A case report of ultrasonic decalcification for calcified bicuspid aortic valve stenosis

Calcified stenotic aortic valve are usually replaced by the artificial valve. Recently, we are trying to decalcify the calcification of the aortic valve by ultrasonic energy. This case report reviewed a small physique, 47 year old female, who had the calcified stenotic bicuspid aortic valve and the narrow aortic valve ring (18 mm diameter). The ultrasonic decalcification was performed by the ultrasonic surgical instrument, SUS-201D (ALOKA), ultrasonic energy output range from 25% to 45%. After the ultrasonic decalcification, the movability of the aortic cusps were improved and the aortic opening was enlarged. The systolic pressure gradient across the aortic valve was improved from 100 mmHg to 20 mmHg. This method "ultrasonic decalcification" is very useful technique for the repair of the calcified aortic valve stenosis.     

Anti-CD45R antibody-treated normal lymphocytes respond to interleukin 2 (IL2) after stimulation by allergens

Interleukin 2 (IL2) responsiveness was specifically induced by Dermatophagoides farinae (Df) antigen in Df-sensitized lymphocytes from asthmatic children, but not in normal lymphocytes. Df-induced IL2 responsiveness was also observed in normal lymphocytes pretreated (Day 0) with anti-CD45R antibody, which recognize suppressor inducer subset among CD4+ T cells. However anti-CD45R antibody was no longer effective when the lymphocytes were cultured for more than one day with the antigen, suggesting its effect in the initial phase of the reaction. The intensity of the response induced in normal lymphocytes by the anti-CD45R was comparable to that of the patients sensitized to the nominal antigen. The response of the patients was no longer augmented by the anti-CD45R antibody. Taken together, these data suggest that even normal lymphocytes have potentiality to elicit Df-induced IL2 responsiveness and it is probably derepressed by inhibiting suppressor inducer subset with the anti-CD45R antibody. Also suggested is a defective suppressor inducer activity in the lymphocytes which may lead to hyperreactivity to allergens in asthmatic children.     

Human thymus-lymphoid tissue antigen and its presence in leukaemia and lymphoma

An antiserum was prepared by immunizing rabbits with human leukaemic tissue homogenate. Prior to immunization, the rabbits had been made tolerant to normal peripheral leucocytes by repeated injections during the neonatal period to suppress the appearance of antibodies against normal tissue components. When the antiserum was tested by gel diffusion precipitation test, it gave one precipitin line against malignant tissue extracts from most leukaemia and lymphoma cases tested, and against normal thymuses and some spleens and lymph nodes as well. It did not react with tissue extracts prepared from normal non-lymphoid tissus. The antigen responsible for the reaction appeared in foetal thymus at 3 months of gestation and persisted throughout life. It appeared in embryonic spleen after 6 months of gestation and in lymph nodes even later, although in spleen and lymph nodes it was not as invariably demonstrated as in the thymus. Neoplasms of other than lymphoid origin were predominantly negative for the antigen; occasional exceptions were probably due to large amounts of infiltrating lymphoid tissue. Antigen localization was studied by the fluorescent antibody method. The cytoplasm of almost all thymocytes, about 30% spleen cells and 20–40% peripheral lymphocytes was stained. Bone marrow, brain, thyroid, liver and kidney cells were negative. The antigen was partially purified from the soluble fraction of thymus homogenate by ion exchange column chromatography and preparative electrophoresis. Its possible use as a marker for thymus derived normal and neoplastic cells has been discussed.     

Only dull CD3+ thymocytes bind to thymic epithelial cells. The binding is elicited by both CD2/LFA-3 and LFA-1/ICAM-1 interactions

In view of the necessity for thymocytes to interact with thymic epithelial cells to differentiate into mature T cells, this study analyzed the binding between human thymocytes, cultured thymic epithelial cells (CTEC) and the required adhesion molecules. Immediately after separation, thymic epithelial cells (TEC) readily expressed ICAM-1, which is one of the ligands of LFA-1 cell adhesion molecules. However, the ICAM-1 expression was gradually lost upon culture of TEC. IFN-gamma re-induced ICAM-1 on the CTEC, and the ability of CTEC to bind to thymocytes was also increased by IFN-gamma treatment. The increase in binding seemed to be caused by the LFA-1/ICAM-1 interaction, since it was inhibited by anti-ICAM-1 monoclonal antibody (mAb) and anti-LFA-1 mAb. This suggests that the LFA-1/ICAM-1 interaction is also involved in vivo with the binding of thymocytes to TEC, which have been shown to express ICAM-1. To better understand the nature of the cells involved in binding, thymocytes were sorted into CD3-, CD3dull+, and CD3bright+ subsets (which are supposed to represent the immature, intermediate and mature stages of differentiation, respectively), and were examined for their binding to IFN-gamma-treated CTEC. The result showed that only the CD3dull+ subset bound to CTEC. CD3-, CD3bright+ cells and peripheral blood T lymphocytes did not bind, but they were induced to bind by neuramidase treatment All these bindings were inhibited by anti-LFA-1 mAb and anti-CD2 mAb. These findings indicate that CD3dull+ cells can bind to TEC via CD2/LFA-3 and LFA-1/ICAM-1 interactions. Other cells seemed not to bind to TEC because of sialylation.     

