An epidemiologic investigation of asthma in welders

To clarify whether asthma may be caused by fume from welding mild steel and to evaluate the possible strength of such an effect, we quantified airway responsiveness among young shipyard workers with different levels of fume exposure. Clinical investigation comprised a cross-sectional survey of 19- to 27-yr-old workers who were completing 3 to 9 yr of employment in various trades, and a control group of 15- to 17-yr-old school leavers who were applying for apprenticeships within the same trades. Both groups were subdivided into negligible-, ambient-, or high-exposure subgroups according to expected levels of fume exposure. Actual exposures were assessed in a parallel environmental survey. Participants were investigated by questionnaire, skin prick tests, spirometry, and methacholine tests. Complete data sets were obtained from 1,024 of the 1,070 eligible subjects (96%). Among the workers but not the school leaver controls, there was an increasing prevalence of positive methacholine tests across the exposure subgroups-negligible 37%, ambient 44%, high 49% (p < 0.05). Regression analyses showed that in males after allowing for the effects of atopy, current smoking, and age, the estimated geometric mean level of airway responsiveness of regular welders was twice that of workers with negligible exposure after 5 yr of work. This implies that fume exposure may have been critical in causing asthma in about 1% of the welders. A lesser effect (though not significantly so) was noted among the workers with ambient exposure.     

Expression and distribution of amyloid precursor protein-like protein-2 in Alzheimer's disease and in normal brain

Amyloid precursor-like protein-2 (APLP-2) belongs to a family of homologous amyloid precursor-like proteins. In the present study we report on the expression and distribution of APLP-2 in fetal and adult human brain and in brains of patients with Alzheimer's disease. We demonstrate that APLP-2 mRNAs encoding isoforms predicted to undergo post-translational modification by chondroitin sulfate glycosaminoglycans are elevated in fetal and aging brains relative to the brains of young adults. Immunocytochemical labeling with APLP-2-specific antibodies demonstrates APLP-2 immunoreactivity in cytoplasmic compartments in neurons and astrocytes, in large part overlapping the distribution of the amyloid precursor protein. In Alzheimer's disease brain, APLP-2 antibodies also label a subset of neuritic plaques. APLP-2 immunoreactivity is particularly conspicuous in large dystrophic neurites that also label with antibodies specific for APP and chromogranin A. In view of the age-dependent increase in levels of chondroitin sulfate glycosaminoglycan-modified forms of APLP-2 in aging brain and the accumulation of APLP-2 in dystrophic presynaptic elements, we suggest that APLP-2 may play roles in neuronal sprouting or in the aggregation, deposition, and/or persistence of beta-amyloid deposits.     

Pudendal nerve terminal motor latency influences surgical outcome in treatment of rectal prolapse

PURPOSE: This study was undertaken to document the effect of pudendal nerve function on anal incontinence after repair of rectal prolapse. METHODS: Patients with full rectal prolapse (n = 24) were prospectively evaluated by anal manometry and pudendal nerve terminal motor latency (PNTML) before and after surgical correction of rectal prolapse (low anterior resection (LAR; n = 13) and retrorectal sacral fixation (RSF; n = 11)). RESULTS: Prolapse was corrected in all patients; there were no recurrences during a mean 25-month follow-up. Postoperative PNTML was prolonged bilaterally (> 2.2 ms) in six patients (3 LAR; 3 RSF); five patients were incontinent (83 percent). PNTML was prolonged unilaterally in eight patients (4 LAR; 4 RSF); three patients were incontinent (38 percent). PNTML was normal in five patients (3 LAR; 2 RSF); one was incontinent (20 percent). Postoperative squeeze pressures were significantly higher for patients with normal PNTML than for those with bilateral abnormal PNTML (145 vs. 66.5 mmHg; P = 0.0151). Patients with unilateral abnormal PNTML had higher postoperative squeeze pressures than those with bilateral abnormal PNTML, but the difference was not significant (94.8 vs. 66.5 mmHg; P = 0.3182). The surgical procedure did not affect postoperative sphincter function or PNTML. CONCLUSION: Injury to the pudendal nerve contributes to postoperative incontinence after repair of rectal prolapse. Status of anal continence after surgical correction of rectal prolapse can be predicted by postoperative measurement of PNTML.     

Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats

Programmed cell death in the myocardium has been linked to ischemia reperfusion injury as well as to excessive mechanical forces associated with increases in ventricular loading. Moreover, hypoxia activates the suicide program of cardiac myocytes in vitro. Because the supplied portion of the ventricular wall is ischemic and subjected to high levels of systolic and diastolic stresses (acutely after coronary artery occlusion), apoptosis and necrosis may contribute independently to myocyte cell death after infarction. Therefore, myocardial infarction was produced in rats, and, after the determination of ventricular hemodynamics, the contribution of apoptotic and/or necrotic myocyte cell death to infarct size was measured quantitatively from 20 minutes to 7 days after coronary artery occlusion. Programmed cell death was assessed by the terminal deoxynucleotidyl transferase assay and by the electrophoretic detection of DNA laddering. Myocyte necrosis was evaluated by myosin monoclonal Ab labeling. Moreover, the expression of Bcl-2, Bax, and Fas proteins in myocytes was examined by immunocytochemistry. Myocyte cell death by apoptosis and necrosis comprised nearly 3 million myocytes at 2 hours. Apoptotic cell death involved 2.8 million cells and necrotic cell death only 90,000 myocytes. Apoptosis continued to represent the major independent form of myocyte cell death, affecting 6.6 million myocytes at 4.5 hours. Myocyte necrosis peaked at 1 day, including 1.1 million myocytes. DNA electrophoretic analysis confirmed these observations by showing nucleosomal ladders at 2-3 hours, 4.5 hours, 1 day, and 2 days after coronary artery occlusion. Myocytes showing both DNA strand breaks and myosin labeling were a prominent aspect of myocardial damage only after 6 hours. Finally, the expression of Bcl-2 and Fas in myocytes increased 18-fold and 131-fold, respectively. In conclusion, programmed myocyte cell death is the major form of myocardial damage produced by occlusion of a major epicardial coronary artery, whereas necrotic myocyte cell death follows apoptosis and contributes to the progressive loss of cells with time after infarction. The enhanced expression of Fas may be implicated in the activation of apoptosis in spite of the increase in Bcl-2, which tends to preserve cell survival.     

Incidence of Toxoplasma and Toxocara antibodies among out-patients in the Ophthalmic Research Institute, Egypt

Infection by Toxoplasma gondii and Toxocara canis is getting much important nowadays. Both are soil transmitted infections. The present study was planned to detect the incidence of T. gondii and T. canis antibodies among 100 patients attending the outpatient clinics in Research Institutes of Ophthalmology (RIO), whose urine and stool were free from other parasitic stages. Patients were classified into two groups, group I; (70 ocular cases) and group II, (30 non-occular cases). Control group (group III); 30 healthy persons. Sera from all individuals were subjected to IFAT and IHAT to detect Toxoplasma antibodies and IFAT to detect Toxocara antibodies. By using IFAT for Toxoplasma revealed, 25% as a total incidence, 21.4% in group I, 33.3% in group II and 6.6% in group III. While IHAT revealed 51% as a total incidence, 51.4% in group I, 50% in group II and 23.3% in group III. Among group I, retinochoroiditis cases showed the highest incidence and titre. While hydrocephalic cases showed highest incidence and titre in group II. T. canis antibodies revealed 23% as a total incidence, 14.3% in group I, 43.3% in group II and 5% in group III. Cases presented with retinal detachment showed the highest incidence and titre in group I while in group II hepatomegalic cases gave the highest incidence and titre. Concomitant infection of both Toxoplasma and Toxocara was detected in 8% of positive cases.     

