PURPOSE: To assess outcomes from patients who underwent radical prostatectomy and had their indwelling urinary catheter removed on postoperative day (POD) 4 or 7. MATERIALS AND METHODS: The medical records of 107 consecutive patients receiving radical prostatectomy (RP), were retrospectively reviewed. Patients were categorized into two groups according to length of catheterization. Group 1 (n=40) had the urethral catheter removed on postoperative day (POD) 4, and group 2 (n=67) had the catheter removed on POD7. Group 1 had urethral catheter removal following no leakage on intraoperative leak testing and POD4 cystography, whilst group 2 exhibited leakage at POD4 and instead had routine POD7 urethral catheter removal if there was evidence of no leakage of POD7 cystography. Incontinence was checked according to the use of protective pad. RESULTS: The mean age of the study population was 67.0 years. acute urinary retension (AUR) following catheter removal occurred in 6 of the cohort (5.6%); 3 patients (7.5%) from group 1 and 3 (4.5%) from group 2 (p=0.669). The overall continence rate was 39.3%, 68.2%, 80.4%, and 91.6% at 1, 3, 6, and 12 months respectively. Importantly, the incontinence recovery pace of group 1 was notably higher than that of group 2 (p=0.001). Neither group exhibited bladder neck contracture. Intraoperative factors influencing the decision to remove catheter at POD4 following RP, are bladder neck reconstruction (OR=3.792, p=0.010) and nerve sparing (OR=6.646, p=0.008). CONCLUSIONS: Selective early urethral catheter removal may shorten the length of incontinence recovery, without increasing the risk of AUR and bladder neck contracture.
Catheterization ; Catheters ; Cohort Studies ; Contracture ; Humans ; Medical Records ; Neck ; Prostatectomy* ; Prostatic Neoplasms ; Retrospective Studies ; Urinary Bladder ; Urinary Catheters*

Some patients with leprosy may present with atypical features, such as isolated peripheral neuropathy without skin lesions, or marked proprioceptive dysfunction. We report a 56-year-old female who presented with predominant proprioceptive loss without skin lesion, but was finally confirmed as leprous neuropathy by sural nerve biopsy. It is postulated that large myelinated fibers were affected by chronic immunological reactions triggered by inactive bacterial particles, producing a peripheral neuropathy presenting as predominant proprioceptive sensory loss without typical skin lesions.
Biopsy ; Female ; Humans ; Leprosy ; Myelin Sheath ; Organic Chemicals ; Peripheral Nervous System Diseases ; Proprioception ; Skin ; Sural Nerve

BACKGROUND/AIMS: The aim of this study was to evaluate targeting the epidermal growth factor receptors (EGFRs) of colon cancer cells with fluorescent magnetic nanoparticles (FMNP) conjugated to anti-EGFR antibodies. METHODS: The expression of EGFRs was evaluated in the HT-29 colon cancer cell lines and the control H-520 lung cancer cells by performing Western blot analysis. We synthesized silica-overcoated iron oxide nanoparticles that contained rhodamine B isothiocyanate (RITC) within a silica shell of a controllable thickness. This FMNP was conjugated to anti-EGFR mouse monoclonal antibody. The cells were treated with this probe conjugate for 4 hours and then the targeting was assessed via confocal microscopy. The fluorescence properties were evaluated for their binding to the expressed EGFRs with using a FACScan flow cytometer. RESULTS: EGFR was expressed in the HT-29 cells, as assessed by Western blot analysis. Red fluorescence was only detected in the membrane regions of the HT-29 cells on the confocal microscope imaging. On the FACS analysis, there was a significant shift of fluorescence intensity for the HT-29 cells. CONCLUSIONS: Our data show the feasibility of targeting colon cancer cells with FMNP conjugated with anti-EGFR antibodies in vitro.
Animals ; Antibodies ; Blotting, Western ; Cell Line ; Colon ; Colonic Neoplasms ; Ferric Compounds ; Fluorescence ; HT29 Cells ; Humans ; Iron ; Lung Neoplasms ; Magnetics ; Magnets ; Membranes ; Mice ; Microscopy, Confocal ; Nanoparticles ; Receptor, Epidermal Growth Factor ; Rhodamines ; Silicon Dioxide

