Hemorrhagic and nonhemorrhagic brain lesions: evaluation with 0.35-T fast MR imaging

Two fast magnetic resonance (MR) imaging techniques, advanced Fourier and partial-flip imaging, were used at 0.35 T to examine 21 patients with suspected intracranial lesions; the results were quantitatively compared with a conventional spin-echo study. Both of the fast MR techniques yielded a fourfold reduction in imaging time per section. The advanced Fourier sequence showed contrast that was identical to the conventional spin-echo study with signal-to-noise ratios of 58% and 57% for the first and second echoes, respectively. The partial-flip sequence showed a contrast of 109% and 57% for lesions versus substantia alba, and 107% and 78% for substantia grisea versus substantia alba relative to the first and second echoes of the conventional spin-echo study. The partial-flip sequence was particularly sensitive to magnetic susceptibility; this produced artifacts that may undermine the usefulness of partial flip for routine screening in certain parts of the brain. However, this susceptibility significantly improved the detection of intracranial hemorrhage when compared with the spin-echo sequence, particularly when combined with phase mapping of the partial-flip study.     

Malignant oncocytoma of the maxillary sinus— An ultrastructural study

A unique case of a malignant oncocytoma of the maxillary sinus is reviewed in detail. The ultrastructural findings are presented. The histologic and ultrastructural criteria that characterize onco-cytes and the clinicopathologic features of benign and malignant oncocytomas are discussed. This case represents the eleventh reported case that would truly qualify as a malignant oncocytoma of the paranasal sinuses.     

HLA polymorphisms in Nigerians

The HLA class I and class II phenotypes of a panel of 114 unrelated Nigerians have been determined. The panel was tested for all the known class I antigens and comparisons of the HLA-A and -B frequencies with those of other African Negroid populations revealed some differences. Only limited comparisons could be made for the HLA-DR and -D frequencies as these are not available for any well-defined African Negroid population. The data concerning the class II antigens of this panel are the most interesting. Half of the DRw11-positive panel members are DQw3 negative and DQw1 positive. In addition, there is dissociation of some HLA-D and -DR specificities, a number of panel members are positive for an HLA-D specificity and are negative for the corresponding HLA-DR specificity. Our results show the value of population studies in the investigation of the relationship between the different HLA class II antigens.     

Missense mutation in a von Willebrand factor type A domain of the alpha 3(VI) collagen gene (COL6A3) in a family with Bethlem myopathy

The Bethlem myopathy is a rare autosomal dominant proximal myopathy characterized by early childhood onset and joint contractures. Evidence for linkage and genetic heterogeneity has been established, with the majority of families linked to 21q22.3 and one large family linked to 2q37, implicating the three type VI collagen subunit genes, COL6A1 (chromosome 21), COL6A2 (chromosome 21) and COL6A3 (chromosome 2) as candidate genes. Mutations of the invariant glycine residues in the triple-helical domain-coding region of COL6A1 and COL6A2 have been reported previously in the chromosome 21-linked families. We report here the identification of a G-->A mutation in the N-terminal globular domain-coding region of COL6A3 in a large American pedigree (19 affected, 12 unaffected), leading to the substitution of glycine by glutamic acid in the N2 motif, which is homologous to the type A domains of the von Willebrand factor. This mutation segregated to all affected family members, to no unaffected family members, and was not identified in 338 unrelated Caucasian control chromosomes. Thus mutations in either the triple-helical domain or the globular domain of type VI collagen appear to cause Bethlem myopathy.      

Pathogenesis of infectious bursal disease in embryonally bursectomised chickens

Embryonally bursectomised and nonbursectomised chickens were infected with infectious bursal disease virus (IBDV) at 36 days of age. Neither clinical signs nor gross lesions were observed in the infected, bursectomised (IB) chickens. No significant changes were observed in carcass, thymus or spleen weights of IB and noninfected bursectomised chickens. A mild lymphocytic necrosis and depletion were found in the spleen, thymus and caecal tonsil of the IB chickens. Neither precipitating nor serum neutralising antibodies were detected in the sera but IBDV was reisolated from the spleen and thymus. Infected, nonbursectomised (IN) chickens developed severe depression with diarrhoea and high mortalities. Haemorrhages were found in the muscles of the breast and thigh, proventriculus and intestines. Significant changes were observed between the carcass, thymus and bursa weights of the IN and noninfected, nonbursectomised chickens. There was severe lymphatic necrosis of the bursa, thymus, spleen and caecal tonsil. Both precipitating and neutralising antibodies were detected in the sera and the virus was reisolated from the bursa, thymus and spleen. It is concluded that the bursa of Fabricius is not essential for the establishment of an IBDV infection but is required for the clinical infection.     

Beckman EL-ISE电解质分析仪准确性及故障的分析判断

0 引言为了克服离子选择电极（ISE）法的微量电位信号极易受环境温度变化及电子噪声的干扰问题,该仪器采用了参考电极,把参考电极与其测定电极装在同一测量室内,保持其相同的物理环境,使干扰源对所有电极的影响相同. 以内参液作为参考电极的测量对象,测得一个参考电极电位值,再测样品的电极电位值,二者相抵就消除了所叠加的干扰信号.     

Rapamycin limits CD4+ T cell proliferation in simian immunodeficiency virus–infected rhesus macaques on antiretroviral therapy

Proliferation of latently infected CD4⁺ T cells with replication-competent proviruses is an important mechanism contributing to HIV persistence during antiretroviral therapy (ART). One approach to targeting this latent cell expansion is to inhibit mTOR, a regulatory kinase involved with cell growth, metabolism, and proliferation. Here, we determined the effects of chronic mTOR inhibition with rapamycin with or without T cell activation in SIV-infected rhesus macaques (RMs) on ART. Rapamycin perturbed the expression of multiple genes and signaling pathways important for cellular proliferation and substantially decreased the frequency of proliferating CD4⁺ memory T cells (TM cells) in blood and tissues. However, levels of cell-associated SIV DNA and SIV RNA were not markedly different between rapamycin-treated RMs and controls during ART. T cell activation with an anti-CD3LALA antibody induced increases in SIV RNA in plasma of RMs on rapamycin, consistent with SIV production. However, upon ART cessation, both rapamycin and CD3LALA–treated and control-treated RMs rebounded in less than 12 days, with no difference in the time to viral rebound or post-ART viral load set points. These results indicate that, while rapamycin can decrease the proliferation of CD4⁺ TM cells, chronic mTOR inhibition alone or in combination with T cell activation was not sufficient to disrupt the stability of the SIV reservoir.