Variation in the histological pattern of nodal involvement by gamma/delta T-cell lymphoma

AIMS: Gamma-delta (gammadelta) T-cell non-Hodgkin's lymphomas (NHLs) usually present with liver, spleen and marrow infiltration. Lymph node involvement by gammadelta T-cell NHL has been rarely documented so far; its histological pattern needs to be further defined. METHODS AND RESULTS: Two cases of nodal gammadelta T-cell NHL are reported: case 1, a 44-year-old man, presented with cytomegalovirus retinitis and superficial lymphadenopathies. Histological analysis of an inguinal lymph node showed complete destruction by a diffuse pleomorphic lymphoid proliferation, which was positive for CD2, CD3, CD43, CD45, TIA-1 and granzyme B, and displayed a gammadelta phenotype (deltaTCR1+, Vdelta1+, Vdelta2-, Vdelta3-, betaF1-). Bone marrow was normal. Case 2, a male 24-year-old patient with a history of renal transplantation, presented with hepatosplenomegaly and supraclavicular lymph node enlargement. Lymph node architecture was globally preserved. Peripheral sinuses contained scattered nests of medium-sized irregular lymphoid cells. Bone-marrow was infiltrated. Phenotype showed positivity for CD2, CD3, CD45 and TIA1 and expression of gammadelta TCR (deltaTCR1+, deltaV1+, deltaV2-, deltaV3-, betaF1-). Both patients died a short time after diagnosis. CONCLUSIONS: These observations suggest that at least two forms of nodal gammadelta T-cell NHL may be encountered: one mimicking classical alphabeta T-cell NHL, with diffuse pleomorphic cell proliferation, and one displaying sinusoidal neoplastic infiltration suggesting a close relationship with hepatosplenic gammadelta T-cell NHL.     

Association analysis of a polymorphism in the G‐protein stimulatory α subunit in patients with major depression*

Growing evidence suggests that G‐proteins may be involved in pathogenesis and treatment of affective disorders. Several studies have reported altered levels and/or activities of stimulatory G‐proteins in depression. The aim of this study was to investigate whether a polymorphism in the stimulatory α subunit of G‐proteins (T/C point mutation in exon 5; ATT → ATC at codon 131) is associated with major depression or response to antidepressant treatment. Therefore, we performed a case‐control association study with 212 depressive patients and 137 healthy, unrelated controls. There was no evidence for an association between the investigated polymorphism in the Gα_s gene and major depression, as well as to treatment response. The results of our study are in concordance with recently published findings which do not support the hypothesis that the gene for the stimulatory α subunit of G‐proteins is a major susceptibility factor in the pathophysiology of major depression. © 2002 Wiley‐Liss, Inc.     

Multiple sclerosis: cell-mediated immunity to human brain gangliosides

Cell-mediated immunity (CMI) to myelin components has been implicated in Multiple Sclerosis (MS) pathogenesis: two targets were suggested, Myelin Basic Protein with controversial results and, more recently, gangliosides. In order to investigate their possible involvement, we have performed Leukocyte Migration inhibition (LMI) tests in the presence of human brain gangliosides. Thirty nine MS patients (twenty four being "definite", according to McDonald and Halliday's classification), twenty nine patients with Other Neurological Diseases (OND), thirty six patients with Inflammatory diseases (ID) and forty healthy controls were tested. MS patients were divided into two groups, depending on the clinical stage of the disease. The mean migration inhibition percentage of the MS-attack group was found to be significantly different from the four others (p less than 0.01) (24.4 +/- 16.2 versus 10.9 +/- 8.5 in MS without attack, 4.4 +/- 12.9 in OND, 3.9 +/- 13.9 in ID and 11.1 +/- 12.1 in healthy subjects). LMI to gangliosides is therefore significantly increased during the attack stage in MS. These results support the notion of a Delayed Type Hypersensitivity to these glycolipids during the active stage of the disease.     

Polysilanes fonctionnels, 3. Synthèse d'α,ω-bis(triméthylsilyl)oligo(méthylphénylsilane)s précurseurs des α,ω-bis(triméthylsilyl)oligo(chlorométhyl-silane)s. Charactérisation des heptaméthyl phényl-2 trisilane et octaméthyl diphényl-2,3 tétrasilane

Low-molecular-weight organosilane polymers were prepared by sodium coupling of dichloro-methylphenylsilane ( 1 ) with chlorotrimethylsilane ( 2 ). Gel permeation chromatography (GPC), IR and NMR (¹H, ¹³C and ²⁹Si) analysis of the crude product ( 3 ) were performed and compared with those of the isolated first oligomers, trisilane ( 3a ) and tetrasilane ( 3b ). The GPC characteristics, especially high resolution ones, in accordance with the α,ω-bis(trimethylsilyl)-oligo(methylphenylsilane) structure are compared with those of hydrocarbon polymers. The relations of the NMR characteristics of the methylphenylsilanediyl unit with the position along the chain and the configuration of the diads are approached. Some spectroscopic indications of the secondary structure are discussed.     

Genomic and proteinic characterization of strain S, a rickettsia isolated from Rhipicephalus sanguineus ticks in Armenia.

Strain S, a spotted fever group (SFG) rickettsia isolated from Rhipicephalus sanguineus ticks collected in Armenia, was identified. Microimmunofluorescence, sodium dodecyl sulfate-polyacrylamide gel protein electrophoresis and Western immunoblotting, PCR and then restriction fragment length polymorphism analysis, pulsed-field gel electrophoresis, and 16S rRNA gene sequencing were used to compare strain S with reference isolates. Strain S was found to possess proteinic, antigenic, and genomic patterns which were unique among SFG rickettsiae. Strain S is characterized by its high degree of pathogenicity for experimental animals, but its role as a potential human pathogen should be determined. The role of R. sanguineus ticks in the epidemiology of SFG rickettsiae is discussed.     

An increase in the number of recombinant molecules and other effects of the simultaneous allotype suppression of trans-chromosomal a VH and n Cmu Ig gene products

The concomitant effects of trans-chromosomal allotype suppression of both an a VH and an n Cmu locus allotype in multiheterozygous rabbits were investigated. For example of the expression of the a2 VH and n81 Cmu allotypes were suppressed in a multiheterozygous rabbit having the a1 chi-y-n81de12,15f73g74/a2 chi 32y33n80de12.14f69g77 genotype. This trans-chromosomal allotype suppression led to the concomitant suppression of other CH allotypes in the same parental haplotype as the suppressed-n81 allotype (i.e. the e15, f73 and g74 allotype) and the partial suppression of the a1 VH allotype (from the normal level of 70% of the total Ig to 10%), and also led to compensation by other VH allotypes from the same parental haplotype as the suppressed-a2 allotype (i.e. the x32 and y33 allotypes). The x32 and y33 allotypes were expressed on Ig molecules with the CH allotypes coded by the same haplotype (i.e. the cis molecules). In a further analysis of the IgG molecules having the partially-suppressed-a1 allotype, one-half (5%) of these molecules were trans-chromosomal recombinant molecules (i.e. a1e14 IgG) and the other half (5%) were cis-chromosomal molecules (i.e. a1e15 IgG). The trans-chromosomal a1e14 IgG molecules probably were derived from the expansion of a limited number of lymphoid clones that normally produce only 1.5% trans-chromosomal recombinant molecules. The cis-chromosomal a1e15 IgG molecules were probably derived either from lymphoid clones that survived the suppression by the anti-n81 Ab, or from lymphoid clones that bore a different subclass of IgM (i.e. n-negative IgM).