Photocatalytic Properties of Plasma-Synthesized Aluminum-Doped Zinc Oxide Nanopowder.

Nano-sized aluminum-doped zinc oxide (AZO) powder was synthesized by a dc thermal plasma process using aluminum nitrate and zinc nitrate as the precursors. The injected precursors were vaporized in the plasma flame followed by vapor-phase reaction and subsequent quenching of the vaporized precursors produced nanosized AZO. XRD results indicate the presence of wurtzite structure without any alumina peaks and SEM micrographs revealed spherical particles. The nanosized AZO would make an excellent material for use as photocatalyst due to high surface to volume ratio. The photocatalytic properties of AZO nanopowder were investigated using the degradation of methylene blue under ultra-violet irradiation. The effects of various parameters, such as catalyst amount, the presence of oxidant, temperature, bubbling of O2 gas, pH, specific surface area, oxygen vacancies, and initial concentration, were studied. The optical study showed that doping leads to a red-shift in band gap. Furthermore, the AZO nanoparticles exhibited superior photocatalytic activity compared with ZnO. The improvement was ascribed to an increase in specific surface area and oxygen vacancies. Kinetic analyses indicated that the photodegradation of methylene blue followed a pseudo-first order kinetic model based on the Langmuir-Hinshelwood (L-H) mechanism.

[Prognostic impact of heart failure with preserved versus reduced ejection fraction in patients with mild symptoms]. / Prognostische Bedeutung der diastolischen versus systolischen Herzinsuffizienz bei Patienten mit klinisch milder Symptomatik.

BACKGROUND AND AIM: Previous studies have found a similarly impaired prognosis in patients with heart failure with preserved ejection fraction (HFpEF) as in patients with systolic heart failure (HFrEF). This study examines the prognosis of HFpEF patients with only mild symptoms and compares two different methods of diagnosing HFpEF. METHODS: Of 670 consecutive patients presenting in our outpatient clinic (57.6 ± 16 years, 50.1 % male), 165 revealed a typical clinical presentation with heart failure NYHA class II-III. The following echocardiographic parameters were assessed: ejection fraction (EF), left atrial size (LA), early and late antegrade mitral flow (E and A), early mitral annular movement (E'). Criteria for HFrEF were typical symptoms (NYHA II-III) and an EF < 50 %, HFpEF was diagnosed in patients with typical presentation, NYHA ≥ 2 and EF ≥ 50 % using 2 different definitions: similarly to the criteria of the I-Preserve study or as recommended by the german association of cardiology (DGK) that imply prove of diastolic dysfunction. Patients were followed-up for up to 2.5 years (mean 1.7±0.7) and the following events were registered: death, hospitalisation (myocardial infarction/coronary intervention/cardiac decompensation), cardiac transplantation (HTX). RESULTS: The majority (93.3 %) of the 165 heart failure patients had mild symptoms NYHA II. Of the 165 patients with typical symptoms, systolic heart failure could be found in 51 (30.9 %) and HFpEF according to I-Preserve criteria in 114 (69.1 %) patients. 56 (33.9 %) patients fulfilled the DGK criteria for HFpEF. Patients with HFpEF were significantly older, more often obese, female and hypertensive. The event rate was higher in patients with systolic heart failure (32 events, 62.7 %) than in patients with HFpEF (I-PRESERVE criteria: 28 events, 24.6 %; DGK criteria: 16 events, 28.6 %; both p < 0,001, log-rank), whereby this difference was mainly caused by increased hospitalisations (43.1 vs. 14.9 and 21,4 %, p < 0.001 and p < 0.016). Significantly more patients with HFrEF reached the combined end point death/HTX (p = 0.019 [I-Preserve] and p = 0.022 [DGK]). Both HFpEF groups showed no significant difference in any of the event types. CONCLUSION: Patients with HFpEF and mild symptoms have a more benign prognosis than those with systolic heart failure. Whether additional echocardiographic measurements are valuable for the diagnosis of HFpEF has to be proved in larger studies.

