Journal of Tongji Medical University

The patients with glaucoma underwent the examination of retinal thickness analyzer (RTA) to explore the diagnostic value of RTA in glaucoma. The retina of 6 mm × 6 mm size (approximately 20°, centered on the macula) at the posterior pole was scanned by using RTA to obtain the images in 35 eyes of 22 patients with glaucoma. The images were processed by using SAS software package. The retinal thickness in the patients with glaucoma showed diffuse or local thinning. Twenty-seven eyes was definitely diagnosed as having glaucoma. There was a very significant difference in retinal thickness measurements by RTA between normal group and glaucomatous group (P= 0.0012). Except the measurements at the detected point 6 having no difference, the measurements at the detected point 3 showed a significant difference and the remaining 7 detected points presented a very significant difference between the two groups. Of the detected 9 points, the changes at the points 4, 8, and 9 were the most obvious. The discrete analysis was performed on the glaucomatous patients by a discriminant function established through the data at the detected points 4, 8 and 9 and the accurate estimate rate for the diagnosis of glaucoma was up to 80.77 %. The measurements of RTA examination was consistent with the results of the vision field test. It was suggested that diffuse or local thinning of retinal thickness exists in the patients with glaucoma. The temporal inferior arcuate fibers and the papillomacular bundle between the macular and optic nerve heads showed a serious damage. The sensitivity of RTA examination was higher than visual field test.

This study examined the mechanism of the inhibitory effect of parthenolide (PTL) on the activity of NF-κB in multiple myeloma (MM). Human multiple myeloma cell line RPMI 8226 cells were treated with or without different concentrations of PTL for various time periods, and then MTT assay was used to detect cell proliferation. Cell cycle and apoptosis were flow cytometrically detected. The level of protein ubiquitination was determined by using immunoprecipitation. Western blotting was employed to measure the level of total protein ubiquitination, the expression of IκB-α in cell plasma and the content of p65 in nucleus. The content of p65 in nucleus before and after PTL treatment was also examined with immunofluorescence. Exposure of RPMI 8226 cells to PTL attenuated the level of ubiquitinated Nemo, increased the expression of IκB-α and reduced the level of p65 in nucleus, finally leading to the decrease of the activity of NF-κB. PTL inhibited cell proliferation, induced apoptosis and blocked cell cycle. Furthermore, the levels of ubiquitinated tumor necrosis factor receptor-associated factor 6 (TRAF6) and total proteins were decreased after PTL treatment. By using Autodock software package, we predicted that PTL could bind to TRAF6 directly and tightly. Taken together, our findings suggest that PTL inhibits the activation of NF-κB signaling pathway via directly binding with TRAF6, thereby suppressing MM cell proliferation and inducing apoptosis.

To study the expression of Dickkopf-1 (DKK-1) in endometrium of pregnant mice during the peri implantation period and the role of DKK-1 during the embryo implantation in mice. Immunohistochemical technique was employed to determine the location of DKK-1 protein in endometrium, and semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) was utilized to determine the levels of DKK-1 mRNA. Our results showed that the expressions of DKK1 mRNA and protein were higher in experimental groups than in control group (P<0.01). and it increased significantly on day 3 and reached its peak on day 4. and then decreased gradually on day 5–7. The levels of DKK-1 mRNA and protein on day 1 was significantly higher than those of other groups (P<0.01). It is concluded that DKK-1 probably plays an important role in signal transudation of embryo implantation and its high expression indicates the opening of implantation window.

By determining the plasma levels of C3, C4, factor B and polymorphonuclear neutrophils (PMNs) of the patients who received CPB, the path of complement activation and changes of PMNs were studied. The results suggest that complement system was activated through alternative pathway during CPB and was activated through classic pathway after CPB. The anaphylatoxin, the products of complement activation may be responsible for the polymorphonuclear neutrocytopenia.

Tumors are believed to consist of a heterogeneous population of tumor cells originating from rare cancer stem cells (CSCs). However, emerging evidence suggests that tumor may also originate from non-CSCs. To support this viewpoint, we are here to present definitive evidence indicating that the number of tumorigenic tumor cells is greater than that of CSCs in tumor, and tumor can also derive from non-CSCs. To achieve this, an idealized mathematical model was employed in the present study and theoretical calculation revealed that non-CSCs could initiate the occurrence of tumor if their proliferation potential was adequate. Further, experimental studies demonstrated that 17.7%, 38.6% and 5.2% of tumor cells in murine B16 solid melanoma, H22 hepatoma and Lewis lung carcinoma, respectively, were potentially tumorigenic. Thus, based on the aforementioned findings, we propose that the scarce CSCs, if exist, are not the sole source of a tumor.

