Cholecystectomy by celioscopy. Experience in two Upper Normandy hospital units. Apropos of 178 procedures]

Laparoscopic cholecystectomy (LC) emerges as an effective alternative to classical cholecystectomy, but its safety, benefits and indications still need to be clarified. From September 1989 to March 1991, 178 LC were performed by 8 surgeons in 2 hospitals, on 142 women and 36 men with a mean age of 48.2 years. The gall bladder wall was thin in 160 cases and thick in 18 cases (with 6 cases acute cholecystitis). We observed no deaths, 147 simple procedures with a hospital stay and drug requirement lower than with the usual cholecystectomy via laparotomy. But in 21 cases, the procedure needed a laparotomy, and in 10 cases complications occurred, requiring laparotomy in 6 cases. Our results suggest: a) LC is an improvement in the treatment of uncomplicated gallstones; b) a trained surgeon and extreme caution are required in complicated cholelithiasis; c) classical cholecystectomy is still useful in many circumstances.     

Human African trypanosomiasis: MRI

We report a case of human African trypanosomiasis caused by Trypanosoma brucei rhodesiense. After the febrile period of parasite dissemination, the patient had meningeal involvement but normal CT. MRI showed the appearances of meningitis. After two periods of arsenical treatment, a severe encephalopathy occurred suggesting post-therapeutic reactive encephalitis (PTRE). Nevertheless, T2-weighted MRI showed no oedema, but focal bilateral high signal areas in the white matter. PTRE was excluded and a third course of treatment was undertaken. The lesions progressively disappeared. Received: 3 September 1996 Accepted: 30 January 1997     

Conception of a decompression table

After a given time at bottom, different tissues become saturated to different extents with nitrogen. In diving back to the surface a hydrostatic decompression occurs first, followed by the desaturation process some time later. It is during this time interval that all important events are taking place, namely: either a monophasic desaturation, whereby inert nitrogen gas is given off at the alveolar capillary interface. or a biphasic desaturation takes place, giving rise to gas bubbles in the blood-stream as well as in the tissues. We may then encounter pathologies which are benign incidents or, worse, lead to decompression sickness grade II. Since Paul Bert dedicated his thoughts in 1878 to this problem, numerous authors tried to explain this time delay, for trying to suppress it would be entirely unrealistic. Unfortunately, mathematical reasoning has too often overshadowed physiological thinking in these matters. We also stuck to Haldane's concept of 1908, in incorporating Workman's improvements of 1965. This method is based on two main principles: 1. all calculations were done with several "tissues" in mind. Their anatomical boundaries are of no importance as, only their desaturation half-times are relevant. 2. a natural limit is given by the critical saturation-coefficient (CS). It expresses the ratio between the partial pressure of the dissolved gas and the reduction of hydrostatic pressure during ascent (given as pressure gradient). Through experience we were able to put up tables which were more and more safe, in examining foremost the CS ratio and the desaturation times of certain tissues. Several examples are given, the values of which are statistically highly significant, as they incorporate the results of more than 60,000 air dives.     

Screening for proteins with polyglutamine expansions in autosomal dominant cerebellar ataxias

Expansion of trinucleotide CAG repeats coding for polyglutamine has been implicated in five neurodegenerative disorders, including spinocerebellar ataxia (SCA) 1 and SCA3 or Machado-Joseph disease (SCA3/MJD), two forms of type I autosomal dominant cerebellar ataxias (ADCA). Using the 1C2 antibody which specifically recognizes large polyglutamine tracts, particularly those that are expanded, we recently reported the detection of proteins with pathological glutamine expansions in lymphoblasts from another form of ADCA type I, SCA2, as well as from patients presenting with the distinct phenotype of ADCA type II. We now have screened a large series of patients with ADCA or isolated cases with cerebellar ataxia, for the presence of proteins with polyglutamine expansions. A 150 kDa SCA2 protein was detected in 16 out of 40 families with ADCA type I. This corresponds to 24% of all ADCA type I families, which is much more frequent than SCA1 in this series of patients (13%). The signal intensity of the SCA2 protein was negatively correlated to age at onset, as expected for an expanded and unstable trinucleotide repeat mutation. The disease segregated with markers closely linked to the SCA2 locus in all identified SCA2 families. In addition, a specific 130 kDa protein, which segregated with the disease, was detected in lymphoblasts of patients from nine families with ADCA type II. It was also visualized in the cerebral cortex of one of the patients, demonstrating its translation in the nervous system. Finally, no new disease-related proteins containing expanded polyglutamine tracts could be detected in lymphoblasts from the remaining patients with ADCA or isolated cases with cerebellar ataxia.      

