Choice of x-ray diagnostic methods in chronic odontogenic sinusitis

On the basis of our experiences the selection of diagnostic methods for chronic odontogenic sinusitis is discussed. The selection is based on the primary sign, the reduced transparency of the sinus, detected with conventional radiography. Its purpose is the determination of the extent and nature of the opacity. Conventional methods, contrast investigations, conventional and computed tomography are used.     

CT tomography of normal parotid and mandibular salivary glands

Computed tomography (CT) allows the differentiation of tissues by measurement of their roentgenologic densities. There are a few controversial literature data on the roentgenologic densities of the parotid and submandibular glands. These differences are, in our opinion, due to several factors: 1. The complex anatomic structure of the facial region of the skull, that demands an exact centering. In daily practice the respective imaging parameters are not always kept constant (including partial volume effects), thus introducing density errors. 2. Metallic prostheses and obturators as well as the high-density bones of the facial skull cause artefacts that impair image quality and density measurements. 3. The small density differences between the salivary glands and the adjacent soft tissues makes their differentiation difficult. 4. Different devices and parameters are used for scanning, resulting in different densities. Considering these facts, we have devised a complex method for the investigation of the parotid and mandibular salivary glands.     

腹部外科常见感染性疾病的病原菌及药敏试验研究

为了了解本地区本医院腹部外科感染性疾病病原菌的构成比和药物敏感率的变化,指导临床用药,我们采用美国BD公司生产的6B和7D两种增菌瓶采集标本和培养细菌,并用该公司生产的生化板和药敏板,对1994～1996年269例常见的普外科感染性疾病患者的手术标本进行前瞻性的细菌培养和药敏试验研究.     

Abrogation of adriamycin-induced cardiotoxicity by selenium in rabbits.

Adriamycin-induced cardiomyopathy in rabbits was produced by intravenous injections of the drug with a short therapeutic schedule (3 mg/kg body wt administered as four intermittent doses). Animals receiving selenium supplementation of Adriamycin showed preservation of the normal pattern of the heart histologic picture. The protective effect of selenium was accompanied by increased selenium levels in the plasma and the heart muscle. An eventual interaction between the antitumor effect of Adriamycin and the protective effect of selenium was ruled out by in vitro experiments using the L1210 cell line. Selenium did not abrogate the antiproliferative effect of Adriamycin when the cells were treated simultaneously with both agents. The results from this study indicate that Adriamycin-induced cardiotoxicity could be prevented by selenium if the animals were pretreated with selenium, rather than simultaneous administration of both agents. The mechanism of this effect is not entirely understood.     

Inefficient formation of a complex among CXCR4, CD4 and gp120 in U937 clones resistant to X4 gp120-gp41-mediated fusion

Certain subclones (designated as minus clones) of the promonocytic U937 cell line do not support efficient infection and fusion mediated by T cell line adapted (TCLA) X4 HIV-1 gp120-gp41 (Env) although the CXCR4 and CD4 concentrations at their surfaces are similar to those at the surfaces of clones susceptible to HIV-1 entry (plus clones) (H. Moriuchi et al., J. Virol. 71, 9664-9671, 1997). To test the hypothesis that inefficient formation of gp120-CD4-CXCR4 complexes could contribute to the mechanism of resistance to Env-mediated fusion in the minus clones, we incubated plus and minus cells with HIV-1 LAI gp120 and coimmunoprecipitated CD4 by using anti-CXCR4 antibodies. The gp120 induced inefficient coimmunoprecipitation of CD4 in the minus clones but not in the plus ones. Overexpression of CD4 resulted in significant restoration of the minus clones' susceptibility to fusion in parallel with an increase in the amount of the gp120-CD4-CXCR4 complexes. These results not only suggest that the resistance to TCLA X4 HIV-1 entry in the U937 minus clones is due to the inability of these cells to efficiently form complexes among CD4, gp120, and CXCR4, but also provide a direct evidence for the correlation between fusion and the cell surface concentration of the complexes among CXCR4, CD4, and gp120. These data and similar recent observations in macrophages suggest that inefficient complex formation among CXCR4, CD4, and gp120 could be a general mechanism of cell resistance to gp120-gp41-mediated fusion and a major determinant of HIV-1 evolution in vivo.