Predicted risk of childhood allergy, asthma, and reported symptoms using measured phthalate exposure in dust and urine.

UNLABELLED: The associated risk of phthalate exposure, both parent compounds in the home and their metabolites in urine, to childhood allergic and respiratory morbidity, after adjusting for exposures of indoor pollutants, especially bioaerosols, was comprehensively assessed. Levels of five phthalates in settled dust from the homes of 101 children (3-9 years old) were measured, along with their corresponding urinary metabolites. Other environmental risk factors, including indoor CO2, PM2.5, formaldehyde, 1,3-ß-D-glucan, endotoxin, allergen and fungal levels, were concomitantly examined. Subject's health status was verified by pediatricians, and parents recorded observed daily symptoms of their children for the week that the home investigation visit took place. Significantly increased level of benzylbutyl phthalate, in settled dust, was associated with test case subjects (allergic or asthmatic children). Higher levels of dibutyl phthalate and its metabolites, mono-n-butyl phthalate, and mono-2-ethylhexyl phthalate were found to be the potential risk factors for the health outcomes of interest. Similarly, indoor fungal exposure remained a significant risk factor, especially for reported respiratory symptoms. The relative contribution from exposure to phthalates and indoor biocontaminants in childhood allergic and respiratory morbidity is, for the first time, quantitatively assessed and characterized. PRACTICAL IMPLICATIONS: For asthmatic and allergic children living in subtropical and highly developed environments like homes in Taiwan, controlling environmental exposure of phthalates may be viewed as equally important as avoiding indoor microbial burdens, for the management of allergy-related diseases. It is also recognized that multidisciplinary efforts will be critical in realizing the true underlying mechanisms associated with these observations.

A dose-dependent relationship between the severity of visible mold growth and IgE levels of pre-school-aged resident children in Taiwan.

UNLABELLED: To demonstrate a dose-dependent relationship between severity of indoor visible mold growth and serum total IgE levels of resident children. A total of 97 children (4-7 years old) identified from previously established birth-cohort, with information pertaining to indoor environmental conditions after child's birth, were successfully recruited while sera were concurrently collected for total IgE and specific IgE analysis during clinical visits. Severity of visible mold growth at homes was scaled into three levels accordingly. A statistically significant dose-dependent relationship was found between severity of indoor visible mold growth and total serum IgE levels. The trend sustains after the model was adjusted for resident child's age, gender, pet-keeping history, number of siblings, atopic history of parents, presence of incense burning, and environmental tobacco smoking (ETS) at home. Further analysis of specific IgE to commonly examined fungal allergens did not substantiate the correlation. Rather, resident child's specific IgE to mite allergens, although without statistical significance, seemed to better associate with the ranked severity of indoor mold growth in this study. An adjuvant role of fungal exposure to enhance sensitization in indoor environment is therefore suggested in Taiwanese population with high prevalence of building dampness. PRACTICAL IMPLICATIONS: The presence of indoor visible mold growth, potentially resulting in fungal exposure, was not associated directly with changing biomarker levels of allergic response in resident children, rather playing an adjuvant role to enhance sensitization. On the other hand, other allergens, such as mite allergen examined in this study, appeared to support a more plausible etiology for directly triggering the ultimate allergic symptoms and diseases of interest. Evidence as such may derive different priority-setting when designing preventive measures for managing indoor air quality.

Cortactin overexpression in the esophageal squamous cell carcinoma and its involvement in the carcinogenesis.

The aim of this study is to examine whether dysregulated expression of cortactin occurs in esophageal squamous cell carcinoma (ESCC) and is involved in the development of ESCCs. An immunohistochemistry study for cortactin expression was performed on 46 pairs of surgically resected non-tumor and ESCC tumor tissues and murine tumors of esophagi induced by a carcinogen. The results show increased cortactin expression in 20 and in 22 to a lesser extent, out of a total 46 ESCC tumor tissues. Increased cortactin was also detected in the premalignant lesions, the early stage dysplasia and carcinoma in situ, of ESCC tumor tissues. Differential polymerase chain reaction results showed slight increases in the EMS1 gene only in two of 10 ESCC tumor tissues, suggesting that EMS1 gene amplification is not the only mechanism for cortactin overexpression. In the mouse model induced by treatment with 4-nitroquinoline 1-oxide and arecoline, increased cortactin was detected in the epithelia with hyperkeratosis, papillomas, and ESCCs with invasion into the submucosa, respectively. Overall, we observed cortactin overexpression in early and late stages of human ESCCs and carcinogen-induced murine ESCCs, suggesting a role for cortactin in esophageal carcinogenesis.