Clinical management of clopidogrel inefficiency by point of care platelet function testing and individual adjustment of anti-platelet therapy--initial experiences.

Insufficient inhibition of ADP dependent platelet aggregation by clopidogrel is associated with an increased risk for adverse coronary events, such as stent thrombosis, after percutaneous coronary intervention. Here, we describe an approach to the clinical management of patients with insufficient inhibition of ADP dependent platelet aggregation by clopidogrel involving dose adjustment or switching of the thienoyridine. We put special emphasize on a patient who experienced recurrent acute myocardial infarction due to stent thrombosis associated with severe clopidogrel non response following elective coronary drug eluting stent implantation. In this patient, an inadequate clopidogrel effect at maintenance doses was confirmed by repeated platelet function assessment with a multiple electrode impedance point of care platelet function test. Subsequent dose adjustments still did not result in sufficient inhibition of ADP dependent platelet aggregation. Only after switching to the then shortly available new thienopyridine prasugrel could a sufficient platelet inhibition be obtained. However, our data from further patients show that although this may overcome inadequate clopidogrel efficiency in many cases, even under prasugrel suboptimal platelet inhibition may occur.

Prothrombotic effects of diclofenac on arteriolar platelet activation and thrombosis in vivo.

BACKGROUND: Diclofenac, like selective cyclooxygenase-2 inhibitors, which alter vascular levels of platelet active prostaglandins, has been reported to increase rates of acute myocardial infarction. OBJECTIVE: The study was performed to investigate, in an animal model of arterial thrombosis in vivo, whether diclofenac differentially influences platelet activation and thrombosis in vessels under non-stimulated conditions or during acute systemic inflammation, such as induced by tumor necrosis factor-alpha (TNF-alpha). METHODS: Platelet-vessel wall interaction (PVWI), firm platelet adhesion and arterial thrombosis following vessel injury were analyzed by intravital microscopy in arterioles of hamsters in the dorsal skinfold chamber model. Prostacyclin [prostaglandin I(2) (PGI(2))] and thromboxane A(2) (TxA(2)) metabolites were measured. In vitro, endothelial adhesion molecule expression in cultured human microvascular endothelial cells was analyzed. RESULTS: Under non-stimulated conditions, diclofenac (1 mg kg(-1)) enhanced PVWI, which was not mediated by increased adhesion molecule expression, but by decreased systemic PGI(2) levels. Following ferric chloride-induced endothelial injury, diclofenac accelerated thrombotic vessel occlusion time, an effect that was reversed by the stable PGI(2) analog iloprost. TNF-alpha, through induction of endothelial adhesion molecule expression, also enhanced PVWI, firm adhesion, and arterial thrombosis, but simultaneous treatment with TNF-alpha and diclofenac did not have an additive effect. CONCLUSIONS: By decreasing levels of PGI(2) without, at the same time, altering prothrombotic TxA(2) levels, diclofenac can exert prothrombotic effects. However, this is not the case when an inflammatory situation is created by TNF-alpha treatment. These data may explain the enhanced risk of acute myocardial infarction observed in patients taking diclofenac.

Early time course of neointima formation and vascular remodelling following percutaneous coronary intervention and vascular brachytherapy of in-stent restenotic lesions as assessed by intravascular ultrasound analysis.

