Peripheral T-cell lymphoma presenting as a soft-tissue mass of the extremity

An 87-year-old man was found to have a lymphoma in the deep soft tissue of the right shoulder with concomitant central nervous system involvement. There was no evidence of cutaneous, peripheral lymph node, mediastinal, abdominal, or bone marrow involvement. Light microscopic, ultrastructural, and immunohistochemical evaluation characterized the neoplasm as a peripheral T-cell lymphoma. Lymphomas presenting in soft tissue are rare, and the few well-documented cases in the literature are of B-cell origin. We report a T-cell lymphoma presenting in the soft tissue of the extremity, and delineate its clinicopathologic features.     

Immunological clearance of 75Se-labelled Trypanosoma brucei in mice. III. Studies in animals with acute infections.

Using trypanosomes labelled with [75Se]-methionine a series of experiments was conducted to investigate antibody production in mice with acute fulminating T. brucei infections. As measured by the hepatic uptake of radiolabelled parasites, we were unable to demonstrate any evidence of antibody-mediated uptake by the liver in such mice. It was concluded that this was not due to impaired macrophage function but was caused by the inability of antibody production to cope with the massive parasitaemias produced by rapidly-replicating infections so that effective opsonization of the parasites did not occur. In contrast, a train of trypanosome which causes a more chronic infection, although initially having a similar replication, although initially having a similar replication rate, subsequently switched t a slower one and thereby allowed antibody to reach levels which permitted effective opsonization. There was no evidence that the parasite caused any significant suppression of antibody responses in these acute infections since inoculation with trypanosomes of one stock at the same time as vaccination with irradiated organisms of a second stock did not prevent the development of antibody to the latter, as measured by the hepatic uptake of radiolabelled parasites.     

Effect of errors in the sequence of optical densities from the Roche AMPLICOR HIV-1 MONITOR assay on the validity of assay results

Specifications for the AMPLICOR HIV-1 MONITOR kit indicate that the results are invalid if the optical densities (ODs) from the PCR-amplified sample that are between 0.1 and 2.3 units are out of sequence. However, among 11,904 assays, results were biased only when ODs of 0.2 to 2.0 units were out of sequence, reducing the rate of invalid results from 3.2 to 0.59%.     

Laboratory infection of the mosquito,Toxorhynchites brevipalpis (Diptera,Culicidae), with bluetongue virus

Summary The use ofToxorhynchites brevipalpis as a system for the propagation and isolation of bluetongue virus (BTV) was investigated.BTV was found to multiply inT. brevipalpis after infection by intrathoracic inoculation. Virus concentrations of up to 6.9 log₁₀ TCID₅₀ per mosquito were found within 7 days of infection and were maintained for at least 6 days. Virus could be detected by an indirect fluorescent antibody test applied to head and thorax tissue smears. These results are comparable to those obtained after inoculation ofCulicoides variipennis with the same virus.Comparison ofT. brevipalpis and baby hamster kidney (BHK) cells as systems for isolation of BTV showed that there was little difference in sensitivity between the two systems for the stock BTV used. Field samples were not available for test. It was concluded that the use ofT. brevipalpis as an isolation system for BTV would have no apparent advantage if BHK cells were available.With 1 Figure     

Analysis of the roles of bluetongue virus outer capsid proteins VP2 and VP5 in determination of virus serotype

Analyses of reassortant and parental strains of BTV serotypes 3 and 10, in serum neutralization tests, confirmed the major role of outer capsid protein VP2 in determination of virus serotype and its involvement in serum neutralization. However, a reassortant BTV strain (R70), containing protein VP5 derived from BTV 3 and VP2 derived from BTV 10, cross-neutralized with both parental virus strains (BTV 3 and BTV 10). It is concluded that VP5 also plays some part in serotype determination of these virus isolates, as analyzed by serum-neutralization, but its role may be less significant than that of VP2.     

On the Shift from Anticipatory Heart Rate Deceleration to Acceleratory Recovery: Revisiting the Role of Response Factors

The influence of inducing motor responses of low and high force at different times in the cardiac cycle was examined. A handgrip response was used which allowed the separation of response initiation from response completion. Based on earlier work, we expected initiation, rather than completion, to initiate poststimulus cardiac acceleration. We also thought that preparation for a high force response might alter preparatory changes of interbeat interval differently from preparation for a low force response. Fifteen college-aged male subjects performed a warned reaction time task in which a visual stimulus signalled a handgrip requiring either a high or a low force to close. NoGo trials in which an inhibit signal was presented occurred on 12% of the trials. Stimuli occurred either on the R-wave of the electrocardiogram or 300 ms later. Reaction speed was varied in different trial blocks by rewarding response times of 200 ms (+/- 50 ms), 300 ms, or 400 ms. Results based on the timing of response initiation were essentially identical to those based on the timing of response completion. High force relative to low force was associated with both earlier response initiation and earlier cardiac acceleration. Force did not alter preparatory cardiac deceleration. Force and response speed did, however, alter the level of heart rate after response occurrence. Thus, response initiation (or an earlier response process) appears to induce a cardiac acceleration whose level is influenced by the speed and force of the motor response.     

The mouse Mid1 gene: implications for the pathogenesis of Opitz syndrome and the evolution of the mammalian pseudoautosomal region

We have recently reported isolation of the gene responsible for X- linked Opitz G/BBB syndrome, a defect of midline development. MID1 is located on the distal short arm of the human X chromosome (Xp22. 3) and encodes a novel member of the B box family of zinc finger proteins. We have now cloned the murine homolog of MID1 and performed preliminary expression studies during development. Mid1 expression in undifferentiated cells in the central nervous, gastrointestinal and urogenital systems suggests that abnormal cell proliferation may underlie the defect in midline development characteristic of Opitz syndrome. We have also found that Mid1 is located within the mouse pseudoautosomal region (PAR) in Mus musculus , while it seems to be X- specific in Mus spretus. Therefore, Mid1 is likely to be a recent acquisition of the M. musculus PAR. Genetic and FISH analyses also demonstrated a high frequency of unequal crossovers in the murine PAR, creating spontaneous deletion/duplication events involving Mid1. These data provide evidence for the first time that genetic instability of the PAR may affect functionally important genes. In addition, we show that MID1 is the first example of a gene subject to X-inactivation in man while escaping it in mouse. These data contribute to a better understanding of the molecular content and evolution of the rodent PAR.      

Determination of the parent of origin in nine cases of prenatally detected chromosome aberrations found after intracytoplasmic sperm injection

Prenatal cytogenetic analysis of 71 fetuses conceived by intracytoplasmic sperm injection (ICSI) resulted in the detection of nine (12.7%) chromosome aberrations including two cases of 47,XXY, four cases involving a 45,X cell line and three autosomal trisomies. Molecular analysis of the parental origin of the deleted or supernumerary chromosome was performed by using polymorphic microsatellite markers. Six cases involving a sex chromosome abnormality were found to be of paternal origin while the two trisomic cases that could be analysed were of maternal origin. Two cases involved the same infertile couple who had two consecutive ICSI pregnancies terminated because of a chromosome abnormality. The replaced embryos in both cases originated from a single batch of ICSI fertilized oocytes of which part was used to initiate the first pregnancy and part was cryopreserved and used to initiate the second pregnancy.