Pulmonary manifestations in cement workers in Jordan

The literature on obsessive-compulsive disorder (OCD) in children and adolescents is reviewed. The disorder is characterized by obsessions (recurrent troublesome thoughts) and compulsions (ritualized thoughts or behaviors performed repetitively in response to an irresistible urge). OCD is far more common among children and adolescents than was previously believed. Good epidemiological studies from different parts of the world are still needed to determine if prevalence is equally high. Boys seem to have an earlier age of onset of OCD than girls. Male female ratio changed with age of onset, with males predominating in early onset and increasing numbers of females occurring during adolescence. Increasing evidence supports a neurobiological theory for etiology of OCD, specifically a frontal lobe--basal ganglia dysfunction.     

Memory-guided saccadic eye movements: effects of cerebellar disease

We compared the accuracy of oblique, memory-guided saccades if the eye is stationary or moves horizontally during the memory period. We studied 11 patients with cerebellar disease and 11 age-matched control subjects. Normal subjects showed similar accuracy of saccades for both conditions. In contrast, all patients showed greater errors if the eye moved horizontally during the memory period; however, errors of both vertical and horizontal components of memory-guided saccades were similar. Thus, inaccuracy of memory-guided saccades could not be simply attributed to failure to internally monitor change in horizontal gaze during the memory period. Instead, we propose that the greater saccadic errors which occurred when gaze changed during the memory period reflected a disruption of predictive mechanisms governing eye movements.     

Directional coronary atherectomy for the treatment of Palmaz-Schatz in-stent restenosis

Management of in-stent restenosis has become a significant challenge in interventional cardiology. The results of balloon angioplasty have been disappointing due to the high recurrence of restenosis at follow-up. Debulking of the restenotic tissue within the stents using directional coronary atherectomy (DCA) may offer a therapeutic advantage. We report the immediate clinical and angiographic outcomes and long-term clinical follow-up results of 45 patients (46 lesions), mean age 63+/-12 years, 73% men, with a mean reference diameter of 2.9+/-0.6 mm, treated with DCA for symptomatic Palmaz-Schatz in-stent restenosis. DCA was performed successfully in all 46 lesions and resulted in a postprocedural minimal luminal diameter of 2.7+/-0.7 mm and a residual diameter stenosis of 17+/-10%. There were no in-hospital deaths, Q-wave myocardial infarctions, or emergency coronary artery bypass surgeries. Four patients (9%) suffered a non-Q-wave myocardial infarction. Target lesion revascularization was 28.3% at a mean follow-up of 10+/-4.6 months. Kaplan-Meier event-free survival (freedom from death, myocardial infarction, and repeat target lesion revascularization) was 71.2% and 64.7% at 6 and 12 months after DCA, respectively. Thus, DCA is safe and efficacious for the treatment of Palmaz-Schatz in-stent restenosis. It results in a large postprocedural minimal luminal diameter and a low rate of both target lesion revascularization and combined major clinical events at follow-up.     

Concanavalin A modulates tyrosine phosphorylation and activation of a type II phosphatidylinositol 4-kinase in rat splenic lymphocytes

Activation of rat splenic lymphocytes by concanavalin A resulted in two-fold increase in Ptdlns 4-kinase activity and rapid tyrosine phosphorylation of the enzyme. The activation kinetics showed a strong correlation with tyrosine phosphorylation state of the enzyme. Characterization of the enzyme activity suggests that it is a type II PtdIns 4-kinase. Kinetic analysis of the enzyme reaction showed three-fold decrease in Km for PtdIns and two-fold increase in Vmax in Con A stimulated cells. These results suggest that a type II PtdIns 4-kinase is an integral component of the early signal transduction machinery during T-cell activation by concanavalin A and is actively regulated by protein tyrosine phosphorylation-dephosphorylation.     

The effect on central dopaminergic structures of various hydrazides of phosphorylated carbonic acids and diaziridines

STUDY OBJECTIVE: To describe the effectiveness of an emergency medical education program in a postwar developing country. METHODS: A prospective, nonrandomized interrupted time-series study was conducted in an emergency department at a national referral hospital in Rwanda immediately after the 1994 civil war. Participants included 11 medical personnel staffing the ED comprising physicians, nurses, and medical assistants. International medical relief workers in the ED identified deficiencies by directly observing routine clinical practices. On the basis of this assessment, formal training programs in trauma resuscitation, airway management, wound care, and blood/fluid precautions were conducted. Subjects were then observed 1 week and 2 months after the educational programs and scored on a standardized data-collection form. Scores before and after intervention were compared with the use of Fisher's exact test to determine program effectiveness. RESULTS: Educational interventions with statistically significantly longer term effects included wound management principles and blood/fluid precautions (before versus after intervention, P < .05). Interventions with the least sustained effect included advanced airway interventions and procedures related to trauma resuscitation. CONCLUSION: Educational seminars proved to have the greatest sustained effect on those behaviors requiring minimal equipment and noncomplex medical decisionmaking.     

Protein tyrosine phosphorylation activates rat splenic type II phosphatidylinositol 4-kinase in vitro

Cystatin A (acid cysteine proteinase inhibitor; ACPI) is a natural inhibitor of cysteine proteinases. It has been suggested that an inverse correlation exists between cystatin A and malignant progression. We wanted to assess the biological and clinical significance of cystatin A in infiltrative breast carcinoma by immunohistochemical staining. Formalin-fixed paraffin-embedded material from 440 cases treated during the years 1988-1991 was used in the study. After exclusion of patients with disseminated disease at diagnosis, previous contralateral breast carcinoma, and absence of follow-up data, 384 patients could be included in the survival analysis. For immunohistochemical analysis of cystatin A, we used monoclonal cystatin A antibody WR-23/2/3/3, the binding of which was detected by the avidin-biotin-peroxidase method. Immunohistochemical analysis of Bcl-2 and p53 was also done, and mitotic activity was evaluated. Positive staining for cystatin A was found in 52 of 440 cases. The staining was irregular but showed irrefutably positive areas within neoplastic tissue. Most of the positive tumors were of the ductal infiltrative type, but two were mucinous carcinomas, one medullary and one squamous cell carcinoma. No lobular carcinomas showed positive staining. Focal cystatin A positivity was seen in myoepithelial cells of benign ducts. Occasional apoptotic bodies within the neoplasm showed strong positivity for cystatin A. Tumors positive for cystatin A were of larger size and had higher mitotic activity than cystatin A-negative tumors. Cystatin A was associated with negative Bcl-2 staining, but there was no statistically significant association between axillary lymph node status or p53 immunostaining. The risk for breast cancer-related death was significantly higher in patients with cystatin A-positive tumors than in those with cystatin A-negative ones. The risk increase was significant also in lymph node-negative patients. After adjusting for the effect of tumor size, histological grade, and lymph node status, cystatin A-positive patients still had a higher risk of death. Patients with cystatin A and p53 coexpression had a higher risk of death than the other patients. The findings reveal a new variant of aggressive breast cancer. This type of carcinoma may develop during tumor progression through genetic instability that allows cystatin A expression and gives growth advantage to a clone of tumor cells.