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The aim of this study was to elucidate the consequences of leisure time physical activities on the one-year results of surgery of lumbar intervertebral disc herniation. Pre- and postoperative leisure time physical activities and severity of occupation handicap were analyzed from 212 patients. Only to a certain degree the findings support the claim that a high preoperative level of physical activities during leisure time is linked with good postoperative results.

Social factors of 179 operated and 97 non-operated patients one year after hospitalization due to low back pain and sciatica were tested by multi-variate regression analysis in relation to the five-year outcome evaluated according to the WHO Handicap Classification. For operated men a subjective working incapacity (relative risk RR = 4.6) and co-morbidity (RR = 2.7) predicted a poor outcome. For operated women the predictive factors were subjective working incapacity (RR = 3.2) and older age (RR = 1.9). For non-operated men an increased occurrence of occupational hazards (RR = 3.6) and for non-operated women co-morbidity (RR = 7.1) indicated a poor outcome

BackgroundObesity is a heritable complex phenotype which can increase the risk of age-related outcomes. Biological age can be estimated from DNA methylation (DNAm) using various “epigenetic clocks.” Previous work suggests individuals with elevated weight also display accelerated aging, but results vary by epigenetic clock and population. Here, we utilize the new epigenetic clock GrimAge, which closely relates with mortality.ObjectivesWe aimed to assess the cross-sectional association of BMI with age acceleration in twins to limit confounding by genetics and shared environment.Methods and ResultsParticipants were from the Finnish Twin Cohort (FTC; n = 1424), including monozygotic (MZ) and dizygotic (DZ) twins, and DNAm was measured using the Illumina 450k array. Multivariate linear mixed effects models including MZ and DZ twins showed an accelerated epigenetic age of 1.02 months (p-value = 6.1 × 10−12) per 1-unit BMI increase. Additionally, heavier twins in a BMI-discordant MZ twin pair (ΔBMI > 3 kg/m2) had an epigenetic age 5.2 months older than their lighter co-twin (p-value = 0.0074). We also found a positive association between log(HOMA-IR) and age acceleration, confirmed by a meta-analysis of the FTC and two other Finnish cohorts (overall effect = 0.45 years, p-value = 0.0025) from adjusted models.ConclusionWe identified significant associations of BMI and insulin resistance with age acceleration based on GrimAge, which were not due to genetic effects on BMI and aging. Overall, these results support a role of BMI in aging, potentially in part due to the effects of insulin resistance.

Increased levels of circulating cell-free DNA (cf-DNA) are associated with and predict poor health outcomes. However, its predictive ability for mortality in population-based samples remains understudied. We analysed the capability of cf-DNA to predict all-cause mortality and assessed whether it adds predictive value on top of the other risk factors in the Health 2000 survey (n = 1,257, 46–76 years of age, 15-years-follow-up, 18% deceased). When analysed in a multivariate model with the other factors that independently predicted mortality in the sample (age, gender, self-rated health, smoking and plasma levels of glucose and adiponectin), increases in cf-DNA levels were associated with increased risk of mortality (hazard ratio [HR] for 0.1 µg increase in cf-DNA: 1.017, 95% confidence interval [CI] 1.008–1.026, p = 0.0003). Inclusion of cf-DNA in the model improved the model fit and discrimination. Stratifying the analysis by cardiovascular disease (CVD) status indicated that cf-DNA predicted mortality equally well in individuals with (HR 1.018, 95% CI 1.008–1.026, p = 0.002) and without (HR 1.018, 95% CI 1.001–1.035, p = 0.033) CVD. In conclusion, our study indicates that cf-DNA level predicts mortality in middle-aged and older individuals, also among those with established CVD, and adds significant value to mortality prediction. Our results thus underscore the role of cf-DNA as a viable marker of health.