In-stent restenosis (ISR) represents the major limitation of stent implantation. Treatment, although of relative technical ease, is unsatisfactory due to a high incidence of recurrent restenosis. Vascular brachytherapy (VBT) has emerged as a powerful adjunct therapeutic modality to treat ISR. Inhibition of neointima formation has been regarded as the relevant mechanism of action. Yet, positive remodelling has been suspected as another contributing factor. Since only very few precise analyses of the extent, distribution and time course of the respective mechanims exist, the goal of the present study was to describe the changes of the vessel geometry at the target lesion and at the reference site following angioplasty and VBT of ISR in 42 patients by means of quantitative coronary angiography (QCA) and intravascular ultrasound (IVUS) before and after the index procedure and at the 3 and 6 month follow-up. By QCA the acute lumen gain measured 2.2+/-0.8 mm, the late lumen loss at 3 months was 0.1+/-0.5 mm and at 6 months 0.4+/-0.7 mm. By IVUS luminal cross-sectional area increased from 1.5+/-1.2 mm(2) to 7.9+/-1.9 mm(2) (p<0.001). The intima hyperplasia cross-sectional area at 3 months was only 0.2+/-1.0 mm(2) (p=0.191), but increased to 0.7+/-0.6 mm(2) (p<0.001) at 6 months resulting in a lumen cross-sectional area of 7.1+/-1.7 mm(2). Stent dimensions did not show any significant changes over time. The external elastic membrane cross-sectional area at 3 months increased by 1.3+/-1.9 mm(2) (p<0.001), and showed a further increase by 0.7+/-2.9 mm(2) at 6 months. Positive remodelling could be demonstrated also at the reference segment. In conclusion the absolute amount of intima hyperplasia during a 6-month follow-up period after VBT of ISR is low and most pronounced between the third and sixth month. Besides this, predominantly within the first 3 months of follow-up, significant positive remodelling could be demonstrated at the target lesion and at the reference site. Both observed effects may contribute to the preservation of the vessel lumen.

[Effect of immunosuppression-induced hypogonadism on bone metabolism after heart transplantation]. / Einfluss des Immunsuppressiva-induzierten Hypogonadismus auf den Knochenmetabolismus nach Herztransplantation.

BACKGROUND AND OBJECTIVE: Accelerated bone loss is a well recognized complication after cardiac transplantation (HTx). The role of an immunosuppressive-induced hypogonadism, a well-known cause of osteoporosis in men and its prevention are less defined after HTx. The aim of this study was first, to evaluate the incidence of hypogonadism after HTx and its influence on bone mineral metabolism and second, to assess the effect of a testosterone replacement therapy in hypogonadal transplants. PATIENTS AND METHODS: Due to hormonal status, 88 male cardiac transplants were randomised to a normogonadal or hypogonadal group. At baseline as well as after 1 and 2 years bone mineral density (BMD g/cm (2), T-score) was measured at the lumbar spine with DEXA. All patients received a basic therapy of calcium and vitamin D. The hypogonadal patients received additional testosterone. RESULTS: 21 patients (24 %) showed an age-independent hypogonadism. Hypogonadal transplants showed a significant lower BMD (p < 0.001) (BMD = 0.8070 g/cm (2), T-value = -2.6514) than normogonadal patients (BMD = 0.9882 g/cm (2), T-value = -1.0568). Despite testosterone replacement hypogonadal patients showed no significant additional increase in BMD over 1 - 2 years compared with the normogonadal. CONCLUSION: Male cardiac transplants in all age groups show an high prevalence of hypogonadism (approximately 25 %) which contributes to a significant bone loss. An additional testosterone substitution did not significantly increase BMD.

Antimicrobial and cytotoxic activity of 18 prenylated flavonoids isolated from medicinal plants: Morus alba L., Morus mongolica Schneider, Broussnetia papyrifera (L.) Vent, Sophora flavescens Ait and Echinosophora koreensis Nakai.

Antimicrobial activity of the 18 prenylated flavonoids, which were purified from five different medicinal plants, was evaluated by determination of MIC using the broth microdilution methods against four bacterial and two fungal microorganisms (Candida albicans, Saccaromyces cerevisiae, Escherichia coli, Salmonella typhimurium, Staphylococcus epidermis and S. aureus). Papyriflavonol A, kuraridin, sophoraflavanone D and sophoraisoflavanone A exhibited a good antifungal activity with strong antibacterial activity. Kuwanon C, mulberrofuran G, albanol B, kenusanone A and sophoraflavanone G showed strong antibacterial activity with 5-30 microg/ml of MICs. Morusin, sanggenon B and D, kazinol B, kurarinone, kenusanone C and isosophoranone were effective to only gram positive bacteria, and broussochalcone A was effective to C. albicans. IC50 values of papyriflavonol A, kuraridin, sophoraflavanone D, sophoraisoflavanone A and broussochalcone A in HepG2 cells were 20.9, 37.8, 39.1, 22.1, and 22.0 microg/ml, respectively. These results support the use of prenylated flavonoids in Asian traditional medicine to treat microbial infection and indicate a high potential for prenylated flavonoids as antimicrobial agents as well as anti-inflammatory agents.

