Risk of empyema in patients with end-stage renal disease: a nationwide propensity-matched cohort study.

BACKGROUND: Empyema is a rare but important complication among patients with end-stage renal disease (ESRD). However, a nationwide, propensity-matched cohort study has never been performed. METHODS: We conducted a retrospective cohort study using data from the National Health Insurance Research Database of Taiwan. The ESRD group consisted of 82 765 patients diagnosed between 2000 and 2008. The comparison group consisted of individuals without kidney disease selected at a 1:1 ratio matched by propensity score estimated with age, gender, year of diagnosis and comorbidities. The occurrence of empyema was monitored until the end of 2011. The hazard ratios (HRs) of empyema were estimated using the Cox proportional hazards model. RESULTS: The incidence of empyema was 2.76-fold higher in the ESRD group than in the comparison group (23.7 vs. 8.19/10 000 person-years, P <0.001), with an adjusted HR of 3.01 [95% confidence interval (CI) = 2.67-3.39]. There was no difference of the incidence of empyema between hemodialysis (HD) and peritoneal dialysis (PD) (adjusted HR = 0.96, 95% CI = 0.75-1.23). In addition, 30-day mortality rate since empyema diagnosis was significantly higher in ESRD group than the comparison group (15.9% vs. 10.9%), with an adjusted OR of 1.69 (95% CI = 1.17-2.44). CONCLUSION: The risk of empyema was significantly higher in patients with ESRD than in those without kidney disease. The occurrence of empyema was without difference in patients undergoing HD compared to those undergoing PD. The 30-day mortality rate since empyema diagnosis was also significantly higher in patients with ESRD.

The GroEL protein of Porphyromonas gingivalis accelerates tumor growth by enhancing endothelial progenitor cell function and neovascularization.

Porphyromonas gingivalis is a bacterial species that causes destruction of periodontal tissues. Additionally, previous evidence indicates that GroEL from P. gingivalis may possess biological activities involved in systemic inflammation, especially inflammation involved in the progression of periodontal diseases. The literature has established a relationship between periodontal disease and cancer. However, it is unclear whether P. gingivalis GroEL enhances tumor growth. Here, we investigated the effects of P. gingivalis GroEL on neovasculogenesis in C26 carcinoma cell-carrying BALB/c mice and chick eggs in vivo as well as its effect on human endothelial progenitor cells (EPC) in vitro. We found that GroEL treatment accelerated tumor growth (tumor volume and weight) and increased the mortality rate in C26 cell-carrying BALB/c mice. GroEL promoted neovasculogenesis in chicken embryonic allantois and increased the circulating EPC level in BALB/c mice. Furthermore, GroEL effectively stimulated EPC migration and tube formation and increased E-selectin expression, which is mediated by eNOS production and p38 mitogen-activated protein kinase activation. Additionally, GroEL may enhance resistance against paclitaxel-induced cell cytotoxicity and senescence in EPC. In conclusion, P. gingivalis GroEL may act as a potent virulence factor, contributing to the neovasculogenesis of tumor cells and resulting in accelerated tumor growth.

Increased risk of chronic obstructive pulmonary disease in patients with rheumatoid arthritis: a population-based cohort study.

BACKGROUND: The role of autoimmune pathology in development and progression of chronic obstructive pulmonary disease (COPD) is becoming increasingly popular. Our aim was to assess the association between patients with rheumatoid arthritis (RA) and subsequent COPD risk in a nationwide population. METHOD: We conducted a retrospective cohort study using data from the National Health Insurance system of Taiwan. The RA cohort included patients who were newly diagnosed and recruited between 1998 and 2008. Each patient was randomly frequency-matched for age, sex and the year of index date with people without RA from the general population. The newly diagnosed COPD was followed up until the end of 2010. The relative risks of COPD were estimated using Cox proportional hazard models after adjusting for age, sex, index year and comorbidities. RESULT: The overall incidence rate of COPD was 1.74-fold higher in the RA cohort than in the non-RA cohort (5.25 vs. 3.01 per 1000 person-years, 95% confidence interval (CI) = 1.68-1.81). Age-related risk analysis showed an increased incidence of COPD with age in both RA and non-RA cohorts. However, adjusted hazard ratio (HR) maximum was witnessed in the age range of 20-34 years (adjusted HR: 7.67, 95% CI=1.94-30.3), whereas adjusted HR minimum was observed in the oldest age group (>65 years). CONCLUSION: Patients with RA have a significantly higher risk of developing COPD than that of the control population. Further, age-related risk analysis indicated much higher adjusted HR in younger patients although COPD incidence increased with age. It can be hypothesized that in addition to cigarette smoke, RA may be a determining factor for COPD incidence and/or facilitates shortening of the time course for developing COPD. However, further investigation is needed to corroborate this hypothesis.