Self-rated health (SRH) is one of the most frequently used indicators in health research. It is easy to use and considered as a valid measure of health because of its robust association with mortality. This association can largely be explained by the fact that in SRH summarized many health factors such as disease, functioning, and symptoms. Yet the biological basis of SRH is poorly understood. We investigated the association of SRH with several biomarkers measured from blood and urine in a large population sample where disease and functioning could be taken into account. Data were from MARK- AGE, a European-wide project on biomarkers of aging. The sample included 3252 individuals aged 18 to 92 years from eight European countries. SRH was categorized as poor&fair, good, very good and excellent. Multinomial logistic regression was used, contrasting “excellent” to “poor&fair”. Altogether 170 biomarkers were included in the preliminary analyses and, adjusted for age and gender, 42 of them showed a significant association with SRH. Adjusted for age, gender and cardiovascular diseases, arthritis, diabetes, elevated blood pressure, hypothyroidism/hyperthyroidism and respiratory diseases, still 33 biomarkers showed a significant association. Of these, the TOP5 strongest SRH-associations were with concentrations of beta-carotene (β=1.7), 25-hydroxyvitamin-D (β=0.03), lutein (β=3.7), beta-cryptoxanthine (β=2.3) and HDL-cholesterol (β=1.3) in plasma (all P

Objective. There is ample evidence demonstrating that accelerated atherosclerosis prevails in autoimmune rheumatic diseases, particularly in SLE, and that the risk is due not only to traditional cardiovascular risk factors but also to the disease itself. ANAs are a hallmark of SLE and are known even to antedate the development of SLE. Our aim was to investigate whether positive ANAs in young adults are associated with risk factors for atherosclerosis or subclinical markers of atherosclerosis. Methods. ANAs were examined by IIF using HEp-2 cells as substrate in 2278 participants in the Cardiovascular Risk in Young Finns Study for whom detailed data on cardiovascular risk factors and markers of subclinical atherosclerosis (including brachial flow-mediated dilatation, carotid compliance and carotid intima-media thickness) were available. Results. In multivariate analyses, adjusted for age, BMI, serum concentrations of CRP, triglycerides, high-density lipoprotein and low-density lipoprotein cholesterol, blood pressure and smoking habits, ANA positivity (titre > 160) was inversely associated (� ¼� 0.145; P ¼ 0.034) with carotid compliance in women. Conclusions. Our results indicate that ANA positivity is associated with decreased carotid elasticity in women, suggesting that mechanisms resulting in ANA production may be involved in the development of early atherosclerosis.

Growing evidence points to a role for inflammation in prostate carcinogenesis. The significance of C-reactive protein (CRP), an inflammatory and innate immunity molecule, has not been evaluated thoroughly in prostate cancer (PC). In this study of 739 Finnish patients with PC and 760 healthy men, we evaluated the associations of CRP genotypes and haplotypes with total PC risk and PC progression, using prostate-specific antigen (PSA) as a marker of metastatic disease. Although the haplotype frequencies were similar in patients and controls, an association between haplotype ACCCA and patients' PSA levels was found. The carriers more often had a high PSA than non-carriers (P=0.0002) and the SNP rs2794521 A-allele and rs1800947 C-allele carriers had a higher PSA than non-carriers (P=0.009 and P=0.0004, respectively). A trend for a younger age at diagnosis was found among the carriers of ACCCA (P=0.07) and the rs1800947 C-allele (P=0.06), as well as a trend for the latter to have more likely metastases (P=0.06), but not after Bonferroni correction (alpha=0.00208). This is the first study to suggest association between PSA and CRP variants in PC and, therefore, further studies are warranted. CRP alleles previously found to protect against increased CRP levels are now suggested to be associated with metastatic PC, indicated by elevated PSA.

1) Two summary tables (a and b) of the results from Spearman correlation analyses between age, the cell counts and the first principal components (PCs). PCs were defined from either the whole methylation data or 1202 a-CpGs using PCA. 2) A table of the GO terms of the bio processes that are enriched to genes with aging-associated CpG-sites. 3) A table of common transcription factors for genes with hypermethylated a-CpGs characterized using Pscan. (DOCX 31 kb)

1) A figure of estimated proportions of CD8T, CD4T, NK, B cell, monocyte and granulocyte cells of peripheral blood samples in YFS. Proportions are visualized as boxplots, categorized by age group and organized to separate panels by sex. 2) A figure of aging-associated CpG site locations in regard to CpG islands (CGIs). Number of aging-associated CpG sites are visualized with stacked bars. 3) A figure (a-c) presenting locations of a-CpGs. 4) A figure showing results for association of DNA methylation level in cg03636183 with smoking. 5) A figure presenting sex specificity of the aging-associated CpG sites (a-CpGs). (DOCX 357 kb)

