The Journal of Bucharest College of Physicians and the Romanian Academy of Medical Sciences

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IPSS Score and IL-6 Before and During Treatment with Dutasteride in Patients with Benign Prostatic Hyperplasia

2015-01

C.V. Ene, Corina Daniela Ene, Ilinca Nicolae, B. Geavlete, Oana Andreia Coman

Benign prostatic hyperplasia (BPH) is one of the most common pathologies in aging men, associated with lower urinary tract symptoms (LUTS). This pathology has a multimodal approach depending on different factors like age, prostate size, prostate-specific antigen level, and severity of the symptoms [1].

Medical treatment is the first option in what patients with low or moderate LUTS are concerned. There are two major drug classes already established in all international treatment guidelines, 5 alpha-reductase inhibitors and alpha-blockers. 5 alpha-reductase inhibitors block the transformation of testosterone in dihydrotestosterone within the prostate, leading to the decrease of prostate volume, increased peak urinary flow rate, improvement of symptoms, decreasing the risk of acute urinary retention. Their main secondary effects are the erectile dysfunction, the decreasing of libido and of the ejaculate volume, and also gynecomastia [2]. Alpha-blockers act on alpha-adrenoceptor sites found particularly at the bladder neck, at the trigone and within the prostate. They have a fast action on the prostate gland, leading quickly to symptom relief, but without reducing the risk of acute retention or surgical treatment. As secondary effects, alpha-blockers can affect blood pressure [3-5].

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Presence of p53 in Tumor Cells - an Indicator of Disease Severity? Retrospective Study in Patients with NSCC (Partial Results)

2015-01

Antonela Dragomir, M. Alexe, Diana Leonte, Florina Vasilescu, Daciana Marta

The lung cancer is the leading cause of death determined by malignancies in the world, followed by breast, prostate and colon cancer. The malignant cells present a variety of genetic aberrations that can be grouped into six essential pathways: (1) the acquisition of self sufficient or autonomous growth signals; (2) insensitivity to growth inhibitory signals; (3) resistance to signals of apoptosis; (4) unlimited proliferation potential; (5) sustained angiogenesis; and (6) invasion and metastasis1.

The p53 protein is a protein with molecular mass of 53 kDa (from where its name derives). The gene p53 encoding the protein p53 is located on the short arm of chromosome 14. The protein p53 is involved in maintaining control cellular genome stability and its disruption can lead to the emergence of malignancies. In about 50% of human cancers, the mutant protein p53 was detected. At the cellular level it regulating the transcription of some genes involved in cell growth control and apoptosis. The gene p53 can be inactivated by punctiform mutations and protein p53 can be inactivated by the formation of complexes with the cellular proteins or by proteolysis.

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NBI Guided TURBT in NMIBC Management - "The Right Path" to Better Tumor Ablation

2015-01

B. Geavlete, C. Ene, C. Bulai, I. Al. Checheriță, P. Geavlete

Over the past few years, the conventional transurethral resection of bladder tumors (TURBT) has undergone increasing criticism among the international urological community due to itsí inability to achieve a complete tumor ablation [1].

This substantial oncologic drawback has been mainly related to the limited sensitivity of the classical white light cystoscopy (WLC) [2]. In other words, the standard endoscopic assessment of the bladder was often outlined as insufficiently capable of accurately identifying all of the existing tumor formations [3].

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Optimal Treatment for Myocardial Revascularization: Surgery or Stenting?

2014-04

S. Wan and M. J. Underwood

Since the introduction of coronary artery bypass grafting (CABG) in 1967, and percutaneous transluminal coronary angioplasty (PTCA) 10 years later, several major clinical trials have been conducted comparing the two therapeutic strategies, such as the Bypass Angioplasty Revascularization Investigation (BARI) (1) and the Coronary Angioplasty versus Bypass Revascularization Investigation (CABRI) (2) trials. The seven-year outcome data of the BARI trial (involving 1,829 patients) demonstrated that CABG carried a significant survival benefit over PTCA and this was particularly pronounced in diabetic patients (1). In addition, nearly 60% of the patients treated with PTCA had to undergo repeat revascularization procedures and half of them relied on CABG as a subsequent therapy (1).

Nevertheless, the past two decades have witnessed a rapid progression of PTCA technology, in particular the development of intra-coronary stents. Drug-eluting stents (DES) especially, appear to have impacted significantly on the current daily practice of treating patients with coronary artery disease (3). These advances and their immediate influence on clinical practice provide a good example of how technology may shift the paradigm of medicine. Consequently, the mechanism and technique of revascularization needs to be redefined in the present era.

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Hepatocyte Growth Factor: Cardiotrophic Roles and Potential Therapeutics for Cardiovascular Diseases

2014-04

S. Mizuno and T. Nakamura

Due to prolonged lifespans, cardiovascular disease is on the increase worldwide and is now the leading cause of death, especially in developed countries. Histologically, it is characterized by coronary atherosclerosis, in which the over-proliferation of vascular smooth muscle cells (VSMC) is evident, associated with endothelial injury and foamy cell-like macrophages (i.e., local inflammation) (1,2). Such a sclerotic event triggers narrowed lumens (i.e., stenosis) and a decrease in coronary blood flow leads to local hypoxia, apoptosis, and eventually the onset of myocardial infarction (MI) (2). Thus, the major approaches proposed to prevent or restore MI are: (i) prevention or restoration of coronary atherosclerosis, the primary cause of heart disease; (ii) induction of cardiac angiogenesis with cytokines/growth factors; (iii) inhibition of cardiomyocyte cell death during heart ischemia (i.e., anti-apoptotic therapy); and, (iv) possible reconstitution of cardiomyocytes via recruitment of intrinsic stem cells, or cell transplantation (i.e., regenerative therapy).

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