Lateral femoral wall thickness. A reliable predictor of post-operative lateral wall fracture in intertrochanteric fractures.

Although the importance of lateral femoral wall integrity is increasingly being recognised in the treatment of intertrochanteric fracture, little attention has been put on the development of a secondary post-operative fracture of the lateral wall. Patients with post-operative fractures of the lateral wall were reported to have high rates of re-operation and complication. To date, no predictors of post-operative lateral wall fracture have been reported. In this study, we investigated the reliability of lateral wall thickness as a predictor of lateral wall fracture after dynamic hip screw (DHS) implantation. A total of 208 patients with AO/OTA 31-A1 and -A2 classified intertrochanteric fractures who received internal fixation with a DHS between January 2003 and May 2012 were reviewed. There were 103 men and 150 women with a mean age at operation of 78 years (33 to 94). The mean follow-up was 23 months (6 to 83). The right side was affected in 97 patients and the left side in 111. Clinical information including age, gender, side, fracture classification, tip-apex distance, follow-up time, lateral wall thickness and outcome were recorded and used in the statistical analysis. Fracture classification and lateral wall thickness significantly contributed to post-operative lateral wall fracture (both p < 0.001). The lateral wall thickness threshold value for risk of developing a secondary lateral wall fracture was found to be 20.5 mm. To our knowledge, this is the first study to investigate the risk factors of post-operative lateral wall fracture in intertrochanteric fracture. We found that lateral wall thickness was a reliable predictor of post-operative lateral wall fracture and conclude that intertrochanteric fractures with a lateral wall thickness < 20.5 mm should not be treated with DHS alone.

Inhibition of peripheral blood natural killer cell cytotoxicity in patients with myasthenia gravis treated with plasmapheresis.

BACKGROUND AND PURPOSE: Myasthenia gravis (MG) is an autoimmune disorder that may involve natural killer (NK) cells. Although NK cells are part of the innate immune system, they also influence adaptive immune responses. Double-filtration plasmapheresis (DFP) is an effective therapy for MG crisis. Thus, we examined the effects of DFP on the cytotoxicity of NK cells. METHODS: A total of 20 patients with MG and 16 healthy controls were recruited for the study. Ficoll-Paque-isolated peripheral blood mononuclear cells (PBMCs) and K562 cells were used as the effector and target cells, respectively. NK cell cytotoxicity was analyzed using flow cytometry immediately before and after DFP and upon course completion. RESULTS: Double-filtration plasmapheresis treatment decreased significantly the NK cell cytotoxicity in patients with MG, especially in good responders, those who were positive for acetylcholine receptor (AChR) antibodies, and those receiving immunosuppressants. CONCLUSIONS: The decrease in NK cell cytotoxicity after DFP and the decline of AChR antibody titer were observed in good responders indicating that this could benefit patients with MG.

Changes in serum cytokine levels during plasmapheresis in patients with myasthenia gravis.

BACKGROUND: The effect of plasmapheresis on cytokine levels in patients with myasthenia gravis (MG) has not been well established. METHODS: Cytokine levels were measured in 19 patients with MG before and after treatment with one course of double-filtration plasmapheresis (DFP). The control group comprised 6 age- and sex-matched healthy volunteers. RESULTS: At baseline, patients with MG had higher levels of IL-10 than normal controls. The levels of IL-2, IL-4, IL-5, and tumor necrosis factor-alpha were almost undetectable in MG patients. After a single session of DFP treatment, IL-10 levels were significantly increased. After three sessions, IL-10 levels were still higher than those at baseline. Elevated IL-10 level was significantly associated with use of immunosuppressant drugs, thymectomy, and good response to DFP treatment. CONCLUSIONS: Interleukin-10 might play a crucial role in the pathogenesis and perpetuation of MG.

Cadmium-induced autophagy and apoptosis are mediated by a calcium signaling pathway.

