The degree of polymerization of inulin-like fructans affects cecal mucin and immunoglobulin A in rats.

Cecal amounts of mucin and immunoglobulin A (IgA) were examined through the cecal fermentation pattern in Wistar (WS) or Sprague-Dawley (SD) rats fed inulin-type fructans differing in their degree of polymerization (DP). The animals were fed a control diet or a diet containing one of the fructans with an average DP of 4, 8, 16, or 23, at 60 g/kg diet for 10 d. Cecal fermentation products substantially differed between WS and SD rats fed DP8 fructan, with short-chain fatty acids (SCFAs) as the major organic acids in the former but lactate predominating in the latter. Cecal fermentability of fructans in both strains generally decreased with increasing DP of fructans, and this was especially manifest in reduction of the amounts of lactate in DP16 and 23. In WS rats, cecal mucin and IgA were greater in all fructan groups than in the control group. In SD rats, cecal mucin was greater only in the DP8, 16, and 23 groups as compared to the control group, while IgA was greater in the DP4 and 8 groups. In both strains, cecal mucin correlated with the sum of cecal SCFAs, but not with lactate, succinate, or total organic acids. In contrast, only cecal lactate correlated with cecal IgA in both strains. The present study shows that the different fermentation patterns of fructans affect cecal mucin and IgA; mucin is likely to respond to cecal SCFA production, whereas IgA increases when fermentation occurs rapidly and lactate is a major fermentation product.

In vitro biocompatibility of a new titanium-29niobium-13tantalum-4.6zirconium alloy with osteoblast-like MG63 cells.

BACKGROUND: Titanium-29niobium-13tantalum-4.6zirconium (TiNb) has recently been developed as a new implant material. TiNb is composed of non-toxic elements and has a lower modulus of elasticity than the other titanium alloys. However, its biocompatibility has not been adequately characterized. The aim of this study was to evaluate the biocompatibility of TiNb using an osteoblast-titanium co-culture system. METHODS: MG63 cells were cultured on three kinds of titanium disks: TiNb, pure titanium (pTi), and titanium-6aluminum-4vanadium (TiAl), prepared with two different surfaces, a polished and acid-etched surface and a machined-grooved surface. The surface topography and roughness were evaluated by scanning electron microscopy (SEM). After 48 hours culture, the number of proliferating cells and prostaglandin E2 (PGE2) production in the culture supernatant were determined. RESULTS: There was no significant difference in surface roughness among the three titanium disks with a polished and acid-etched surface. After 48 hours of culture, the number of cells was significantly reduced on pTi and TiAl compared to TiNb and the control. PGE2 production was significantly higher on pTi than on TiAl, TiNb, and the control. We further examined the effect of surface roughness on PGE2 production using machine-grooved titanium disks. While pTi and TiAl stimulated the production of PGE2 depending on surface roughness, roughened TiNb did not affect PGE2 production. CONCLUSIONS: These results suggest that TiNb may exhibit favorable biocompatibility because it has an efficient surface topography for cell proliferation, and the level of PGE2 production does not depend on surface roughness. We conclude that TiNb may be useful as an implant material.

Inhibition of experimental bone resorption and osteoclast formation and survival by 2-aminoethanesulphonic acid.

