38 research outputs found

    Additional file 1 of Development and validation of a model and nomogram for breast cancer diagnosis based on quantitative analysis of serum disease-specific haptoglobin N-glycosylation

    No full text
    Additional file 1: Figure S1. Aggregation plots of missing values of clinical variables. The first plot shows the proportion of missing values in each variable. The second plot shows patterns of missing values. The frequencies of the corresponding combinations are demonstrated to the right. The blue bars represent missing values, while the orange bars represent observed values. Figure S2. Strip plots of observed and imputed data of clinicopathological variables. The strip plots display the distribution of imputed values (orange points) over observed values (blue points) in a combined way. In total, 5 multiple imputed data sets were created. Column 1 represents the original data set, while column 2-6 represent the 5 imputed data sets. The second imputed data set (column 3) was used. Most of its imputations were in a plausible range, and properly accounted for the distribution of the missing data. Figure S3. Histogram plots displaying propensity score distributions for the malignant and benign groups before and after propensity score matching (caliper = 0.333). Figure S4. Heatmap of the correlations of DSHp-β N-glycopeptides and tumor markers. The numbers in grid show the Spearman correlation coefficients. Blank indicates a Bonferroni correction p-value of ≥ 0.05. Table S1. Identified N-glycopeptides of DSHp-β, their potential structures, and intensities between benign breast diseases and breast cancer

    Description of an obese mouse model established after 10 weeks on HFD.

    No full text
    <p>(A) Representative picture of 15-week old obese and control mice. (B) Comparison of time-dependent increases in body weight between CD (n = 27) and HFD groups (n = 30). (C) Weekly food consumption by mice in CD and HFD groups. (D) Hematoxylin and eosin-stained hepatic sections from mice both fed control diet (CD) and high-fat diet (HFD). (D2) and (D4) are two-fold enlarged views of (D1) and (D3). Scale bars = 50 μm. Data are expressed as mean ± SEM. * <i>P</i><0.05, ** <i>P</i><0.01.</p

    Image_1_Breast-conserving surgery without axillary surgery and radiation versus mastectomy plus axillary dissection in elderly breast cancer patients: A retrospective study.jpeg

    No full text
    BackgroundThe high relative mortality rate in elderly breast cancer patients is most likely the result of comorbidities rather than the tumor load. Foregoing axillary lymph node dissection or omitting radiotherapy after breast-conserving surgery (BCS) does not affect the prognosis of elderly breast cancer patients. We sought to assess the safety of breast-conserving surgery without axillary lymph node dissection as well as breast and axillary radiotherapy (BCSNR) in elderly patients with early-stage breast cancer.MethodsWe retrospectively included 541 consecutive breast cancer patients aged over 70 years with clinically negative axillary lymph nodes in one clinical center. Of these patients, 181 underwent mastectomy plus axillary lymph node dissection (MALND) with negative axillary cleaning and 360 underwent BCSNR.ResultsAfter a median follow-up of 5 years, there was no significant difference between the BCSNR and MALND groups in either distant recurrence-free survival (DRFS) (p=0.990) or breast cancer-specific survival (p=0.076). Ipsilateral axillary disease was found in 11 (3.1%) patients in the BCSNR group and 3 (1.7%) patients in the MALND group; this difference was not significant (p=0.334). We did not observe a significant difference in distant recurrence between the groups (p=0.574), with 25 (6.9%) patients in the BCSNR group experiencing distant recurrence compared to 15 (8.3%) patients in the MALND group. Our findings did show a significant difference in ipsilateral breast cancer recurrence (IBTR), with 31 (8.6%) patients in the BCSNR group experiencing IBTR compared to only 2 (1.1%) patients in the MALND group (p=0.003).ConclusionBCSNR is a safe treatment option for elderly breast cancer patients with clinically negative axillary lymph nodes.</p

    Effects of HFD on sperm acrosome reaction in mice.

    No full text
    <p>(A) Status of the mouse sperm acrosome stained with Commassie blue G250 in HFD and CD groups; the arrow indicates the intact acrosome stained with intensive blue. Scale bar = 20 μm. (B) Status of the mouse sperm acrosome stained with FITC-PNA, the arrow indicates the intact acrosome exhibiting green fluorescence. The red fluorescence indicates sperm nuclei stained with Propidium Iodide. Scale bar = 10 μm. A1 and B1: spermatozoa from CD mice; A2 and B2: spermatozoa from HFD mice. AR: acrosome reaction; CBG250: Commassie blue G250. Data are expressed as mean ± SEM. **<i>P</i><0.01.</p

    HFD-induced androgen receptor, clathrin, ZO-1 and occludin expression changes in mice.