Recent studies suggested that the prostate cancer may arise from prostate cancer stem cells that share some same characteristics with normal stem cells. The purpose of this study was to detect the differences of Nanog expression between PC3 prostate cancer cell line and its tumor stem cells, and the relationship was preliminarily examined between Nanog and prostate cancer and its tumor stem cells. By using magnetic active cell sorting (MACS), we isolated a population of CD44+/CD133+ prostate cancer cells that display stem cell characteristics from PC3 cell line. Immunohistochemistry revealed positive expressions of CD44, CD133 and α2β1-integin in the isolated cells. CCK-8 analysis showed that isolated cells had a strong proliferative ability. The formation of the cell spheres in serum-free medium and holoclones in serum-supplied medium showed that the cells were capable of self-renewing, indicating that the isolated cells were a population of cancer stem-like cells derived from PC3 cell line. Western blotting exhibited that the isolated cells had higher experession of Nanog, an embryonic stem marker, as compared with PC3 cells. Our study showed that Nanog might be helpful in sustaining the self-renewal and the undifferentiation of prostate cancer stem cells, and may serve as a marker for prostate cancer stem cells for isolation and identification.

T cell subsets and immunoglobulin (Ig) were observed sequentially with the OKT monoclonal antibodies rosette test and the rate scattering turbidimetry in 13 patients who underwent open heart surgery under cardiopulmonary bypass (CPB) for rheumatic heart diseases (RHD) and congenital heart diseases (CHD), before and after operation. Compared with preoperative values, in the early period after CPB, T helper cells, T helper cells to T suppressor cells ratio and IgG decreased significantly; whereas T suppressor cells increased, in RHD and CHD. The T cell subsets returned to the preoperative levels two weeks after CPB in RHD and CHD. The IgG came back to the preoperative levels two weeks after CPB in RHD and only one week after CPB in CHD.

This study examined the association of polymorphisms in angiotensin II receptor genes (AT 1 R and AT 2 R) with the risk for aldosterone-producing adenoma (APA) in a Chinese Han population. Four polymorphisms including rs5182 (573T/C) in exon 4, rs5186 (1166A/C) in 3′-untranslated region (3′-UTR) in AT 1 R gene and rs5194 (2274G/A) in 3′-UTR, rs1403543 (1675G/A) in intron 1 in AT 2 R gene were detected in 148 APA patients and 192 normal subjects (serving as control) by using a MGB-Taqman probe. The distribution of genotypes of each locus was in accordance with Hardy-Weinberg Equilibrium (HWE) in the APA and control groups (P>0.05). The allele A frequency at rs5194 was significantly higher in the APA group (0.49) than in the control group (0.35) (χ 2=12.08, P=0.001). Subjects with homozygotic genotype AA and heterozygotic genotype GA were at an increased risk for APA as compared to those with GG genotype (OR=2.66, 95% CI=1.45–4.87; OR=1.67, 95% CI=1.02–2.74). Furthermore, rs5194 single-nucleotide polymorphism (SNP) at AT 2 R gene was significantly associated with APA in additive (OR=1.64, 95% CI=1.21–2.20, P=0.001), dominant (OR=1.94, 95% CI=1.23–3.06, P=0.003), and recessive model (OR=2.01, 95% CI=1.17–3.45, P=0.01). It was concluded that rs5194 polymorphism at AT 2 R gene was associated with the risk for APA, which may constitute a genetic marker of APA.

Th2 cytokines play a pivotal role in the pathogenesis of allergic rhinitis. To investigate the effect of p38 mitogen-activated protein kinase (MAPK) on the production of Th2 cytokines such as IL-4 and IL-5 in allergic rhinitis, a model of allergic rhinitis was established in SD rats. The expression level of p38 MAPK mRNA in PBMCs was detected by means of real time quantitative RT-PCR. The p38 MAPK activity in PBMCs was detected by Western blotting. PBMCs were cultured with various concentrations of p38 MAPK inhibitor SB 239063 or without the treatment, and then IL-4, IL-5 levels of the supernatant were determined by using sandwich ELISA. The results showed that mRNA expression and activity of p38 MAPK in PBMCs were significantly higher in allergic rhinitis rats than in control rats (P<0.05). The p38 MAPK inhibitor SB 239063 decreased the production of IL-4 and IL-5 in a dose-dependent manner. It is concluded that p38 MAPK plays an important role in the pathogenesis of allergic rhinitis which is associated with Th2 cytokines release.