Adult Flat Foot With Multiple Accessory Navicular Bones Treated Surgically: A Case Report and Review of the Literature.

Multiple accessory navicular bones is an extremely rare condition. To the best of our knowledge, only 8 cases in 2 imaging studies have been published. We report a case of a patient with flat foot with 2 accessory navicular bones. This patient needed to be treated surgically, and the surgery was successful, with short-term follow-up. We believe this is the first case of multiple accessory navicular bones to be treated surgically in English literature. The incidence of multiple accessory navicular bones might be higher. There is a risk to remaining ossicles without resection or fixation during surgery; therefore, we strongly recommend using not only radiographs, but also 3-dimensional computed tomography scans or magnetic resonance imaging scans to confirm the type of accessory navicular bone, at least before surgery, for both painful accessory navicular bone and flat foot with accessory navicular bone.

[Thymic basaloid carcinoma].

This is a case of a 72-year-old male whose chest computed tomography (CT) revealed a 2.0 x 1.6 cm anterior mediastinal solid tumor during follow-up of an abnormal shadow of the lung. The tumor increased its size during preoperative follow-up, and multilocular cyst was also observed. Radical thymectomy was performed, and histopathologically the tumor was diagnosed as thymic basaloid carcinoma. Thymic basaloid carcinoma is a rare tumor and is often associated with multilocular thymic cyst. There are only 32 cases reported both locally and internationally. Surgical resection is the general treatment for this disease. Adjuvant radiotherapy can be considered in cases of incomplete resection and invasive tumor. In our case, no recurrence of the tumor was noted 12 months post-operative. Generally, the malignancy of thymic basaloid carcinomas are regarded as low-grade compared with other thymic carcinomas, however, since mortality and recurrence have been reported, careful follow-up is required.

[Third-line CPT-11 chemotherapy for gastric cancer cases of non-curative gastrectomy or recurrence].

BACKGROUND: There have been few case reports of 3rd-line chemotherapy for gastric cancer. So we reported the results of CPT-11 therapy as the 3rd-line chemotherapy for gastric cancer. PATIENTS AND METHODS: 549 cases underwent gastrectomy from Jan. 2004 to Aug. 2007 in our hospital. In 76 of these cases, which underwent non-curative resection or evidenced a recurrence until July 2009, were analyzed in this study. CPT -11 3rd-line chemotherapy was administered to 11 cases. RESULTS: The mean survival time of non-curative or recurrent cases was 16.9 months. Mean survival times of the non-chemotherapy group, the group administered only 1st-line chemotherapy, the group administered until 3rd-line chemotherapy, the group administered 3rd-line chemotherapy were 7.9 , 11.3 , 21.4 and 28.9 months, respectively(p=0.000 ). Adverse effects occurred in 90.9% of 3rd-line CPT-11, however, all cases were categorized in GradeI. CONCLUSION: The group administered 3rd-line chemotherapy survived the longest. It is probably correct to administer 3rd-line chemotherapy, if the patient maintains a good performance status.

A sodium hyaluronate carboxymethylcellulose bioresorbable membrane prevents postoperative small-bowel adhesive obstruction after distal gastrectomy.

PURPOSE: It is predictable that since distal gastrectomy (DG) with Billroth I anastomosis involves no procedures caudal to transverse colon, the effects of the surgical wound are the main cause of adhesive obstruction. Thus, it is an appropriate operation to test the efficiency of a synthetic absorbable adhesion barrier (Seprafilm). METHODS: The subjects were 282 patients diagnosed with gastric cancer who underwent open DG with Billroth I anastomosis between 2001 and August, 2005. Seprafilm was not used in any patients operated on before April, 2003 (n = 169), but it was used in all patients operated on from May 2003 onward (n = 113). We retrospectively compared the incidences of adhesive obstruction in the Seprafilm group and the non-Seprafilm group. RESULTS: The cumulative incidence of adhesive obstruction was significantly lower in the Seprafilm group than in the non-Seprafilm group (P = 0.021). The respective incidences of adhesive obstruction 2 years after surgery were 0.9% and 6.5%. Multivariate analysis of the occurrence of adhesive obstruction revealed no significant differences in sex, age, body mass index, operation time, blood loss, or degree of lymph-node dissection; however, it revealed a significant difference in relation to the use of Seprafilm (P = 0.049). CONCLUSION: In this series, Seprafilm reduced the incidence of adhesive obstruction after DG significantly; however, a prospective randomized study will be necessary to confirm this result.

Breast cancer resistant protein (BCRP) is a molecular determinant of the outcome of photodynamic therapy (PDT) for centrally located early lung cancer.