FHIT loss confers cisplatin resistance in lung cancer via the AKT/NF-κB/Slug-mediated PUMA reduction.

This corrects the article DOI: 10.1038/onc.2014.184.

Overexpression of ribonucleotide reductase in transfected human KB cells increases their resistance to hydroxyurea: M2 but not M1 is sufficient to increase resistance to hydroxyurea in transfected cells.

Ribonucleotide reductase (RR) is a rate-limiting enzyme in DNA synthesis. The enzyme consists of two subunits, M1 and M2. Hydroxyurea (HU) is an M2-specific inhibitor. It has been shown that a HU-resistant clone derived from stepwise exposure to HU overexpresses the M2 mRNA and the RR protein (Y. Yen et al., Cancer Res., 54: 3868-3691, 1994). In this study, we established stable clones by transfecting human KB cells with the cDNA of human wild-type RR in which each subunit was overexpressed by a SV40 promoter. The mammalian cell expression vector ph beta APr-1 was used for constructing M1, M2, and M1/M2 subunit cDNA. The transfected cells were selected with G418. The clones designated M2-D, M1-D, X-D, and KB-V represent transfectant clones which contain M2 cDNA, M1 cDNA, M1/M2 cDNA, and vector alone, respectively. The parental KB cells and clones containing vector plasmid KB-V express equally low amounts of M2 and M1 mRNA from the endogenous genes. The expression of M2 mRNA and M1 mRNA is elevated 2-3 fold in the X-D transfectants. M2-D clone demonstrated a 6-fold higher M2 mRNA level although the M1 mRNA expression remains the same as parental cells. M1-D transfectants have a 3-fold increase in M1 mRNA expression relative to parental cells, but reveal no alteration of M2 mRNA. Southern analysis of genomic DNA suggested the incorporation of the plasmid into the genome. The X-D clone revealed both integration of the M2 and M1 gene while the M2-D clone only showed M2 gene integration. The M1-D clone revealed M1 gene integration relative to the parental cells. The Western blot of M2 protein showed a 3-fold increase in the X-D and M2-D clones whereas the M2 protein level in M1-D was the same as it was in parental cells. The M1 protein was increased 3-fold in X-D and 1.5-fold in M1-D over that of parental cells. However, lower M1 protein levels were identified in the M2-D clone. The specific activity of the RR enzyme from each transfectant showed a 3-fold increase in both the X-D and M2-D clones and slightly increased in M1-D clone over that of parental cells. However, X-D and M2-D both demonstrated a 3-fold increase in resistance to HU as compared to M1-D which showed the same sensitivity as the parental enzyme.(ABSTRACT TRUNCATED AT 400 WORDS)

Overexpression of dihydrodiol dehydrogenase as a prognostic marker of non-small cell lung cancer.

By using mRNA differential display to examine specimens of non-small cell lung cancer (NSCLC), we have identified overexpression of dihydrodiol dehydrogenase (DDH) that was not detected in the corresponding normal lung tissue. Normally DDH is associated with catalysis of polycyclic aromatic hydrocarbons (PAHs) in the liver; in NSCLC cells, DDH expression would implicate an association with disease progression. In this study we investigated the prognostic significance of DDH expression in patients with NSCLC. By using immunohistochemistry, we measured DDH expression in 381 patients with NSCLC. The relationship between DDH expression and clinicopathological parameters (age, gender, smoking history, mitotic index, histological type, stage, cell differentiation, and lymphovascular invasion) was analyzed by chi2 analysis. Survival curves were plotted with the method of Kaplan-Meier, and statistical difference of survivals between different groups was compared by a log-rank test. Our results showed that DDH overexpression could be detected in 317 (83.2%) of 381 pathological sections and in 77.9% (60 of 77) of metastatic lymph nodes. Expression of DDH was confirmed by immunoblotting. Compared with patients with DDH overexpression in tumors, patients with low DDH expression had significantly lower incidence of early tumor recurrence and distant organ metastasis (46.7 versus 29.7%; P = 0.045). Interestingly, survival was also significantly better in patients with low DDH expression than in those with DDH overexpression (P = 0.0017). Using univariate analysis, we correlated three important factors, DDH overexpression, tumor stages, and gender, with poor prognosis for NSCLC patients. Nevertheless, biological function and involvement of DDH in the disease progression of NSCLC require additional studies.