BACKGROUND: Apolipoprotein E (apoE) polymorphism plays a central role in lipid metabolism, but has recently also been suggested to regulate inflammation, as judged by levels of serum C-reactive protein (CRP). OBJECTIVE: To establish whether polymorphism of the apoE genes affects susceptibility to primary Sjogren's syndrome (pSS), degree of inflammation or age of onset of pSS. METHODS: ApoE genotype distribution and allelic frequencies were analysed using PCR and the TaqMan system in 63 Finnish Caucasian patients with pSS and in 64 healthy controls matched for sex, ethnic origin and area of residence. The clinical and immunological data on the pSS patients were analysed in relation to the apoE genotypes. RESULTS: There was no difference between pSS patients and controls in apoE genotype and allelic frequencies. The apoE epsilon4 allele was significantly associated with early onset of pSS in the entire population and in female patients (Kaplan-Meier log rank test, P = 0.0407 and P = 0.0168, respectively). The average age (+/- S.D.) of onset of pSS in all apoE epsilon4 allele carriers was 46 +/- 12 and in other genotypes it was 53 +/- 10 yr (P = 0.031, t-test). ApoE polymorphism was not associated with signs of inflammation evaluated by such markers as concentration of plasma CRP, plasma interleukin-6, plasma TNF-alpha, immunoglobulin G and haemoglobin, or leucocyte count or ESR. CONCLUSIONS: ApoE polymorphism does not affect susceptibility to pSS or levels of plasma inflammatory indices in patients with pSS. However, a clear association prevails between apoE epsilon4 and early onset of pSS.

Objectives To determine whether plasma matrix metalloproteinase 9 (MMP-9) and MMP9 (-1562C-->T) polymorphism have an effect on the disease phenotype in primary Sjogren's syndrome (pSS). Methods Plasma MMP-9 concentrations and polymorphism of the MMP9 gene were analysed in 66 patients with pSS. These data were studied in relation to the clinical data of the patients. The genetic data of patients were compared with the data of 66 healthy subjects. Results Plasma MMP-9 was higher in patients with definite pSS than in patients with possible pSS. This association was principally caused by higher plasma MMP-9 in patients with a positive Schirmer test and keratoconjunctivitis sicca. pSS patients with purpura, SS-A autoantibodies and RF had significantly lower plasma MMP-9 than patients without these characteristics. The overall MMP9 (-1562C-->T) allele frequencies were similar in patients and control subjects. The frequency of the allele T was higher in patients without Raynaud's phenomenon than in the control group. Conclusions MMP9 (-1562C-->T) could not be used for risk assessment in pSS. The presence of the rarer allele T may decrease the risk of Raynaud's phenomenon in pSS. High plasma MMP-9 is indicative of definite pSS but may paradoxically have a preventive effect on the eruption of purpura and on the development of autoantibody reaction in pSS.

Objectives. To determine whether plasma interleukin-6 (IL-6) and G/C base exchange polymorphism at position -174 of the IL6 gene have an effect on the clinical manifestations of primary Sjogren's syndrome (pSS). Methods. Levels of circulating IL-6 protein and polymorphism of the IL6 gene were analysed in 66 patients with pSS and in 400 healthy subjects. These data were studied in relation to clinical data on the pSS patients. Results. Plasma IL-6 was elevated in pSS patients compared with healthy controls, pSS patients with coeliac disease, pulmonary fibrosis or alveolitis or peripheral nervous system symptoms had significantly higher IL-6 levels than patients without these manifestations. IL-6 levels increased in parallel with the histological grade of minor salivary gland biopsy and the number of pSS criteria fulfilled. IL6 allele frequencies were similar in patients and normal subjects. Plasma IL-6 levels were regulated by the IL6 genotype in pSS patients. Conclusions. The G/C polymorphism of the IL6 gene does not predispose patients to pSS, but the circulating IL-6 concentration is related to specific manifestations of the disease and the levels of IL-6 are regulated by the IL6 promoter polymorphism in pSS.