The cytotoxicity of cadmium (Cd) induced autophagy and apoptosis in MES-13 cells was determined by flow cytometry. Autophagy was also assessed by formation of autophagosomes and processing of LC3. Pharmacological inhibition of autophagy resulted in increased of cell viability, suggesting autophagy plays a role in cell death in Cd-treated mesangial cells. Cd also induced a rapid elevation in cytosolic calcium ([Ca(2+)](i) ), and modulation of [Ca(2+)](i) via treatment with IP (3)R inhibitor or knockdown of calcineurin resulted in a change in the proportion of cell death, suggesting that the release of calcium from the ER plays a crucial role in Cd-induced cell death. Inhibition of Cd-induced ERK activation by PD 98059 suppressed Cd-induced autophagy, and BAPTA-AM eliminated activation of ERK. BAPTA-AM also inhibited Cd-induced mitochondrial depolarization and activation of caspases. These findings demonstrated that Cd induces both autophagy and apoptosis through elevation of [Ca(2+)](i), followed by Ca(2+)-ERK and Ca(2+)-mitochondria-caspase signaling pathways.

Autoantibodies against tumour suppressor protein p53 in pleural effusions of patients with tuberculosis pleurisy.

BACKGROUND: Autoantibodies against the p53 proteins (p53 Abs) can be detected in the serum, ascites, saliva and pleural effusions of various malignant patients. It is suggested that p53 Abs in pleural effusions might have some value for tumour diagnosis, prognosis or monitoring. The present study investigated the prevalence of p53 Abs in the pleural effusions of 90 patients with various diseases. METHODS: Patients with suspicious pleural effusions in chest film received thoracocentesis and their pleural effusions were collected. The presence of p53 Abs in effusion was detected by immunoblotting. Differences of p53 Abs with respect to the patient's age, gender, white blood cell count, lactate dehydrogenase, total proteins and adenosine deaminase scores were calculated by chi2-test. RESULTS: p53 Abs were detected in 14.4% (13/90) of our patients, with prevalences of 10.5% (6/57) and 21.2% (7/33) among patients with benign and malignant diseases, respectively. Notably, 16.1% (5/31) of patients with tuberculosis pleurisy were positive for p53 Abs. These five patients had no history of cancer and, so far, have had no manifestations related to tumorigenesis. CONCLUSIONS: As far as we know, this is the first report regarding the detection of p53 Abs in pleural effusions from patients with tuberculosis pleurisy.

Midazolam attenuates adenosine diphosphate-induced P-selectin expression and platelet-leucocyte aggregation.

BACKGROUND AND OBJECTIVE: The expression of P-selectin on the surface of platelets and platelet-leucocyte conjugate formation are considered to be an indicator of platelet activation in thrombotic and inflammatory disease. Midazolam is a widely used sedative and anaesthetic induction agent. It may inhibit platelet aggregation and suppress interleukin-6 and -8 response in human leucocytes, but any effect on the adhesion of activated platelets to leucocytes remains obscure. We have examined the influence of midazolam on adenosine diphosphate (ADP)-induced platelet surface P-selectin expression and platelet-leucocyte aggregation in whole blood. METHODS: Human whole blood was stimulated with 2 x 10(-5)M ADP in the presence of midazolam (3 x 10(-4) to 3 x 10(-6)M). Samples were stained with a fluorochrome-conjugated CD62P and CD41a antibody for detecting human platelet P-selectin antigens. The leucocyte subpopulations were separately gated and platelet-leucocyte aggregates were defined as cells found positive for CD45 and CD62P. All samples were analysed and were electronically separated into specific cell types (platelets, neutrophils, monocytes and lymphocytes) according to their typical forward/side scattering by flow cytometry. RESULTS: Midazolam significantly inhibited ADP-induced platelet P-selectin expression and attenuated platelet-leucocyte aggregation (mainly in neutrophils and monocytes) in a dose-dependent manner with a maximum inhibitory effect at 3 x 10(-4)M (P < 0.01). CONCLUSIONS: This study demonstrated that midazolam decreases the ADP-induced expression of platelet surface P-selectin and platelet-leucocyte aggregation.

Using technetium-99m tetrofosmin chest imaging to predict taxol-based chemotherapy response in non-small cell lung cancer but not related to lung resistance protein expression.