[Hepatitis of unknown origin with protracted liver failure in a 48-year-old patient with significantly increased pANCA titer]. / Unklare Hepatitis mit protrahiertem Leberversagen bei einem 48-jährigen Patienten mit deutlich erhöhtem pANCA-Titer.

In spite of intense diagnostic testing, no cause for the chronically aggressive hepatitis of a 48-year old male patient was found. Evidence for an autoimmune process, however, could be derived from a high titer of pANCA. Only according to the revised criteria of the working group on autoimmune hepatitis, but not to the first version, it was possible to classify this as an autoimmune hepatitis. Despite of high-dose steroid treatment and accelerated preparation for liver transplantation the patient died of the complications of rapid liver failure. Thus, in case of unclear rapid progressive hepatitis, the revised criteria of autoimmune hepatitis should be reviewed early and with high priority and consequent high-dose steroid therapy and preparation for liver transplantation should be initiated. The prognostic impact of a high titer of pANCA in patients with autoimmune hepatitis remains to be established.

A new process for converting SO2 to sulfur without generating secondary pollutants through reactions involving CaS and CaSO4.

Nonferrous smelters and coal gasification processes generate environmentally harmful sulfur dioxide streams, most of which are treated to produce sulfuric acid with the accompanying problems of market shortage and transportation difficulties. Some sulfur dioxide streams are scrubbed with an alkali solution or a solid substance such as limestone or dolomite, which in turn generates wastes that pose other pollution problems. While the conversion of sulfur dioxide to elemental sulfur has many environmental advantages, no processes exist that are environmentally acceptable and economically viable. A new method for converting sulfur dioxide to elemental sulfur by a cyclic process involving calcium sulfide and calcium sulfate without generating solid wastes has been developed. In this process, calcium sulfate pellets as the starting raw material are reduced by a suitable reducing agent such as hydrogen to produce calcium sulfide pellets, which are used to reduce sulfur dioxide producing elemental sulfur vapor and calcium sulfate. The latter is then reduced to regenerate calcium sulfide. Thermodynamic analysis and experimental results indicated that the CaS-SO2 reaction produces mainly sulfur vapor and solid calcium sulfate and that the gaseous product from the CaSO4-H2 reaction is mainly water vapor. The rates of the two reactions are reasonably rapid in the temperature range 1000-1100 K, and, importantly, the physical strengths and reactivities of the pellets are maintained largely unchanged up to the tenth cycle, the last cycle tested in this work. Sulfur dioxide-containing streams from certain sources, such as the regenerator off-gas from an integrated gasification combined cycle desulfurization unit and new sulfide smelting plants, contain much higher partial pressures of SO2. In these cases, the rate of the first reaction is expected to be proportionally higher than in the test conditions reported in this paper.

Differential role of angiotensin II receptor subtypes on endothelial superoxide formation.