Summary Human cytomegalovirus (CMV) infection is associated with a higher risk of cardiovascular disease in immunocompromised organ transplant patients. It has been linked with the pathogenesis of elevated arterial blood pressure. However, controversy exists as to whether CMV infection is associated with endothelial function, and little is known about its role as a potential risk factor for early atherosclerosis development at a young age. We aimed to discover if CMV antibody titres are associated with early vascular changes (carotid intima-media thickness, carotid artery distensibility and brachial artery flow-mediated dilation), blood pressure elevation or other traditional cardiovascular risk factors. CMV antibody titres were measured in 1074 women and 857 men (aged 24–39 years) taking part in the Cardiovascular Risk in Young Finns study. CMV antibody titres were significantly higher in women compared to men. In men, high CMV antibody titres were associated directly with age (P

Alzheimer's disease (AD) and Parkinson's disease (PD) are the two most common neurodegenerative conditions characterised by the presence of abnormal accumulation of proteins and loss of neurones in specific regions of the brain. The aetiology and pathogenesis of AD and PD still remain largely unknown. Evidence has emerged that immune mediated mechanisms may be important in the development of these disorders,1,2 and cytokine interleukin 1 (IL1) is one of the mediators suggested to be involved. The IL1 family comprises three proteins, the proinflammatory IL1α and IL1β and their inhibitor IL1 receptor antagonist (IL1Ra), which are encoded by the IL1A , IL1B , and IL1RN genes respectively.3 Since IL1 may have a role in AD4–8 and in PD,9,10 variation in the IL1A , IL1B , and IL1RN genes may be of importance in the development of these disorders. There is already some evidence in support of this, including the postulated association of the IL1A (−889) \*2/\*2 genotype with AD11 and the influence of the IL1B (−511) \*1/\*1 genotype on age at onset of PD.12 However, validation in different population groups is needed to determine whether polymorphisms located in the IL1A , IL1B , and IL1RN genes represent actual susceptibility factors for AD and PD. In the present study, our purpose was to investigate whether polymorphisms of the IL1 cluster genes are associated with the risk of AD or PD in Finnish patients. Ethical approval for the investigation was obtained from the local Hospital Ethical Committees. All patients and controls enrolled in the study were from western Finland. The AD group consisted of 92 sporadic late onset (>65 years) patients (63 women, 29 men). Thirty-eight patients (mean age at onset 73.7 years (SD 4.9)) met the clinical diagnostic criteria of the NINCDS-ADRDA Work …

Urokinase-type plasminogen activator receptor (uPAR) is expressed on a variety of different immune cells and vascular endothelial cells during inflammation. Previous studies indicate that a high plasma concentration of the soluble form of the receptor (suPAR) predicts poor outcome in infectious diseases.A prospective cohort study.Plasma suPAR levels were measured in 132 patients with bacteraemia caused by Staphylococcus aureus, Streptococcus pneumoniae, ß-haemolytic streptococcae or Escherichia coli using a commercial enzyme-linked immunosorbent assay (ELISA). Values were measured on days 1-4 after a positive blood culture, on days 13-18 and on recovery.The maximum suPAR values on days 1-4 were markedly higher in nonsurvivors compared to survivors (15.8 vs. 7.3 ng mL(-1) , P0.001) and the area under the receiver operating characteristic curve (AUC(ROC) ) in the prediction of case fatality was 0.84 (95% confidence interval (CI) 0.76-0.93, P0.001). At a cut-off level of 11.0 ng mL(-1) , the sensitivity and specificity of suPAR for fatal disease was 83% and 76%, respectively. A high level of suPAR (≥ 11 ng mL(-1) ) was associated with hypotension (mean arterial pressure70 mmHg) (odds ratio (OR) 6.5; 95% CI 2.9-14.6) and high sequential organ failure assessment score (≥ 4) (OR 9.3; 95% CI 4.0-21.9). A high suPAR level remained an independent risk factor for case fatality in a logistic regression model adjusted for potential confounders.Plasma suPAR level is a sensitive and specific independent prognostic biomarker in patients with bacteraemia.

Activin A/erythroid differentiation factor (EDF), a dimeric polypeptide hormone composed of two beta A subunits, regulates growth and erythroid differentiation of human hematopoietic progenitor and erythroleukemia cells. We have identified activated human peripheral blood monocytes as a natural source of activin A/EDF. In these cells, lipopolysaccharide (LPS) induced rapidly the expression of the beta A subunit mRNAs through protein kinase C-dependent transcriptional regulation. The beta A subunit mRNA expression was also increased by 1,25-dihydroxyvitamin D3, an inducer of macrophage maturation of monocytes. Western analysis with an anti-beta A antibody and an erythroid differentiation bioassay confirmed that the conditioned media of LPS-activated monocytes contained the activin A/EDF protein. We suggest that monocyte/macrophage-derived activin A/EDF may not only modulate hematopoiesis but may also act as a mediator molecule in the diverse physiologic and pathogenetic events in which these cells are involved.