In vitro studies have shown that technetium-99m tetrofosmin (Tc-99m TF) is a transport substrate for the P-glycoprotein (Pgp) pump. Therefore, Tc-99m TF uptake of tumors can be used to predict chemotherapy response in lung cancers. However, whether lung resistance-related protein (LRP) expression affects tumor accumulation and efflux of Tc-99m TF in lung cancers is not known. Our aim was to use Tc-99m TF uptake of tumors to predict paclitaxel-based chemotherapy response of non-small cell lung cancer (NSCLC) and to compare Pgp or LRP expression. Twenty patients with advanced NSCLC received Tc-99m TF chest images before Taxol-based chemotherapy was used in this study. The chemotherapy response was evaluated by clinical and radiological methods in the third month after completion of treatment. No significant differences of prognostic factors (age, sex, body weight loss, performance status, tumor size, tumor stage, and tumor cell type) were found between the patients with good and those with poor responses. Early and delayed tumor/normal lung (T/L) uptake ratios were calculated on Tc-99m TF chest images. Immunohistochemical analyses were performed on multiple nonconsecutive sections of the biopsy specimens to detect Pgp and LPR expressions. The early and delayed T/L uptake ratios of 10 patients with good response were significantly higher than those of the other 10 patients with poor response. Significantly higher early and delayed T/L uptake ratios were found in patients with negative than those with positive Pgp expression ( p < 0.05). However, no significant differences of early and delayed T/L uptake ratios were found between patients with negative and positive LRP expressions ( p > 0.05). We found that Tc-99m TF imaging could accurately predict Taxol-base chemotherapy response. In addition, the Tc-99m TF tumor uptake was related to Pgp but not LPR expression in NSCLC.

Hepatitis B viral polymerase fusion proteins are biologically active and can interact with the hepatitis C virus core protein in vivo.

Hepadnaviruses and retroviruses are evolutionarily related families because they both require a process of reverse transcription for genome replication. However, hepadnaviruses produce polymerase (pol) and core proteins separately, while retroviruses synthesize a gag-pol fusion protein that is subsequently cleaved by a virally encoded protease to release a functional polymerase. To test whether an additional sequence at the N-terminus of pol in hepatitis B virus (HBV) interferes with its function, we created two plasmids expressing core-pol fusion proteins, core144-pol and core31-pol. Secreted particles obtained from HuH-7 cells, which were cotransfected with a core-pol fusion protein-expressing plasmid and a core-expressing plasmid, showed a positive signal of HBV DNA by the endogenous polymerase assay, indicating that the core-pol fusion proteins retain DNA priming, polymerization and RNase H activities. The fusion protein was detected in the cytoplasm of transfected cells and in secreted virions by immunoprecipitation. Furthermore, we found by immunofluorescence staining that the HBV core-pol fusion protein colocalized with the hepatitis C virus (HCV) core protein in cytoplasm and in lipid droplets. Immunoprecipitation studies showed that the anti-HCV core complex contained the HBV core-pol fusion protein while the anti-HBV pol complex contained the HCV core protein, which supports the hypothesis that the HCV core protein can form a complex with the HBV core-pol fusion protein.

Growth inhibition of cultured smooth muscle cells by corrosion products of 316 L stainless steel wire.

The potential cytotoxicity on vascular smooth muscle cells of corrosion products from 316 L stainless steel, one of most popular biomaterials of intravascular stents, has not been highlighted. In this investigation, 316 L stainless steel wires were corroded in Dulbecco's modified eagle's medium with applied constant electrochemical breakdown voltage, and the supernatant and precipitates of corrosion products were prepared as culture media. The effects of different concentrations of corrosion products on the growth of rat aortic smooth muscle cells were conducted with the [3H]-thymidine uptake test and cell cycle sorter. Both the supernatant and precipitates of corrosion products were toxic to the primary culture of smooth muscle cells. The growth inhibition was correlated well with the increased nickel ions in the corrosion products when nickel concentration was above 11.7 ppm. The corrosion products also changed cell morphology and induced cell necrosis. The cell growth inhibition occurred at the G0/G1 to S transition phase. Similar to our recent study of nitinol stent wire, the present investigation also demonstrated the cytotoxicity of corrosion products of 316 L stainless steel stent wire on smooth muscle cells, which might affect the poststenting vascular response.

Endovascular aortic graft exclusion of abdominal aortic aneurysm.

Endovascular repair of abdominal aortic aneurysms has evolved dramatically within the past few years. This study reports the first successful case in Taiwan area of infrarenal abdominal aortic aneurysm treated with endovascular aortic bifurcational stent-graft. Minimally invasive surgery leading to early recovery, mobilization and shortened hospital day was promising. In addition, there were no local, remote or systemic complications during a 18-month follow-up. Thus, the procedure is an attractive alternative in its potential to reduce morbidity and mortality associated with open surgical repair, especially for patients who are not surgical candidates because of comorbidities. Careful patient selection and more experiences with refined endograft models will elucidate the feasible alternative to conventional surgical repair.