BACKGROUND: Mac-2 binding protein (Mac-2BP) is a secreted glycoprotein from the culture fluid of several human cancer cells, especially breast, lung, and gastric cells. Mac-2BP plays a role in immune response and cell adhesion activity in patients with various cancer and infectious diseases. In this study, we attempted to identify the regulators of Mac-2BP expression at the transcriptional level. METHODS: To determine the effect of epidermal growth factor (EGF) to Mac-2BP expression in gastric cancers, we constructed the different lengths of Mac-2BP promoter plasmids and measured the promoter activity and Mac-2BP expression. In addition to investigating the role of signal transducer and activator of transcription3 (STAT3) or human telomerase reverse transcriptase (hTERT) as a regulator of Mac-2BP, we transfected the small interfering RNA (siRNA) specific for STAT3 or hTERT, and Mac-2BP level was observed by a quantitative ELISA. RESULTS: EGF treatment could suppress the Mac-2BP transcription in HEK293 or gastric cancer cell lines (SNU-638 or AGS). In 5'-deleted promoter experiment, pGL3-Mac Pro-2377 transfected cells showed a decreased luciferase activity compared to pGL3-Mac Pro-2277. We also identified that (-2,366/-2,356) on Mac-2BP promoter is a putative STAT3 binding site and suppression of STAT3 with STAT3 specific siRNA increased the Mac-2BP level, suggesting the role of STAT3 as a negative regulator, in contrast to hTERT, which is known as a positive regulator. CONCLUSIONS: EGF signal is critical for the Mac-2BP expression, and more importantly, STAT3 could work as a negative regulator, while hTERT as a positive regulator in Mac-2BP transcription.
Antigens, Neoplasm/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Down-Regulation ; Epidermal Growth Factor/metabolism ; Humans ; Membrane Glycoproteins/genetics/*metabolism ; RNA, Small Interfering ; STAT3 Transcription Factor/genetics/*metabolism ; Telomerase/metabolism ; Transfection

BACKGROUND: Human telomerase reverse transcriptase (hTERT) is a catalytic enzyme that is required for telomerase activity (TA) and cancer progression. Telomerase inhibition or inactivation increases cellular sensitivity to UV irradiation, DNA-damaging agents, the tyrosine kinase inhibitor, imatinib, and pharmacological inhibitors, such as BIBR1532. hTERT is associated with apoptosis. Some patients show drug-resistance during anti-cancer drug treatment and the cancer cell acquire anti-apoptotic mechanism. Therefore, we attempted to study correlation between hTERT and drug-resistance. METHODS: To study the correlation between protein level and activity of hTERT and drug-resistance, Western blotting and telomerase repeat amplification protocol (TRAP) assays were performed. To investigate whether hTERT contributes to drug resistance in tumor cells, we transiently decreased hTERT levels using small interfering RNA (siRNA) in T24/R2 cells. RESULTS: hTERT knockdown increased Bax translocation into the mitochondria and cytochrome C release into the cytosol. Caspase inhibitors, especially Z-VAD-FMK, rescued this phenomenon, suggesting that the stability or expression of hTERT might be regulated by caspase activity. CONCLUSIONS: These data suggest that hTERT might be a target molecule for drug-resistant tumor therapy.
Amino Acid Chloromethyl Ketones/pharmacology ; Antineoplastic Agents/*pharmacology ; Caspases/antagonists & inhibitors/metabolism ; Cell Line, Tumor ; Cisplatin/*pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; Cytochrome c Group/metabolism ; Drug Resistance, Neoplasm/genetics ; Humans ; Neoplasms/therapy ; RNA, Small Interfering ; Telomerase/*antagonists & inhibitors/genetics/metabolism ; bcl-2-Associated X Protein/metabolism

Although N-myc downstream regulated gene 2 (NDRG2) has been known to be a tumor suppressor gene, the function of this gene has not been elucidated. In the present study, we investigated the expression and function of NDRG2 in human gastric cancer. Among seven gastric cancer and two non-cancer cell lines, only two gastric cancer cell lines, SNU-16 and SNU-620, expressed NDRG2, which was detected in the cytoplasm. Interestingly, NDRG2 was highly expressed in normal gastric tissues, but gastric cancer patients were divided into NDRG2-positive and -negative groups. The survival rate of NDRG2-negative patients was lower than that of NDRG2-positive patients. We confirmed that the loss of NDRG2 expression was a significant and independent prognostic indicator in gastric carcinomas by multivariate analysis. To investigate the role of NDRG2 in gastric cancer cells, we generated a NDRG2-silenced gastric cancer cell line, which stably expresses NDRG2 siRNA. NDRG2-silenced SNU-620 cells exhibited slightly increased proliferation and cisplatin resistance. In addition, inhibition of NDRG2 decreased Fas expression and Fas-mediated cell death. Taken together, these data suggest that inactivation of NDRG2 may elicit resistance against anticancer drug and Fas-mediated cell death. Furthermore, case studies of gastric cancer patients indicate that NDRG2 expression may be involved in tumor progression and overall survival of the patients.
Apoptosis/*physiology ; Cell Line, Tumor ; Down-Regulation ; Fas Ligand Protein/*physiology ; Gene Expression Regulation, Neoplastic ; Humans ; Stomach Neoplasms/metabolism/*mortality/pathology ; Tumor Markers, Biological/*metabolism ; Tumor Suppressor Proteins/biosynthesis/genetics/immunology/*metabolism