It is known that bone resorption is mediated by osteoclasts, and lipopolysaccharide (LPS) and inflammatory mediators such as interleukin-1 (IL-1) and prostaglandin E2 (PGE2) induce osteoclast differentiation from haemopoietic cells, 2-aminoethanesulphonic acid, which is known as taurine, is an important nutrient and is added to most synthetic human infant milk formulas. In this study, it was found that 2-aminoethanesulphonic acid inhibits the stimulation of bone resorption mediated by LPS of the periodontopathic microorganism Actinobacillus actinomycetemcomitans Y4 in organ cultures of newborn mouse calvaria. The effect of 2-aminoethanesulphonic acid on the development and survival of osteoclast-like multinucleated cells produced in a mouse bone-marrow culture system was also examined. 2-aminoethanesulphonic acid (100 microg/ml) suppressed the formation of these osteoclast-like cells in the presence of LPS of A. actinomycetemcomitans Y4, IL-1alpha or PGE2 in mouse marrow cultures. On the other hand, 2-aminoethanesulphonic acid did not inhibit 1alpha, 25-dihydroxyvitamin D3-mediated osteoclast differentiation. Although IL-1alpha elongated the survival of the osteoclast-like cells, 2-aminoethanesulphonic acid blocked the supportive effect of IL-1alpha on osteoclast survival. 2-aminoethanesulphonic acid showed no effect on the growth of mouse osteoblasts. Finally, it was found that 2-aminoethanesulphonic acid inhibited alveolar bone resorption in experimental periodontitis in hamsters. These results suggest that 2-aminoethanesulphonic acid is an effective agent in preventing inflammatory bone resorption in periodontal diseases.

1,25-Dihydroxyvitamin D3 induces differentiation of a retinoic acid-resistant acute promyelocytic leukemia cell line (UF-1) associated with expression of p21(WAF1/CIP1) and p27(KIP1).

Retinoic acid (RA) resistance is a serious problem for patients with acute promyelocytic leukemia (APL) who are receiving all-trans RA. However, the mechanisms and strategies to overcome RA resistance by APL cells are still unclear. The biologic effects of RA are mediated by two distinct families of transcriptional factors: RA receptors (RARs) and retinoid X receptors (RXRs). RXRs heterodimerize with 1, 25-dihydroxyvitamin D3 [1,25(OH)2D3] receptor (VDR), enabling their efficient transcriptional activation. The cyclin-dependent kinase (cdk) inhibitor p21(WAF1/CIP1) has a vitamin D3-responsive element (VDRE) in its promoter, and 1,25(OH)2D3 enhances the expression of p21(WAF1/CIP1) and induces differentiation of selected myeloid leukemic cell lines. We have recently established a novel APL cell line (UF-1) with features of RA resistance. 1,25(OH)2D3 can induce growth inhibition and G1 arrest of UF-1 cells, resulting in differentiation of these cells toward granulocytes. This 1, 25(OH)2D3-induced G1 arrest is enhanced by all-trans RA. Also, 1, 25(OH)2D3 (10(-10) to 10(-7) mol/L) in combination with RA markedly inhibits cellular proliferation in a dose- and time-dependent manner. Associated with these findings, the levels of p21(WAF1/CIP1) and p27(KIP1) mRNA and protein increased in these cells. Northern blot analysis showed that p21(WAF1/CIP1) and p27(KIP1) mRNA and protein increased in these cells. Northern blot analysis showed that p21(WAF1/CIP1) and p27(KIP1) transcripts were induced after 6 hours' exposure to 1,25(OH)2D3 and then decreased to basal levels over 48 hours. Western blot experiments showed that p21(WAF1/CIP1) protein levels increased and became detectable after 12 hours of 1,25(OH)2D3 treatment and induction of p27(KIP1) protein was much more gradual and sustained in UF-1 cells. Interestingly, the combination of 1, 25(OH)2D3 and RA markedly enhanced the levels of p27(KIP1) transcript and protein as compared with levels induced by 1, 25(OH)2D3 alone. In addition, exogenous p27(KIP1) expression can enhance the level of CD11b antigen in myeloid leukemic cells. In contrast, RA alone can induce G1 arrest of UF-1 cells; however, it did not result in an increase of p21(WAF1/CIP1) and p27(KIP1) transcript and protein expression in RA-resistant cells. Taken together, we conclude that 1,25(OH)2D3 induces increased expression of cdk inhibitors, which mediates a G1 arrest, and this may be associated with differentiation of RA-resistant UF-1 cells toward mature granulocytes.

Actinobacillus actinomycetemcomitans toxin induces both cell cycle arrest in the G2/M phase and apoptosis.