Virus infection in patients with histiocytic necrotizing lymphadenitis in Taiwan. Detection of Epstein-Barr virus, type I human T-cell lymphotropic virus, and parvovirus B19.

The relationship of Epstein-Barr virus (EBV), type I human T-cell lymphotropic virus (HTLV-I), and parvovirus B19 to histiocytic necrotizing lymphadenitis was studied prospectively in 10 Taiwanese patients using materials obtained by fine-needle aspiration and lymph node biopsy. The presence of EBV was detected by in situ hybridization for EBV-encoded RNA expression. Immunocytochemistry was used to detect virus-encoded protein for EBV and parvovirus B19. DNA in situ hybridization and polymerase chain reaction were performed to determine the existence of HTLV-I provirus. Expressions of EBV-encoded RNA and Fas ligand were detected in all cases. Expression of EBV-encoded protein was identified in only 1 case. Neither HTLV-I nor parvovirus B19 was detected in any case.

Lack of evidence of association of p21WAF1/CIP1 polymorphism with lung cancer susceptibility and prognosis in Taiwan.

An association between the Arg allele of the p21WAF1/CIP1 codon 31 polymorphism and lung cancer has been reported. However, the genotype distribution of the p21 codon 31 polymorphism, as well as the association of this polymorphism with lung cancer risk and prognosis, remain undefined in the Taiwanese population. Therefore, we investigated the genotype distribution of the p21 codon 31 polymorphism in 155 lung cancer patients and 189 non-cancer controls. The genotype frequencies in the Taiwanese non-cancer controls were 0.51 (Ser) and 0.49 (Arg). Chi2 analysis indicated significant differences in Taiwanese genotype distribution of p21 from those reported for Swedes (P=0.001), Caucasians (P=0.001), Indians (P=0.001), and African-Americans (P=0.001). However, our data did not demonstrate an association of the Arg allele of the p21 polymorphism with lung cancer risk in Taiwan. Lung cancer patients with Ser/Arg and Arg/Arg genotypes were at a nonsignificant 1.15-fold increased risk of lung cancer when compared to individuals with the Ser/Ser genotype (95%CI, 0.70-1.86). In addition, although p21 is a downstream target of p53, we found no significant correlation of the p21 polymorphism with the p53 polymorphism and p53 gene mutation in lung cancer patients. We further investigated the association of the p21 polymorphism with prognosis in 154 lung cancer patients. Patients with the Ser/Ser genotype tended to have a poorer prognosis than those with the Ser/Arg and Arg/Arg genotypes (P=0.097, by the log rank test). Our data suggest that the p21 codon 31 polymorphism may not play a significant role in cancer susceptibility and the prognosis of lung cancer patients in Taiwan.

Partial or complete circular duodenectomy with highly selective vagotomy for severe obstructing duodenal ulcer disease: an initial experience.

OBJECTIVE: To evaluate partial and complete circular duodenectomy combined with highly selective vagotomy (HSV) for relief of gastric retention. DESIGN: A retrospective, case-comparison study. SETTING: University hospital referral center. PATIENTS: Eighteen patients with severe obstructing duodenal ulcer disease defined by failure of a saline load test and endoscopic narrowing of the gastric outlet to 5 mm or less. METHODS: In patients with severe obstructing ulcer the diseased duodenal segment was excised with electrocautery (partial excision, 10 patients; complete excision, 8 patients). An HSV was then done. Postoperative fasting gastric residuum measurement and measurement of the emptying of liquids and solids was done at 3 months and patients were weighed at 3 and 12 months. RESULTS: No patient experienced postoperative gastric retention or required reoperation in a 2-year follow up. The early emptying of liquid (20 minutes) in complete circular duodenectomy plus HSV was more rapid than in normal subjects and duodenal ulcer patients. The emptying of solids was slightly delayed in partial duodenectomy plus HSV compared with duodenal ulcer patients but not with normal controls. The emptying of solids in duodenal ulcer patients was more rapid than in normal controls. Weight gain was excellent at 3 and 12 months. CONCLUSION: Partial duodenectomy and complete circular duodenectomy plus HSV are more efficacious than alternative nonresective procedures in restoring gastric emptying to near normal and restoring weight in patients with obstructing duodenal ulcer.

