorable and unfavorable outcomes., Conclusion: Our results support that in traumatic brain injury patients with impaired CPA, CPP should not be elevated.

It is reported that between 65-91% of elite soccer players in Sweden have at least one injury per year. Several studies define different physiological and psychological factors affecting athletic injury-risk. A number of models contain proposals that specify relationships between psychological factors and an increased athletic injury-risk. Examples include Williams and Andersen's stress-injury model and Johnson and Ivarsson's empirical model of injury risk factors which proposes that factors such as trait anxiety and ineffective coping skills are influential. The purpose of this study was to examine the relationship between (a) personality factors, b) coping variables, and (c) stress and injury risk. Participants were 48 male soccer players from 3 Swedish teams ranging in age from 16 to 36 years (M = 22 years). Participants completed 5 questionnaires: Football Worry Scale, Swedish universities Scales of Personality, Life Events Survey for Collegiate Athletes, Daily Hassle Scale and Brief COPE. Information on injuries was collected by athletic trainers of the teams over 3-months. Results suggest injury was significantly predicted by 4 personality trait predictors: somatic trait anxiety, psychic trait anxiety, stress susceptibility, and trait irritability. Collectively, the predictors self-blame and acceptance could explain 14.6% of injury occurrence. More injuries were reported among players who score high in daily hassles. These results support previous findings. Recommendations are given for both the athletes and the trainers on working to prevent sport injuries. Key pointsA number of psychological factors, such as high stress levels and ineffective coping could increase the injury risk among athletes.The two coping factors, self - blame and acceptance could together explain 14.6 % of injury occurrence.Results of the current study suggest that the factors; somatic trait anxiety, psychic trait anxiety, stress susceptibility and trait irritability could increase injury risk among soccer players.Suggestion for future research is to investigate how daily hassles affects injury risk among soccer players in larger samples and on premiership levels. Moreover, to investigate the effects of a preventive intervention designs for a representative sample of soccer players.

Attention deficit hyperactivity disorder (ADHD) is a prevalent childhood psychiatric condition. This study was a qualitative investigation with parents and professionals conducted in two north London boroughs, using focus groups as well as semi-structured and narrative interviews. The aim was to explore parents' and professionals' beliefs regarding the causes of ADHD and their perceptions of service provision. The sample was drawn purposively from GP practices and voluntary support groups. Professionals were recruited via professional networks. Analysis was thematic. It was found that the views of parents and professionals differed. Professionals were more likely to see ADHD as a medical condition, while parents were more likely to see ADHD in association with socio-environmental causes. Delayed diagnosis, inadequate access to information and a lack of co-ordinated care are stated as some of the reasons for parental dissatisfaction with services. Professionals emphasised the need for multidisciplinary input into the management of ADHD. The implications of these findings were that parents often battled with professionals to encourage them to see their viewpoint, access to treatment was influenced by the views of parents and professionals, and noncompliance occurred when parents had different views from professionals.

Serum samples were collected from healthy blood donors in 5 regions in Sweden in 1999, i.e. from the local Blood Centres (collecting facilities) in Boden, Jönköping, Lund, Skövde, and Uppsala. In total, 498 serum samples (63% males, 37% females) were received and tested by immunofluorescence assay for antibodies against B. elizabethae, B. grahamii, B. henselae (Houston-1), B. henselae (Marseille), B. quintana, and B. vinsonii subsp. vinsonii. An overall Bartonella spp. seroprevalence of 16.1% was found, with a predominance of immunoreactivity to B. elizabethae, at 14.1%; B. grahamii, 2.6%; B. henselae (Houston-1), 1.2%; B. henselae (Marseille), 1.8%; B. quintana, 0.2%; and B. vinsonii subsp. vinsonii, 0.0%. Univariate and multivariate analyses of epidemiological and demographical information revealed an increased rate of B. elizabethae seropositivity in blood donors working outdoors, being out in the wild a minimum of once a week, hunting moose, having cat contact, and travelling to Eastern Europe. Living in the southern region of Sweden (Lund area) was associated with decreased seropositivity to B. elizabethae.