The physiological role of the angiotensin II AT2 receptor subtype is not fully characterized. We studied whether AT2 receptor could antagonize AT1 mediated superoxide formation in endothelial cells. In quiescent human umbilical vein endothelial cells (HUVEC) superoxide formation was measured after long-term incubation (6 h) with angiotensin II in the presence or absence of its receptor blocker candesartan (AT1) or PD123319 (AT2) using the cytochrome c assay. In separate experiments, the effects of AT2 mediated effects on activities of cellular phosphates including the src homology 2 domain containing phosphatases (SHP-1) was studied. The basal superoxide formation (0.19+/-0.03 nmol superoxide mg protein(-1) min(-1)) in HUVEC was increased by 37.1% after exposure to angiotensin II (100 nM,) which was due to an activation of a NAD(P)H oxidase. This was abolished by candesartan (1 microM) as well as the tyrosine kinase inhibitor genistein. In contrast, blockade of AT2 receptors by PD123319 enhanced the superoxide formation by 73.7% in intact cells. Stimulation of AT2 went along with an increased activity of tyrosine phosphatases in total cell lysates (29.8%) and, in particular, a marked stimulation of src homology 2 domain containing phosphatases (SHP-1, by 293.4%). The tyrosine phosphatase inhibitor vanadate, in turn, prevented the AT2 mediated effects on superoxide formation. The expression of both angiotensin II receptor subtypes AT1 and AT2 was confirmed by RT - PCR analysis. It is concluded that AT2 functionally antagonizes the AT1 induced endothelial superoxide formation by a pathway involving tyrosine phosphatases.

Ultradian oscillation of Saccharomyces cerevisiae during aerobic continuous culture: hydrogen sulphide mediates population synchrony.

Saccharomyces cerevisiae showed an ultradian respiratory oscillation during aerobic continuous culture. Analysis of the off-gas revealed that hydrogen sulphide production also oscillated. Production was first detected at the onset of low respiration and reached a maximum (1.5 microM) prior to minimum respiratory activity. Then H(2)S concentration fell rapidly to below 0.2 microM before the onset of high respiration. Injection of respiratory oscillation perturbation agents, such as glutathione (50 microM), NaNO(2) (50 microM) or acetaldehyde (4.5 mM),() transiently increased H(2)S production above 6 microM. The synchronization properties of H(2)S were analysed to reveal that changes of oscillation period and amplitude were dependent on H(2)S concentration in culture. It is concluded that H(2)S produced during oscillation produces population synchrony by respiratory chain inhibition.

The small G-protein Rac mediates depolarization-induced superoxide formation in human endothelial cells.

Superoxide anions impair nitric oxide-mediated responses and are involved in the development of hypertensive vascular hypertrophy. The regulation of their production in the vascular system is, however, poorly understood. We investigated whether changes in membrane potential that occur in hypertensive vessels modulate endothelial superoxide production. In cultured human umbilical vein endothelial cells, changes in membrane potential were induced by high potassium buffer, the non-selective potassium channel blocker tetrabutylammonium chloride (1 mm), and the non-selective cation ionophore gramicidin (1 micrometer). Superoxide formation was significantly elevated to a similar degree by all three treatments (by approximately 60%, n = 23, p < 0.01), whereas hyperpolarization by the K(ATP) channel activator Hoe234 (1 micrometer) significantly decreased superoxide formation. Depolarization also induced an increased tyrosine phosphorylation of several not yet identified proteins (90-110 kDa) and resulted in a significant increase in membrane association of the small G-protein Rac. Accordingly, the Rac inhibitor Clostridium difficile toxin B blocked the effects of depolarization on superoxide formation. The tyrosine kinase inhibitor genistein (30 micrometer, n = 15) abolished depolarization-induced superoxide formation and also prevented depolarization-induced Rac translocation associated with it. It is concluded that depolarization is an important stimulus of endothelial superoxide production, which involves a tyrosine phosphorylation-dependent translocation of the small G-protein Rac.

Pitfalls of using lucigenin in endothelial cells: implications for NAD(P)H dependent superoxide formation.

Since an increased endothelial superoxide formation plays an important role in the pathogenesis of endothelial dysfunction its specific detection is of particular interest. The widely used superoxide probe lucigenin, however, has been reported to induce superoxide under certain conditions, especially in the presence of NADH. This raises questions as to the conclusion of a NAD(P)H oxidase as the major source of endothelial superoxide. Using independent methods, we showed that lucigenin in the presence of NADH leads to the production of substantial amount of superoxide (approximately 15-fold of control) in endothelial cell homogenates. On the other hand, these independent methods revealed that endothelial cells without lucigenin still produce superoxide in a NAD(P)H-dependent manner. This was blocked by inhibitors of the neutrophil NADPH oxidase diphenyleniodonium and phenylarsine oxide. Our results demonstrate that a NAD(P)H-dependent oxidase is an important source for endothelial superoxide but the latter, however, cannot be measured reliably by lucigenin.

