Efficacy and safety of three different analgesic methods for patients undergoing transrectal ultrasound-guided prostate biopsy: a prospective, randomized controlled trial.

BACKGROUND: Recent evidence suggests that additional analgesic regimens to periprostatic nerve block (PPNB) anesthesia provide substantial pain relief during transrectal ultrasound-guided prostate biopsy. In this regard, we investigated the efficacy and safety of tramadol alone or in combination with parecoxib as adjunct regimens to PPNB anesthesia. MATERIAL AND METHODS: A total of 51 participants were randomly allocated into three study groups: Group 1 received PPNB anesthesia, Group 2 received tramadol and PPNB anesthesia, whereas Group 3 received both tramadol and parecoxib as adjunct regimens to PPNB anesthesia. The pain was evaluated at three different time points during biopsy: at the time of probe insertion (NRS1), at the time of PPNB anesthesia (NRS2), and at the time of the actual biopsy itself (NRS3), using a numeric rating scale (NRS) of pain. Safety was evaluated by the occurrence of complications and adverse effects. RESULTS: The mean NRS1 score was statistically significantly different in Groups 2 and 3 than in Group 1 (2.4 ± 1.3 and 1.1 ± 1.2 vs. 4.5 ± 1.8; p <0.0167). We found a statistically significant difference regarding NRS 2 score in Groups 2 and 3 than in Group 1 (2.6 ± 1.4 and 1.1 ± 1.3 vs. 4.1 ± 1.3; p <0.0167). The mean NRS1 and NRS2 scores were found to be statistically significantly different in Group 3 than in Group 2 (1.1 ± 1.2 vs. 2.4 ± 1.3 as well as 1.1 ± 1.3 vs. 2.6 ± 1.4; p <0.0167). Also, a statistically significant difference was found between Groups 2 and 3 regarding hematuria episodes [0 (0.0) vs. 5 (29.4); p <0.0167]. CONCLUSION: Tramadol as an adjunct regimen to PPNB anesthesia is a safe and straightforward technique that provides a significant analgesic effect. The effectiveness is even higher when tramadol is combined with parecoxib. HIPPOKRATIA 2020, 24(4): 166-172.

Post-eruptive flooding of Santorini caldera and implications for tsunami generation.

Caldera-forming eruptions of island volcanoes generate tsunamis by the interaction of different eruptive phenomena with the sea. Such tsunamis are a major hazard, but forward models of their impacts are limited by poor understanding of source mechanisms. The caldera-forming eruption of Santorini in the Late Bronze Age is known to have been tsunamigenic, and caldera collapse has been proposed as a mechanism. Here, we present bathymetric and seismic evidence showing that the caldera was not open to the sea during the main phase of the eruption, but was flooded once the eruption had finished. Inflow of water and associated landsliding cut a deep, 2.0-2.5 km3, submarine channel, thus filling the caldera in less than a couple of days. If, as at most such volcanoes, caldera collapse occurred syn-eruptively, then it cannot have generated tsunamis. Entry of pyroclastic flows into the sea, combined with slumping of submarine pyroclastic accumulations, were the main mechanisms of tsunami production.

Expression patterns of the E-cadherin-catenin cell-cell adhesion complex in gastric cancer.

BACKGROUND/AIMS: The E-cadherin-catenin complex plays a key role in intercellular adhesion of epithelial cells. Aberrant expression and/or function of its components have been implicated in tumor progression and metastasis. We evaluated the expression of the E-cadherin-catenin complex in gastric cancer by immunohistochemistry and investigated its relationship to histopathological features. METHODOLOGY: The expression of E-cadherin, alpha-, beta-, and gamma-catenin, and p120 protein was evaluated by immunohistochemistry in 36 formalin-fixed, paraffin-embedded specimens of gastric cancer. RESULTS: In benign gastric mucosa all five molecules co-localized at the cell membrane. Reduced E-cadherin, alpha-, beta-, and gamma-catenin, and p120 expression was found in 67%, 61%, 50%, 64%, and 56% of cases, respectively. The expression of E-cadherin and beta-catenin correlated significantly with the histological type and the degree of tumor differentiation. gamma-Catenin expression correlated only with the histological type of the tumor. The expression of E-cadherin correlated significantly with alpha-, beta- and gamma-catenin, and p120 expression, respectively. The expression of E-cadherin and alpha-catenin showed the highest concordance. CONCLUSIONS: In gastric cancer, reduced E-cadherin, catenin and p120 expressions are related events with E-cadherin showing the most frequent aberrations.

Sequential and morphological analyses of aberrant crypt foci formation in mice of differing susceptibility to azoxymethane-induced colon carcinogenesis.

Aberrant crypt foci (ACF), putative preneoplastic lesions, are early morphological changes induced by the colon carcinogen azoxymethane (AOM). Although inbred mice differ markedly in their susceptibility to AOM carcinogenesis, we have previously shown that ACF develop in both resistant and sensitive mouse strains after AOM treatment. The purpose of this study was to examine the sequential development and identify the morphological characteristics of ACF induced by AOM in the distal colon of sensitive and resistant mice. A/J (highly susceptible), SWR/J (relatively susceptible) and AKR/J (resistant) mice were treated with 10 mg/kg AOM or saline i.p. once a week for 6 weeks and were killed at 1, 2, 4, 6, 9 and 24 weeks after the last injection. The distal colons were stained with methylene blue and the numbers of ACF and tumors determined. Tumors were present as early as 4 weeks after AOM exposure in SWR/J and A/J mice and increased in frequency throughout the study in both strains. No tumors developed in the AKR/J mice. ACF, however, formed in all strains of mice. The greatest difference between susceptible and resistant strains was in the number of large ACF that developed at later time points. Furthermore, morphometric analysis revealed that A/J mice had the highest percentage of dysplastic ACF, followed by SWR/J mice. These data indicate that the difference in cancer risk from AOM may be due to the lack of progression of smaller ACF in the resistant mice and to the development of dysplasia in a higher percentage of ACF from susceptible strains.

E-cadherin expression correlates with tumor differentiation in colorectal cancer.

BACKGROUND/AIMS: Epithelial cadherin (E-cadherin) is the main cell-cell adhesion molecule in all epithelia. Aberrant expression of this molecule has been implicated in tumor invasion and metastasis. We evaluated E-cadherin expression and cellular localization in colorectal cancer and investigated its relationship to histopathological features. METHODOLOGY: The expression of E-cadherin was evaluated in 57 formalin-fixed, paraffin-embedded specimens of colorectal cancer by immunohistochemistry. RESULTS: In normal colonic mucosa, E-cadherin was expressed uniformly at the cell membrane. Abnormal E-cadherin expression and/or cellular distribution was found in 46% of tumors. There was a significant correlation between E-cadherin expression and tumor grade with a trend towards reduced E-cadherin expression as the tumor grade increased. The association between E-cadherin expression and tumor stage was not significant. CONCLUSIONS: Abnormal E-cadherin expression in colorectal cancer correlates with loss of differentiation.