We found that the culture supernatant of the periodontopathic bacterium Actinobacillus actinomycetemcomitans had a cytotoxic effect on several cell lines. In this study, we purified the toxin from the culture supernatant of A. actinomycetemcomitans Y4 by a four-step procedure: ammonium sulfate precipitation, POROS HQ/M column chromatography, polymyxin B matrix column chromatography, and Mono-Q column chromatography. The purified toxin gave two major bands of protein with molecular masses of 80 and 85 kDa upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The mechanism of cell death of the B-cell hybridoma cell line HS-72 was examined by observing changes in nuclear morphology, an increase in the proportion of fragmented DNA, and the typical ladder pattern of degraded chromosomal DNA, indicating the induction of apoptosis. Overexpression of human Bcl-2 suppressed apoptosis in HS-72 cells, indicating that the toxin from A. actinomycetemcomitans induces apoptosis by a Bcl-2-inhibitable mechanism. Flow cytometric analysis revealed that the toxin caused cell cycle arrest in the G2/M phase and apoptosis in HS-72 cells. In addition, aurintricarboxylic acid, a DNA endonuclease inhibitor, markedly decreased the percentage of apoptotic cells but had no effect on cell cycle arrest in the G2/M phase. Taken together, these findings suggest that the toxin from A. actinomycetemcomitans could mediate the development of periodontal diseases through cell cycle arrest in the G2/M phase and apoptosis in B lymphocytes of periodontal tissue.

Smad7 is an activin-inducible inhibitor of activin-induced growth arrest and apoptosis in mouse B cells.

Members of the transforming growth factor-beta (TGF-beta) family, which includes the activins, relay signals from serine/threonine kinase receptors in membrane to nucleus via intracellular Sma- and Mad-related (Smad) proteins. Inhibitory Smad proteins were found to prevent the interaction between the serine/threonine kinase receptors and pathway-restricted Smad proteins. Smad7 was identified as a TGF-beta-inducible antagonist of TGF-beta signaling, and it may participate in a negative feedback loop to control TGF-beta signaling. Here we demonstrate that the mRNA expression of Smad7 is induced by activin A in mouse B cell hybridoma HS-72 cells, which undergo growth arrest and apoptosis upon exposure to activin A. The ectopic expression of mouse Smad7 in HS-72 cells suppressed the activin A-induced cell cycle arrest in the G1 phase by abolishing the activin A-induced expression of p21(CIP1/WAF1) and hypophosphorylation of retinoblastoma protein. Furthermore, Smad7 expression suppressed activin A-induced apoptosis in HS-72 cells. Thus, our data indicate that Smad7 is an activin A-inducible antagonist of activin A-induced growth arrest and apoptosis of B lineage cells.

Activin A regulates the production of mature interleukin-1beta and interleukin-1 receptor antagonist in human monocytic cells.

Activin A, a member of the transforming growth factor-beta (TGF-beta) family, is produced by a variety of cells and implicated in the regulation of the reproductive endocrine system, mesoderm induction, and erythropoiesis. In the present study, we showed that activin A inhibited the production of interleukin-1beta (IL-1beta), a potent proinflammatory cytokine, and enhanced the production of IL-1 receptor antagonist (IL-1ra), in activated THP-1 and U-937 human monocytic cells, resulting in the reduction of IL-1 biologic activity. Northern blot analysis revealed that activin A had no effect on mRNA accumulation of IL-1beta and IL-1ra, indicating that activin A regulates IL-1beta and IL-1ra production at a posttranscriptional level. As it is well known that an inactive precursor form of IL-1beta (pro-IL-1beta) is converted to an active mature form (mature IL-1beta), we examined the expression levels of pro-IL-1beta and mature IL-1beta by immunoblot analysis. Although activin A inhibited the production of mature IL-1beta in activated U-937 cells, the relative protein expression of pro-IL-1beta was unaltered by activin A, suggesting that activin A inhibits IL-1beta production by blocking proteolytic conversion of pro-IL-1beta into mature IL-1beta. Taken together, these findings suggest that activin A may function as an anti-inflammatory cytokine by modulating mature IL-1beta and IL-1ra production in inflammatory sites.

