Renal compensatory growth, after the loss of functioning parenchyme due to nephrectomy or hydronephrosis, is an important clinical phenomenon which often eventually results in glomerulosclerosis and renal failure. Thus numerous efforts have been made to elucidate the mechanism of compensatory growth and to discover the methods which can impede the compensatory process. Compensatory renal growth in mature animals is mainly by cellular hypertrophy, the increase in cellular component without increase in number of cells. But small portion of growth is composed of hyperplasia, the increase in total number of cells. To evaluate hyperplasia and hypertrophy, flowcytometry is employed. The DNA ploidy pattern of each kidney cell is analyzed, and the proportion of synthetic and replicating cells is calculated. For evaluation of hypertrophy, the presumed causative metabolite, nitric oxide, is indirectly titrated by measuring the activity of its key enzyme, nitric oxide synthase. The results of the experiment are as follows. 1. The increase in fraction of synthetic and replicating cells in flow cytometry is a definite evidence of cellular hyperplasia, thus hyperplasia is involved in neonatal compensatory renal growth. 2. Cellular hyperplasia is profound after 48 to 72 hours of injury 3. A statistically significant difference was noted at 12 hours after nephrectomy between control and experimental groups in G, + M phase (mitotic phase). 4. Nitric oxide is an important messenger of early (within 48 hours) renal compensatory growth in neonatal rats. 5. In view of the adult model experiment of nitric oxide synthase, where nitric oxide is confirmed to be involved in renal compensatory hypertrophy, nitric oxide is also related to the renal hypertrophy in neonatal periods. In conclusion, the compensatory renal growth in neonatal period is due to both hyperplasia and hypertrophy. Nitric oxide is a key signaling messenger of early compensatory renal growth, it can be stated that if the process of hypertrophy could be selectively blocked, prevention of renal failure as a consequence of glomerulosclerosis can be a reality.
Adult ; Animals ; Cell Division ; Cell Proliferation* ; DNA ; Flow Cytometry* ; Humans ; Hydronephrosis ; Hyperplasia ; Hypertrophy ; Kidney ; Nephrectomy ; Nitric Oxide Synthase* ; Nitric Oxide* ; Ploidies ; Rats* ; Renal Insufficiency

No abstract available.
Evidence-Based Medicine/methods ; Humans ; Male ; Minimally Invasive Surgical Procedures/methods ; Prostatectomy/*methods ; Robotic Surgical Procedures/*methods

No abstract available.
Aneurysm* ; Renal Artery*

Since the beginning of the 21st century, the emergence of innovative technologies has made further advances in minimal access surgery possible. Robotic surgery and telepresence surgery effectively addressed the limitations of laparoscopic procedures, thus revolutionizing minimal access surgery. Surgical robots provide surgeons with technologically advanced vision and hand skills. As a result, such systems are expected to revolutionize the field of surgery. In that time, much progress has been made in integrating robotic technologies with surgical instrumentation. However, robotic surgery will not only require special training, but it will also change the existing surgical training pattern patters and reshape the learning curve by offering new solutions, such as robotic surgical simulators and robotic telementoring. This article provides an introduction to medical robotic technologies, describesdevelops a possible classification, reviews the evolution of a surgical robot, and discusses future prospects for innovation. In the future, surgical robots should be smaller, less expensive, easier to operate, and should seamlessly integrate emerging technologies from a number of different fields. We believe that, in the near future Aas robotic technology continues to develop in the near future, we believe that almost all kinds of endoscopic surgery will be performed by this technology.
Hand ; Learning Curve ; Robotics ; Surgical Instruments ; Vision, Ocular

PURPOSE: Laparoscopic radical prostatectomy is an alternative to open prostatectomy in the surgical management of prostate cancer. The introduction of surgical robot to assist laparoscopic surgery served as a mechanical device to enhance the laparoscopic skills and improve surgical maneuverability with enhanced visual systems and the multi-axis articulating instruments. This review will introduce the evolution of surgical technique and current status of robotic-assisted laparoscopic prostatectomy. MATERIALS AND METHODS: A review of literatures is conducted with the homepage of Korean Urologic Association and PubMed, a search tool of the National Library of Medicine and the National Institutes of Health, including the MEDLINE database. RESULTS: After its approval by the United States FDA in 2000, the robotic technology has revolutionized the treatment of surgical management of prostate cancer. Robotic-assisted laparoscopic radical prostatectomy offers benefits of minimally invasive surgery with comparable oncological functional outcomes compared to standard surgical options. CONCLUSIONS: This technique is expected to evolve into one of the standard of care in treatment of localized prostate cancer.
Laparoscopy ; National Institutes of Health (U.S.) ; National Library of Medicine (U.S.) ; Prostatectomy ; Prostatic Neoplasms ; Standard of Care ; United States

Reference 14 on page 104 was accidentally omitted in the article, "Robot-Assisted Laparoscopic Radical Prostatectomy" authored by Koon Ho Rha, in the Korean Journal of Urology (Volume 50, Number 2). The following reference should be added to the REFERENCES section: 14. Lee SY, Jeong W, Park SY, Kim JH, Mah SY, Rha KH. Time to obtain continence after robot-assisted laparoscopic radical prostatectomy. Korean J Urol 2008;49(Suppl 1):211, abstract p-182.