BACKGROUND: Bcl-2 family proteins play a central role in regulating apoptosis. In human, over 20 members of this family have been identified to date. Bfl-1, a member of the Bcl-2 family, has been known to retard apoptosis in various cell lines. However, the function of Bfl-1 remains unclear. METHODS: In order to investigate the Bfl-1 function, we employed yeast two-hybrid system to identify the proteins which are capable of interacting with Bfl-1. The interaction of inhibitor kappaB kinase-beta (IKK-beta) and Bfl-1 was confirmed using glutathione S-transferase pull down assays. To determine which regions of IKK-beta were required for interaction with Bfl-1, we constructed 12 deletion mutants of IKK-beta and 5 deletion mutants of Bfl-1. RESULTS: Bfl-1 interacted with the C-terminal region of IKK-beta which is a subunit of IKK complex, and IKK-beta activity is very important in the NF-kappaB related pathway. In addition, the amino acids 673-745 of IKK-beta were important for Bfl-1 interactions, and amino acids 1-484 of Bfl-1, including Bcl-2 homology domains (BH1, BH2, BH3, BH4), were crucial for IKK-beta interactions. CONCLUSIONS: IKK beta C-terminus contains many serine residues as binding partner of Bfl-1. Our results suggested that Bfl-1 is involved in the NF-kappaB activation through interaction of IKK-beta and Bfl-1. Further studies need to be performed to understand functions of the IKK-beta and Bfl-1 associated with the regulation of the NF-kappaB activation pathway.
Amino Acids ; Apoptosis ; Cell Line ; Glutathione Transferase ; Humans ; I-kappa B Kinase ; NF-kappa B ; Serine* ; Two-Hybrid System Techniques

BACKGROUND: Neuronal death in acute-phase cerebral ischemic injury is caused by necrosis. However, neuronal injury after reperfusion can be associated with apoptosis. METHODS: We used Sprague-Dawley rats whose brains were reperfused after middle cerebral artery occlusion for either 30 min or 2 h. We examined a relationship between apoptosis and the expression of inducible nitric oxide synthase (iNOS) in the brain tissue from 3 h to 14 days after reperfusion in both groups. RESULTS: TUNEL and iNOS positivity were closely related in both groups. The 2-h ischemia group exhibited increases in the amount of TUNEL and iNOS-positive cells for up to 3 days after reperfusion, at which the TUNEL and iNOS-positive cells decreased. The 30-min ischemia group exhibited peak positivity 24 h after reperfusion, followed by a similar decrease. iNOS mRNA expression peaked 3 h after reperfusion in the 30-min ischemia group, at which time it decreased. In the 2-h ischemia group, iNOS mRNA increased 3 h after reperfusion, peaked 24 h after reperfusion, and then decreased. CONCLUSION: These results indicated the occurrence of delayed apoptosis in transient cerebral ischemia. Increased expression of iNOS is closely associated with this apoptosis, and oxygen free radical-producing materials, such as nitric oxide, may play an important role in the induction of this apoptosis.
Apoptosis* ; Brain ; Brain Ischemia* ; In Situ Nick-End Labeling ; Infarction, Middle Cerebral Artery ; Ischemia ; Ischemic Attack, Transient ; Necrosis ; Neurons* ; Nitric Oxide ; Nitric Oxide Synthase Type II* ; Oxygen ; Rats, Sprague-Dawley ; Reperfusion ; RNA, Messenger

Congenital duodenal web in adult life is an extremely rare condition, which results from an incomplete recanalization of the duodenum during early embryologic development. We report a case of congenital duodenal web in a 23-year-old man who complained of postprandial epigastric pain and fullness, as well as nausea since childhood. The plain abdomen showed a double-bubble sign. The UGI study showed a marked dilatation of the proximal duodenum and a delayed passage of barium into the third portion of the duodenum. Abdominal ultrasonography and CT revealed a marked dilatation of the proximal duodenum and a duodenal web with windsock deformity, which originated from the ampulla of Vater and extended to the third portion of the duodenum. A winsock web with a 0.9 cm eccentric aperture and a healed ulcer proximal to the ampulla of Vater were observed during a longitudinal duodenotomy. The web was excised circumferentially and the duodenum was closed transversely in a Heineke-Mikulicz fashion.
Abdomen ; Adult ; Ampulla of Vater ; Barium ; Congenital Abnormalities ; Dilatation ; Duodenum ; Humans ; Nausea ; Ulcer ; Ultrasonography ; Young Adult*

With the increasing number of interventional angiographic procedures, iodinated contrast induced nephropathy has become an important cause of iatrogenic acute renal failure. Gadopentetate dimeglumine, gadolinium chelated by DTPA, are widely used in magnetic resonance imaging without adverse effect on renal function in patients with renal insufficiency. It also has sufficient radiographic density to allow visualization and has been described as an alternative contrast agent for angiography. Here we report a case of successful angioplasty using gadopentetate dimeglumine as a contrast agent in a patient with both renal artery stenosis and renal insufficiency. The patient had a history of iodinated contrast induced acute renal failure. Using this contrast agent, angioplasty was successfully performed and contrast induced acute renal failure did not occur after this procedure.
Acute Kidney Injury ; Angiography ; Angioplasty* ; Gadolinium ; Gadolinium DTPA* ; Humans ; Magnetic Resonance Imaging ; Pentetic Acid ; Renal Artery Obstruction* ; Renal Artery* ; Renal Insufficiency*