Baseline C-reactive protein (CRP) concentrations are indicative of persons prone to cardiovascular diseases and are about 40-50% heritable. We have previously shown that interleukin (IL)-1B +3954 allele T is associated with lower CRP concentration. In this study, we aimed to examine the effect of this polymorphism together with the CRP +1059 gene polymorphism on baseline CRP concentrations, and genotyped 336 healthy blood donors for CRP +1059 (G--C) and IL-1B +3954 (C--T) polymorphisms. In men, the carriers of the CRP +1059 C-allele had significantly lower CRP values than GG homozygotes (0.66 versus 0.43 mg l(-1), up to -35%, P = 0.009). No significant difference was found in women. When the data were stratified for both of these polymorphisms in men, CRP +1059 GG homozygotes had low CRP concentrations only if they were allele-T carriers of IL-1B +3954 simultaneously (0.93 versus 0.50 mg l(-1), P = 0.013). Genotype CRP +1059 GG/IL-1B +3954 CC was associated with an almost 3-fold risk of a higher baseline CRP value [odds ratio (OR) 2.84 (CI 1.03-6.07)]. Thus, both IL-1B +3954 (C--T) and CRP +1059 (G--C) polymorphisms influence baseline CRP values and act independently of each other in male subjects. These polymorphisms might be predictive markers of persons prone to cardiovascular diseases.

The capacity of neonatal T cells to secrete interleukin-2 (IL-2) has been reported to be variable. We analysed IL-2 production in purified neonatal and adult T cells using polyclonal activator phorbol ester + calcium ionophore (PDBu + iono) or receptor-mediated anti-CD3/anti-CD3+ anti-CD28 stimulation. PDBu + iono induced equally high IL-2 levels in both groups and, when stimulated with plate-bound anti-CD3 monoclonal antibody (mAb), the IL-2 secretion by neonatal cells was undetectable and adult cells produced low amounts of IL-2 (mean 331 +/- 86 pg/ml). The addition of anti-CD28 mAb to anti-CD3-stimulated cells markedly increased IL-2 production in both cell types, but levels of IL-2 in neonatal T cells remained clearly lower than those of adult T cells (respective mean values: 385 +/- 109 pg/ml and 4494 +/- 1199 pg/ml). As NF-kappa B is a critical transcription factor in the control of IL-2 expression, we next analysed its nuclear translocation in neonatal and adult T cells using the electrophoretic mobility shift assay and, because induction of reactive oxygen intermediates (ROI) is required for the activation of NF-kappa B, we also analysed levels of intracellular ROI in these cells using the ROI-reactive fluorochrome DCFH-DA and flow cytometry. In neonatal T cells NF-kappa B activation and ROI formation after anti-CD3 stimulation were low compared with adult T cells and, although addition of anti-CD28 mAb increased induction of NF-kappa B and ROI formation, levels similar to those of adults were not achieved. After PDBu + iono stimulation, the cells showed similar ROI formation and IL-2 secretion. Our results suggest that reduced IL-2 production by neonatal T cells is specific for anti-CD3 and anti-CD3+ anti-CD28-mediated stimulation and that these activators cannot effectively activate the ROI-NF-kappa B signalling pathway in neonatal T cells.

