Clinimetric properties of sacroiliac joint mobility tests: A systematic review.

BACKGROUND: Previous systematic reviews revealed poor reliability and validity for sacroiliac joint (SIJ) mobility tests. However, these reviews were published nearly 20 years ago and recent evidence has not yet been summarised. OBJECTIVES: To conduct an up-to-date systematic review to verify whether recommendations regarding the clinical use of SIJ mobility tests should be revised. STUDY DESIGN: Systematic review. METHOD: The literature was searched for relevant articles via 5 electronic databases. The review was conducted according to the PRISMA guidelines. COSMIN checklists were used to appraise the methodological quality. Studies were included if they had at least fair methodology and reported clinimetric properties of SIJ mobility tests performed in adult patients with non-specific low back pain, pelvic (girdle) pain and/or SIJ pain. Only tests that can be performed in a clinical setting were considered. RESULTS: Twelve relevant articles were identified, of which three were of sufficient methodological quality. These three studies evaluated the reliability of eight SIJ mobility tests and one test cluster. For the majority of individual tests, the intertester reliability showed slight to fair agreement. Although some tests and one test cluster had higher reliability, the confidence intervals around most reliability estimates were large. Furthermore, there were no validity studies of sufficient methodological quality. CONCLUSION: Considering the low and/or imprecise reliability estimates, the absence of high-quality diagnostic accuracy studies, and the uncertainty regarding the construct these tests aim to measure, this review supports the previous recommendations that the use of SIJ mobility tests in clinical practice is problematic.

Risk factors for exercise-related acute cardiac events. A case-control study.

BACKGROUND: In spite of the benefits of physical activity, exercise may provoke acute cardiac events in susceptible individuals. Understanding risk factors of exercise-related acute cardiac events may identify opportunities for prevention. METHODS: A case-control study was conducted to examine determinants of acute cardiac events in athletes. The cases were athletes who suffered an acute cardiac event during or shortly after vigorous exercise. Athletes who visited a hospital because of a minor sports injury were selected as controls. Information on cardiovascular disease, family history of cardiovascular disease, cardiovascular symptoms and other potential risk factors was collected through questionnaires. RESULTS: 57 cases (mean age 41.8 years, range 11-73) and 57 controls (mean age 40.9 years, range 13-68) were included in the study. Athletes with a history of cardiovascular disease were at a markedly increased risk for cardiac events during exercise (OR = 32; 95% CI 7.4 to 143). Smoking (OR 5.9; 95% CI 1.9 to 18), fatigue (OR = 12; 95% CI 1.2 to 118) and flu-like symptoms (OR 13; 95% CI 1.4 to 131) in the month preceding the event were related to acute cardiac events in athletes. CONCLUSIONS: Prior cardiovascular disease, smoking, and a recent episode of fatigue or flu-like symptoms are associated with an increased risk of exercise-related acute cardiac events. Athletes and physicians should pay careful attention when these factors exist or occur.

The diallelic locus encoding the minor histocompatibility antigen HA-1 is evolutionarily conserved.

The polymorphic minor histocompatibility antigen HA-1 induces powerful T-cell alloreactivities with important consequences for graft-vs-tumor activity and development of graft-vs-host disease in patients after human leukocyte antigen-matched stem-cell transplantation (SCT). In view of possible translational animal studies, we analyzed the evolutionary conservation of the diallelic HA-1 locus in four mammalian species. Our results show that rodents do not encode the HA-1(H) allele, neither show polymorphism in this position on the HA-1 gene. Contrariwise, the HA-1(H) allele is present in non-human primate species and dogs. Interestingly, both the HA-1(H) T-cell epitope and its non-immunogenic counterpart HA-1(R) are present in the latter species. Thus, the HA-1 allelic polymorphism is conserved in evolution in primates and dogs.

Allele specific PCR for the minor Histocompatibility antigen HA-2.

The hematopoietic system restricted minor Histocompatibility antigen (mHag), HA-2, is encoded by the novel human class I Myosin gene, MYO1G, located on the short arm of chromosome 7. The HA-2 encoding region is di-allelic and comprises the HLA-A2 restricted T cell epitope YIGEVLVSV (HA-2V) and its allelic counterpart YIGEVLVSM (HA-2M). We designed a sequence specific PCR (SSP) for both HA-2 alleles. The HA-2 genomic typing results were compared with the HA-2 CTL phenotyping in three families and revealed exact correlation. The mHag HA-2 SSP can be incorporated in DNA based typing protocols.