Mechanism of rethrombosis after thrombolytic therapy: angioscopic findings and investigation of the coagulation system in dogs.

The purpose of this study was to angioscopically observe the process of thrombolysis after intracoronary administration of thrombolytic agents and to investigate the effects of these agents on coagulation/fibrinolysis systems in dogs. The coronary endothelium was removed and thrombus formation was confirmed by angioscopy. In the tissue plasminogen activator (tPA) group (n=8), complete thrombolysis occurred in all animals, but thrombolysis was incomplete in the urokinase (UK) group (n=6). The plasma level of plasmin alpha2-plasmin inhibitor complex peaked at 15 minutes after treatment in both the tPA and UK groups. Plasma thrombin-antithrombin III (TAT) complex decreased transiently at 15 minutes after tPA administration but increased at 30 and 60 minutes (P<0.05). In the UK group, plasma TAT also showed a transient decrease followed by an increase, which was minimal compared with that in the tPA group. Plasma TAT decreased transiently after infusion of tPA and subsequently increased to above the pretreatment level, suggesting a risk of rethrombosis after successful recanalization.

Asynergy of the noninfarcted left ventricular inferior wall in anterior wall acute myocardial infarction secondary to isolated occlusion of the left anterior descending artery.

There are patients in whom left ventricular (LV) wall motion decreases in the noninfarcted region and LV systolic function declines globally despite the presence of a localized myocardial infarct attributable to narrowing or occlusion of a single coronary artery. This study examines angiographic characteristics of patients with chronic hypokinesia of noninfarcted myocardium after anterior wall acute myocardial infarction (AMI) due to narrowing of a single coronary artery, namely, the left anterior descending (LAD) artery. The LV ejection fraction, abnormalities in the motion of the noninfarcted LV inferior wall (SD/chord value by Sheehan's technique), the angiographic characteristics of the infarct-related coronary artery, the effect of acute reperfusion therapy, and presence of coronary risk factors were examined in 85 consecutive patients. The SD/chord value in the noninfarcted region showed a positive correlation with the LV ejection fraction (r = 0.505, p <0.0001). By multivariate analysis, hypertension (odds ratio = 0.53, 95% confidence interval [CI] 0.36 to 0.80), an infarct-related narrowing proximal to the origin of the first diagonal branch (odds ratio = 0.56, 95% CI 0.38 to 0.84), and patency of the infarct-related lesion during AMI (odds ratio = 1.56, 95% CI 1.03 to 2.30) were independent predictors of wall motion in the noninfarct region. In some patients with single-vessel anterior wall AMI, the motion of the noninfarcted inferior LV wall decreases during the chronic stage and cardiac function declines severely. In most of these patients, the infarct-related narrowing or occlusion is proximal to the origin of the first diagonal branch of the LAD artery.

Gallium-67-citrate scintigraphy of primary renal lymphoma.

We present a case of primary renal lymphoma, which is a rare entity and poses diagnostic challenge. Ultrasound and CT scan demonstrated a nonspecific solid tumor in the left kidney. 67Ga-citrate scintigraphy demonstrated an intense uptake in the tumor, which led to a correct diagnosis, so that we could spare unnecessary laparotomy and possible nephrectomy.

Increase in Bcl-2 level promoted by CD40 ligation correlates with inhibition of B cell apoptosis induced by vacuolar type H(+)-ATPase inhibitor.