The cellular basis of dilated cardiomyopathy in humans

The present investigation was designed to evaluate whether end-stage cardiac failure in patients affected by dilated cardiomyopathy (DC) was dependent upon extensive myocyte cell death with reduction in muscle mass or was the consequence of collagen accumulation in the myocardium independently from myocyte cell loss. In addition, the mechanisms of ventricular dilation were analysed in order to determine whether the changes in cardiac anatomy were important variables in the development of intractable congestive heart failure. DC is characterized by chamber dilation, myocardial scarring and myocyte hypertrophy in the absence of significant coronary atherosclerosis. However, the relative contribution of each of these factors to the remodeling of the ventricle is currently unknown. Moreover, no information is available concerning the potential etiology of collagen deposition in the myocardium and the changes in number and size of ventricular myocytes with this disease. Morphometric methodologies were applied to the analysis of 10 DC hearts obtained from patients undergoing cardiac transplantation. An identical number of control hearts was collected from individuals who died from causes other than cardiovascular diseases. DC produced a 2.2-fold and 4.2-fold increase in left ventricular weight and chamber volume resulting in a 48% reduction in mass-to-volume ratio. In the right ventricle, tissue weight and chamber size were both nearly doubled. Left ventricular dilation was the result of a 59% lengthening of myocytes and a 20% increase in the transverse circumference due to slippage of myocytes within the wall. Myocardial scarring represented by segmental, replacement and interstitial fibrosis occupied approximately 20% of each ventricle, and was indicative of extensive myocyte cell loss. However, myocyte number was not reduced and average cell volume increased 2-fold in both ventricles. In conclusion, reactive growth processes in myocytes and architectural rearrangement of the muscle compartment of the myocardium appear to be the major determinants of ventricular remodeling and the occurrence of cardiac failure in DC.     

Observer agreement on interpreting colposcopic images of CIN

The purpose of this work was to study intraobserver and interobserver variation in the interpretation of colposcopic images of cervical intraepithelial neoplasia (CIN). Twenty-three experienced colposcopists were asked to assess colposcopic images presented on slides and to select the biopsy site. Eleven cases were independently interpreted twice with an interval of 2-3 months by all observers. No information about the cytological classification was available. In each case the "majority assessment" was considered as the standard, being "no CIN" in 2 cases, CIN I in 4 cases, CIN II in 3 cases, and CIN III in 2 cases. Intraobserver concordance was 66.7%, the kappa value was 0.54. Interobserver agreement was found to be 52.4 and 51.0% in the first and second sessions, respectively, while the mean kappa values were 0.41 and 0.33, respectively. In selecting the site for biopsy, 77.4% of all observers agreed while the same site was selected in 85.3% of cases by the individual colposcopist in the two sessions. Overall, CIN I and II interpretations revealed lower levels of agreement than no CIN or CIN III interpretations. It is concluded that observer variability in interpreting colposcopic images and selecting the site for biopsy is in the same range as observer variation in other subjective diagnostic tests such as cytology and histopathology. This variation should be taken into account in the colposcopical management of patients with abnormal cytology.     

A comparison of the investment in hospital-based obstetrical ultrasound in Wales and Washington state

The purpose of this study was to examine differences in the way Britain and the United States invest in and deploy a new medical technology. We used structured interviews to obtain information on the technical sophistication and approximate replacement value of all hospital-based obstetrical ultrasound machines in every maternity hospital in Washington state and Wales. The supply of hospital-based ultrasound machines--approximately two machines per 1,000 births--was similar in both countries. Wales had fewer advanced ultrasound machines than Washington state, and they were based exclusively in high-volume district general hospitals; there were no obstetric ultrasound machines in the private sector. In Washington state, the majority of advanced machines were in small and medium-sized hospitals, and many private offices had ultrasound machines. The approximate replacement value of hospital-based machines was three times as high per birth in Washington state as in Wales. In the case of obstetrical ultrasound, centralization of facilities, a relatively small private sector, and global budgeting lead to lower expenditures per patient within the National Health Service without compromising access to care.