Novel transmembrane GTPase of non-small cell lung cancer identified by mRNA differential display.

The technique of differential display was used previously to profile the gene expression patterns of non-small cell lung cancer, and several genes differentially expressed were thus identified. In this report, we demonstrate that a DNA fragment of 347-bp length, up-regulated in tumor tissues, showed 100% sequence similarity to human cDNA FLJ20693 for a 370-residue protein. The gene product of cDNA FLJ20693 was postulated to be a shorter isoform of transmembrane GTPase, termed TG370, based upon the results of searching for sequence homology. The nucleotide sequence alignment also indicated that the cDNA FLJ20693 and the cDNA for 741-residue human mitofusin 1 (TG741) possibly resulted from the event of alternative splicing from which a 127-bp region was retained in the latter. Analysis of the genome sequence confirmed the speculation that both cDNAs were mapped to the same chromosomal position composing of 18 exons, of which the 127-bp region of TG741 constituted exon 11. The alternative splicing in all lung cancer cell lines was also observed to occur nearly in all tissue specimens examined. The up-regulated expression of transmembrane GTPase was subsequently found in tumor tissues from at least five of seven non-small cell lung cancer patients. Also, a distinct PCR product was initially detected in cell line H520, and further sequence analysis identified the presence of the 86-bp region mapped to the genome sequence immediately followed by exon 10. To evaluate the retention of 86-bp region, it was found that, besides the predicted 486-bp product, an unexpected 332-bp product was concomitantly observed and identified as the result of exon 8 deletion. The expression and subcellular localization of the full-length TG741 and other shorter isoforms were detected by flow cytometry using three polyclonal antibodies. It was concluded that the full-length TG741 located at plasma membrane with its NH(2)-terminal domain exposed extracellularly and the shorter isoforms retained at cytosol. Finally, the up-regulation of transmembrane GTPase in tumor tissues was further illustrated using immunohistochemical staining.

Pre-tracheal lymph node metastasis in squamous cell carcinoma of the thoracic esophagus.

AIMS: To clarify the incidence of pre-tracheal lymph node metastasis in squamous cell carcinoma of the esophagus, and their impact on survival. METHODS: A cohort of 101 patients with squamous cell carcinoma of the thoracic esophagus who underwent esophagectomy together with 2-field lymphadenectomy including the pre-tracheal region was analysed, retrospectively. The p-TNM staging included stage I in 9, stage IIa in 33, stage IIb in 4, stage III in 43, and stage IV in 12 cases. RESULTS: Nodal metastases were identified in 56 patients (55.4%). Subcarinal lymph node and pre-tracheal lymph-node metastases were found in 24 patients (23.8%) and 15 patients (14.9%), respectively. The 5-year cumulative survival rates were 26.5 and 2.5% in nodal negative and nodal positive patients, respectively. Patients with pre-tracheal nodal metastasis all died within 2 years. Cox proportional hazards model in patients with nodal involvement revealed T-factor (p=0.0017), pre-tracheal nodal involvement (p=0.0055) and distant metastasis (p=0.0024) as independent prognostic factors. CONCLUSIONS: Our findings suggest that pre-tracheal lymph node metastasis indicates a dismal prognosis. Its occurrence is not unusual, especially in tumour of upper or middle thoracic esophagus. The subcarinal node cannot be regarded as a sentinel node of the pre-tracheal nodal station. Complete lymphadenectomy excluding the pre-tracheal lymph nodes in treating esophageal cancers is only a myth.

Expression of nm23 in the primary tumor and the metastatic regional lymph nodes of patients with gastric cardiac cancer.