Modulation of the trans-suppression activity of hepatitis C virus core protein by phosphorylation.

We previously demonstrated that the core protein of hepatitis C virus (HCV) can suppress gene expression and replication of hepatitis B virus (HBV) in a human hepatoma cell line (HuH-7). In this study, we have characterized the phosphorylation property of HCV core protein and examined the effect of phosphorylation on its suppressive activity of HBV. Our results indicated that both the full-length HCV core protein (22 kDa) and its processed or degraded forms (14 to 18 kDa) were phosphorylated in insect cells. As demonstrated by using the glutathione S-transferase fusion protein expression system and in vitro transcription and translation system, the phosphorylation of HCV core protein was carried out by protein kinase A (PKA) and protein kinase C (PKC) in vitro. In both kinase reactions, it was determined that the phosphorylated amino acid was a serine residue. The potential phosphorylated sites in core protein were identified as residues Ser-53 and Ser-116 for PKA and Ser-53 and Ser-99 for PKC. Comparison of the phosphorylation intensities of the wild type and Ser mutants suggested that Ser-99 and Ser-116 were the major phosphorylation sites for PKC and PKA, respectively. The phosphorylation of Ser-99 and Ser-116, but not Ser-53, in HCV core protein was essential for the suppressive activity of HCV core protein on HBV gene expression and replication in HuH-7 cells. Mutation of the former two serine residues to alanine or aspartate residues led to a drastic loss of the inhibitory effects of HCV core protein on HBV gene expression (both transcription and antigen production) and pregenomic RNA encapsidation, as well as the release of HBV virus particles. In contrast, the Ser-53 mutant conferred the same level of suppressive activity as the wild type did. This property is in accordance with the observation that Ser-99 and Ser-116 are the predominant phosphorylation sites in the HCV core construct. All serine mutants (including those with mutations in PKA, PKC, and both kinase recognition sites) of HCV core protein retained the ability to translocate into the nucleus. Furthermore, wild-type HCV core protein diminished its suppressive activity when cells were treated with PKA or PKC inhibitor. In conclusion, HCV core protein is a phospho-protein and in HuH-7 cells, its trans suppression of HBV gene expression and replication is positively regulated by PKA and PKC. The role of phosphorylation in the control of trans-suppressive activity cannot be reproduced by introducing an acidic residue.(ABSTRACT TRUNCATED AT 250 WORDS)

Ultrasound-guided biopsy of thoracic masses.

BACKGROUND: Fine needle aspiration cytologic examination may be sufficient for managing patients with primary lung cancer. However, the procedure is not reliable for benign lesions and metastatic lung cancers. An attempt was made to find the influence of cell type on the results of fine needle aspiration and cutting biopsy. METHODS: One hundred and sixteen patients with thoracic nodules or masses underwent chest ultrasound examination and percutaneous ultrasound-guided needle biopsy. All patients underwent ultrasound-guided fine needle aspiration biopsy (UGAB) and thirty-eight of them also underwent ultrasound-guided cutting biopsy (UGCB). Thoracic lesions were divided into seven groups. RESULTS: Using UGAB alone, the diagnostic rate varied from 56% (mediastinal tumor) to 91% (lung mass). When both methods of UGAB and UGCB were evaluated, the diagnostic rate varied from 67% (pulmonary nodule) to 100% (collapsed lung with mass and pancoast tumor). When thoracic lesions were divided into carcinomatous neoplasms (n = 88) and noncarcinomatous lesions (n = 21), a higher diagnostic rate was found in the carcinomatous group than in the noncarcinomatous group (92% versus 53%, p < 0.001). Correct histologic results between both groups had no statistical significance (64% versus 56%, p > 0.05). CONCLUSIONS: Ultrasound-guided needle biopsy has a high diagnostic yield of thoracic tumors, and carcinomatous masses can be easily diagnosed by UGCB. Noncarcinomatous masses and benign tumors frequently need UGAB to obtain a histologic diagnosis.

Use of signal-distinguishable probes in differential or sequential autoradiography in hybridization analysis.

To avoid the time-consuming reprobing process in hybridization analysis, signal-distinguishable probes (32P, 35S or antigenic hapten-labeled DNA) can be added to the same hybridization mixture. After hybridization, an unambiguous result can be obtained by differential or sequential autoradiography.