Telomeres, the protective caps of chromosomes, shorten with age, as telomerase, the enzyme responsible for the compensation of telomere erosion, is inactive in the majority of cells. Telomere shortening and subsequent cell senescence lead to tissue aging and age-related diseases. Neurodegenerative disorders, characterized by the progressive loss of neurons among other hallmarks of aged tissue, and poor cognitive function, have been associated with a short telomere length. Thus, telomerase activity has emerged as a therapeutic target, with novel agents being under investigation. The present study aimed to examine the effects of a novel natural telomerase activator, 'Reverse™', containing Centella asiatica extract, vitamin C, zinc and vitamin D3 on the brains of 18-month-old rats. The administration of the 'Reverse™' supplement for 3 months restored telomerase reverse transcriptase (TERT) expression in the brains of rats, as revealed by ELISA and immunohistochemistry. In addition, the findings from PCR-ELISA demonstrated an enhanced telomerase activity in the cerebellum and cortex cells in the brains of rats treated with the 'Reverse™' supplement. The histopathological findings confirmed a structural reversibility effect close to the differentiation observed in the young control group of rats treated with two capsules/kg body weight of the 'Reverse™' supplement. On the whole, the findings of the present study provide a strong indication that an increased telomerase activity and TERT expression may be achieved not only in the postnatal or embryonic period, but also in the brains of middle-aged rats through nutraceutical supplementation. The use of the 'Reverse™' supplement may thus contribute to the potential alleviation of a number of central nervous system diseases.
Clinical and pathological aspects of condyloma acuminatum -review of literature and case presentationDAMIAN DIŢESCU 1) , ANCA-MARIA ISTRATE-OFIŢERU 2-4) , GABRIELA-CAMELIA ROŞU 2,3) , LARISA IOVAN 2-5) , ILONA MIHAELA LILIAC 2,3,5) , GEORGE-LUCIAN ZORILĂ 4) , MARIA BĂLĂŞOIU 6) , LILIANA CERCELARU 7)
Hepatocellular carcinoma (HCC) is the main primary liver malignancy, being associated with both health and economic burden worldwide. Recently, novel molecular markers and possible therapeutic targets were identified. Different adhesion molecules, as well as possible angiogenesisassociated targets can be prime candidates when investigating novel therapies. Considering these premises, our goal was to study the coexistence of E-cadherin and aquaporin 1 (AQP1) in a series of HCC diagnosed patients. Utilizing archived tissue fragments from 17 patients diagnosed with well-to-moderate and poorly differentiated HCC, as well as four samples of normal liver tissue and using a highly specific biotinfree tyramide amplification technique, we have assessed here the expression of E-cadherin and AQP1 during HCC carcinogenesis. Moreover, as we have observed that some of the AQP1 expression seems membrane-bound, we have sought to evaluate their co-localization. Our data showed, as expected, that E-cadherin decreases from control tissue to low-grade and respectively, high-grade HCC. AQP1 was expressed, also as already known, at the level of endothelial blood vessels and bile ducts epithelia, however, we have showed here for the first time that this water pore is also expressed in the cytoplasm and membranes of hepatocytes, both in control and HCC tissue. Moreover, AQP1 expression parallels the decrease of E-cadherin expression during carcinogenesis, but together with this downregulation, we have also found a spatial decrease in the colocalization of the two proteins. Altogether, utilizing a biotin-free tyramide signal amplification technique, this study shows for the first time that AQP1 is expressed at the level of liver epithelia, in both control and HCC tissue.
The validation of histological prognostic markers in colorectal cancer not only for survival parameters but also for early postoperative outcomes is of paramount importance. The aim of our study was to search for the tumor histopathological (HP) characteristics that may influence the postoperative morbidity, especially the occurrence of anastomotic leakage. Our results indicated that peritumoral inflammatory cell infiltrate appeared to correlate with both anastomotic fistula and overall postoperative complications. Likewise, high-grade and undifferentiated colorectal tumors seemed to be correlated with a higher incidence of postoperative leakage and complications. No relation could be established between the other HP features and the postoperative untoward outcomes.
The potential renoprotective effects of vardenafil (VAR) have been evaluated in a very limited number of studies using acute kidney injury animal models other than contrast-induced nephropathy (CIN) with promising results, while avanafil (AVA) has not been evaluated in this respect before. The purpose of this study was to evaluate for the first time the potential renoprotective effect of VAR and AVA in a rat model of CIN. Twenty-five male Wistar rats were equally assigned into five groups: control, CIN, CIN+N-acetyl cysteine (NAC) (100 mg/kg/day) as a positive control, CIN+VAR (10 mg/kg/day) and CIN+AVA (50 mg/kg/day). CIN was induced by dehydration, inhibition of prostaglandin and nitric oxide synthesis as well as exposure to the contrast medium (CM). Serum Cr (sCr) levels were measured at 24 and 48 h after CIN induction. At 48 h of CM exposure, animals were sacrificed. Matrix metalloproteinase (MMP) 2 (MMP-2) and MMP-9, kidney injury molecule 1 (KIM-1) and cystatin-C (Cys-C) were measured on renal tissue. Histopathological findings were evaluated on kidney tissue. All treatment groups had close to normal kidney appearance. sCr levels subsided in all treatment groups compared to CIN group at 48 h following CIN induction. A significant decline in the levels of MMP-2, MMP-9, KIM-1 and Cys-C compared to CIN group was observed. These results provide emerging evidence that VAR and AVA may have the potential to prevent CIN.
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