Lipoprotein(a) concentrations in Mexican Americans and non-Hispanic whites: the San Antonio Heart Study.

There is considerable evidence that lipoprotein(a) (Lp(a)) is a strong independent risk factor for coronary heart disease. Based on their risk factor profile, Mexican Americans have an increased risk of coronary heart disease, yet Mexican Americans have coronary heart disease mortality similar to or lower than that of non-Hispanic whites. The authors therefore attempted to determine whether Mexican Americans had decreased Lp(a) concentrations relative to non-Hispanic whites in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Lp(a) concentrations (mg/dl) were significantly lower in Mexican Americans (n = 316) than in non-Hispanic whites (n = 242) (men: 10.4 vs. 16.3; women: 11.5 vs. 16.4). In addition, the proportion of persons with Lp(a) concentrations of > or = 30 mg/dl (the threshold at which increased risk of coronary heart disease is believed to occur) was significantly higher in non-Hispanic whites than in Mexican Americans (18.6% vs. 7.6%; Mantel-Haenszel odds ratio (adjusted for sex) = 2.79). Age, obesity, body fat distribution, cigarette smoking, alcohol consumption, and glucose and insulin concentrations were not significantly related to Lp(a) levels. Decreased Lp(a) concentrations may account in part for Mexican Americans' relative protection from coronary heart disease mortality.     

Role of technetium-99m planar bone scanning in the evaluation of low back pain

The records of 1018 patients with low back pain in a tertiary spine referral practice were reviewed. One hundred thirty-nine out of 1018 (13.6%) underwent technetium-99m planar bone scanning as part of their investigation. Seventy-three out of 139 scans (52%) showed increased uptake in some area, but only 27 out of 139 (19.4%) showed increased uptake specifically in the low back. Scans consistently yielded no findings with reference to the back when the prescan diagnosis was spinal stenosis, lumbar pain syndrome, herniated nucleus pulposus, or postlaminectomy syndrome. Some scans gave positive findings in patients with a diagnosis of degenerative disc disease, pseudarthrosis, spondylolisthesis, fracture, infection, metabolic disorder, or tumor. Positive scans were generally obtained early after presentation (within 3 months) and negative scans obtained later (after 6 months), suggesting that clinical suspicion is still the main indication for early scanning. Planar bone scanning was helpful in both diagnosis and therapeutic decisionmaking in many conditions.     

Long-term in vivo depletion of functional CD4+ T lymphocytes from calves requires both thymectomy and anti-CD4 monoclonal antibody treatment

In vivo depletion of lymphocyte subsets is a direct approach used for dissection of the mechanisms of protective immunity. Long-term in vivo depletion of bovine T lymphocyte subpopulations with monoclonal antibody (mAb) treatment alone has been difficult to achieve. The objective of this study was to determine whether both thymectomy and anti-CD4 mAb treatment would optimize long-term in vivo depletion of functional bovine CD4+ T lymphocytes. Calves were thymectomized and treated with high doses of anti-CD4 mAb (approximately 5 mg/kg) over 4 days followed by subsequent lower doses (approximately 0.3 mg/kg) administered twice weekly for an additional 7 weeks. Depletion of CD4+ T lymphocytes from blood, spleen and peripheral lymph nodes was significantly improved in thymectomized calves compared to thymus-intact anti-CD4 mAb-treated calves. Significant differences in percentages of CD4+ T lymphocytes between thymectomized and thymus-intact calves were sustained for the duration of the 8-week study. Depletion of CD4+ T lymphocytes from thymectomized calves resulted in complete abrogation of lymphoproliferative responses to ovalbumin. In addition, thymectomized calves treated with anti-CD4 mAb had significantly reduced immunoglobulin G1 and no detectable immunoglobulin G2 ovalbumin-specific antibody responses compared to thymus-intact anti-CD4 mAb-treated calves. The results of this study demonstrate that both thymectomy and treatment with anti-CD4 mAb are required for long-term in vivo depletion of functional bovine CD4+ T lymphocytes.     

Reduced suppressor cell response to Mycobacterium leprae in lepromatous leprosy.

We have previously shown that concanavalin A (ConA) induction of suppressor cell activity is impaired in patients with lepromatous leprosy (LL). In this study, we demonstrated that the proportion of cells bearing the Leu8 antigen (associated with suppressor-inducer cells) is low in LL patients and tends to normalize during the erythema nodosum leprosum (ENL) episode. Antigen-induced suppressor cell function was evaluated by a two-stage assay. In the first stage, peripheral blood mononuclear cells (PBMC) were cultured for 5 days either in the presence of gamma-irradiated Mycobacterium leprae or in tissue culture medium as a control. In the second stage, mitomycin C-treated suppressor or control cells were added to phytohemagglutinin (PHA)- or ConA-stimulated autologous PBMC. The results indicate that the ability of M. leprae to induce suppressor activity was lower in LL patients than in patients with tuberculoid (TT) and intermediate clinical (BB, BL, BT) forms and Mycobacterium bovis BCG-immunized normal controls. In ENL patients, the percent suppression was between that of TT and normal individuals. M. leprae-induced suppression was more effective on ConA- than on PHA-triggered T-cell proliferation in all groups. In contrast, normal PBMC cultured for 5 days in RPMI 1640 medium (N-C) and cells from patients with leprosy (TT-C and LL-C) had effects of their own on PHA- or ConA-induced proliferation. LL-C depressed the response to ConA and enhanced PHA-induced proliferation of autologous cells. Conversely, TT-C reduced PHA-induced proliferation and increased the ConA response. Suppression of proliferation could not be overcome with exogenous interleukin-2 and was not related to the induction of the Tac antigen. The abilities of LL, TT, ENL, and normal cells to proliferate upon PHA or ConA stimulus were similar, indicating that the defect in the generation of in vitro suppression by M. leprae in LL patients occurred during the induction period (step 1 of assay).     

