Phenotypic Cytoskeletal Heterogeneity in Melanoma, a Challenge to the Surgical Pathologist Evaluating a Poorly Differentiated Neoplasm: An Illustrative Case

Characterization of poorly differentiated neoplasms can be a challenging task for the surgical pathologist. It is essential that the entire spectrum of immunomorphologic findings of various tumors be recognized to avoid improper characterization of a given neoplasm, which may in turn adversely affect patient management. Tumor characterization is complicated by the immunomorphologic transformations that malignant cells may undergo by virtue of which they may depart from expression of expected features and acquire new, unexpected characteristics. Traditionally, amelanotic melanomas have been difficult to characterize because of the diversity of their light microscopic morphology (epithelioid, spindle, and combined varieties). As a result, several other neoplasms are usually considered in the differential diagnosis. This report describes a primarily spindle-cell amelanotic melanoma that created a diagnostic dilemma, which could only be resolved by combining the information obtained from extensive evaluation by means of several diagnostic techniques. This case also stresses the phenotypic heterogeneity of the cytoskeleton of malignant melanomas and therefore their varied immunomorphologic characteristics.     

Epithelial cell proliferation in the rat urinary system induced by parenteral injection of lead salts.

In Wistar rats a single intravascular injection of lead nitrate causes substantial cellular proliferation in the proximal tubules of the kidneys and in the epithelium of the renal pelvis, ureters and urinary bladder. The tritiated thymidine labelling index (LI) reaches a peak 18 to 24 h after injection and the mitotic index (MI) increases to a comparable extent 6 to 10 h later. The proliferation is most prominent in the bladder and proximal tubules and is virtually complete at 48 h. After a single intraperitoneal injection the proliferative changes are confined to the ureteric and bladder epithelium. In all affected tissues the proliferation develops without preceding necrosis and appears to be a hyperplastic phenomenon. After intravascular administration the volume of urine and its total protein content are significantly increased and certain proteins were detected which were not present in the urine of saline controls.     

Seizure Disorders: The Changes With Age

Summary: Age has a profound influence on our approach to the convulsive disorders. Age is a variable which is an important determinant for risk factors for epilepsy. Age, as a surrogate of brain maturation, is a determinant of the specific characteristics of the seizure disorder in those with epilepsy, and age-related changes in these manifestations can be identified. Age is a determinant for the occurrence of acute symptomatic seizures in several types of metabolic or central nervous system insults. Age is a determinant for prognosis, whether one considers remission, medication withdrawal in those entering remission, relapse following prolonged remission, or mortality. Last, age per se seems to be a risk factor for epilepsy independent of other factors. This seems particularly true for partial seizures.     

Causes of blindness in children attending four schools for the blind in Thailand and the Philippines

Using WHO definitions of visual loss and a standardised methodology, 256 children were examined in schools for the blind in Thailand (1 school) and the Philippines (3 schools). 244 (95%) were blind (BL) or severely visually impaired (SVI). Causes of SVI and blindness were classified anatomically and aetiologically, and avoidable causes identified. Causes of visual loss in Khon Kaen, Thailand (n = 65) and Manila, Philippines, (n = 113) were similar, with conditions of the whole globe accounting for 27.7 and 27.4% of SVI/BL; retinal disease 29.2 and 23.0%; cataract 16.9 and 16.8%; corneal disease 12.3 and 13.4%; and optic nerve disease and glaucoma 6.2 and 8.8%. Perinatal factors accounted for 20.0 and 23.0% of SVI/BL; hereditary disease 13.8 and 17.7%; and 12.3 and 15.0% was due to events occurring during childhood. The underlying aetiology could not be determined in 50.8 and 41.6% of cases, respectively. In the two schools together twenty six children (15%) were blind from retinopathy of prematurity (ROP) and 16 (9%) from corneal scarring attributed to Vitamin A deficiency. 103 of 178 (58%) children had avoidable causes of visual loss. In the Filipino towns of Baguio and Davao (n = 66), the causes of visual loss were different from those in Khon Kaen and Manila, with 54.8 and 42.9% of SVI/BL being due to corneal disease, and only 3.2 and 8.5% to retinal disease. Childhood factors were more important (61.3 and 57.1%) than hereditary (9.7 and 17.1%) or perinatal factors (0 and 2.9%). Thirty one children (47%) had SVI/BL attributed to Vitamin A deficiency. No child was blind from ROP. 42 of 66 (64%) of children had avoidable causes of blindness. Overall 60% of children with SVI/BL had avoidable causes of visual loss in these 4 schools. Approximately half could have been prevented by primary health and eye care services and half could have been managed by surgical ophthalmological procedures. The causes of blindness identified in this blind school study suggest that the major causes are different for schools serving rural populations compared to those serving urban communities. Different control strategies are required for the different situations.     

Family physicians' perceptions of academic detailing: a quantitative and qualitative study

Background  

The efficacy of academic detailing in changing physicians' knowledge and practice has been the subject of many primary research publications and systematic reviews. However, there is little written about the features of academic detailing that physicians find valuable or that affect their use of it. The goal of our project was to explore family physicians' (FPs) perceptions of academic detailing and the factors that affect their use of it.     

Mutational analysis of familial and sporadic hyperekplexia

Hyperekplexia is a rare, autosomal dominant neurological disorder characterized by hypertonia, especially in infancy, and by an exaggerated startle response. This disorder is caused by mutations in the ?1 subunit of the inhibitory glycine receptor (GLRA1). We previously reported two GLRA1 point mutations detected in 4 unrelated hyperekplexia families; both mutations were at nucleotide 1192 and resulted in the replacement of Arg²⁷¹ by a glutamine (R271Q) in one case and a leucine (R271L) in the other. Here, 5 additional hyperekplexia families are shown to have the most common G-to-A transition mutation at nucleotide 1192. Haplotype analysis using polymorphisms within and close to the GLRA1 locus suggests that this mutation has arisen at least twice (and possibly four times). In 2 additional families, a third mutation is also presented that changes a tyrosine at amino acid 279 to a cysteine (Y279C). Five patients with atypical clinical features and equivocal or absent family history of hyperekplexia and 1 patient with a classical presentation but no family history are presented in whom a mutation in the GLRA1 gene was not detected. Thus, only clinically typical hyperekplexia appears to be consistently associated with GLRA1 mutations, and these affect a specific extracellular domain of the protein.     

Community psychiatry then and now: An introduction

Allen R. Dyer is Professor of Psychiatry at Albany Medical College and Professor of Health Policy and Management at the State University of New York at Albany, Albany, New York. Effective March 1, 1992, he becomes Professor and Chairman, Department of Psychiatry and Behavioral Sciences, James H. Quillen College of Medicine, East Tennessee State University.