The HA-2 minor histocompatibility antigen is derived from a diallelic gene encoding a novel human class I myosin protein.

Human minor histocompatibility Ags (mHag) present significant barriers to successful bone marrow transplantation. However, the structure of human mHag and the basis for antigenic disparities are still largely unknown. Here we report the identification of the gene encoding the human mHag HA-2 as a previously unknown member of the class I myosin family, which we have designated MYO1G. The gene is located on the short arm of chromosome 7. Expression of this gene is limited to cells of hemopoietic origin, in keeping with the previously defined tissue expression of the HA-2 Ag. RT-PCR amplification of MYO1G from different individuals led to the identification of two genetic variants, designated MYO1G(V) and MYO1G(M). The former encodes the peptide sequence previously shown to be the HA-2 epitope (YIGEVLVSV), whereas the latter shows a single amino acid change in this peptide (YIGEVLVSM). This change has only a modest effect on peptide binding to the class I MHC-restricted element HLA-A*0201, and a minimal impact on recognition by T cells when added exogenously to target cells. Nonetheless, as detected using either T cells or mass spectrometry, this amino acid change results in a failure of the latter peptide to be presented at the surface of cells that express MYO1G(M) endogenously. These studies have thus identified a new mHag-encoding gene, and thereby provide additional information about both the genetic origins of human mHag as well as the underlying basis of an Ag-positive vs Ag-negative state.

Clinical significance of alpha1-adrenoceptor selectivity in the management of benign prostatic hyperplasia.

Alpha1-adrenoceptor antagonists have been shown to provide effective relief from symptoms of benign prostatic hyperplasia (BPH) with attendant improvements in quality of life. Although the alpha1A-adrenoceptor subtype predominates over other subtypes of alpha1 adrenoceptors in the prostate gland, there is no evidence that a subselective alpha-adrenoceptor antagonist provides a clinical advantage over a selective alpha1-adrenoceptor antagonist in the treatment of patients with BPH. The pharmacokinetic profiles of alpha1A-adrenoceptor antagonists and their documented penetration of the blood-brain barrier (CNS adverse effects) preclude a clinical benefit of subselective alpha-adrenoceptor blockers over selective alpha1 blockers.

Accidents among drillers in the Venezuelan oil industry in 1993.

In 1993 a total of 356 accidents with injuries occurred in workers of 26 companies of oil and gas extraction in the eastern coast of Maracaibo Lake in Venezuela. 288 of them worked in drilling tasks. With the purpose of analyzing the factors that are associated with the drilling activities, the data base of the Venezuela Institute of Social Security, was reviewed. Only the first two digits of the Standard Industrial Classification were used in this study. For preventive reasons this study focused on six variables: unsafe condition or mechanical cause, insecure action, external agent, type of the accident, part of the body injured and the nature of the injury. The following results were obtained: the frequency rate was 222.3 by 1,000, most of them were minor and were caused by not paying attention when walking on or around labor areas (37%), thus favoring being struck by lifting machines (14%); also 62% occurred in non-classified conditions that injured the upper and lower extremities (48% and 24%) producing contusions and crushing (39%). In conclusion, most injuries occurring in the activity of oil and gas extraction are due to factors controllable with preventive strategies.

Interpretation of the ALLHAT interim analysis and implications for the treatment of patients with BPH.

The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) was designed to see if the effects of doxazosin, amlodipine and lisinopril were superior to those of chlorthalidone on the incidence of cardiovascular disease in high-risk patients with hypertension. Earlier this year, following an interim analysis of 24,335 patients, the doxazosin treatment arm was stopped amid reports of an increased incidence of secondary cardiovascular endpoints relative to chlorthalidone. This paper will offer some insight into the interpretation of the ALLHAT interim data, and clarify any issues around the use of alpha-1 adrenoceptor antagonists, such as doxazosin, in the management of patients with benign prostatic hyperplasia. Prostate Cancer and Prostatic Diseases (2000) 3, 152-156

The minor histocompatibility antigen HA-1: a diallelic gene with a single amino acid polymorphism.

