Jean Côté

Parametrization of the deuteron wave function of the Paris NN potential

Abstract We present a convenient analytical parametrization, in both configuration and momentum spaces, of the deuteron wave-function calculated with the Paris potential.

Variability in hepatic iron concentration measurement from needle-biopsy specimens

BACKGROUND/AIM Quantitative measurement of hepatic iron by biochemical analysis of liver biopsy samples is required to assess hepatic iron stores accurately. Cirrhotic livers, however, contain variable amounts of fibrous tissue and the distribution of iron within the hepatic parenchyma is not always uniform. The aim of this study was to assess the variability in hepatic iron concentration measurement from needle-biopsy specimens. METHODS The livers from eight patients with cirrhosis selected because of elevated serum ferritin were obtained at the time of liver transplantation (n = 6) or at autopsy (n = 2). Multiple needle biopsies were done, and hepatic iron concentration was measured by atomic absorption spectroscopy. The hepatic iron index was calculated as iron concentration divided by age. RESULTS Four cases had a mean hepatic iron index above 2.0, in the range of that reported in patients with homozygous genetic hemochromatosis, whereas the other four had an hepatic iron index of less than 2.0. The intra-individual coefficient of variation for hepatic iron concentration ranged from 11.3 to 43.7%, averaging 24.9%. The coefficient of variation was smaller in biopsy samples > 4 mg dry weight than in samples < 4 mg (19.8% vs 28.6%, p < 0.05). Histological examination of surgical biopsies from these livers showed large amounts of fibrous tissue, and inhomogeneous distribution or iron in the hepatic parenchyma. CONCLUSIONS This study demonstrates an important variability in the measurement of hepatic iron content from needle biopsy specimens in patients with severe cirrhosis.

Autoimmune cholangiopathy: the result of consecutive primary biliary cirrhosis and autoimmune hepatitis?

Autoimmune cholangiopathy is a recently proposed entity that describes a specific group of patients presenting overlapping features of primary biliary cirrhosis and autoimmune hepatitis, i.e., clinical and/or biochemical cholestasis, high titer antinuclear antibody, negative antimitochondrial antibody, and elevated immunoglobulin G. Liver histology shows primary biliary cirrhosis coexisting with varying degrees of parenchymal inflammation. In addition, these patients achieve remission on corticosteroid therapy. The patient in this report fulfilled the above criteria. However, preceding the autoimmune cholangitis stage, a typical antimitochondrial antibody-positive primary biliary cirrhosis was documented with favorable response to ursodeoxycholic acid treatment. Twenty months later, the patient developed autoimmune hepatitis with elevated aspartate aminotransferase and immunoglobulin G and high titer antinuclear antibody as well as corticosteroid dependency, whereas the antimitochondrial antibody disappeared. The patients sera initially showed reactivity to three mitochondrial proteins, the 74-, 64-, and 56-kilodalton autoantigens of the 2-oxo acid dehydrogenase complexes, which was characteristic of primary biliary cirrhosis. After developing autoimmune hepatitis, reactivity to the 74- and 64-kilodalton antigens disappeared, whereas reactivity to the 56-kilodalton antigen decreased to low levels. Autoimmune cholangitis and probably other forms of the overlap syndrome may result from the association of two diseases: primary biliary cirrhosis and autoimmune hepatitis.

Interhemispheric EEG Coherence before and after Partial Callosotomy

Measures of interhemispheric EEG coherence during REM and NREM sleep reflect the functional connectivity of the right and left hemispheres mediated by the corpus callosum. Surface recordings of interhemispheric coherence in two patients reflected fairly accurately the degree of anatomical section produced by partial callosotomy. With further development, EEG coherence may prove useful as a noninvasive method for assessing interhemispheric integration under different physiological and experimental conditions.

Neurobiological characterization of an azoxymethane mouse model of acute liver failure.

Molecular biological approaches continue to lead to the identification of alterations in expression of genes coding for key central nervous system proteins involved in water homeostasis, energy metabolism and neurotransmitter regulation in acute liver failure (ALF). However, studies aimed at elucidating the pathophysiological consequences of these changes in gene expression are impeded by the lack of a suitable mouse model of ALF. A previous report described hepatic pathology characteristic of ALF resulting from the administration of azoxymethane (AOM) in mice [Matkowskyj, K.A., Marrero, J.A., Carroll, R.E., Danilkovich, A.V., Green, R.M., Benya, R.V., 1999. Azoxymethane-induced fulminant hepatic failure in C57BL/6J mice: characterization of a new animal model. Am. J. Physiol. 277, G455-G462]. In a series of experiments to further assess this treatment as an effective model of ALF, the effects of administration of AOM to male C57BL mice on hepatic and cerebral function were studied. With maintenance of body temperature at 37 degrees C and control of hypoglycemia, mice developed signs of encephalopathy (decreased locomotor activity followed by loss of righting and corneal reflexes) within 16 h of AOM treatment. AOM-treated mice were hyperammonemic, developed spontaneous hypothermia and brain edema. Brain ammonia concentrations were increased to 0.98+/-0.12 mM at coma stages of encephalopathy. Brain amino acid profiles determined by HPLC were typical of ALF in other species including humans. Mild hypothermia (35 degrees C) led to significant attenuation of brain edema, ammonia, and amino acid changes. These findings demonstrate that AOM treatment affords a simple, reproducible mouse model of ALF which may be suitable for the study of the effects of gene manipulation on the cerebral complications of ALF.