We have previously demonstrated that cell death of WEHI-231 cells induced by specific inhibitors of vacuolar type H(+)-ATPase (V-ATPase) occurs through apoptosis. CD40 is involved in regulating activation, differentiation, and apoptosis of B cells. Here we show that the CD40 ligation rescues WEHI-231 cells from apoptotic cell death induced by a specific V-ATPase inhibitor, concanamycin A. CD40 signaling with anti-CD40 antibody resulted in the induction of Bcl-2 and Bcl-XL proteins in WEHI-231 cells. Constitutive expression of Bcl-2 but not Bcl-XL inhibited concanamycin A-induced apoptosis. These findings suggest that the expression of Bcl-2 mediated through CD40 signaling rescues the apoptotic cell death induced by blockade of V-ATPase. Interestingly, the acidification of intracellular acidic compartments was completely inhibited when WEHI-231 cells were cultured with concanamycin A, even in the presence of anti-CD40 antibody. In addition, apoptosis in WEHI-231 cells induced by concanamycin A was strongly suppressed when cultured with imidazole, a cell-permeable base, suggesting that apoptosis induced by concanamycin A is preceded by intraacidification.

Involvement of prostaglandin E2 and interleukin-1 alpha in the differentiation and survival of osteoclasts induced by lipopolysaccharide from Actinobacillus actinomycetemcomitans Y4.

Lipopolysaccharide (LPS) is a bacterial cell component that plays multifunctional roles in inflammatory reactions. LPS from various periodontal pathogens is supposed to be a major virulence factor of periodontal diseases. In the present study, we demonstrated that LPS from periodontopathic bacterium Actinobacillus actinomycetemcomitans Y4 (Y4 LPS) stimulated osteoclast formation in mouse bone marrow culture systems. Addition of anti-interleukin-1 alpha (IL-1 alpha) antibody or indomethacin in the marrow cultures resulted in the suppression of osteoclast differentiation. Quantitative analyses revealed that Y4 LPS stimulated the production of IL-1 alpha and prostaglandin E2 (PGE2) by bone marrow cells. Furthermore, an immunoblot analysis showed that Y4 LPS stimulated bone marrow cells to upregulate the expression of cyclooxygenase-2, a rate-limiting enzyme for the conversion of arachidonic acid to prostanoids. These findings suggest that both IL-1 alpha and PGE2 are involved in the LPS-mediated osteoclast differentiation. In addition, we found that Y4 LPS supported the survival of osteoclasts. Addition of anti-IL-1 alpha antibody in the osteoclast culture resulted in a reduction of osteoclast survival. Indomethacin, however, showed no effect on osteoclast survival. These findings suggest that the increased PGE2 and IL-1 alpha synthesis by bone marrow cells may play an important role in the differentiation and survival of osteoclasts induced by A. actinomycetemcomitans LPS.

The role of activin type I receptors in activin A-induced growth arrest and apoptosis in mouse B-cell hybridoma cells.

Activins transduce their signals by binding to activin type I receptors and activin type II receptors, both of which contain a serine/threonine kinase domain. In this study, we established stable transfectants expressing two types of activin receptors, ActRI and ActRIB, to clarify the role of these receptors in activin signalling for growth inhibition in HS-72 mouse B-cell hybridoma cells. Over-expression of ActRI suppressed activin A-induced cell-cycle arrest in the G1 phase caused by inhibition of retinoblastoma protein phosphorylation through induction of p21CIP1/WAF1, a cyclin-dependent kinase inhibitor, and subsequent apoptosis. In contrast, HS-72 clones that over-expressed ActRIB significantly facilitated activin A-induced apoptosis. These results indicate that ActRI and ActRIB are distinct from each other and that the ActRI/ActRIB expression ratio could regulate cell-cycle arrest in the G1 phase and subsequent apoptosis in HS-72 cells induced by activin A.

Gingival crevicular interleukin-1 and interleukin-1 receptor antagonist levels in periodontally healthy and diseased sites.