Tumor recurrence and distant metastasis are major causes of treatment failure in gastric cardiac cancer (GCC). Rapid growth of tumor cells and reduced expression of nm23, a metastatic suppressor gene, in tumor cells have been suggested as two important mechanisms for disease progression of GCC. Therefore, to determine the prognostic value of nm23 expression in GCC, we used immunohistochemistry to examine the expression of nm23 in the pathological sections of both gastric cancer and metastatic lymph nodes from 24 stage III patients. Twenty-two patients had total gastrectomy, and two patients had proximal subtotal gastrectomy with a D2 dissection. Postoperative adjuvant therapy was provided, and the clinical responses were followed routinely. Clinical correlation was evaluated by chi2 with Fisher's exact test and survival by log-rank test. Our results show that the reduced nm23 expression in the primary tumor and in the nodal metastasis is the most useful marker for the poor prognosis of GCC following surgery.

FHIT loss confers cisplatin resistance in lung cancer via the AKT/NF-κB/Slug-mediated PUMA reduction.

Correction to: Oncogene (2015) 34, 2505­2515; doi:10.1038/onc. 2014.184; published online 7 July 2014. Since the publication of the above paper, the authors found a misplacing band in Figure 2e. The correct version of the figure is given below. The correction does not affect the validity of the data presented and does not limit the conclusions drawn in the paper. The authors apologize for this mistake.

c-Myc suppresses microRNA-29b to promote tumor aggressiveness and poor outcomes in non-small cell lung cancer by targeting FHIT.

The dual role of the microRNA-29 (miR-29) family in tumor progression and metastasis in solid tumors has been reported. Evidence for the role of miR-29 in tumor malignancy and its prognostic value in overall survival (OS) and relapse-free survival (RFS) in non-small cell lung cancer (NSCLC) remains conflicting. Mechanistic studies presented herein demonstrated that c-Myc suppressed the expression of miR-29b, promoting soft agar growth and invasion capability in lung cancer cells. Interestingly, the decrease in the expression of miR-29b by c-Myc is responsible for soft agar growth and invasiveness mediated by FHIT loss due to promoter methylation. Among patients, low expression of miR-29b and FHIT was more common in tumors with high c-Myc expression than in tumors with low c-Myc expression. Kaplan-Meier and Cox regression analysis showed that tumors with high c-Myc, low miR-29b and low FHIT expression had shorter OS and RFS periods than their counterparts. In conclusion, the decrease in the expression of miR-29b by c-Myc may be responsible for FHIT loss-mediated tumor aggressiveness and for poor outcome in NSCLC. Therefore, we suggest that restoration of the miR-29b expression using the c-Myc inhibitor might be helpful in suppressing tumor aggressiveness mediated by FHIT loss and consequently improving outcomes in NSCLC patients with tumors with low expression of FHIT.

FHIT loss confers cisplatin resistance in lung cancer via the AKT/NF-κB/Slug-mediated PUMA reduction.

Fragile histidine triad (FHIT) loss by the two-hit mechanism of loss of heterozygosity and promoter hypermethylation commonly occurrs in non-small cell lung cancer (NSCLC) and may confer cisplatin resistance in NSCLC cells. However, the underlying mechanisms of FHIT loss in cisplatin resistance and the response to cisplatin-based chemotherapy in NSCLC patients have not yet been reported. In the present study, inhibition concentration of 50% cell viability induced by cisplatin (IC50) and soft agar growth and invasion capability were increased and decreased in FHIT-knockdown and -overexpressing cells, respectively. Mechanistically, Slug transcription is upregulated by AKT/NF-κB activation due to FHIT loss and, in turn, Slug suppresses PUMA expression; this decrease of PUMA by FHIT loss is responsible for cisplatin resistance. In addition, cisplatin resistance due to FHIT loss can be conquered by AKT inhibitor-perifosine in xenograft tumors. Among NSCLC patients, low FHIT, high p-AKT, high Slug and low PUMA were correlated with shorter overall survival, relapse-free survival and poorer response to cisplatin-based chemotherapy. Therefore, the AKT inhibitor perifosine might potentially overcome the resistance to cisplatin-based chemotherapy in NSCLC patients with low-FHIT tumors, and consequently improve the outcome.

Bronchioloalveolar carcinoma.