Our aim was to corroborate previous findings that HLA-DR4 carriers are characterized by higher levels of mutans streptococci in saliva than are individuals expressing other HLA-DR types. Of 68 subjects (dental students, staff, and faculty) who were sampled for salivary counts of mutants streptococci, 13 subjects with the lowest counts of mutans streptococci and 15 subjects with the highest counts were selected for HLA-typing. Of the 13 who expressed HLA-DR4, 8 were heavily colonized by mutants streptococci. Although a trend towards a relationship was found between HLA-DR4 carriage and high levels of mutans streptococci, it was not statistically significant. In this selected population, knowledge of how to minimize the risk of caries and mutans streptococci level may have influenced the results.

Objective: Evaluation of the prognostic value of immunogenetic markers in early rheumatoid arthritis (RA)., Methods: Ninety-nine patients with definite RA and disease duration 24 months or less were followed with standardized assessment. Disability was assessed by the HAQ index and radiographic changes in hands and feet by the Larsen method. The frequencies of HLA-DR genes were determined by serological typing, Gm allotype distribution by classical hemagglutination inhibition test, and occurrence of anti-Gm allotypes by use of anti-Rh coats. The immunogenetic findings were related to disease severity after 2 years' followup., Results: Functional capacity was well preserved, disease activity was less, but radiographic changes in hands and feet had increased considerably at study finish. A group of 13 patients had developed rapidly progressive changes of hip and/or shoulder joints, all requiring arthroplasty. There was a significantly increased frequency of HLA-DR4. Twenty-seven of the 68 HLA-DR4 positive patients were putatively homozygous. HLA-DR4 was not related to disability or to severe small joint destruction. However, progressive large joint damage was significantly more prevalent in homozygous patients (p < 0.01). Gm allotype distribution was normal and not related to clinical findings. Anti-Gm antibodies were common and frequently specific for nonhost Gm allotype. Fifty-six patients carried anti-G1m(a), and occurrence of this antibody was significantly associated with radiographic progression of small joints (p = 0.01), presence of nodules (p < 0.01) and number of active joints (p = 0.001)., Conclusion: Immunogenetic markers aided in identifying patients with early RA with more severe disease.

Clinical data suggest the involvement of hereditary factors in children susceptible to recurrent acute otitis media. That relationships of varying degree exist between the frequencies of certain HLA antigens and various disease entities is well established. In the present study, we investigated the frequencies of a number of HLA antigens in 45 patients with clinical recurrent acute otitis media and compared these frequencies with those in a control group from the same district. The HLA-A2 antigen occurred in 80% (36/45) of the group with recurrent acute otitis media, as compared with 56% of controls. Of a subgroup of 11 children with recurrent acute otitis media who were prospectively followed up, 10 (91%) were HLA-A2 positive. The HLA-A3 antigen occurred in only 11% (5/45) of the group with recurrent acute otitis media as a whole (n = 45) in comparison with 28% of controls. Among 22 prospectively followed up children without any episode of acute otitis media during the first 3 years of life, the frequency of HLA-A2 was 45% (10/22) and that of HLA-A3, 32% (7/22). The results indicate the existence of a relationship between recurrent acute otitis media and the HLA-A locus, suggesting the involvement of genetic factors in the disease.

Mutans streptococci are well established as caries-inducing microorganisms in man. Most humans carry the bacteria, but in highly different numbers. This cannot be explained by environmental factors only. The aim of this study was to investigate a possible association between levels of colonization by mutans streptococci and the presence of certain B and DR human leukocyte antigens (HLA). Altogether, 170 subjects who had their HLA antigens determined (76 renal transplant patients and 94 healthy blood donors) were selected for the investigation. Paraffin-stimulated saliva samples were taken using the wooden spatula method with subsequent cultivation of mutans streptococci on mitis salivarius bacitracin agar plates. An association between the absence of HLA-DR 4 antigens and low, or undetectable, levels of mutans streptococci was found. This was statistically significant for the immunosuppressed renal transplant subjects. The same trend was observed among the healthy blood donors.

HLA and Gm allotypes of 99 consecutive Swedish patients with rheumatoid arthritis were determined. Ninety-two of the 198 haplotypes contained DR4, a significant increase. The patients' sera from 3 different occasions were studied for anti-immunoglobulin profile as judged by 6 selected anti-Rh coats, 4 of them being monoclonal anti-Ds restricted as to allotype. Ninety-two of the patients were reactive with a polyclonal anti-Rh Ri as against 10 with the monoclonal carrying the G1m(f) allotype. Antibodies to Ig coats carrying defined allotypes were more frequently observed in patients not carrying the allotype in question than in those individuals possessing it. The difference was significant or highly significant as regards presence/absence of G1m(a), G3m(b) and G3m(g), respectively. Anti-G1m(a) and anti-G3m(g) cooccurred in 17 of the patients. Results consistent with presence/absence of particular anti-immunoglobulins at the 3 examinations were observed in 74 of the patients. Gm allotypes or antiallotypes were not statistically related with DR4 status. In conclusion, alloimmunization to Gm markers frequently occurs in early rheumatoid arthritis.