The 67-kDa laminin-binding protein is involved in shear stress-dependent endothelial nitric-oxide synthase expression.

It has been suggested that the mechanical forces acting on endothelial cells may be sensed in part by cell-matrix connections. We therefore studied the role of different matrix proteins, in particular laminin I, on a shear stress-dependent endothelial response, namely nitric-oxide synthase (eNOS) expression. Primary porcine aortic endothelial cells were seeded onto glass plates either noncoated (NC cells) or precoated with fibronectin (FN cells), laminin (LN cells), or collagen I (CN cells). Western blots were used to detect differences in the final matrix composition of these cells. A shear stress of 16 dyn/cm2 was applied for 6 h. Only LN cells showed detectable amounts of laminin I in their underlying matrix when they reached confluence. They reacted with a 2-fold increase of eNOS expression (n = 16, p < 0.001) to the exposure of shear stress, which went along with enhanced eNOS protein and NO release. In contrast, neither FN cells (n = 9) nor NC cells (n = 13) showed a significant increase of eNOS expression under shear stress. The increase in CN cells was borderline (1.4-fold; n = 9, p < 0.05) and was not associated with an increase of eNOS protein. The shear-induced increase in eNOS expression of LN cells was abolished by the peptide YIGSR, which blocks the cellular binding to laminin I via a 67-kDa laminin-binding protein, whereas a control peptide (YIGSK) had no effect. The induction of eNOS expression by shear stress is stimulated by an interaction of endothelial cells with laminin which is, at least in part, mediated by a 67-kDa laminin-binding protein.

Sensitive superoxide detection in vascular cells by the new chemiluminescence dye L-012.

The detection superoxide production in vascular cells is usually limited by a low sensitivity of available assays. We tested the applicability of the luminol derivate L-012 ¿8-amino-5-chloro-7-phenylpyridol¿3,4-dpyridazine-1,4(2H,3H)dione to measure superoxide production in cultured endothelial cells (human umbilical vein endothelial cells) and rat aortic segments. Following stimulation with the protein kinase stimulator phorbol 12-myristate 13-acetate (PMA, 1 microM) there was an 2.8-fold increase of L-012 chemiluminescence, whereas incubation with angiotensin II (100 nM) did not result in a measurable increase. Addition of vanadate (100 microM) considerably increased the chemiluminescence (up to 17-fold) after PMA and made possible the detection of an enhanced superoxide production after stimulation with angiotensin II (by 1.7-fold). This was due to a approximately 9-fold increase in signal intensity of L-012 in the presence of vanadate. Prolonged incubation with vanadate also led to a tyrosine phosphorylation-dependent increase in superoxide formation which was predominantly produced by an NAD(P)H oxidase. Short-term vanadate-enhanced L-012 chemiluminescence represents a highly sensitive assay making it possible to detect small changes of superoxide formation in intact vascular cells.

Clinical predictors of unstable coronary lesion morphology.

We evaluated prospectively clinical and angiographic data in 400 patients, 200 with unstable and 200 with stable angina in order to determine which clinical markers could reliably predict unstable coronary artery lesions. Comparison of the angiogram of 200 patients with unstable and 200 with stable angina revealed a high-grade lesion (42% vs 23%, P < 0.0001), complex lesion morphology (49% vs 20%, P < 0.0001) and thrombus-containing lesions (7% vs 1%, P = 0.006) as typical findings in patients with unstable angina. A high-grade lesion and/or complex lesion (including thrombotic lesions but excluding total occlusion) was found in 61% of unstable and 34% of stable patients (P < 0.0001). Clinical features including the Braunwald classification of unstable angina were then evaluated by means of a multivariate approach with regard to their ability to predict the presence of unstable coronary artery lesions. Multivariate analysis revealed an abnormal ECG as the single most predictive clinical indicator of complex lesion morphology (P < 0.0001, odds ratio 4,2). The clinical presentation of recent onset of angina was highly predictive of a high grade lesion (P = 0.0003, odds ratio 3,2). The endpoint of a high-grade and/or a complex lesion was identified by an abnormal ECG (P = 0.0015, odds ratio 3,0) and recent onset angina (P = 0.0119, odds ratio 2,5). Thus, a high grade and/or complex lesion, typical of patients with unstable angina, was best identified by the clinical feature of recent onset angina and/or abnormal ECG changes.