PURPOSE: Carbon monoxide (CO) is produced during the degradation of hemoglobin to heme (iron protoporphyrin) and present in various tissues including brain. CO is believed to activate soluble guanylate cyclase to exert its action on the smooth muscles. the effects of CO and its relationships to adrenergic or cholinergic mechanisms were studied using the isolated rabbit corpus cavernosal strips, and the effects of CO and NO were further investigated. MATERIALS AND METHODS: Using adult New Zealand rabbits, the corpus cavernosal strip was carefully prepared from rabbit penis and suspended in an 10ml organ bath containing Tyrode solution. When a stable tension level of the strip had been attained, drugs were added to the organ bath the change of motility of the strip was recorded on a computerized polygraph. RESULTS: The NO donor, sodium nitroprusside (SNP) and CO caused a dosedependent relaxation of the cavernosal strip of the rabbit penis. Pretreatment of SNP and CO had no effect on contraction induced by adrenergic drugs and the effects of SNP and CO was not affected by atropine. The relaxation effects of SNP were inhibited by NO scavenger pyrogallol, inhibitor of soluble guanylate cyclase 1H-[1,2,4] oxadiazolo[4,3-a] quinoxalin-1-one (ODQ) and methylene blue. The relaxation effects of CO were significantly inhibited by ODQ and methylene blue. the relaxation effects by acetylcholine were inhibited by NO synthase inhibitor L-nitroarginine methyl ester (NAME) and deendothelialization, but not affected by zinc protoporphyrin (ZnPP), the heme oxidase inhibitor. On the immunostaining of heme oxidase (HO) in corpus cavernosal smooth muscle strip, the positive staining for HO was observed in the perivascular nerve fibers. CONCLUSIONS: The relaxation effect of NO was confirmed, and CO exerts an endothelium dependent relaxing effect on the cavernosal strip of the rabbit penis similar to NO. This action is seem to be mediated by soluble guanylate cyclase, and the actions of CO is also mediated by similar guanylate cyclase system.
Acetylcholine ; Adrenergic Agents ; Adult ; Atropine ; Baths ; Brain ; Carbon Monoxide* ; Carbon* ; Endothelium ; Guanylate Cyclase ; Heme ; Humans ; Male ; Methylene Blue ; Muscle, Smooth ; Nerve Fibers ; Nitric Oxide ; Nitric Oxide Synthase ; Nitroprusside ; Oxidoreductases ; Penis ; Pyrogallol ; Rabbits ; Relaxation ; Tissue Donors ; Zinc

PURPOSE: The increased incidence of urologic malignancy, especially transitional cell carcinoma in patient after renal allograft is well known. The aim of this study was to analyze the development of transitional cell carcinoma and its management. MATERIALS AND METHODS: Of 2,092 patients who underwent renal allograft at Severance hospital between April 1986 and August 2003, 10 (0.48%) had urologic malignancies. The clinical variables collected were patient age, age at renal allograft, cancer diagnosis time since renal allograft, cancer site, TNM stage, pathology and grade, treatment, recurrence and follow up tool. RESULTS: There were 6 men (median age at renal allograft 49.6, median age at cancer diagnosis 57.6) and 4 women (median age at renal allograft 54.5, median age at cancer diagnosis 62.8). There were two adenocarcinoma of prostate patients (0.10%), six transitional cell carcinoma patients (0.29%) and two squamous cell carcinoma of penis patients (0.10%). Sites of transitional cell carcinoma were bladder in five patients, renal pelvis in three patients, ureter in two patients, respectively. As a treatment, nephroureterectomy with bladder cuff resection for transitional cell carcinoma of renal pelvis or ureter, transurethral resection of bladder tumor with mitomycin C intravesical instillation for transitional cell carcinoma of bladder were done. No recurrence or metastasis was observed except transitional cell carcinoma of bladder. In four of five transitional cell carcinoma of bladder patients, multiple recurrences more than three times were observed. CONCLUSIONS: In patients after renal allograft, the transitional cell carcinoma always should be highly suspected. Aggressive follow up and management are indicated.
Adenocarcinoma ; Administration, Intravesical ; Allografts* ; Carcinoma, Squamous Cell ; Carcinoma, Transitional Cell* ; Diagnosis ; Female ; Follow-Up Studies ; Humans ; Incidence ; Kidney Pelvis ; Male ; Mitomycin ; Neoplasm Metastasis ; Pathology ; Pelvis ; Penis ; Prostate ; Recurrence ; Ureter ; Urinary Bladder ; Urinary Bladder Neoplasms

No abstract available.

To investigate the possibility of in vivo transplantation of Leydig cells as a new biologic androgen replacement therapy, the Leydig cells procured from 6 week-old male Sprague-Dawley rats were autotransplanted, and the level of testosterone secretion and histostructural changes were observed. The renal subcapsular and intraperitoneal transplant showed higher levels of testosterone compared to subcutaneous or scrotal counterparts, and the number of transplanted cells was correlated with the level of measured testosterone. Furthermore, if the Leydig cells were transplanted intraperitoneally after the uptake on synthetic collagen, testosterone levels were higher than the ones simply transplanted without synthetic collagen uptake, resulting in 27 fold increase at 3 months. The activity of 125I-hCG decreased 20 to 40% at each month after transplantation compared to the normal levels, but no statistical significance was noted among different periods. The histologic examination revealed neovascularized capillaries and well demarcated sheet-like group of eosinophilic Leydig cells were observed at 4 weeks. But the evidence of destructive changes such as a focal inflammation with central dystropic ossification could be noted after 3 month. On electron microscopy, the marked indentation of nucleus and presence of lipochrome pigment were seen, and the number and size of smooth endoplasmic reticulum and mitochondria were reduced after 3 month. In conclusion, testosterone output could be increased to the physiologic range by increasing the number of transplant cells or utilizing collagen uptake but further effort is necessary on delaying or preventing the structural and functional decrement of Leydig cells.
Animal ; Cell Count ; Leydig Cells/cytology/metabolism/*transplantation ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, LH/metabolism ; Support, Non-U.S. Gov't ; Testosterone/*biosynthesis ; Transplantation, Autologous