Under specified conditions purified C1q, activated C1r and C1s and C1r-C1s complexes were bound independently of Ca2+, to heparin-Sepharose, and could be eluted by an increasing salt gradient. Zymogen C1r and C1s, C1r-C1s complexes, C1 inactivator, and C1r-C1s-C1 activator complexes were not bound. However, at lower conductance Ca2+ independent binding of C14 occurred, which was utilized in the purification of C14 and C1s. In the presence of C1t (serum amyloid P component), C1s was firmly retained on heparin-Sepharose, which was probably due to formation of a C1s-C1t complex.

Beta 2-microglobulin aggregated with glutaric dialdehyde was efficiently bound to C1q in fluid and solid phase assay systems. Furthermore, affinity chromatography experiments suggested reactivity of monomeric beta 2-microglobulin with C1q. In spite of its C1q binding capacity, the aggregated beta 2-microglobulin did not activate the C1 complex in serum. This however, might have been due to the mode of aggregation.

In a retrospective study of 138 HLA-typed patients with primary glomerulonephritis progressing to terminal uraemia, a bimodal curve of age at onset of disease was observed among males. An initial peak occurred between 16 and 25 years of age, and a second peak between the ages of 46 and 55. The prevalence of HLA B40 was found to be high among males in the first group, and a relationship was found to exist between the presence of HLA B40 and increased titres of ASO (antistreptolysin O). No such findings were made either in the second group of males or in the female group. Among females, a single peak for age of onset occurred between 6 and 15 years. The frequency of HLA B40 did not differ significantly from that of the controls. The results of this study suggest a relationship to exist, predominantly in younger males, between primary glomerulonephritis with fatal outcome and HLA B40-related alterations in the immunological response to beta-streptococcal infection.

The pedigree of a family where three of nine siblings had suffered from aneurysmal subarachnoid haemorrhage (SAH) was explored, by means of interviews and revisions of population and medical records. We thus found two nephews with previously ruptured intracranial aneurysms. Subsequently high resolution computerised tomography (CT) scans were performed in the remaining six siblings, one of which was shown to harbor an intracranial aneurysm. This individual was subjected to uncomplicated clipping of the aneurysm. Typing of human leukocyte antigen (HLA) was performed in 15 individuals of the pedigree. Three of the six HLA-antigens recently reported to occur in increased frequently in a series of (non-familial) patients with ruptured aneurysm were found, namely B7, DR2 and Cw2. Most noteable was the expression of the antigen B7 in five of the six individuals with aneurysm in the investigated family. At present HLA-typing is not a useful screening tool to identify individuals in the general population with an increased risk of developing intracranial aneurysms. The present study shows that HLA-typing could neither be used to predict the occurrence of intracranial aneurysms in the siblings in the investigated family. HLA-typing may provide further clues to our understanding of the etiology of intracranial aneurysms, especially concerning possible genetic factors. The authors thus would like to encourage HLA-typing in previously known and newly detected families with accumulation of intracranial aneurysms.

Twenty children with acute pneumococcal otitis media were studied. In 6 children the infection ran a normal course and healed after the first episode and in 14 it relapsed. The serum levels of the immunoglobulins IgG, IgA and IgM were normal in all 20 children. Specific antibodies to pneumococcal polysaccharide were found in all cases, with no differences in the titers between the relapsed cases and those that healed. The complement components were quantitated with electroimmuno assay. G1q proved depressed in 60 per cent of the relapsed cases and in 16 per cent of the healed cases. C1r and C1s were disproportionally high compared with the C1q levels. Furthermore, crossed immunoelectrophoresis revealed abnormal complexes composed of C1r and C1s, and complexes composed of C1r, C1s and C1 IA. These complexes were more pronounced in sera from the children with relapsing otitis media.