The interleukin (IL)-1 gene cluster within chromosome 2 contains genes coding for both anti- and proinflammatory cytokines, including IL-1alpha, IL-1beta, IL-1Ra, and several novel cytokines designated IL-1F5 - IL-1F10.1 Proinflammatory cytokines IL-1alpha and beta are involved in the enhancement of inflammation and host defence. Anti-inflammatory IL-1Ra counteracts the function of IL-1alpha and IL-1beta. These cytokines are produced by a variety of cell types, for example, monocytes, magrophages, and keratinocytes. All IL-1 family genes are polymorphic and several of these polymorphisms have been shown to be associated with either susceptibility to or severity of inflammatory conditions and diseases.2 Atopy is a familial syndrome underlying atopic eczema, allergic rhinoconjuctivitis, and bronchial asthma. The skin prick test (SPT) is used to examine specific IgE mediated allergic responses and the results are generally in line with anamnestic data on atopy.3 Both IL-1alpha and beta have been shown to play a role in the regulation of allergen induced early and late reactions.4,5 IL-1alpha has also been found to accelerate cutaneous inflammation,6 whereas IL-1beta is involved in the regulation of contact sensitisation.7 In asthmatic bronchial epithelium, the expression of both IL-1beta and IL-1Ra is increased.8 Cytokines function as a network and thus the net effect on allergic inflammation may be dependent on allele combinations of individual cytokine genes. Recently in our population based case control study, we showed that IL1A (SNP +4845) genotype influences the SPT results.9 The carriers of the rarer allele 2 had a significantly lower SPT positive rate than that of non-carriers. Now we have expanded the study by analysing two additional SNPs ( IL1B SNP +3954 C>T and IL1RN VNTR in intron 2) in the IL-1 gene cluster from the same cohort. Altogether 254 females and 151 males (mean age 60 years, age range …

We read with interest the paper by Joos et al 1 on the association of IL-1 gene haplotypes with decline in lung function in smokers and share their view on a possible role of IL-1 genetics in inflammatory respiratory diseases. We have analysed the same polymorphism by the same methods in adult incident non-smoking asthmatic patients and non-smoking controls. Our results indicate that the association of IL-1 genetics with rate of decline in lung function is not limited to smokers. New adult asthma cases and controls were selected from a cohort of the Mini-Finland Health Survey (MFHS) and later re-evaluated. A more detailed description of the methods used in MFHS has been published elsewhere.2 The accuracy of the method of asthma case ascertainment has also recently been described.3 IL-1 haplotypes …

The secondary cytotoxic responses to the male specific antigen (H-Y) in in mice show H-2 restrictions so that cytotoxic female cells must share K and/or D end antigen with the male target cells. The production of cytotoxic cells is under the control of Ir genes, thus offering the possibility of studying the function of Ir genes in H-2-restricted cytotoxic responses. There are two kinds of Ir genes regulating this response; the dominant gene in the H-2b haplotype and complementary genes in other haplotypes. Now we have been able to map the dominant gene and some of the complementary genes: the dominant genes is in IAb, and in H-2k/H-2d complementation, the Ir genes are in ICk and ICd, and in H-2k/H2s and H-2k/H-2q complementations, at least the H-2k gene is in IC.

Cross-reactive T-cell cytotoxicity is seen when cytotoxic responses are generated in mixed lymphocyte cultures either between mouse strans which differ at the major histocompatibility complex, H-2, or between H-2b mutant strains and the strain from which they were derived. This cross-reactivity can be measured with [51Cr] labeled target cells from a number of different H-2 haplotypes, and the pattern of cross-reaction indicates that the target antigens are unlikely to be any of the serologically defined public specificities. In contrast, the specificity of H-2 restricted cytotoxic responses, such as that to the male-specific antigen, H-Y, is exquisite, and male cells from strains of mice carrying H-2 haplotypes other than the responder have never been found to act as appropriate targets. The contrast between the specificity of anti-H-2 and H-2 restricted responses may argue for a greater idiotypic homogeneity of the cells makiing H-2 restricted responses, and the greater specificity of these responses may be necessary for their biological function.

To develop monoclonal reagents for antigenic analysis and serotyping of Campylobacter spp., hybridoma cell lines were produced by fusion of mouse myeloma cells and spleen cells from mice immunized with Formalin-treated Campylobacter jejuni organisms. An enzyme immunoassay was used for preliminary screening of the cell culture supernatants and ascites. Twenty-nine clones which reacted with the immunogen were obtained. Seven of these clones were positive in passive hemagglutination tests with sheep erythrocytes coated with boiled saline extract of whole bacteria; four of these reacted with the purified polysaccharide preparation and with the autoclaved saline extract, but not with lipopolysaccharide prepared from the immunogen strain. Two of the antipolysaccharide clones agglutinated live bacteria in slide tests. Four additional clones gave positive slide agglutination tests with live bacteria, but in tube testing no clones agglutinated Formalin-treated bacteria. No cross-reactions with unrelated bacteria were seen, but several clones reacted in the enzyme immunoassay with many of the 24 Campylobacter strains studied. The clone which gave the highest mean enzyme immunoassay values with Campylobacter coli and C. jejuni strains also reacted with Campylobacter fetus subsp. veneralis and C. fetus subsp. fetus strains. This clone also gave the highest enzyme immunoassay value with an acid glycine extract of the immunogen, which indicates the presence of common antigens in the extract. The results suggest that monoclonal antibodies may be used to devise serotyping schemes for Campylobacter spp.