Interleukin-1 (IL-1) molecules, IL-1 alpha and IL-1 beta are cytokines involved in the acute-phase response against infection and in the pathogenesis of periodontal destruction. Administration of exogenous IL-1 receptor antagonist (IL-1ra) is effective in reducing the inflammatory reactions mediated by IL-1. However, the relationship between these three naturally occurring IL-1 molecules and periodontal diseases has been poorly characterized. We investigated the correlation of gingival crevicular IL-1 molecules and the clinical status of patients with different severities of periodontitis. IL-1 alpha, IL-1 beta, IL-1ra and the total IL-1/IL-1ra ratio (IL-1 activity index; IL-1AI) were measured in 75 gingival crevicular fluid (GCF) samples from non-inflamed gingiva sites in 2 healthy subjects and diseased sites in 7 patients with several types of periodontitis. IL-1 alpha, IL-1 beta and IL-1ra were measured by specific non-cross-reactive enzyme linked immunosorbent assay. The probing depth, gingival index and alveolar bone loss of each site was recorded at the time of GCF sampling. The total amount of IL-1 alpha, IL-1 beta and the IL-1AI, but not total IL-1ra, were found to be correlated with alveolar bone loss score. Three IL-1 molecules were also measured in the gingival tissue of patients with periodontitis. A similar progressive decrease of the IL-1AI was detected in gingival tissue with periodontitis. These results suggest that the amounts of both crevicular IL-1 and IL-1AI are closely associated with periodontal disease severity.

Activin A induction of cell-cycle arrest involves modulation of cyclin D2 and p21CIP1/WAF1 in plasmacytic cells.

Activins, members of the transforming growth factor-beta family, have been implicated in the regulation of growth and differentiation of various types of cells. We have recently found that activin A induces apoptotic cell death of plasmacytic cells including B cell hybridoma cells and myeloma cells. In the present study, we demonstrated that activin A caused cell-cycle arrest in the G1 phase before appearance of apoptotic cells in mouse B cell hybridoma cells. Phosphorylation of retinoblastoma protein (Rb) and in vitro Rb kinase activity of cyclin-dependent kinase (CDK)4 was inhibited in activin A-treated cells. Analysis of expression of genes regulating Rb phosphorylation revealed that activin A suppressed cyclin D2, the sole D-type cyclin gene expressed in the hybridoma cells, and activated p21CIP1/WAF1 but had no effect on expression of cyclin-dependent kinases (CDK2, CDK4, CDK6) and other CDK inhibitors (p27KIP1, p16INK4a, p15INK4b). Modulation of cyclin D2 and p21CIP1/WAF1 expression resulted in a decrease in level of cyclin D2-CDK4 complex and an increase in level of CDK4 complexed with p21CIP1/WAF1. Moreover, overexpression of cyclin D2 partially abrogated inhibition of Rb phosphorylation and G1 arrest in the hybridoma cells.

Technetium-99m tetrofosmin uptake in lung cancer: comparison with thallium-201.

Technetium-99m tetrofosmin and thallium-201 lung SPECT imaging were performed in a patient with adenocarcinoma of the lung. Significant activities in the lung lesion were clearly depicted on both technetium-99m tetrofosmin and thallium-201 SPECT imaging. The early uptake, delayed uptake ratios and retention indices of the tumor were 2.75, 2.39 and -1.31 for thallium-201 imaging and 3.09, 2.27 and -26.5 for technetium-99m tetrofosmin imaging, respectively. This preliminary report suggests that technetium-99m tetrofosmin may have potential as a tumor imaging agent.

[A study on the dosage of carboplatin for bronchial arterial infusion in combination with radiation therapy].

Radiation therapy holds an important position as one of the multidisciplinary methods of treating lung cancer (non-small cell carcinoma). As a result of the development of platinum preparations such as cisplatin (CDDP) and wide use of digital subtraction angiography (DSA), selective bronchial arterial infusion (BAI) therapy made possible more effective use of anti-lung cancer drugs. The use of radiation therapy in combination with BAI is now recommended as a more effective method. Meanwhile carboplatin (CBDCA) has recently been developed as a second generation platinum preparation with less side effects, and is being used for BAI, too. However, the maximum tolerated dose (MTD) of CB DCA for BAI to be used in combination with radiation therapy is not known yet. We, therefore, carried out a phase-study to determine MTD of CBD CA for combination with radiation therapy. The results show that the MTD of CBDCA is 400 mg/m2, and that clinically recommendable infusion limit is 350 mg/m2. In an angiographic study performed at the same time, a plural number of tumor affected blood vessels were found in 81.3% of the patients with lung cancer. Therefore, infusion of a drug for such patients should be carefully applied.