Increased concentrations of C3dg were demonstrated in plasma from patients with primary biliary cirrhosis (PBC), indicating in vivo activation of C3. Rapid spontaneous C3 cleavage by the classical pathway was observed in vitro in serum and in EDTA plasma reconstituted with Ca++ and Mg++, suggesting the presence of complement-activating substances. On incubation with fresh normal serum, purified polyclonal IgM from patients with PBC induced C1 activation, C4 cleavage, and C3dg formation. No C3 cleavage was observed when PBC-IgM was incubated with a C2-deficient serum. We suggest that the complement activation in vivo in PBC, which occurs predominantly by the classical pathway and is characterized by increased concentrations of C1 activation complexes, decreased C4 concentrations, and hypercatabolism of C3, is attributable to an abnormal IgM population.

Samples of blood were obtained from 100 healthy full-term women in labour and, after delivery, from the umbilical cord of their infants. By electroimmunoassay, complement components were quantitated in serum (C1q, C1r, C1s, C1 IA, C2, P, D. I, H, C6 and C7) or in EDTA-plasma (C4, C3, B, C5. and C). The concentrations of C7 in cord serum was twice that found by others using a functional assay. Concentrations of C1r, I and C6 in the cord sample were 50-60 per cent of those in healthy blood donors used as reference, and that of D was about 130 per cent. The cord serum and plasma concentrations of the remaining components agreed with previously reported values. The maternal levels of C2, C4, C3, B, H, C5 were 40-60 per cent higher than those of the reference.

Sixteen complement components were analysed at three different occasions during a normal pregnancy. Samples were also obtained at delivery and six weeks post partum. All factors but C1 IA and D increased during the pregnancy. Six weeks after the delivery, the levels of all components but C1s, C4 and C6 showed a beginning normalisation. In 15 per cent of the women, C1 IA was functionally inactive at delivery.

A simple procedure for isolating C-reactive protein is presented. The method consists of two chromatographic separations on diethylaminoethyl (DEAE)-cellulose columns and utilized the difference between the binding of C-reactive protein to DEAE in the presence and absence of calcium. Electrophoretically pure C-reactive protein can be recovered from serum or ascitic fluid with a yield of approx. 50--60% within one day.

In plasma and serum samples, ageing results in excessive C3dg/d values when measured by electroimmunoassay. The use of polyethylene glycol, either in the preparation of the samples or in the electrophoretic gels, gives falsely low values.

The influence of activated C1s, C1r and properdin in the fluid phase initiation of the C3b-dependent feedback mechanism of the human complement was studied. It was found that C1s caused conversion of C3 and factor B in a normal serum, but not in a serum genetically deficient in C4 or in a serum to which Na2EDTA had been added. When a normal serum was incubated with C1r before incubation with C1s, only C3 was converted, whereas factor B remained in the unaltered native state. Properdin did not influence the C1s mediated conversion of C3 and factor B. When activated properdin was added to a properdin-depleted serum, both C3 and factor B were converted. Activated properdin was also incubated with purified C3 and purified C3b. It was shown that C3 was converted to C3b, but C3b was not degraded despite prolonged incubation.

Complement activation, as shown by increased amounts of complexes composed of C1r-C1s-C1 IA, and abnormal complexes of C1r-C1s were demonstrated in serum from patients with acute pneumococcal and chronic otitis media, serous or mucoid respectively. C1q binding substances were shown in middle ear effusions and in sera from patients with chronic serous otitis media. Presence of immune complexes and/or bacterial products capable of binding c1q results in formation of C1r-C1s-C1 IA complexes and may also cause the generation of C1r-C1s complexes. Such a dissociation of the C1 component will compromise the important opsonic function of the classical pathway.

Cell division in log-phase cultures of the unicellular, biflagellate alga, Chlamydomonas reinhardi, has been studied with the electron microscope. The two basal bodies of the cell replicate prior to cytokinesis; stages in basal body formation are presented. At the time of cell division, the original basal bodies detach from the flagella, and the four basal bodies appear to be involved in the orientation of the plane of the cleavage furrow. Four sets of microtubules participate in cell division. Spindle microtubules are involved in a mitosis that is marked by the presence of an intact nuclear envelope. A band of microtubules arcs over the mitotic nucleus, indicating the future cleavage plane. A third set of microtubules appears between the daughter nuclei at telophase, and microtubules comprising the "cleavage apparatus" radiate from the basal bodies and extend along both sides of the cleavage furrow during cytokinesis. Features of cell division in C. reinhardi are discussed and related to cell division in other organisms. It is proposed that microtubules participate in the formation of the cleavage furrow in C. reinhardi.