乳腺管状小叶癌

乳腺管状小叶癌（Tubulolobular carcinoma，TLC）最初是被作为小叶癌的管状变型。作者总结了27例TLC的组织学、免疫表型和临床特征，并与纯小管癌和经典型小叶癌进行了比较。此组患者年龄43-79岁（中位年龄60岁）。1例双侧乳腺受累，5例病变为多灶性。肿瘤直径0．5-2．5cm，色灰褐，质硬。组织学观察：TLC的肿瘤细胞形成管状和条索状两种结构模式并相互混杂，且两者比例相当（统称为管状小叶模式）。     

Composite germ cell tumor and B-cell non-Hodgkin's lymphoma arising in the sella turcica

We report the case of a composite malignant neoplasm consisting of germ cell tumor and B-cell non-Hodgkin's lymphoma occurring in the sella turcica of a young girl who presented with hypopituitarism. Routine hematoxylin and eosin-stained sections of a resected suprasellar tumor demonstrated a neoplasm composed of 2 distinct morphologies. A panel of immunohistochemical markers was used to confirm the morphologic impression of germinoma (cytokeratin AE1/AE3-CAM 5.2, cytokeratin 7, neuron-specific enolase, and focally placental alkaline phosphatase positive) and mature B-cell lymphoma (CD20 positive; pancytokeratin, placental alkaline phosphatase, and terminal deoxynucleotidyl transferase negative). To the best of our knowledge, this is the first reported case of such a composite tumor in the central nervous system.     

The effect of yoghurt on the cytotoxic and phagocytic activity of macrophages in tumour‐bearing mice

In a previous paper, it was demonstrated that feeding yoghurt was able to inhibit the growth of an intestinal tumour induced chemically with 1,2‐dimethylhydrazine (DMH). This effect was due to the increase in IgA‐producing cells and a diminution of the inflammatory immune response. In this paper the phagocytic and cytotoxic capacity of macrophages both involved and not involved in the target organ are studied. The study was aimed at determining whether in the intestinal tumour inhibition demonstrated previously the systemic immune response was also increased. The cytotoxic capacity and ß‐glucuronidase enzyme levels of the peritoneal macrophages were analyzed together with the cytolytic effect of the serum on tumour cells and the phagocytic activity of the macrophages infiltrating the intestinal mucosa. Groups of mice were split into three experimental groups. One group was treated with DMH. The others were treated with DMH, and their diets were supplemented with yoghurt for 7 or 10 consecutive days, during 24 weeks. It was demonstrated that feeding yoghurt for 7 or 10 days increased cytotoxic and ß‐glucuronidase levels in peritoneal macrophages, and also the cytolytic capacity of serum, reaching values significantly higher than those in the DMH control. Enhancement of the phagocytic activity of the macrophages associated with the large intestine was also observed. This increase in the macrophage activity involved in the systemic and mucosal immune responses could also be responsible for the tumour inhibition observed in the group of mice fed with yoghurt. The presence in the serum of lytic factors (cytokines) which were released by immune cells activated by feeding yoghurt may also have had a role in tumour inhibition.     

Germline mutations of the CDKN2 gene in UK melanoma families

Germline mutations in CDKN2 on chromosome 9p21, which codes for the cyclin D kinase inhibitor p16, and more rarely, mutations in the gene coding for CDK4, the protein to which p16 binds, underlie susceptibility in some melanoma families. We have sequenced all exons of CDKN2 and analysed the CDK4 gene for mutations in 27 UK families showing evidence of predisposition to melanoma. Five different germline mutations in CDKN2 were found in six families. Three of the mutations (Met53Ile, Arg24Pro and 23ins24) have been reported previously. We have identified two novel CDKN2 mutations (88delG and Ala118Thr) which are likely to be associated with the development of melanoma, because of their co-segregation with the disease and their likely functional effect on the CDKN2 protein. In binding assays the protein expressed from the previously described mutation, Met53Ile, did not bind to CDK4/CDK6, confirming its role as a causal mutation in the development of melanoma. Ala118Thr appeared to be functional in this assay. Arg24Pro appeared to bind to CDK6, but not to CDK4. No mutations were detected in exon 2 of CDK4, suggesting that causal mutations in this gene are uncommon. The penetrance of these mutant CDKN2 genes is not yet established, nor is the risk of non-melanoma cancer to gene carriers.