    No full text
    <p>(A) Western blot analyses of androgen receptor, clathrin, ZO-1 and occludin expression levels in testicular protein from CD and HFD mice. (B) Summary plot showing densitometric readings of the corresponding protein blots. Data are expressed as mean ± SEM. *<i>P</i><0.05, **<i>P</i><0.01.</p

    Hydroxysteroid Sulfotransferase SULT2B1b Promotes Hepatocellular Carcinoma Cells Proliferation <i>In Vitro</i> and <i>In Vivo</i>

    Get PDF
    <div><p>Hydroxysteroid sulfotransferase 2B1b (SULT2B1b) is highly selective for the addition of sulfate groups to 3β-hydroxysteroids. Although previous reports have suggested that SULT2B1b is correlated with cell proliferation of hepatocytes, the relationship between SULT2B1b and the malignant phenotype of hepatocarcinoma cells was not clear. In the present study, we found that SULT2B1 was comparatively higher in the human hepatocarcinoma tumorous tissues than their adjacent tissues. Besides, SULT2B1b overexpression promoted the growth of the mouse hepatocarcinoma cell line Hepa1-6, while Lentivirus-mediated SULT2B1b interference inhibited growth as assessed by the CCK-8 assay. Likewise, inhibition of SULT2B1b expression induced cell-cycle arrest and apoptosis in Hepa1-6 cells by upregulating the expression of FAS, downregulating the expression of cyclinB1, BCL2 and MYC <i>in vitro</i> and <i>in vivo</i> at both the transcript and protein levels. Knock-down of SULT2B1b expression significantly suppressed tumor growth in nude mouse xenografts. Moreover, proliferation rates and SULT2B1b expression were highly correlated in the human hepatocarcinoma cell lines Huh-7, Hep3B, SMMC-7721 and BEL-7402 cells. Knock-down of SULT2B1b inhibited cell growth and cyclinB1 levels in human hepatocarcinoma cells and suppressed xenograft growth <i>in vivo</i>. In conclusion, SULT2B1b expression promotes proliferation of hepatocellular carcinoma cells <i>in vitro</i> and <i>in vivo</i>, which may contribute to the progression of HCC.</p></div

    Alteration of serum lipids and sex hormone levels in HFD mice.

    No full text
    <p>(A) Comparison of serum lipid levels between CD and HFD groups; TG: triglycerides, TC: total cholesterol, LDL: low density lipoprotein, HDL: high density lipoprotein. (B) Comparison of serum sex hormone levels between CD and HFD groups, including testosterone, estradiol, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Data are expressed as mean ± SEM. * <i>P</i><0.05, ** <i>P</i><0.01.</p

    SULT2B1b knock-down suppressed the growth of human hepatocarcinoma cells <i>in vivo</i> and <i>in vitro</i>.

    No full text
    <p>(A) qPCR analysis of SULT2B1b mRNA levels in BEL-7402 and SMMC-7721 cells with SULT2B1 or SULT2B1b-specific siRNA treatment. Cell proliferation rates of BEL-7402 (B) and SMMC-7721 (C) cells treated with SULT2B1 or SULT2B1b-specific siRNA was assessed by CCK-8 assay. (D) cyclinB1 mRNA levels in BEL-7402 and SMMC-7721 cells with SULT2B1b-specific siRNA treatment was detected by qPCR assay. (E) cyclinB1 protein levels in BEL-7402 and SMMC-7721 cells with SULT2B1b-specific siRNA treatment detected by Western-blot analysis, β-actin as internal control. *<i>P</i><0.05 vs. NC group<b>.</b> BEL-7402 cells (1×10<sup>6</sup>) infected with NC-RFP-LV or hSULT2B1-RNAi-LV were injected subcutaneously into right subaxillary region of each nude mouse. The xenograft tumor growth curve (F), representative images (G) and the weights (H) of dissected xenografts were shown. *<i>P</i><0.05 vs. NC-RFP-LV control group.</p

    Model accounting for declines in male fertility in mice fed HFD.

    No full text
    <p>However, in mice on HFD, what is the impact of BTB integrity disruption on spermatogensis or subsequent sperm maturation? We found that these mice generally have decreased sperm motility and progressive motility, increased rate of teratozoospermia and even lowering of the sperm fertility index. Undoubtedly, the disruption of BTB integrity is one of the crucial factors for this pathogenesis. A possible reason accounting for why mice on a HFD have a disrupted BTB, but without any sperm concentration alteration is that preleptotene/leptotene spermatocytes merely traverse the BTB in advance of BTB integrity disruption rather than later at spermatogenic arrest prior to meiosis onset. Therefore, spermatozoa of HFD mice within the cauda epididymides may be immature eventually, and sperm abnormality rates will also dramatically increase more in the HFD group than in the CD group [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0120775#pone.0120775.ref016" target="_blank">16</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0120775#pone.0120775.ref018" target="_blank">18</a>].</p
    corecore