The minor histocompatibility antigen (mHag) HA-1 is the only known mHag for which mismatching is correlated with the development of severe graft versus host disease (GvHD) after human leukocyte antigen-identical bone marrow transplantation. HA-1 was found to be a nonapeptide derived from an allele of the KIAA0223 gene. The HA-1-negative allelic counterpart encoded by KIAA0223 had one amino acid difference from HA-1. Family analysis with HA-1 allele-specific polymerase chain reaction showed an exact correlation between this allelic polymorphism and the HA-1 phenotype. HA-1 allele typing of donor and recipient should improve donor selection and allow the determination of bone marrow transplantation recipients with high risk for HA-1-induced GvHD development.

Alpha adrenoceptor blockade in the treatment of benign prostatic hyperplasia: past, present and future.

The treatment of BPH by alpha blockade is built upon a sound anatomical, physiological and pharmacological rationale. The theory is borne out in clinical practice; alpha adrenoceptor antagonists have been shown in placebo-controlled studies to improve symptoms of BPH and increase urinary flow rate. In hypertensive patients, there is a clinically significant reduction in blood pressure, with little or no effect on the blood pressure of normotensive patients with BPH. The development of selective alpha-1 adrenoceptor antagonists with a gradual onset and long duration of action has improved the tolerability and makes this class of drug a valuable alternative to surgery in many cases. Further refinements in the selectivity of alpha-1 adrenoceptor antagonists may enable even better targeted alpha blockade for BPH in the future by specific antagonism of the alpha-1 A adrenoceptor, although this hypothesis has yet to be confirmed clinically.

Heart rate variability from short electrocardiographic recordings predicts mortality from all causes in middle-aged and elderly men. The Zutphen Study.

Low heart rate variability is associated with high risk of sudden death in myocardial infarction patients. This has been attributed to unfavorable autonomic cardiac control. In the present study, the predictive value of heart rate variability for sudden death, mortality from coronary heart disease, and from all causes was investigated in the general population, using brief electrocardiographic recordings. From 1960 to 1985, 878 middle-aged Dutch men, aged 40-60 years, were followed and repeatedly examined as part of the Zutphen Study. In 1985 the remaining cohort was extended to 885 elderly men, aged 65-85 years, and followed until 1990. Heart rate variability (standard deviation of duration of normal RR intervals) was determined from the resting 12-lead electrocardiogram. The 5-year age-adjusted relative rate of total mortality of men with heart rate variability of < 20 milliseconds (msec) compared with men with heart rate variability of 20-39 msec was 2.1 (95 percent confidence interval 1.4-3.0) in middle-aged men and 1.4 (95% confidence interval 0.9-2.2) in elderly men. Death from noncoronary causes, especially cancer, contributed significantly to this elevated risk. The association of low heart rate variability with sudden death or coronary heart disease mortality was less consistent. In conclusion, in middle-aged men and probably in elderly men, low heart rate variability is predictive of mortality from all causes. This suggests that low heart rate variability is an indicator of compromised health in the general population.

Conservation of minor histocompatibility antigens between human and non-human primates.

It is well accepted that minor histocompatibility antigens (mHag) can function as transplantation barriers between HLA-matched individuals. Little is known about the molecular nature and evolutionary conservation of mHag. It is only very recently that the first human mHag were identified. The HLA-A2.1-restricted mHag HA-2 and the HLA-B7-restricted mHag H-Y appeared to be peptides derived from polymorphic self proteins. Here we show that the HLA-A2.1-restricted mHag HA-1, HA-2, and the H-Y peptides are conserved between man, chimpanzees and rhesus macaques. Human cytotoxic T cell clones specific for the HLA-A2.1-restricted mHag HA-1, HA-2, and H-Y recognized HLA-A2.1 gene-transfected chimpanzee and rhesus macaque cells. High-pressure liquid chromatography fractionation of HLA-A2.1-bound peptides isolated from the HLA-A2.1-transfected chimpanzee cells revealed that the chimpanzee HA-1 and HA-2 co-eluted with the human HA-1 and HA-2. Subsequent amino acid sequencing showed that the chimpanzee HA-2 peptide is identical to the human HA-2 peptide. Our functional and biochemical results demonstrate that mHag peptides are conserved for over 35 million years.