Bronchioloalveolar carcinoma is a subtype of adenocarcinoma of the lung with a relatively better prognosis. We reviewed the cases of 50 consecutive patients with bronchioloalveolar carcinoma treated during a 10-year period and attempted to analyze factors related to prognosis. During the 10-year study period, the prevalence of bronchioloalveolar carcinoma relative to adenocarcinoma of the lung remained steady. The subjects included 32 male and 18 female patients with mean ages of 64.7 years and 55.1 years, respectively (p = 0.0030). The preoperative radiographic findings included 40 cases of localized and 10 cases of diffuse bronchioloalveolar carcinoma. The clinicopathologic TNM staging included 20 patients with stage I cancer, 4 with stage II cancer, 11 with stage IIIa cancer, 3 with stage IIIb cancer, and 12 with stage IV cancer. Forty patients with clinical stage I, II, or III disease underwent operation (operability 80%). The resectability rate was 90% (36 of 40). Thirty-four procedures were considered as curative. The overall cumulative survival at 5 years was 22.2% (46.4% for stage I). Different TNM stages showed significant differences in survival time (p = 0.0001). The median survival times were 64.6 months for stage I, 48.0 months for stage II, 24.7 months for stage IIIa, 9.0 months for stage IIIb, and 4.5 months for stage IV disease. The median survival time for localized bronchioloalveolar carcinoma was 27.5 months, and the median survival time for diffuse bronchioloalveolar carcinoma was 4.3 months (p = 0.0002). The median survival time for the curative resection group was 30.6 months, and the median survival time for the noncurative resection or nonresection group was 5.8 months (p = 0.0001). On the basis of this study we conclude that (1) the prevalence of bronchioloalveolar carcinoma is quite steady, (2) bronchioloalveolar carcinoma presents at an earlier age in women, (3) bronchioloalveolar carcinoma frequently presents with lymphatic spread or systemic metastasis at diagnosis, (4) most localized bronchioloalveolar carcinomas are resectable and the prognosis with this type is better than that of the diffuse type, and (5) long-term survival correlates closely with initial roentgenographic appearance, TNM stage, and completeness of surgical resection.

Clinical experience in radical lymphadenectomy for adenocarcinoma of the gastric cardia.

OBJECTIVES: We evaluated the pattern of nodal metastasis and its prognosis after radical lymphadenectomy in adenocarcinoma of the gastric cardia. METHODS: We conducted a retrospective cohort study of 70 patients (52 men and 18 women; mean age 63.6 years) with adenocarcinomas of the gastric cardia who underwent extended gastrectomy (65 total gastrectomies and 5 proximal gastrectomies) and radical lymphadenectomy (D2 to D4) at Taichung Veterans General Hospital between 1989 and 1995. RESULTS: Twenty-four complications developed in 22 (31.4%) patients, and seven (10.0%) hospital deaths occurred. An overall 5-year cumulative survival of 37.6% was obtained. Lymph node metastases were identified in 53 (75.7%) patients. Nodal involvement was closely related to the depth of tumor invasion (p = 0.005). When the gastric wall invasion was limited to the subserosal layer (T1 and T2, n = 15), no patient had N4 group nodal metastasis. Once the serosal layer had been involved (beyond T3), N4 group nodal metastasis was frequently seen (30.9%, 17 of 55 patients). A multivariable analysis revealed that the level of nodal involvement, the depth of tumor invasion, and the presence of complications were independent prognostic factors. Cumulative 5-year survivals of curability A (n = 12), B (n = 19), and C (n = 32) resections were 100%, 21.2%, and 27.5%, respectively (p = 0.0001). The long-term survival of the patients after resection was also closely related to their pTNM stages (p = 0.0004). CONCLUSIONS: We conclude that gastrectomy accompanied by radical lymphadenectomy provides a reasonable long-term survival expectancy that is closely related to the stage of the disease and the curability of resection.

Thymic carcinoma. Ten years' experience in twenty patients.

