Intravenous treatment with liposome-encapsulated dichloromethylene bisphosphonate (C12MBP)suppresses nitric oxide production and reduces genetic resistance to Marek's disease

In this study the functional effectiveness of in vivo macrophage depletion using liposome-encapsulateddichloromethylene bisphosphonate (C12MBP) was examined in the chicken. The main target organs forsystemic liposome-encapsulated C12MBP treatment are the spleen and the liver. Intravenous treatment withC12MBP of B²¹/B²¹ chickens, genetically resistant to Marek's disease (MD), before challenge with the very virulent strain RB-lB, increased viral load in the blood and spleen after the first week and up to 6 weeks postinfection. In addition, C12MBP treatment dramatically increased tumour incidence and tumour load, especially in the spleens and livers of sick animals, but without affecting MD-specific mortality of B²¹/B²¹ cickens infected with RB-1B at 12 days of age. Nitric oxide (NO) is an important effector of the macrophage and has antiviral and antitumoural properties. NO has been shown to be one of the mechanisms triggered in resistance to Marek's disease. Intravenous treatment with Cl2MBP before infection with RB-1B induced a long-lasting decrease in numbers of macrophages and reduction in splenic inducible NO production associated with an absence of nitrate induction in the serum (up to 6 weeks pi). These results do not identify macrophage and NO production as major effector components in genetic resistance to Marek's disease, but underline their roles in limiting viraemia and tumour development in organs such as the spleen and the liver.     

TRIO amplification and abundant mRNA expression is associated with invasive tumor growth and rapid tumor cell proliferation in urinary bladder cancer

Studies by comparative genome hybridization have suggested that 5p amplification is related to tumor progression in urinary bladder cancer. In this study seven genes (TAS2R, ADCY2, DNAH5, CTNND2, TRIO, ANKH, and MYO10) located to 5p15.31-5p15.1 were analyzed by fluorescence in situ hybridization using a tissue microarray containing samples from tumors and cell lines with known 5p amplification by comparative genome hybridization. Amplification frequency was highest for TRIO, which maps to 5p15.2 and encodes a protein with a putative role in cell-cycle regulation. To further investigate the role of TRIO amplification in bladder cancer, a tissue microarray containing samples from 2317 bladder tumors was used for fluorescence in situ hybridization analysis. TRIO amplification was strongly associated with invasive tumor phenotype, high tumor grade, and rapid tumor cell proliferation (Ki67 LI) (P < 0.0001 each). Only 7 of 456 pTaG1/G2 tumors (1.5%) but 62 of 485 pT1-4 carcinomas (12.8%) had TRIO amplification. TRIO amplification was not associated with poor prognosis. Using a frozen bladder tumor tissue microarray RNA in situ hybridization confirmed that TRIO is up-regulated in amplified tumors. It is concluded that TRIO up-regulation through amplification has a potential role in bladder cancer progression.     

Placental candidiasis: report of four cases, one with villitis

Four cases of placental candidiasis, an uncommon complication of rupture of the membranes, are presented. In addition to chorioamnionitis, in one of these cases villitis was also observed. Villitis is a rare occurrence in Candida infection and this represents only the second case in the literature. The involvement of villi may be suggestive of blood-borne infection. However, since neither the mother nor the foetus presented any signs of systemic dissemination, the authors suggest a hypothesis of contamination of the villi from foci of chorioamnionitis.     

Liposome-mediated gene transfer to fetal human ventral mesencephalic explant cultures

To clarify how Abeta deposits induce secondary tauopathy, the presence of phosphorylated tau, glycogen synthase kinase 3alpha (GSK3alpha), GSK3beta, cyclin-dependent kinase 5 (CDK5), mitogen-activated protein kinase (MAPK) and fyn were examined in the Tg2576 brain showing substantial brain Abeta amyloidosis and behavioral abnormalities. Phosphorylated tau at Ser199, Thr231/Ser235, Ser396 and Ser413 accumulated in the dystrophic neurites of senile plaques. The major kinase for tau phosphorylation was GSK3beta. Smaller contributions of GSK3alpha, CDK5 and MAPK were suggested. Thus, brain Abeta amyloidosis has a potential role in the induction of tauopathy leading to the mental disturbances of Alzheimer's disease.     

Evolution of health care utilization and expenditure during the year before death in 2015 among people with cancer: French snds-based cohort study

The European Journal of Health Economics - Cancer patients have one of the highest health care expenditures (HCE) at the end of life. However, the growth of HCE at the end of life remains poorly...     