Flow cytometric analysis of DNA ploidy in primary non-small cell carcinoma of the lung in Korea.

Flow cytometrically determined nuclear DNA content has been measured on 74 formalin-fixed, paraffin embedded specimens of non-small cell carcinoma of the lung. Of the 60 tumors that were successfully analyzed, 32 (53%) were diploid and 28 (47%) were aneuploid. The mean DNA index of aneuploid tumor was 1.5 +/- 0.25, ranging from 1.1 to 2.0. There was no significant correlation between DNA ploidy and the patient's clinical characteristics, histology of tumor, nodal status or tumor stage. Tumor ploidy was not found as a prognostic determinant in non-small cell carcinoma of the lung in this study.

Tuberculous bronchial stenosis: CT findings in 28 cases.

Bronchial stenosis is a complication of tuberculous parenchymal or lymph node disease and may adversely affect its treatment. Findings on plain radiographs may be nonspecific or simulate malignancy. The purpose of this study was to evaluate the role of CT in diagnosing this abnormality. We reviewed the findings in 28 patients who underwent CT to evaluate bronchial stenosis proved by bronchoscopy. Eighteen had evidence of tuberculosis on bronchial biopsy. In the other 10 the biopsy findings were nonspecific, but tuberculous lesions were elsewhere in the thorax. Twelve patients (43%) had CT findings of concentric bronchial stenosis, uniform thickening of the bronchial wall, and involvement of a long segment of the bronchi. In 14 patients (50%), CT showed obliteration of bronchial outlines by adjacent lymphadenopathy, parenchymal consolidation, and absence of intraluminal air. In two patients, the abnormality was not visible on CT. Our experience shows that CT is useful for identifying bronchial stenosis caused by tuberculosis. However, the findings vary, and in more than half of the patients concentric narrowing and uniform thickening of the bronchi are not seen.

Phase II study of cyclophosphamide, doxorubicin, and vincristine (CAV) and etoposide plus cisplatin (EP) alternating chemotherapy combined with radiotherapy in small cell lung cancer.

The development of drug resistance is the major limiting factor influencing the survival of patients with small cell lung cancer (SCLC). We have thus examined the activity of cyclophosphamide, doxorubicin and vincristine (CAV) alternating with etoposide and cisplatin (EP) in 35 patients with SCLC. The treatment courses were alternated every 3 or 4 weeks. After induction chemotherapy, patients with limited disease (LD) received thoracic radiotherapy (5000 cGy), prophylactic cranial irradiation (3000 cGy) and maintenance chemotherapy and patients with extensive disease (ED) received maintenance chemotherapy only. In this group of 35 patients, 13 had limited disease (LD) and 22 had extensive disease (ED). After completion of the therapy, 100% of the patients with LD achieved complete plus partial remission (CR + PR) and 68% of the patients with ED achieved CR + PR. The median survival time was 66 weeks (15.3 months) in patients with LD and 44 weeks (10.2 months) in patients with ED. The over all survival for patients with LD was superior to that for patients with ED (p less than 0.05). Also, median response duration for patients with LD (35 wks) was longer than that for patients with ED (17 weeks) (p less than 0.05). The primary site was the most vulnerable site to relapse (18 patients). Toxicity was mild to moderate and acceptable, and there were no treatment-related deaths. These results suggest that the alternation of CAV and EP is effective treatment strategy in the management of SCLC. A randomized controlled study will be required to discriminate the actual effect of this alternating regimen.