Thymic carcinoma is a rare neoplasm with extremely poor prognosis. To evaluate the outcome of treatment in thymic carcinoma, we reviewed a 10-year (1982 to 1992) experience with 20 consecutive patients in Taichung Veterans General Hospital. There were 9 men and 11 women: ages ranged from 34 to 70 years old (mean 51.4 years). None of these patients had concomitant myasthenia gravis. All of the patients received surgical intervention, and the diagnosis was made by pathologic study. Postoperative staging was made according to the modified Masaoka staging system. None of our patients were in stage I. One patient (5%) had stage II disease, 12 (60%) stage III, and 7 (35%) stage IV. The pathologic subtypes of thymic carcinoma included eight squamous cell carcinomas, seven undifferentiated carcinomas, one lymphoepithelioma-like carcinoma, one clear-cell carcinoma, 1 mucoepidermoid carcinoma, and two carcinoid tumors. Curative resection could be done in seven patients (35%). The overall cumulative survival was 45.9% at 3 years and 34.4% at 5 years. The median survival times for patients with complete and incomplete resection were 39.0 months and 14.3 months, respectively (p = 0.1752). The median survival times of patients with postoperative radiotherapy and without postoperative radiotherapy were 39.3 months and 15.0 months, respectively (p = 0.0738). The median survival times of patients with squamous cell carcinoma and undifferentiated carcinoma were 25.4 months and 11.3 months, respectively (p = 0.1464). Our data show that complete resection, postoperative radiotherapy, and squamous cell carcinoma do not indicate a significantly favorable result, even though they result in longer median survival times. Yet a positive trend of favorable outcome in patients who received postoperative radiotherapy is ambiguously shown.

Surgical experience in treating T4 lung cancer: its resectability, morbidity, mortality and prognosis.

Extensive experience in the treatment of locally advanced lung cancers is rare. The aim of this study is to show the rationality and effectiveness of an aggressive surgical approach in T4 lung cancers. Between 1984 and 1994, 111 consecutive cases of T4 lung cancers were operated on. The patients included 91 males and 20 females, with mean ages of 61.8 years and 55.3 years, respectively. The cell types included 57 squamous cell carcinomas, 42 adenocarcinomas, and 12 miscellaneous malignancies. Fifty-three (47.7%) procedures were non-resectional. The remaining 58 (52.3%) procedures had various extents of pulmonary resection. These surgical procedures included 24 (21.6%) pulmonary resections with gross residual tumour (R2), nine (8.1%) pulmonary resections with microscopic residual tumour (R1), and 25 (22.5%) curative pulmonary resections without residual tumour (R0). Post-operative adjuvant therapy included radiotherapy ( > or = 3000 rads) in 53 patients (47.7%), and cisplatin-based chemotherapy in 15 patients (13.5%). The overall median survival time of these 111 patients was 9.1 months. The overall cumulative survival rates at 1, 2, 3 and 5 years were 38.0%, 20.4%, 15.3%, and 5.5%, respectively. There were 24 (21.6%) complications and eight (7.2%) hospital mortalities. Most of the pleural seedings were caused by adenocarcinomas, while most of the curatively resected tumours were squamous cell carcinomas. Our data demonstrate that: (1) Almost a quarter (22.5%) of T4 lung cancers could be curatively resected, and the cumulative 5-year survival rate was 23.4%; (2) squamous cell carcinoma had a higher curative resection rate (P = 0.0381), while adenocarcinoma showed higher possibility of pleural seeding (P = 0.0000); (3) the prognosis of T4 lung cancers did not relate to their nodal status (P = 0.7978), and cell type (P = 0.4169); (4) complete surgical resection provided the best rates for long-term survival (P = 0.0263); (5) the complication rate was higher in the resectional group (P = 0.0221); (6) post-operative irradiation did not lengthen survival times (P = 0.1720); and (7) post-operative chemotherapy did not improve survival (P = 0.1577). We conclude that surgery to T4 lung cancers should only be performed in highly selected patients due to their poor prognosis, and the associated high complication and mortality rates.

Detection of esophageal carcinoma using single-photon emission computed tomography of thallium-201: a preliminary report.

The aim of this preliminary study was to evaluate the potential usefulness of thallium-201 (Tl-201) in detecting esophageal carcinoma. A total of 15 patients with esophageal carcinoma were arranged for Tl-201 single-photon emission computed tomography (SPECT) of the chest. Thirteen of the patients had epidermoid carcinoma and two had adenocarcinoma. Meanwhile, 7 normal controls without any history of esophageal disease also accepted Tl-201 SPECT of the chest for comparison. From the 15 patients, Tl-201 chest SPECT detected esophageal carcinoma in 13 (86.7%) but not in 2 (13.3%) patients with epidermoid carcinoma. In contrast, all 7 normal controls (100.0%) had negative results of Tl-201 chest SPECT. Our study showed that the Tl-201 chest SPECT scan could be considered as a non-invasive useful imaging method in detection of esophageal carcinoma.