[Bronchial arterial hemodynamics after thoracic irradiation therapy in lung cancer patients].

We evaluated bronchial arterial hemodynamics after thoracic irradiation therapy. We performed bronchial arteriography in 9 patients (8 males and 1 female) with lung cancer who received thoracic irradiation (58-72 Gy). Three patients had adenocarcinoma, 3 squamous cell carcinoma, 2 small cell carcinoma and 1 large cell carcinoma. Their clinical stages were 6 in stage IIIB and 3 in stage IV. Eight of these cases also received chemotherapy by intra-bronchial arterial infusion of anti-cancer agents (Carboplatin and/or Cisplatin). The bronchial arterial supply was patent except in the one complete remission case (small cell carcinoma of stage IIIB). In the five cases developing radiation pneumonitis, bronchial arteries demonstrated angiogenesis in the radiation fields, despite which pulmonary arteriography and/or pulmonary perfusion scintigrams showed a decreased pulmonary arterial supply. Bronchial arterial hemodynamics demonstrated no significant damage in the bronchial arteries by the thoracic irradiation therapy and/or bronchial arterial infusion of anti-cancer agents. It is suggested that patent bronchial arteries after radiation therapy promote local recurrences of lung cancer. In 5 cases, including 2 local relapsed cases and 3 cases showing no remarkable response to radical radiation therapy, we performed bronchial arterial infusion of anti-cancer agents after radiation therapy, with good responses obtained. We conclude that thoracic irradiation did not damage bronchial arteries as compared with pulmonary arteries, and that in local relapsed and radio-resistant cases bronchial arterial infusion of anti-cancer agents after radiation therapy is a useful approach.

[A case of radiation pneumonitis caused by treatment of lung cancer which revealed marked hypervasculality on bronchial arteriography].

A 44-year-old man was admitted to our hospital because of hemoptysis. He had been admitted to our ward in June 1991, after resection of a brain tumor at another hospital due to cerebral metastasis of lung cancer (adenocarcinoma). Systemic chemotherapy and pulmonary irradiation therapy were performed during the first hospitalization. Radiation pneumonitis occurred 1 month after the completion of radiotherapy, which responded to administration of corticosteroids. One year and 4 months later after the completion of radiotherapy, he was readmitted to our hospital because of hemoptysis. Chest computed tomogram and bronchoscopy showed no recurrence of lung cancer, so pulmonary arteriography and bronchial arteriography were performed to investigate the cause of hemoptysis. Pulmonary arteriograms showed diminished vascularity in the area of radiation fibrosis, but a bronchial arteriogram showed inflammatory hypervascularization in the same field. We considered that the bronchial arterial angiogenesis induced by radiation pneumonitis was the cause of hemoptysis. Bronchial arteriography is necessary in cases of radiation pulmonary fibrosis with hemoptysis without obvious recurrence of tumor. If the growth of new blood vessels in the bronchial artery can be induced by radiation therapy, the administration of anti-cancer agents to the bronchial artery should be considered in the treatment of recurrent lung cancer after radiation therapy.

[Relationship between Ga-67 uptake and radiotherapeutic response of primary lung cancer (squamous cell carcinoma)].

This investigation was undertaken to evaluate the relationship between Ga-67 uptake and radiotherapeutic response to primary lung cancer (squamous cell carcinoma), Ga-67 uptake of tumor was estimated on 16 patients with untreated primary lung cancer (squamous cell carcinoma). Ga-67 uptake was then compared with the response to radiation therapy (tumor reduction ratio). There was statistically significant inverse correlation between Ga-67 uptake and response to radiation therapy (r = -0.701, p less than 0.01). The fewer the Ga-67 accumulation in the tumor, the more effective radiotherapy in reducing tumor size. In conclusion, Ga-67 scintigraphy appears to be able to predict the response of primary lung cancer (squamous cell carcinoma) to radiation therapy.