Effects of rope-jump training on the os calcis stiffness index of postpubescent girls

PURPOSE: The specific aims of the study were to 1) determine what effects dose-dependent rope jumping had on os calcis stiffness index (OCSI) and 2) determine whether OCSI values measured by quantitative ultrasound (QUS) were dependent or independent of the values of bone mineral content (BMC) determined by dual energy x-ray absorptiometry (DXA) at the lumbar spine and proximal femur (femoral neck; greater trochanter). METHODS: Upon study entry, girls were randomly assigned to either one of two treatment groups (high volume; low volume) or a control group. Thirty-seven high school girls were recruited to participate in the study. QUS and DXA measurements were made at baseline and at 4-month follow-up. Students in the high-volume and low-volume groups jumped rope for 10 and 5 min, respectively. RESULTS: The follow-up mean OCSI values for the high-volume, low-volume, and control conditions were 103.95 +/- 12.55, 102.09 +/- 12.70, and 99.05 +/- 9.84, respectively. A statistically significant difference (P = 0.033) was identified between the high-volume and control groups. Baseline and follow-up OCSI values were significantly correlated with baseline and follow-up BMC measures of the femoral neck (r = 0.60, r = 0.59), greater trochanter (r = 0.47, r = 0.40), and lumbar spine (r = 0.56, r = 0.56). CONCLUSIONS: High-volume rope jumping increases the OCSI more than the control condition in postpubescent girls. Furthermore, the OCSI measured by QUS is moderately related to proximal femur and lumbar spine BMC measured by DXA.     

High-grade gliomas and solitary metastases: differentiation by using perfusion and proton spectroscopic MR imaging

PURPOSE: To determine whether perfusion-weighted and proton spectroscopic MR imaging can be used to differentiate high-grade primary gliomas and solitary metastases on the basis of differences in vascularity and metabolite levels in the peritumoral region. MATERIALS AND METHODS: Fifty-one patients with a solitary brain tumor (33 gliomas, 18 metastases) underwent conventional, contrast material--enhanced perfusion-weighted, and proton spectroscopic MR imaging before surgical resection or stereotactic biopsy. Of the 33 patients with gliomas, 22 underwent perfusion-weighted MR imaging; nine, spectroscopic MR imaging; and two underwent both. Of the 18 patients with metastases, 12 underwent perfusion-weighted MR imaging, and six, spectroscopic MR imaging. The peritumoral region was defined as the area in the white matter immediately adjacent to the enhancing (hyperintense on T2-weighted images, but not enhancing on postcontrast T1-weighted images) portion of the tumor. Relative cerebral blood volumes in these regions were calculated from perfusion-weighted MR data. Spectra from the enhancing tumor, the peritumoral region, and normal brain were obtained from the two-dimensional spectroscopic MR acquisition. The Student t test was used to determine if there was a statistically significant difference in relative cerebral blood volume and metabolic ratios between high-grade gliomas and metastases. RESULTS: The measured relative cerebral blood volumes in the peritumoral region in high-grade gliomas and metastases were 1.31 +/- 0.97 (mean +/- SD) and 0.39 +/- 0.19, respectively. The difference was statistically significant (P <.001). Spectroscopic imaging demonstrated elevated choline levels (choline-to-creatine ratio was 2.28 +/- 1.24) in the peritumoral region of gliomas but not in metastases (choline-to-creatine ratio was 0.76 +/- 0.23). The difference was statistically significant (P =.001). CONCLUSION: Although conventional MR imaging characteristics of solitary metastases and primary high-grade gliomas may sometimes be similar, perfusion-weighted and spectroscopic MR imaging enable distinction between the two.     

Inhibiting activin‐A signaling stimulates bone formation and prevents cancer‐induced bone destruction in vivo

Cancers that grow in bone, such as myeloma and breast cancer metastases, cause devastating osteolytic bone destruction. These cancers hijack bone remodeling by stimulating osteoclastic bone resorption and suppressing bone formation. Currently, treatment is targeted primarily at blocking bone resorption, but this approach has achieved only limited success. Stimulating osteoblastic bone formation to promote repair is a novel alternative approach. We show that a soluble activin receptor type IIA fusion protein (ActRIIA.muFc) stimulates osteoblastogenesis (p < .01), promotes bone formation (p < .01) and increases bone mass in vivo (p < .001). We show that the development of osteolytic bone lesions in mice bearing murine myeloma cells is caused by both increased resorption (p < .05) and suppression of bone formation (p < .01). ActRIIA.muFc treatment stimulates osteoblastogenesis (p < .01), prevents myeloma‐induced suppression of bone formation (p < .05), blocks the development of osteolytic bone lesions (p < .05), and increases survival (p < .05). We also show, in a murine model of breast cancer bone metastasis, that ActRIIA.muFc again prevents bone destruction (p < .001) and inhibits bone metastases (p < .05). These findings show that stimulating osteoblastic bone formation with ActRIIA.muFc blocks the formation of osteolytic bone lesions and bone metastases in models of myeloma and breast cancer and paves the way for new approaches to treating this debilitating aspect of cancer. © 2010 American Society for Bone and Mineral Research.     

Human papillomavirus molecular biology and pathogenesis

Human papillomavirus (HPV) infection is the most common sexually transmitted disease in the world and accounts for an estimated 11% of the global cancer incidence in women. HPV-16 is the most prevalent type detected in cervical cancer and along with types 18, 31, 33 and 45 has been classified as a class I carcinogen. In addition to cervical cancer, HPVs are also associated with the malignant transformation of other mucosal and skin cancers. Thus, the combination of the malignant potential of HPV and its high prevalence of infection confers to it an importance of generalized clinical and virological significance. The natural history of HPV infection with or without treatment varies from spontaneous regression to persistence. The most important mechanism for wart regression appears to be cell-mediated immunity. Cytokines released by keratinocytes or cells of the immune system may play a part in the induction of an effective immune response against HPV infection and the subsequent regression of lesions. This review discusses the molecular biology, pathogenesis and immunology of HPV infections.     

Coinduction of granulocyte-macrophage colony-stimulating factor release and lymphokine-activated killer cell susceptibility in monocytes by interleukin-2 via interleukin-2 receptor beta

Human monocytes express interleukin-2 receptor beta (IL-2R beta) constitutively; however, the function of these receptors has not been fully delineated. We discovered that IL-2R beta directs two biologic activities in human monocytes, the release of granulocyte-macrophage colony-stimulating factor (GM-CSF) and increased susceptibility to lysis by lymphokine-activated killer cells (LAK) cells. Human monocytes were purified from peripheral blood mononuclear cells by plastic adherence and anti-CD2 plus complement lysis. By a 5-hour 51Cr-release assay, monocytes cultured in IL-2 were found to gain increasing susceptibility to LAK cells with time and this effect was dose dependent. Maximal susceptibility was obtained with a 4-day culture in 1,000 U/mL of IL-2. Monocytes were also found to release GM-CSF in response to IL-2 using a CSF-dependent cell line, Mo7e. Because IL-2- induced GM-CSF release coincides with LAK lysis of IL-2-cultured monocytes, we treated monocytes with anti-GM-CSF and anti-IL-2R beta to determine whether GM-CSF release and LAK susceptibility were dependent or independent events. We found that both phenomena were inhibited by either antibody. Therefore, we conclude that IL-2-induced release of GM- CSF is mediated by IL-2R beta, which then acts to modulate the susceptibility of monocytes to lysis by LAK cells.