Composable security of CV-MDI-QKD with secret key rate and data processing.

We provide a rigorous security proof of continuous-variable measurement-device-independent quantum key distribution which incorporates finite-size effects and composable terms. In order to use realistic and optimized parameters and be able to derive results close to experimental expectations, we run protocol simulations supported by a Python library, including all the protocol operations, from simulating the quantum communication till the extraction of the final key.

Parameter Estimation with Almost No Public Communication for Continuous-Variable Quantum Key Distribution.

One crucial step in any quantum key distribution (QKD) scheme is parameter estimation. In a typical QKD protocol the users have to sacrifice part of their raw data to estimate the parameters of the communication channel as, for example, the error rate. This introduces a trade-off between the secret key rate and the accuracy of parameter estimation in the finite-size regime. Here we show that continuous-variable QKD is not subject to this constraint as the whole raw keys can be used for both parameter estimation and secret key generation, without compromising the security. First, we show that this property holds for measurement-device-independent (MDI) protocols, as a consequence of the fact that in a MDI protocol the correlations between Alice and Bob are postselected by the measurement performed by an untrusted relay. This result is then extended beyond the MDI framework by exploiting the fact that MDI protocols can simulate device-dependent one-way QKD with arbitrarily high precision.

Cellular distribution of human tissue kallikreins: immunohistochemical localization.

We have studied the immunohistochemical expression (IE) of eight non-tissue-specific human kallikreins (hKs) (hK5, 6, 7, 10, 11, 12, 13, and 14) in different normal tissues. The IE was always cytoplasmic, showing a characteristic pattern in some tissues. Comparison of the IE of all hKs studied in the different tissues revealed no major differences, suggesting that they share a common mode of regulation. Furthermore, hKs were immunohistochemically revealed in a variety of tissues, indicating that no protein is tissue-specific (except for hK2 and hK3, which have tissue-restricted expression). In general, our results correspond well with data from RT-PCR and ELISA assays. Glandular epithelia constitute the main kallikrein IE sites, and the staining in their secretions confirms that these proteases are secreted. A variety of other tissues express the proteins as well. We have also immunohistochemically evaluated all the above hKs in several malignant tissues. Tumors arising from tissues expressing kallikreins tested positive. Corresponding to the IE in normal glandular tissues, most hKs were expressed in adenocarcinomas. The prognostic value of several hKs was studied in series of prostate, renal cell, colon and urothelial carcinomas.

Prognostic implications of the immunohistochemical expression of human kallikreins 5, 6, 10 and 11 in renal cell carcinoma.

Human kallikreins 5, 6, 10 and 11 (hK5, 6, 10 and 11) are expressed by many normal tissues, and it has been suggested that they may represent candidate tumor-diagnostic or -prognostic markers. In patients with renal cell carcinoma (RCC), outcome is unpredictable despite the use of conventional prognostic factors. The aim of this study is to evaluate the immunohistochemical expression and the prognostic value of the above kallikreins in RCC. The study comprised 95 patients who underwent radical nephrectomy for RCC. The median follow-up period was 60 months (range 1-180 months). Fifty-seven RCC cases were immunostained for hK5, 70 for hK6, 70 for hK10 and 69 for hK11. The streptavidin-biotin-peroxidase method of immunostaining was performed using anti-hK5, anti-hK6, anti-hK10 and anti-hK11 monoclonal and polyclonal antibodies. The immunohistochemical expression of these kallikreins was correlated with tumor size, histological type, histological malignancy according to the Fuhrman four-grade scale, mitotic index, pathological stage and disease survival. For the statistical analysis, four grades were collapsed into two by which RCC cases were categorized as low malignant (LM) and high malignant (HM). In the normal renal parenchyma adjacent to the tumors, the renal tubular epithelium showed a cytoplasmic expression of all four kallikreins. In RCC, immunohistochemical expression was decreased: 33 of 57 cases (58%) were positive for hK5, 27 of 70 (39%) for hK6, 46 of 70 (66%) for hK10 and 32 of 69 (46%) for hK11. A statistically significant positive correlation was observed among the immunohistochemical expression of all kallikreins. HM-RCC expressed all kallikreins in a higher percentage of cases than LM-RCC, but statistically significant differences were only observed for hK6 and hK10 (55 vs. 27%, p = 0.016, and 79 vs. 56%, p = 0.044, respectively). hK6 and hK11 expression showed a positive correlation to pathological stage: hK6 with both Robson and TNM 2002 staging systems (p = 0.010 and p = 0.017, respectively), and hK11 only with the Robson staging system (p = 0.045). In both the Kaplan-Meier and the univariate Cox regression analyses, hK6 expression was negatively correlated with disease-specific survival (p = 0.05 and p = 0.038, respectively). In univariate analysis, nuclear grade, Robson stage and TNM stage also correlated with disease-specific survival. However, in the multivariate analysis, TNM stage was the only independent prognostic factor. In conclusion, although the immunohistochemical expression of hK5, hK6, hK10 and hK11 was downregulated in RCC, tumors of high grade and late stage expressed one or more of the above kallikreins in a higher percentage of cases, and hK6 may predict a poor disease outcome in RCC.

Prostate cancer with small-cell morphology: an immunophenotypic subdivision.