A history of the Neurological Institute of New York and its Department of Neurological Surgery.

The neurological institute of New York was founded in 1909 as the first hospital in North America devoted exclusively to the care of patients afflicted with neurological diseases. The Institute amalgamated with Columbia University's College of Physicians and Surgeons and The Presbyterian Hospital in New York City in 1928. The Department of Neurological Surgery developed under the successive leadership of Charles Elsberg, Byron Stookey, J. Lawrence Pool, Lester Mount, Edward Schlesinger, and Bennett Stein, each of whom brought unique qualities to the role of Department Chairman. This article traces the history of the Institute and its affiliates, present activities, and future plans.

Doxazosin: a new approach to hypertension and benign prostatic hyperplasia.

Doxazosin, a selective alpha 1-adrenoceptor antagonist, is an established first-line antihypertensive agent that is being introduced for the management of benign prostatic hyperplasia. Hypertension and benign prostatic hyperplasia are linked by the sympathetic nervous system, which has an aetiologic role in both conditions. The alpha 1-adrenoceptor is a mediator of increased tension, both in vascular and prostatic smooth muscle. Studies have shown that doxazosin, through its balanced action on alpha 1-adrenoceptor subtypes, reduces blood pressure and improves other risk factors for coronary heart disease, such as lipid profile, insulin sensitivity, left ventricular hypertrophy, platelet aggregation and fibrinolysis. Data are now accumulating to show that doxazosin improves urinary flow rates and symptoms in patients with benign prostatic hyperplasia. These effects have been demonstrated in controlled clinical studies, within weeks, and long term. Since hypertension and benign prostatic hyperplasia are widespread and often undiagnosed in the community, particularly with increasing age, doxazosin may be a particularly appropriate therapy for the considerable number of older men with both conditions.

Mismatches of minor histocompatibility antigens between HLA-identical donors and recipients and the development of graft-versus-host disease after bone marrow transplantation.

BACKGROUND: Graft-versus-host disease (GVHD) can be a major complication of allogeneic bone marrow transplantation even when the donor and recipient are siblings and share identical major histocompatibility antigens. The explanation may be a mismatch of minor histocompatibility antigens. We previously characterized five minor histocompatibility antigens, HA-1, 2, 3, 4, and 5, that are recognized by T cells in association with the major histocompatibility antigens HLA-A1 an A2. METHODS: We collected peripheral-blood leukocytes from 148 bone marrow recipients and their sibling donors, who were genotypically HLA identical. Fifty pairs were positive for HLA-A1, 117 were positive for HLA-A2, and 19 were positive for both. The pairs were typed with cytotoxic-T-cell clones specific for minor histocompatibility antigens HA-1, 2, 3, 4, and 5. RESULTS: Mismatches of HA-3 were equally distributed among recipients in whom GVHD developed and those in whom it did not. By contrast, a mismatch of only HA-1 was significantly correlated with GVHD of grade II or higher (odds ratio, infinity; P = 0.02) in adults. One or more mismatches of HA-1, 2, 4, and 5 were also significantly associated with GVHD (odds ratio, infinity; P = 0.006) in adults. These associations were not observed in children. CONCLUSIONS: A mismatch of minor histocompatibility antigen HA-1 can cause GVHD in adult recipients of allogeneic bone marrow from HLA-identical donors. Prospective HA-1 typing may improve donor selection and identify recipients who are at high risk for GVHD.

Cytokines restore MHC class I complex formation and control antigen presentation in human cytomegalovirus-infected cells.