Mice were injected with a sublethal dose of cyclophosphamide (Cy) (300 mg/kg), and the appearance of the capacity of the regenerating spleen to form cytotoxic T lymphocytes (CTL) in response against 2,4,6 trinitrophenyl-coupled syngeneic cells or against allogeneic cells was followed. It was found that 8 da after Cy injection, the spleen contained cells that could give rise to CTL, but only 2,4,6 trinitrophenyl-specific CTL responses could be obtained at this stage. A low alloresponse was first seen 2 wk after Cy injection.

A series of surgically treated patellar tendon lesions among athletes is presented. The material was collected during 5 years from three sports injury clinics and from two hospitals. During this period the authors treated about 150 cases of jumper's knee, of which 34 cases were treated by operation. The athletes were mostly volley ball players, jumpers or runners. The operation revealed a necrotic focus of the patellar tendon in 21 cases, the retinaculum was thick and adherent in 16 patients and an exostosis of the patellar insertion was seen in two cases. The necrotic areas were excised, the thick and adherent retinaculum was divided and the exostoses were excised and drilled. Surgical treatment of chronic patellar tendon pains may give good results in selected cases.

Monoclonal antibodies directed against Uukuniemi virus glycoproteins G1 and G2 in combination with polyclonal antibodies against the nucleoprotein (N) were used to study the maturation of the virus in Golgi complexes of infected chicken embryo fibroblasts and BHK cells. Of 25 monoclonal antibodies obtained, 10 were shown to be G1 specific and 15 were shown to be G2 specific by immunoblotting and immunoprecipitation. In double-staining experiments, some of the monoclonal antibodies gave similar distributions of fluorescence as compared with the staining obtained from polyclonal rabbit anti-G1-G2 antibodies. Others, however, preferentially stained either the glycoproteins in the Golgi complex or those at the cell surface. This may indicate that the glycoproteins underwent conformational changes during their transport. Uukuniemi virus infection resulted in the vacuolization of the membranes of Golgi complexes where the maturation of the virus was taking place. Double-staining experiments with monoclonal antibodies which preferentially stained the Golgi-associated viral glycoproteins and with anti-N polyclonal rabbit antiserum showed a correlation between the progressive vacuolization of the Golgi complex and the accumulation of viral nucleoprotein in the Golgi region, suggesting that a morphological alteration of the Golgi complex may be a prerequisite for intracellular maturation of the virus. Treatment of Uukuniemi virus-infected cells with tunicamycin, a drug which inhibits N-linked glycosylation, resulted in the accumulation of both glycoproteins at an intracellular location, apparently representing the endoplasmic reticulum. Double-staining experiments showed a parallel accumulation of nucleoprotein at these sites, indicating that local accumulation of glycoproteins is required for nucleoprotein binding to intracellular membranes.

A DISTINCTIVE characteristic of IgA is its polymorphic nature with regard to the molecular size. It occurs in secretions mostly as a dimer or tetramer1,2 while serum IgA has a polydisperse weight distribution in many species1. It is mostly monomeric in human serum (7S) (ref. 3), mostly polymeric in the mouse4 and in the dog5, but in both these and other species several molecular sizes occur in the blood1.

Spleen cells from cyclophosphamide-treated mice responded in vitro to allogeneic stimulator cells but not to TNP-coupled syngeneic spleen cells. Similarly, cells from female mice, primed in vivo with syngeneic male cells, could not respond in vitro to male spleen cell stimulation if the mice were pretreated with cyclophosphamide. These results suggest that the precursor cells for H-2-restricted cytotoxic responses belong to a different T-cell subpopulation than the precursor cells for allogeneic responses.