Human lymphocyte subpopulations. Human thymus-lymphoid tissue (HTL) antigen-positive lymphocytes forming rosettes with sheep erythrocytes and HTL antigen-negative lymphocytes interacting with antigen-antibody-complement complexes

Human lymphocytes from various lymphoid tissues were studied for the relationship between the existence of HTL (human thymus-lymphoid tissue) antigen, and binding of sheep erythrocytes (E) or sheep erythrocyte–antibody-complement complexes (EA(IgM)C43). E adhered to the majority of thymus lymphocytes and formed rosettes. These lymphocytes were shown to be HTL antigen positive by immunofluorescence performed simultaneously. In the peripheral lymphoid tissues, 10–30% of lymphocytes formed E rosettes and almost all E rosette-forming lymphocytes were HTL antigen positive. Conversely HTL antigen-negative cells did not form E rosettes.

In contrast, the cells binding EA(IgM)C43 were always HTL antigen negative.

There were very few HTL antigen-positive or rosette-forming lymphocytes either with E or EA(IgM)C43 in bone marrow.

From these data we conclude that E-rosette-forming and HTL antigen-positive lymphocytes are of thymus origin and EA(IgM)C43-rosette-forming cells are not thymus-dependent cells.

     

A rapid isolation technique of unmodified human T cells on a polystyrene resin column

An easy and rapid isolation technique of human T cells on a polystyrene resin particle column has been developed. The cells of the effluent fraction contained more than 90% sheep erythrocyte (SRBC) rosette-forming cells and less than 1% of cells bearing surface immunoglobulin (Ig) or peroxidase. The T cell (SRBC rosette-forming cells) recovery rate was 80%. The distribution of OKT antigen T cell subsets was essentially the same as that of T cells separated by rosette sedimentation. Cell functions such as tritiated thymidine uptake by T cells and helper activity in Ig production were also the same as that of T cells separated by SRBC rosette sedimentation. Natural killer-like activity of the T cells isolated by the present method increased more than that of T cells obtained by the conventional method. Moreover, it was free from functional modification which tends to result from stimulation such as by the SRBC antigen in the SRBC centrifugation method. The combination of a T cell population offered by the present method and B cells depleted of SRBC-binding B cells minimized background plaque formation and enabled us to quantify the plaque-forming cell number in an antigen-specific plaque-forming assay. Furthermore, these populations produced relatively pure interleukin 2 (IL 2) by stimulation of an autologous mixed lymphocyte reaction without any absorption of IL 2 produced in the same culture. It seemed to be useful to evaluate the ability of lymphocytes from normal individuals and patients to produce IL 2.     

Blockade of Rho/Rho-associated coiled coil-forming kinase signaling can prevent progression of hepatocellular carcinoma in matrix metalloproteinase-dependent manner

Aim:  There is growing evidence that the Rho/Rho-associated coiled coil-forming kinase (ROCK) signaling pathway is upregulated in tumors and plays a key role in cancer invasion and metastasis. Our aim was to test the anticancer effects of Rho/ROCK inhibitor, Y-27632, including possible mechanisms in a highly-metastasizing hepatocellular carcinoma (HCC) mouse model on its secretion of matrix metalloproteinase (MMP) and tumor progression.
Methods:  Following orthotopic implantation of CBO140C12 HCC tumor fragments into the liver of mice, the mice were randomly assigned to a Y-27632-treated group or control group. After treatment for 4 weeks, specimens were obtained to evaluate tumor size, metastases, and immunohistochemical findings. In vitro , we examined the effects of Y-27632 and RhoC siRNA on MMP-2 and -9 expressions, invasiveness, and apoptosis in cultured tumor cells.
Results:  Both RhoA and RhoC were upregulated in HCC-bearing livers, and Y-27632 significantly inhibited not only tumor growth and intrahepatic metastasis ( P  < 0.05), but also tumoral MMP-9 expression. Moreover, Y-27632 treatment resulted in large necrotic areas in tumors. In vitro , Y-27632 and RhoC siRNA reduced MMP-2 and -9 expressions, as well as the chemotactic migration of tumor cells dose-dependently, and increased apoptosis eight times.
Conclusion:  Y-27632 suppresses progression and limits the intrahepatic metastasis of established HCC. This could be linked to the decreased MMP expression and induction of apoptosis in tumor cells. Rho signaling may prove to be a productive target in anticancer therapy.     

Nanostructure lipid carriers enhance alpha-mangostin neuroprotective efficacy in mice with rotenone-induced neurodegeneration

Metabolic Brain Disease - Neurodegenerative disease, for instance, Parkinson’s disease (PD), is associated with substantia nigra dopaminergic neuronal loss with subsequent striatal dopamine...