CD8+ cytotoxic T cell (CTL) clones with specificity for defined minor and major histocompatibility (H) antigens were used to monitor antigen presentation in human cytomegalovirus (HCMV)-infected skin fibroblasts. At the immediate early stage of virus replication antigen presentation was intact, but was abolished during the early and late phase. Lack of CTL recognition was not selective for certain antigens but was associated with decreased steady state levels of nascent MHC class I complexes and unassembled MHC class I heavy chains, whereas free beta 2-microglobulin remained abundant. HCMV also affected the stability of both immature endoglycosidase H (Endo H)-sensitive and mature Endo H-resistant MHC class I molecules, suggesting that the virus interferes with antigen presentation at more than one step during maturation of the MHC class I complex. The action of interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) lifted the block of MHC class I complex formation by stimulating synthesis, assembly and stability of MHC class I molecules. This resulted in restored antigen presentation provided that cells were exposed to the factors before HCMV infection. Because few MHC molecules suffice for CTL recognition these cytokines compensated for the negative viral effect on the antigen presentation function. Nevertheless, the viral interference with MHC class I complex formation was still active. The data imply that specific cytokines limit the immune evasion potential of HCMV from CD8+ T lymphocyte control.

Effects of doxazosin on coronary heart disease risk factors in the hypertensive patient.

Hypertension often exists as part of a syndrome of cardiovascular, neuroendocrine and metabolic abnormalities. While antihypertensive pharmacotherapy has reduced the rates of stroke, congestive heart failure and renal failure, a disappointing benefit in terms of the reduction in coronary heart disease (CHD) mortality has been seen as a result of the adverse effects of some of the traditional antihypertensive agents on serum lipids and other factors. Doxazosin, a selective alpha 1-adrenoceptor inhibitor, is an effective antihypertensive agent with beneficial effects on an array of atherogenic risk factors. Treatment with doxazosin can lower blood pressure, reduce the levels of atherogenic lipids, increase the levels of cardioprotective lipids, reduce hyperinsulinaemia, insulin resistance and glucose intolerance, increase fibrinolysis, inhibit platelet aggregation, attenuate the adverse haemodynamic and haemostatic effects of smoking, and regress cardiac and smooth muscle hypertrophy. This unique combination of risk factor modifications should produce a reduction in CHD events.

Role of the sympathetic nervous system in hypertension and benign prostatic hyperplasia.

Hypertension and benign prostatic hyperplasia (BPH) have a number of features in common. For example, both occur with increasing frequency in the elderly, and both are a major source of health expenditure worldwide. However, the most striking feature linking hypertension and BPH is the aetiological role of the sympathetic nervous system. Sympathetic tone mediated by the alpha-receptor is vital in the control of blood pressure. By selectively inhibiting the alpha 1-adrenoceptors in the vasculature, thereby inhibiting the response to epinephrine and norepinephrine and thus reducing peripheral resistance, selective alpha 1-inhibitors such as doxazosin produce a physiological reduction in blood pressure. Receptors of the alpha 1 subtype are also found in the prostate, the urethra and bladder neck. Doxazosin, by reducing the tone of the prostatic smooth muscle, has the potential to improve urinary flow rate, as well as the obstructive and irritative symptoms characteristic of BPH.

Month-related variability in immunological test results; implications for immunological follow-up studies.

This longitudinal study was originally designed to detect changes in the in vitro immune response of healthy subjects as a result of a psychological intervention. In this study a significant proportion, about 70%, of the immunological variability in the test results was accounted for by the differences in immunological response levels of the subjects. Apart from this between-subject-effect, a significant proportion of the variability in test results was related to the month of data sampling. The month-effect was computed in such a way that the between-subject variation was taken into account. This resulted in a more accurate estimation of the month-effect. Even after correction for the intervention, i.e. the defence of the PhD thesis, the effect of month of data sampling remains significant for mean corpuscular haemoglobin, mean corpuscular haemoglobin concentration, percentage of CD4 and CD8 cells, and for the response to the mitogens phytohaemagglutinin, pokeweed mitogen and concanavalin A as well as the results for the mixed lymphocyte culture for one pool out of three. In contrast, no significant month-effect was observed for the whole blood cell counts, for the differential white blood cell counts as determined by monoclonal antibody staining for cell surface markers CD3, CD16, TAC and OKM1, nor for the immunoglobulin IgM and IgG serum levels. Likewise the cell-mediated lympholysis activities measured against three pools of stimulator cells remained unaltered. We discuss the implications for future immunological follow-up studies of the observation that a significant proportion of the variability in immunological test results is related to differences between subjects and to the month of data sampling.