Comparison between the right side and subxiphoid bilateral approaches in performing video-assisted thoracoscopic extended thymectomy for myasthenia gravis.

BACKGROUND: This study aimed to compare the efficacy of the right thoracoscopic (RtT) approach and the subxiphoid bilateral thoracoscopic (SxBiT) approach in performing thymectomy for myasthenia gravis. METHODS: Between March 2001 and April 2003, 27 myasthenic patients were enrolled in this prospective study. The operations were conducted by two surgical teams in a single institute. The surgical procedures included RtT for 12 patients and SxBiT for 15 patients. The operation time, resected thymus weights, and thoracic drainage periods were compared. RESULTS: Subxiphoid video-assisted thoracoscopic extended thymectomy (SxVATET) and right-side thoracoscopic extended thymectomy (RtVATET) were performed for 27 consecutive myasthenic patients. The mean operation time, weights of resected specimens, and duration of hospital stay for the SxVATET and RtVATET groups were, respectively, 151.3 min (range, 120-200 min) versus 191.5 min (range, 120-225 min) (p = 0.0012), 73.3 g (range, 40-90 g) versus 50.8 g (range, 5-90 g) (p = 0.0029), and 3.1 days (range, 2-4 days) versus 3.8 days (range, 2-4 days) (p = 0.914). Ten patients (37%) had complete remission, observed during a mean follow-up period of 18.5 months (range, 6-30 months). CONCLUSIONS: During this consecutive experience, both the RtT and SxBiT approaches showed satisfactory results for nonthymomatous myasthenic patients. However, a better view of the bilateral pleural cavities and more radical thymectomy could be achieved only by the SxBiT approach.

Detection of k-ras point mutations in codons 12 and 13 in non-small cell lung cancers.

Point mutations of the K-ras gene have been reported in a wide variety of human tumors. By using polymerase chain reaction followed by direct DNA sequencing, we screened for point mutations at codons 12 and 13 of the K-ras gene in specimens obtained from fresh frozen tumors in 38 patients with non-small cell lung cancers. Point mutations were detected in two of 38 (5.3%) resected non-small cell lung cancers. Both of them were G to T transversions. One patient was found to have a K-ras codon 13 point mutation (GGC to TGC, gly to cys), while the other had a codon 12 point mutation (GGT to GTT, gly to val). Based on the limited numbers in this study, we found that the frequency of K-ras point mutations in codons 12 and 13 among Asian patients with lung adenocarcinomas was lower than that detected among Caucasian patients.

Comparison of different diagnostic methods for lupus pleuritis and pericarditis: a prospective three-year study.

BACKGROUND AND PURPOSE: Pleural or pericardial effusions, or both, are commonly encountered, but the differential diagnosis is sometimes difficult. We evaluated the diagnostic value of effusion immunofluorescent antinuclear antibody (ANA) titer, systemic lupus erythematosus (SLE) latex agglutination slide test, and cytologic LE cell examination in patients with pleural and/or pericardial effusions of various etiologies. METHODS: A total of 153 pleural and/or pericardial effusion specimens were collected by aspiration from 152 patients (14 SLE and 138 non-SLE patients). All specimens were sent for routine biochemistry testing, determination of ANA titer, SLE latex agglutination slide test, and LE cell examination. RESULTS: Ten of the 14 SLE patients had lupus serositis and all of them had high ANA titers (> or = 1:160) in their effusions. SLE latex and LE cell tests were positive in seven and eight patients with lupus serositis, respectively. The remaining four SLE patients with effusion of etiologies other than lupus serositis had low or negative effusion ANA titers. Among the non-SLE patients, 29 of 112 patients (26%) with pleural effusion and six of 26 patients (23%) with pericardial effusion had positive ANA tests (> or = 1:40). None of them had a positive SLE latex or LE cell test result. Thirteen of the 138 non-SLE patients (11%) had high effusion ANA titers (> or = 1:160). Effusion in 11 of 13 non-SLE patients (85%) was due to malignancy. CONCLUSIONS: Effusion ANA titer detection is a very sensitive but nonspecific test for the diagnosis of lupus serositis. SLE latex and cytologic LE cell tests can aid in the differential diagnosis as complementary tools. The specificity, positive and negative predictive values of these two tests are excellent for the diagnosis of lupus serositis.