Detection of Antiendothelial Cell Antibodies by an Enzyme-Linked Immunosorbent Assay Using Antigens from Cell Lysate: Minimal Interference with Antinuclear Antibodies and Rheumatoid Factors

The objective of the present work was to set up a routine test adapted to screening for antiendothelial cell antibodies (AECAs) in serum samples with minimal interference from antinuclear antibodies (ANAs) or rheumatoid factors (RFs). We compared the titers of AECAs titrated following two enzyme-linked immunosorbent assays (ELISAs): (i) an ELISA with ethanol-fixed EA.hy926 monolayers as the antigenic substrate and (ii) an ELISA with nucleus-depleted lysates prepared from EA.hy926 cells and normalized for protein (1.0 to 1.7 mg/ml) and DNA (≤0.1 μg/ml) contents as a surrogate substrate (postnuclear supernatant ELISA [PNS-ELISA]). The AECA titers in 51 serum samples, including 28 samples containing ANAs, were compared. A significantly positive correlation (r = 0.77; P < 0.001) between the two series was shown only for the ANA-negative serum samples. Conversely, ANAs or RFs in samples were shown not to interfere in tests for AECAs by the PNS-ELISA. AECAs recognize their antigenic targets in postnuclear supernatants, which is representative of the endothelial antigenic content, with improvement of the reliability of the assay, a prerequisite to application of the assay for their evaluation in clinical practice.     

Saccharomyces boulardii interferes with enterohemorrhagic Escherichia coli-induced signaling pathways in T84 cells

Enterohemorrhagic Escherichia coli (EHEC) infections are associated with the modification of tight-junction permeability and synthesis of proinflammatory cytokine interleukin-8 (IL-8). In a previous study, it was demonstrated that EHEC-induced IL-8 secretion is due to the involvement of the mitogen-activated protein kinase (MAPK), AP-1, and NF-kappaB pathways. In this study, we investigated the effect of the yeast Saccharomyces boulardii on EHEC infection in T84 cells. For this purpose, cells were (i) incubated with bacteria and yeast at the same time or (ii) incubated overnight with yeast cells that were maintained during infection or eliminated by several washes before infection. Coincubation is sufficient to maintain the transmonolayer electrical resistance (TER) of EHEC-infected cells, whereas the preincubation of cells with the yeast without elimination of the yeast during infection is necessary to significantly decrease IL-8 secretion. We thus analyzed the mechanisms of S. boulardii action. We showed that S. boulardii has no effect on EHEC growth or on EHEC adhesion. Kinetics studies revealed that EHEC-induced myosin light chain (MLC) phosphorylation precedes the decrease of TER. ML-7, an MLC kinase inhibitor, abolishes the EHEC-induced MLC phosphorylation and decrease of TER. Studies show that S. boulardii also abolishes EHEC-induced MLC phosphorylation. We demonstrated that the preincubation of cells with S. boulardii without washes before EHEC infection inhibits NF-kappaB DNA binding activity, phosphorylation and degradation of IkappaB-alpha, and activation of the three members of a MAPK group (extracellular signal-regulated protein kinases 1 and 2, p38, and c-jun N-terminal kinase). These findings demonstrate that S. boulardii exerts a preventive effect on EHEC infection by (i) interfering with one of the transduction pathways implicated in the control of tight-junction structure and (ii) decreasing IL-8 proinflammatory secretion via inhibition of the NF-kappaB and MAPK signaling pathways in infected T84 cells.     

Simian virus 40 T antigen is detected only in cells in the G2 phase of the cell cycle in one group of rat transformants

The relationship between the cell cycle and the presence of the nuclear T antigen in simian virus 40-transformed rat cells independently derived from FR 3T3 cells has been investigated using a fluorescence-activated cell sorter and a combination of stainings for cellular DNA (4',6-diamidine-2-phenylindole dihydrochloride, DAPI) and for the viral T antigen (fluorescein-labeled IgG). Such an analysis revealed that in three out of six lines, T antigen could be detected only in the G2 phase of the cell cycle. In the other three lines, the accumulation of T antigen appeared to be independent of the position of the cell in the cycle. The emergence of either phenotype was strictly correlated with the physiological state of the cell (growing versus resting, respectively) at the time the transformants were established.     

Myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML) with myelofibrosis.

Acute myeloid leukemias (AML) and myelodysplastic syndromes (MDS) enter rarely in the differential diagnosis of myelofibrosis (MF). MF of marked intensity, resulting in either "dry taps" or non-representative smears, is encountered in approximately 10% of cases. MF may be observed in any type of AML, most frequently in acute megakaryoblastic leukemia (M7). Apart from some typical cases of MDS, MF is associated with cases of acute myelodysplasia with myelofibrosis (and a major megakaryocytic component). This syndrome has been described under various headings: acute or malignant myelosclerosis, and acute MF. It should be distinguished from M7 and from myeloproliferative syndromes.