Retinoblastoma and p53 gene product expression in breast carcinoma: Immunohistochemical analysis and clinicopathologic correlation

We examined 100 breast cancers for retinoblastoma (Rb) and p53 protein expression by immunohistochemistry using the PMG3.245 and PAb 1801 antibodies. We assessed percentages of reactive cells and their intensity, as well as staining patterns. The results were correlated with neu protein reactivity and a panel of variables, including age, tumor size and type, nuclear grade, estrogen receptor/progesterone receptor content, and lymph node status. Retinoblastoma protein negativity, either partial or complete, was noted in 47% of cases. Surprisingly, a relatively stronger Rb reaction was seen in some high nuclear grade tumors. p53 positivity was found in 23% of cases and was a significant predictor of Rb loss. p53 also was correlated with poorly differentiated (nuclear grade III) neoplasms and neu expression but not with negative ER status. Tissue distribution profiles for Rb-negative and p53-positive cells were variable in this series, with both uniform and heterogeneous patterns observed. This suggests that Rb and p53 alterations may represent early or late events in transformation. Our findings further implicate Rb and p53 derangements in mammary oncogenesis.

Hartree-Fock calculations of surface-symmetry properties with finite-range forces

Abstract Complete Hartree-Fock calculations on asymmetric semi-infinite nuclear matter have been performed with a family of finite-range Gogny-type forces. For one of these forces all the computed values of the droplet-model symmetry coefficients J , L , M and Q are in good agreement with recent mass-formula fits.

A structural motif is the recognition site for a new family of bacterial protein O‐glycosyltransferases

The Escherichia coli Adhesin Involved in Diffuse Adherence (AIDA‐I) is a multifunctional protein that belongs to the family of monomeric autotransporters. This adhesin can be glycosylated by the AIDA‐associated heptosyltransferase (Aah). Glycosylation appears to be restricted to the extracellular domain of AIDA‐I, which comprises imperfect repeats of a 19‐amino‐acid consensus sequence and is predicted to form a β‐helix. Here, we show that Aah homologues can be found in many Gram‐negative bacteria, including Citrobacter rodentium. We demonstrated that an AIDA‐like protein is glycosylated in this species by the Aah homologue. We then investigated the substrate recognition mechanism of the E. coli Aah heptosyltransferase. We found that a peptide corresponding to one repeat of the 19‐amino‐acid consensus is sufficient for recognition and glycosylation by Aah. Mutagenesis studies suggested that, unexpectedly, Aah recognizes a structural motif typical of β‐helices, but not a specific sequence. In agreement with this finding, we observed that the extracellular domain of the Bordetella pertussis pertactin, a β‐helical polypeptide lacking the 19‐amino‐acid consensus sequence, could be glycosylated by Aah. Overall, our findings suggest that Aah represents the prototype of a new large family of bacterial protein O‐glycosyltransferases that modify various substrates recognized through a structural motif.

Treatment of benign breast disease with vitamin A

Twelve patients with benign breast disease (BBD) were treated with 150,000 IU of vitamin A daily taken orally. All patients were symptomatic and had measurable or evaluable breast masses. At 3 months of treatment, complete or partial responses were observed in five patients, and marked pain reduction in nine was observed. Side effects were generally mild in nature, consisting mostly of skin and mucosal changes, and were rapidly reversible upon discontinuation of the drug. Treatment was interrupted or discontinued in only two patients, and the dosage of vitamin A was reduced in one on account of toxicity. No hepatotoxicity was observed. Investigation of the chemopreventive role of either vitamin A or retinoids in patients with BBD who are at high risk of developing breast cancer is suggested.

T cell chronic lymphocytic leukemia with bullous manifestations

Among chronic lymphocytic leukemias (CLLs), the B cell variant is the most common phenotype. The T cell is rare. A variety of cutaneous manifestations have been reported with B and T cell leukemias. We report a patient who presented with a bullous eruption and who was found to have T cell CLL. Despite different therapeutic approaches, the patient died. The cutaneous histology and autopsy findings are reviewed.