The ATP-binding cassette (ABC) transporter protein, BCRP (breast cancer resistance protein)/ABCG2 pumps out some types of photosensitizers used in photodynamic therapy (PDT) and causes resistance to the antitumor effect of PDT. The purpose of this study was to investigate the association between the expression of BCRP and the efficacy of PDT using Photofrin, or the second-generation photosensitizer, NPe6, for centrally located early lung cancers. Using human epidermoid carcinoma cells, A431 cells and the BCRP-overexpressing A431/BCRP cells, we examined the effects of BCRP expression on the effect of PDT by cell viability assay in vitro, and investigated the expression of BCRP by immunohistochemical analysis in 81 tumor samples obtained from patients with centrally located early lung cancers. The A431/BCRP cells were more resistant to Photofrin-PDT than A431 cells in vitro, and Fumitremorgin C, a specific inhibitor of BCRP, reversed the resistance. However, there was no significant difference in the antitumor effect of NPe6-PDT between these cells. All of the 81 centrally located early lung cancer lesions were BCRP-positive (2+, 45 lesions; 1+, 30 lesions) and all the patients were male and heavy smokers (>30 pack-years). The expression of BCRP significantly affected the efficacy of Photofrin-PDT in cancer lesions > or =10mm in diameter (P=0.04). On the other hand, NPe6-PDT exhibited a strong antitumor effect, regardless of the expression status of BCRP. Photofrin may be a substrate of BCRP and be pumped out from the cells, therefore, BCRP may be a molecular determinant of the outcome of Photofrin-PDT.

Photodynamic therapy for lung cancers based on novel photodynamic diagnosis using talaporfin sodium (NPe6) and autofluorescence bronchoscopy.

BACKGROUND: We had previously developed the possibility of use of a photodynamic diagnosis (PDD) system using a tumor-selective photosensitizer and laser irradiation for the early detection and photodynamic therapy (PDT) for centrally located early lung cancers. Recently, we established the autofluorescence diagnosis system integrated into a videoendoscope (SAFE-3000) as a very useful technique for the early diagnosis of lung cancer. PATIENTS AND METHODS: Twenty-nine patients (38 lesions) with centrally located early lung cancer received PDD and PDT using the second-generation photosensitizer, talaporfin sodium (NPe6). Just before the PDT, we defined the tumor margin accurately using the novel PDD system SAFE-3000 with NPe6 and a diode laser (408nm). RESULTS: Red fluorescence emitted from the tumor by excitation of the photosensitizer by the diode laser (408nm) from SAFE-3000 allowed accurate determination of the tumor margin just before the PDT. The complete remission (CR) rate following NPe6-PDT in the cases with early lung cancer was 92.1% (35/38 lesions). We also confirmed the loss of red fluorescence from the tumors immediately after the PDT using SAFE-3000. We confirmed that all the NPe6 in the tumor had been excited and photobleached by the laser irradiation (664nm) and that no additional laser irradiation was needed for curative treatment. CONCLUSIONS: This novel PDD system using SAFE-3000 and NPe6 improved the quality and efficacy of PDT and avoided misjudgement of the dose of the photosensitizer or laser irradiation in PDT. PDT using NPe6 will become a standard option of treatments for centrally located early lung cancer.

Lysosomal cathepsin initiates apoptosis, which is regulated by photodamage to Bcl-2 at mitochondria in photodynamic therapy using a novel photosensitizer, ATX-s10 (Na).

ATX-s10 is a novel and second-generation photosensitizer for photodynamic therapy (PDT). In order to conduct clinical trials of ATX-s10-PDT and/or extend its clinical applications, it is very important to elucidate the mechanisms of the action of ATX-s10-PDT. We examined the apoptic response against ATX-s10-PDT using a Bcl-2 or Bcl-2 mutant overexpressing cells. Using fluorescent microscopy, ATX-s10 localized not only to mitochondria but also to lysosomes and possibly other intracellular organelles, but not to the plasma membrane or the nucleus. These results suggest that ATX-s10-PDT can damage mitochondria and lysosomes. By Western blot analysis, ATX-s10-PDT damaged Bcl-2, which localized preferentially at mitochondrial membranes, and caused Bcl-2 to cross-link immediately after laser irradiation. However, ATX-s10-PDT was not able to rapidly induce morphologically typical apoptosis (i.e. chromatin condensation and fragmentation) as PDT using mitochondria targeted photosensitizers, such as phthalocyanine 4 (Pc 4). Pharmacological inhibitions of lysosomal cytokine protease cathepsins, such as cathepsin B and D, protected MCF-7c3 cells (human breast cancer cells expressing stably transfected procaspase-3) from apoptosis caused by ATX-s10-PDT. Overexpression of wild-type Bcl-2 or Bcl-2Delta33-54 resulted in relative resistance of cells to ATX-s10-PDT, as assessed by the degree of morphological apoptosis or loss of clonogenicity. We conclude that lysosomal damage by ATX-s10-PDT can initiate apoptotic response and this apoptotic pathway can be regulated by photodamage to Bcl-2 via mitochondrial damage.