Immunogenicity of herpes simplex virus glycoprotein gB-1-related protein produced in yeast

A protein related to glycoprotein B of herpes simplex virus type 1 (HSV-1) produced in yeast (ygB-1) was purified with an immunoadsorbent. The molecular weight of the purified ygB-1 as determined by sodium dodecyl sulphate polyacrylamide gel electrophoresis was 96,000. Mice injected twice with ygB-1 adsorbed to alum developed ELISA antibody to ygB-1, neutralizing antibody to HSV-1 and a lymphoproliferative response to ygB-1 and HSV-1. The immunized mice were protected against intraperitoneal and corneal challenge with HSV-1. Latent infection in the trigeminal ganglia after corneal challenge was also inhibited by immunization with ygB-1. Guinea-pigs pigs immunized with ygB-1 adsorbed to alum also developed ELISA antibody to to ygB-1 and neutralizing antibody to both types of HSV. After the second dose, strong lymphoproliferative responses were seen upon stimulation with HSV-2. Animals were protected against intravaginal challenge with HSV type 2.     

Three-dimensional architecture of elastic tissue in athero-arteriosclerotic lesions of the rat aorta

The overall three-dimensional architecture of elastic tissue in athero-arteriosclerotic lesions of the ascending aorta of the rat was studied, using scanning electron microscopy (SEM), after hot-formic acid extraction followed by a freeze-drying method. The lesions were induced by feeding the rats a diet containing 2% cholesterol for 6 weeks and administering massive doses of vitamin D2 for the first 4 days. SEM revealed the synthesis of elastins mainly in the intima and the degradation in the internal elastic lamina (IEL) and medial concentric elastic lamellae. Intimal elastic elements involved in atherosclerotic lesions were composed of an intricately tangled network of fibrous elastins or a row of elastic laminae that surrounded many rectangular compartments, which were separated by fenestrated septum-like elastins and were assumed to be the sites of smooth-muscle-cell proliferation. These observations indicated remodelling of the elastic laminae in the intima. Degradation in the IEL and media was attributed to either vitamin D2 intoxication, which was characterized by the formation of a large degraded portion, or an enhanced elastolytic process. These alterations of elastic elements probably reflect the exact frame of the modes of migration of aortic smooth muscle cells in the development of athero-arteriosclerotic lesions, thereby indicating the role of smooth muscle cells in the progress of atherosclerosis.     

ALPHA FETOPROTEIN and GARGINOEMBRYONIC ANTIGEN PRODUCING HEPATOCELLULAR CARCINOMA

Hepatocellular carcinoma (HCC) showing marked elevation of serum alpha fetoprotein (AFP) (maximum; 70942.0 ng/ml at the end stage) and serum carcinoembryonic antigen (CEA)(maximum; 7368.4 ng/ml at the end stage) was surgically resected. In the resected liver, there were two different tumor nodules which were adjacent to each other but clearly separated by a thin connective tissue. One of the nodules was a well differentiated and the other was poorly differentiated HCC. Immunoperoxidase study revealed that both CEA and AFP were localized in the tumor cells of the poorly differentiated HCC. This is the first report which clearly proved CEA synthesis in the cells of HCC. Serial staining showed that there was simultaneous synthesis of CEA and AFP in some of the tumor cells. ACTA PATHOL. JPN. 35: 969–974, 1985.     

Effects of TSH receptor mutations on binding and biological activity of monoclonal antibodies and TSH.

The effects of an extensive series of mutations in the TSH receptor (TSHR) leucine-rich domain (LRD) on the ability of thyroid-stimulating monoclonal antibodies (TSMAbs) and TSH to bind to the receptor and stimulate cyclic AMP production in TSHR-transfected CHO cells has been investigated. In addition, the ability of a mouse monoclonal antibody with blocking (i.e., antagonist) activity (RSR-B2) to interact with mutated receptors has been studied. Several amino acids distributed along an extensive part of the concave surface of the LRD were found to be important for binding and stimulation by the thyroid-stimulating human MAb M22 but did not appear to be important for TSH binding and stimulation. Most of these amino acids important for M22 interactions were also found to be important for the stimulating activity of six different mouse TSMAbs and a hamster TSMAb. Furthermore, most of these same amino acids were important for stimulation by TSHR autoantibodies in a panel of sera from patients with Graves' disease. Amino acid R255 was the only residue found to be unimportant for TSH stimulation but critical for stimulation by all thyroid-stimulating antibodies tested (23 patient serum TSHR autoantibodies, M22, and all seven animal TSMAbs). About half the amino acids (all located in the N-terminal part of the LRD) found to be important for M22 activity were also important for the blocking activity of RSR-B2 and although the epitopes for the two MAbs overlap they are different. As the two MAbs have similar affinities, their epitope differences are probably responsible for their different activities. Overall our results indicate that different TSMAbs and different patient sera thyroid-stimulating autoantibodies interact with the same region of the TSHR, but there are subtle differences in the actual amino acids that make contact with the different stimulators.     

Primary megaureter which showed aplasia of the muscle bundles on all dilated portions: a case report

A case of primary megaureter in a 59-year-old man which might shed light on the etiology and pathology is described. Intravenous urography and the computed tomography showed a left marked hydro-nephro-ureter which compressed the bladder and right ureter. In the left ureter, dilated portions stretched beyond dilated portions; that is, five non-dilated portions lay among four dilated portions. On histological examination of this specimen, all dilated portions showed aplasia of muscle in which muscle bundles were not observed, while all non-dilated portions including ureterovesical junction showed normal muscle layers. A case presentation and brief review of the literature were made.     

Fusogenic oncolytic vaccinia virus enhances systemic antitumor immune response by modulating the tumor microenvironment

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Influence of monoclonal antiplatelet glycoprotein antibodies on in vitro human megakaryocyte colony formation and proplatelet formation

The influence of antiplatelet glycoprotein (GP) antibodies on megakaryocytopoiesis in patients with idiopathic or immune thrombocytopenic purpura (ITP) has been well studied. However, the influence of GP antibodies on proplatelet formation is poorly understood. Here we investigated whether in vitro human megakaryocyte colony formation and proplatelet formation are affected by various monoclonal antiplatelet GP antibodies (MoAb). The megakaryocyte colony formation inhibition assay was performed by methylcellulose culture with modifications, using peripheral blood nonadherent mononuclear cells. The proplatelet formation inhibition assay was performed by megakaryocytes derived from CD34(+) cells, stimulated with thrombopoietin + stem cell factor, which were then incubated with antiplatelet GP MoAb for 24 or 48 hours. Anti-GP-Ibalpha MoAb (CD42b; HIP1) slightly inhibited megakaryocyte colony formation (P < .05). and strongly inhibited proplatelet formation (after 24 hours incubation, P < .0002; after 48 hours incubation, P < .0007). Anti-GP-IIb MoAb (CD41; 5B12) inhibited only proplatelet formation (only after 24 hours incubation, P <. 03). Anti-integrin alphavbeta3 MoAb (CD51/CD61; 23C6) only slightly inhibited colony size (P < .05). However, anti-GP-IIIa MoAb (CD61; Y2/51) did not inhibit either colony formation or proplatelet formation. These results suggest that antiplatelet GP MoAbs have differing effects on in vitro megakaryocyte colony formation and proplatelet formation.     

Anisakiasis confirmed by radiography of the large intestine

As yet, there has been no report of acute anisakiasis of the large intestine diagnosed by radiographic demonstration of the larvae. We present such a case, in which roentgenologic examination revealed Anisakis larvae in the ascending colon.