Jin-Shyr Chen

Recurrence after skin-sparing mastectomy and immediate transverse rectus abdominis musculocutaneous flap reconstruction for invasive breast cancer

BackgroundThe aim of this study was to evaluate the recurrence pattern after skin-sparing mastectomy (SSM) and immediate breast reconstruction (IBR) using transverse rectus abdominis musculocutaneous (TRAM) flap in patients with invasive breast cancer.MethodsFrom 1995 to 2010, patients with invasive breast cancer who underwent SSM followed by IBR using TRAM flap were retrospectively reviewed. The pattern of the first recurrence event was recorded.ResultsWe identified 249 consecutive patients with invasive breast cancer, two-thirds of whom (67.1%) were diagnosed with stage II or stage III disease. During a median follow-up period of 53 months, three (1.2%) local, 13 (5.2%) regional, 34 (13.7%) distant, and five (2.0%) concurrent locoregional and distant recurrences were observed. The median time to recurrences was 26 months (range, 2 to 70 months) for all recurrences, 23 months (range, 2 to 64 months) for locoregional recurrences, and 26 months (range, 8 to 70 months) for distant recurrences. All local recurrent lesions were detectable by careful physical examination, and detection of local recurrence suggested the presence of distant metastasis (60.0%). In contrast to distant metastasis, the risk of locoregional recurrence did not increase significantly with an increase in disease stage. The 5-year overall, locoregional relapse-free, and distant relapse-free survival rates were 89.7%, 90.8%, and 81.6%, respectively.ConclusionsSSM followed by immediate reconstruction using TRAM flap is an oncologically safe procedure even in patients with advanced-stage disease. Detection of local recurrence is crucial and can be aided by a thorough physical examination.

Effect of calmidazolium on Ca2+ movement and proliferation in human osteosarcoma cells

1. In human MG63 osteosarcoma cells, the effect of calmidazolium on [Ca2+]i and proliferation was explored using fura‐2 and ELISA, respectively.

Short waves-induced enhancement of proliferation of human chondrocytes: involvement of extracellular signal-regulated map-kinase (erk).

1 Short‐wave diathermy (SWD) is a form of radiofrequency radiation that is used therapeutically by physiotherapists. The cellular mechanisms of SWD are unclear. The present study was performed to explore the effect of different conditions of short‐wave exposure on the proliferation of cultured human chondrocytes. 2 Cells exposed to short waves once per day for seven consecutive days exhibited a significant increase in proliferation by 42% compared with the control cells. In cells that were treated with short waves twice per day for seven consecutive days, or only once on Day 1 and then examined for proliferation on Day 7, cell proliferation was greater than the control cells by 40% and 30%, respectively. 3 Given the importance of mitogen‐activated protein kinases (MAPK) in the proliferation of different cell types, efforts were extended to explore the role of three major types of MAPK; that is, extracellular signal‐regulated kinase (ERK), c‐Jun NH2‐terminal protein kinase (JNK) and p38. 4. It was found that the level of phosphorylated ERK (phospho‐ERK 1 and ERK 2) increased significantly within 5–120 min following consecutive exposure to short waves for 7 days. Exposure to short waves failed to alter the intensity of phosphorylated JNK and p38 within 0–240 min. 5 Cells were exposed to short waves once for seven consecutive days in the presence of 0, 10 µmol/L, 20 µmol/L or 50 µmol/L PD98059 (an ERK inhibitor). PD98059 totally inhibited short waves‐induced enhancement of proliferation without altering normal control viability. In the presence of short waves and PD98059, the cell viability was lower than the normal control. Together, the data suggest that short waves could increase proliferation in human chondrocytes through activation of the ERK pathway, which is also involved in maintaining normal cell proliferation under physiological conditions.

Effect of the antidepressant maprotiline on Ca2+ movement and proliferation in human prostate cancer cells

1. The effect of maprotiline, an antidepressant, on human prostate cells is unclear. In the present study, the effect of maprotiline on [Ca2+]i and growth in PC3 human prostate cancer cells was measured using the fluorescent dyes fura‐2 and tetrazolium, respectively.

Ketoconazole-evoked [Ca2+]i rises and non-Ca2+-triggered cell death in rabbit corneal epithelial cells (SIRC).

