Assessment of CD43 expression in adenoid cystic carcinomas, polymorphous low-grade adenocarcinomas, and monomorphic adenomas.

OBJECTIVE: Distinguishing between adenoid cystic carcinoma (ACC), polymorphous low-grade adenocarcinoma (PLGA), and monomorphic adenoma (MA) can occasionally pose a diagnostic challenge. It is of interest to identify a marker that can differentiate between these tumors. CD43 is a sialoglycoprotein that is typically expressed by hematopoietic cells and their derivative neoplasms, although positivity in epithelial tumors has been recently recognized. Our aim was to investigate CD43 immunoreactivity in ACCs, PLGAs, and MAs. STUDY DESIGN: Formalin-fixed paraffin-embedded sections from 40 salivary gland tumors (12 ACCs, 14 PLGAs, and 14 MAs) accessioned from 1989 to 2002 were retrieved from the files at the Department of Pathology, Long Island Jewish Medical Center. Immunohistochemical staining with anti-CD43 monoclonal antibody was performed. RESULTS: Cytoplasmic and membranous immunoreactivity was detected in 12/12 ACCs (100%), 1/14 PLGAs (7.1%), and 3/14 MAs (21.4%). CONCLUSIONS: CD43 appears to be preferentially expressed in salivary gland ACCs compared to PLGAs and MAs. Although the mechanism of this overexpression remains obscure at this time, our results suggest that the use of CD43 immunostaining as an adjunct to histological examination may be helpful in differentiating ACC from its mimics.     

Medical Necessity in Canadian Health Policy: Four Meanings and . . . a Funeral?

Four meanings of medical necessity have emerged, evolved, and dominated past and current health policy debates about the appropriate level of service coverage under Canada's health insurance program. To explore the shift in definition, provincial government and national health care association position papers responding to federal legislative and policy reviews of Canada's health insurance program from 1957 to 1984 were examined, as were more current reports on medical necessity. Four meanings of medical necessity predominated: "what doctors and hospitals do"; "the maximum we can afford"; "what is scientifically justified"; and "what is consistently funded across all provinces." These meanings changed with time as different stakeholder associations and governments redefined the concept of medical necessity to achieve different policy objectives for health service coverage under Canada's health insurance program.     

Hydrocarbon poisoning: a review

This article reviews the mechanisms of pulmonary injury associated with hydrocarbon poisoning. The evolution of clinical and radiographic changes is discussed, along with appropriate treatment. Preventing aspiration in the emergency department is the most effective therapy for these children in the first few hours after ingestion.     

Chylous Ascites Caused by Constrictive Pericarditis

Chylous ascites is an uncommon clinical entity associated with lymphatic obstruction usually caused by underlying malignancy. The authors describe a patient with chylous ascites caused by constrictive pericarditis in the absence of mechanical lymphatic obstruction. Pathophysiological mechanisms for the development of chylous ascites in constrictive pericarditis include augmented lymph production and high impedance to lymph drainage caused by central venous hypertension. After pericardiectomy, the patient's ascites and edema resolved. Constrictive pericarditis should be considered a rare but potentially curable cause of chylous ascites.     

Surface treatment of indirect resin composite surfaces before cementation

Statement of problem. Controversy surrounds the use of hydrofluoric acid to prepare precementation surfaces of indirect composites.Purpose. This study was conducted to compare effects of combining hydrofluoric or orthophosphoric acid with microetching as precementation treatments.Material and methods. Nine specimens of three composite materials were prepared to simulate heat-cured indirect restorations. The specimen surfaces were prepared with one of three treatments. Adhesive Bond II and Twinlook cements were used to bond a phosphoric acid-etched disk of P50 to the treated surface. Analysis of variance and Scheffé tests were used to assess the bond strength data. Scanning electron microscopy and microscopic analysis of the fractured and treated surfaces were also performed.Results. Bond strengths for all surface treatments did not significantly differ. Hybrids had a higher bond strength with etching than microfills, and mechanical roughening produced the greatest bond strengths with microfills. Microetching with orthophosphoric acid produced higher bond strengths than microetching with hydrofluoric acid on hybrids.Conclusions. Acid etching alone is not sufficient to produce effective bond strengths, and hydrofluoric acid treatments are detrimental to the resin composite. (J Prosthet Dent 1997;77:568-72.)     

Disease associations and altered immune function in CD45 138G variant carriers

The CD45 antigen is a haemopoietic cell specific tyrosine phosphatase essential for antigen receptor mediated signalling in lymphocytes. Expression of different patterns of alternatively spliced CD45 isoforms is associated with distinct functions. We recently identified a polymorphism in exon 6 (A138G) of the gene encoding CD45 (PTPRC) that results in altered CD45 splicing. The 138G allele is present at a high frequency among Japanese (23.7%), with 5.1% individuals homozygous for the G allele. In this study we show that the A138G polymorphism is the cause of altered CD45 isoform expression, promoting splicing towards low molecular weight CD45 isoforms. We further report that the frequency of A138G heterozygotes is significantly reduced in number in cohorts of patients with autoimmune Graves' disease or hepatitis B infection, whereas G138G homozygotes are absent from a cohort of Hashimoto's thyroiditis patients. We also show that 138G individuals exhibit altered cytokine production in vitro and an increased proportion of memory T cells. These data suggest that the 138G variant allele strongly influences these diseases by modulation of immune mechanisms and may have achieved its high frequency as a result of a natural selection probably related to pathogen resistance.     

Dosage compensation, the origin and the afterlife of sex chromosomes

Over the past 100 years Drosophila has been developed into an outstanding model system for the study of evolutionary processes. A fascinating aspect of evolution is the differentiation of sex chromosomes. Organisms with highly differentiated sex chromosomes, such as the mammalian X and Y, must compensate for the imbalance in gene dosage that this creates. The need to adjust the expression of sex-linked genes is a potent force driving the rise of regulatory mechanisms that act on an entire chromosome. This review will contrast the process of dosage compensation in Drosophila with the divergent strategies adopted by other model organisms. While the machinery of sex chromosome compensation is different in each instance, all share the ability to direct chromatin modifications to an entire chromosome. This review will also explore the idea that chromosome-targeting systems are sometimes adapted for other purposes. This appears the likely source of a chromosome-wide targeting system displayed by the Drosophila fourth chromosome.     

A severe form of amyloidotic polyneuropathy in a Costa Rican family with a rare transthyretin mutation (Glu54Lys)

Four affected siblings in a Costa Rican family presented an aggressive polyneuropathy with widespread involvement of many visceral organs and onset during the third decade of life with rapid loss of muscle mass in the lower limbs and severe dysautonomy. The medical histories include vitreous opacity, cardiac enlargement, dermal and gastrointestinal infiltration, and autonomic dysfunction including circulatory compromise and gastrointestinal disturbances. Histological studies using Congo red stain and immunohistochemical assays with antibodies against the transthyretin (TTR) protein showed widespread deposition of amyloid in extracellular areas, including dermis and gastrointestinal lamina propia, endo- and perineural spaces, and vascular walls. A mutation search in the transthyretin (ttr) gene was performed seeking the cause of this severe form of familial amyloidotic polyneuropathy (FAP). We applied single-stranded conformational polymorphism (SSCP)-analyses followed by sequencing of the four exons of the ttr gene, revealing a point mutation in exon 3, a G to A transition that causes a Glu54Lys codon change. Western blots of plasma proteins incubated with anti-transthyretin antibodies after gel electrophoresis provided separation of wild-type and mutant TTR protein in affected family members.