OBJECTIVE: To study the immunophenotypic characteristics and clinical outcome of morphologically undifferentiated prostatic carcinoma with small-cell morphology (U-PC-SCM). MATERIAL AND METHODS: Sixteen patients with U-PC-SCM were enrolled. The streptavidin-biotin complex immunohistochemical method was used on paraffin-embedded tissue sections to test positivity for prostate-specific antigen, prostate-specific acid phosphatase, CD57, androgen receptors, CK8-18, epithelial membrane antigen, carcinoembryonic antigen, CD56, neuron-specific enolase, chromogranin, synaptophysin, serotonin, various hormones, thyroid transcriptional factor-1 and Ki-67/MIB1. RESULTS: Based on immunophenotypic criteria, we identified two groups of patients. The final diagnosis was U-PC (Gleason score 10) in Group 1 (n=9) and pure or mixed neuroendocrine small-cell carcinoma in Group 2 (n=7). Group 1 underwent total androgen blockade (TAB) with no major response and had a median survival of 9 months. In Group 2, three patients underwent TAB, two of whom died of progressive disease. The third patient showed a partial response (PR) for 18 months but eventually relapsed with liver metastatic lesions. He was then treated with cisplatin + etoposide and showed a PR for 3 months and survived for 5 months after the initiation of the second-line chemotherapy (CTH) treatment. The other four patients received six cycles of cisplatin + etoposide. There were two complete responses of >14 and >22 months, respectively and 2 PRs of 11 and 17 months, respectively, the partial responders surviving for 14 and 21 months, respectively. CONCLUSION: U-PC-SCM with a neuroendocrine immunophenotype is a histogenetically distinct entity with different clinical and laboratory manifestations which responds well to a cisplatin + etoposide CTH regimen.

p27(kip1) and Ki-67 (MIB1) immunohistochemical expression in radical prostatectomy specimens of patients with clinically localized prostate cancer.

The immunohistochemical expressions (IE) of p27(kip1) and Ki-67 (MIB-1), both involved in cell cycle regulation and cell proliferation, and their ability to predict biochemical failure, were assessed in patients with clinically localized prostate cancer who had underdone radical prostatectomy of curative intent. In addition, p27(kip1) and Ki-67 (MIB1) expressions were correlated with several pre-operative and post-operative parameters, such as Gleason score, extracapsular extension, seminal vesicle involvement, pelvic lymph nodes metastasis, positive surgical margins, coexistence of high-grade prostatic intraepithelial neoplasia, tumour size, prostate volume and PSA levels. Our analysis involved 130 consecutive radical prostatectomy specimens. A statistically significant correlation of low p27(kiP1) IE with seminal vesicles involvement, increased tumour volume and high pre-operative PSA values was documented. Low p27(kiP1) IE was significantly correlated with an increased likelihood of biochemical failure after radical prostatectomy. In addition, the increased IE of Ki-67 (MIB1) correlated significantly with metastatic disease in the pelvic lymph nodes and was a significant predictor of biochemical failure. Cox regression analysis, which included p27(kip1) expression, Ki-67 (MIB1) expression and all the pre-operative and post-operative parameters, showed that pelvic lymph node involvement and Ki-67 (MIB1) IE were independent prognostic markers of biochemical failure after radical prostatectomy.

Immunohistochemical expression of Bcl2 is an independent predictor of time-to-biochemical failure in patients with clinically localized prostate cancer following radical prostatectomy.

BACKGROUND: Whether the immunohistochemical expression (IHCE) of the bcl2, the p53 and of the prostate apoptosis response-4 (PAR4) proteins is associated with pre-operative PSA levels, post-operative parameters of prostate cancer (PC) pathology, surgical staging or biochemical failure (BF) of patients with clinically localized PC who underwent radical prostatectomy (RP) of curative intent, was investigated. PATIENTS AND METHODS: A retrospective analysis of clinical data evaluating surgical specimens of 131 patients with PC, consecutively treated with RP for clinically localized disease, was performed. The IHC method of streptavidin biotin peroxidase on paraffin tissue sections was used to detect bcl2 and p53 oncoproteins and PAR4 pro-apoptotic protein expression in surgical specimens. RESULTS: Statistically significant relationships were detected between: (i) p53 IHC expression and infiltration of periprostatic tissue (IPT; p = 0.011); (ii) tumor volume (TV; p = 0.027); and (iii) bcl2 IHCE and absence of prostatic intraepithelial neoplasia (PIN) (p = 0.004). Biochemical failure (BF) was documented in 37% of these patients. Kaplan-Meier survival curves showed that the IHCE of bcl2 and p53 was significantly related to BF. Taking the hazard ratio (HR) estimated from the Cox proportional hazard regression model to be 1.00 for patients with negative bcl2 IHCE, a value of 2.82 was found for patients with positive bcl2 IHCE (p = 0.015, 95% CI = 1.22-6.47). The HR for patients with positive p53 IHCE was 2.05 (p = 0.048, 95% CI = 1.00-4.19). Multivariate analysis showed that only seminal vesicle invasion (SVI), pelvic lymph node metastasis (PLNM) and bcl2 IHCE were independent predictors for BF (HR = 3.06, 3.31 and 3.15; p = 0.048, p = 0.031 and p = 0.031 for SVI, PLNM and bcl2 IHCE, respectively). CONCLUSION: Bcl2 immunohistochemical overexpression in specimens of RP suggests high risk for BF in clinically localized PC.