The effect of ketoconazole on cytosolic free Ca2 + concentrations ([Ca2 +]i) and proliferation has not been explored in corneal cells. This study examined whether ketoconazole alters Ca2 + levels and causes cell death in SIRC rabbit corneal epithelial cells. [Ca2 +]i and cell viability were measured by using the fluorescent dyes fura-2 and WST-1, respectively. Ketoconazole at concentrations of 5 μ M and above increased [Ca2 +]i in a concentration-dependent manner. The Ca2 + signal was reduced partly by removing extracellular Ca2 +. The ketoconazole-induced Ca2 + influx was insensitive to L-type Ca2 + channel blockers and protein kinase C modulators. In Ca2 +-free medium, after pretreatment with 50 μ M ketoconazole, thapsigargin-(1 μ M)-induced [Ca2 +]i rises were abolished; conversely, thapsigargin pretreatment nearly abolished ketoconazole-induced [Ca2 +]i rises. Inhibition of phospholipase C with 2 μ M U73122 did not change ketoconazole-induced [Ca2 +]i rises. At concentrations between 5 and 100 μ M, ketoconazole killed cells in a concentration-dependent manner. The cytotoxic effect of 50 μ M ketoconazole was not reversed by prechelating cytosolic Ca2 + with BAPTA. In summary, in corneal cells, ketoconazole-induced [Ca2 +]i rises by causing Ca2 + release from the endoplasmic reticulum and Ca2 + influx from unknown pathways. Furthermore, the cytotoxicity induced by ketoconazole was not caused via a preceding [Ca2 +]i rise.

Defect in Regulation of Ca2+ Movement in Platelets from Patients with Systemic Lupus erythematosus

The differences in the intracellular Ca²⁺ responses to hormones in platelets from systemic lupus erythematosus (SLE) patients compared to normal humans have not been explored. This study examined the Ca²⁺ signaling and density of platelets in normal, inactive and active SLE patients. The platelet number per µl in inactive and normal groups did not differ, whereas the number in active SLE patients was smaller than the other two groups by 60%. The intracellular free Ca²⁺ levels ([Ca²⁺]_i) in response to stimulation of four endogenous Ca²⁺ mobilizing hormones, 100 µM arachidonic acid (AA), 10 µM ADP, 10 nM platelet activation factor (PAF) and 1 µM thrombin, were investigated using the Ca²⁺-sensitive fluorescent dye, fura-2. The AA-induced [Ca²⁺]_i rises in normal and inactive groups were similar. In contrast, the AA-induced [Ca²⁺]_i rises in the active SLE group were significantly smaller than in the normal and inactive groups. The defect in the AA-induced [Ca²⁺]_i rises in active SLE groups appears to be caused by defective Ca²⁺ influx and Ca²⁺ releasing pathways because the AA-induced responses were not altered by removal of extracellular Ca²⁺, whereas the AA-induced responses in normal and inactive SLE groups were reduced by removal of extracellular Ca²⁺, and the AA-induced Ca²⁺ release was smaller in the active SLE group. PAF, ADP and thrombin all induced [Ca²⁺]_i rises in the three groups, but no significant differences were found among the three groups. Together, the results indicate that cell density and Ca²⁺ signaling in platelets from active SLE patients are altered in response to particular stimulators. In these regards, platelets from inactive SLE patients appear to be similar to those from normal humans.

Median Nerve Recovery after Carpal Tunnel Release

Objective: Reports of nerve conduction studies following treatment for carpal tunnel syndrome are uncommon. To better understand the improvement of median nerve after release of compression over wrist in carpal tunnel syndrome patients, we studied the recovery from preoperative to postoperative period using neurophysiological methods. Design: prospective, early postoperative intervals neurophysiological investigations Materials and methods: From March 1999 to March 2000, seventeen carpal tunnel syndrome patients received minimal invasive carpal tunnel release surgery in Kaohsiung Veterans General Hospital. We compared the data of median nerve motor and sensory distal latencies, motor nerve conduction velocity, amplitudes of motor and sensory action potentials between preoperative and postoperative period. Results: We found the following: (1) The preoperative motor latency, sensory distal latency, and sensory amplitude of the median nerve of the carpal tunnel syndrome patients showed significantly abnormal in comparison with those of the normal groups. (2) The minimal invasive carpal tunnel release produced constant good result in carpal tunnel syndrome patients. (3) The median motor latency significantly improved 4wk after minimal invasive carpal tunnel release, but it took at least 8 wk for the median motor latency recovery back to normal. (4) The median sensory latency and amplitude significantly improved and back to normal since 8 wk after the operation. Conclusions: Minimal invasive carpal tunnel release is a useful method in treating carpal tunnel syndrome. The recovery of the median motor and sensory on the electrophysiological point of views is not apparent until 8 wk after operation.