Eribulin combined with radiation therapy in a young patient re-irradiated for a new lesion of breast cancer

Eribulin is widely used in the treatment of metastatic breast cancer, with a manageable toxicity profile. This aggressive disease often requires systemic and local treatments, comprising surgery or radiotherapy. However, eribulin is usually discontinued during radiation therapy due to the lack of data concerning the safety of this combination, especially in the setting of repeat locoregional radiation therapy. Our patient was diagnosed with ER positive invasive ductal carcinoma of the left breast initially treated by surgery, radiation therapy, chemotherapy, and hormone therapy. She then received various lines of chemotherapy for multiple triple-negative relapses in the left axillary region. Since October 2020, she has been treated by eribulin. In order to improve local control, it was decided to add local radiation therapy to the region of recurrence in addition to systemic therapy. She underwent radiation therapy concomitantly with eribulin from February to March 2021. Treatment was very well tolerated, and no acute toxicity was reported. This is the first published case of repeat locoregional radiation therapy in combination with eribulin.     

Imaging of chest wall disorders.

Pathologic processes that may involve the chest wall include congenital and developmental anomalies, inflammatory and infectious diseases, and soft-tissue and bone tumors. Many of these processes have characteristic radiologic appearances that allow definitive diagnosis. Sternal deformities can be visualized at radiography and their severity quantified with computed tomography (CT). In cervical rib, CT with multiplanar reconstruction may demonstrate relevant anatomic detail and the relationship between bone deformity and arterial compression. In Poland syndrome, radiography reveals an area of hyperlucency on the affected side, whereas CT demonstrates the absence of the greater pectoral muscle and clearly depicts associated musculoskeletal anomalies. Tuberculosis typically manifests at radiography and CT as osseous and cartilaginous destruction and soft-tissue masses with calcification and rim enhancement. Aspergillosis involving the chest wall manifests as pulmonary consolidations and permeative osteolytic changes of the rib and spine at CT and as an area of increased signal intensity at T2-weighted magnetic resonance (MR) imaging. Neurogenic tumors and hemangiomas also typically have high signal intensity at T2-weighted MR imaging. Apparent mass extension or unequivocal bone destruction seen at CT or MR imaging may indicate chest wall involvement by lymphoma. Radiologically, soft-tissue sarcomas typically appear as areas of soft-tissue density or attenuation, often associated with necrotic areas of low density or attenuation. At radiography, plasmacytoma typically manifests as well-defined, "punched-out" lytic lesions with associated extrapleural soft-tissue masses. Chondrosarcoma frequently appears as a large, lobulated excrescent mass arising from a rib with scattered flocculent calcifications characteristic of its cartilaginous mix. Familiarity with these radiologic features facilitates accurate diagnosis and optimal patient treatment.     

Sexual and pharmacostimulated erections are proportional

Even complex diagnostic tests may not establish aetiology and degree of erectile dysfunction (ED) in many patients. Therefore, we evaluated a self-report method with a restrictive focus to quality of erections which may yield information sufficient to make an aetiologic diagnosis. We studied 74 patients 25 to 75 years of age with untreated ED. Sexually stimulated erections were quantified and compared to duplexsonographically and clinically evaluated data from pharmacostimulated erections. Patients reported that there was a marked decrease in ability to penetrate the partner, to sustain an erection and of penile rigidity (p < 0.001). Parameters from duplexsonography and clinically assessed response to pharmacostimulation correlated (r = 0.72). Direct comparison of these data with quantified history showed no relation (r = 0.05). Using change in penile volume due to erection as a basis to compare with, showed significant correlation with quantified data from history (r = 0.26-0.34; p < 0.03) and measured parameters from pharmacostimulated erections (r = 0.44-0.55; p < 0.0001). Sexually- and pharmacostimulated erections are proportional to change in penile volume. Although there is a relation between erections emerging from both stimulations, quantifying history on sexually stimulated erections does not qualify to make an aetiologic diagnosis without using complex tests.     

A histochemical study of glycosidases in benign prostatic hyperplasia and in prostatic carcinoma in the human

Summary In benign hyperplasia marked -glucuronidase and N-acetyl--glucosaminidase activity was seen in the prostatic epithelium whereas the reactions for 5 other glycosidases were only slight or negative. The intensity of the reaction for the glycosidases in prostatic carcinoma was dependent upon the degree of the differentiation. The possible importance of glycosidases for the invasiveness of prostatic carcinoma is briefly discussed.