Image quality and radiation exposure in CT of the pancreas: 320-MDCT with and without adaptive iterative dose reduction versus 64-MDCT.

AIM: To compare the image quality and radiation exposure in computed tomography (CT) of the pancreas acquired using 320-multidetector (MD)CT versus 64-MDCT and to demonstrate the effects of adaptive iterative dose reduction (AIDR) on 320-MDCT. MATERIALS AND METHODS: One hundred and fifty patients were randomized into three groups including 320-section volume imaging using AIDR (group A), 320-slice volume scan without AIDR (group B), and 64-section helical imaging without AIDR (group C). Transaxial arterial, pancreatic phase, and volume-rendered CT angiographic images were reconstructed. CT radiodensity of the abdominal aorta, pancreas, signal-to-noise ratios (SNR), dose-length products (DLPs; mGy cm), and image quality were measured. RESULTS: No significant difference in CT radiodensity of the abdominal aorta or pancreas was noted between groups. Mean DLPs were 600.9 ± 145.8, 681.6 ± 97.5, and 1231.5 ± 271.4 in groups A, B, and C, respectively. The DLP was reduced by 51% in group A and 45% in group B compared to group C (p < 0.001). SNRs of the pancreas during the pancreatic phase were comparable between groups A and C, but were significantly lower in group B (p < 0.001). Image quality, including the depiction of some small arterial branches on the arterial and CT angiographic images and the main pancreatic duct on the pancreatic-phase images, were significantly lower in group B than in groups A and C (p = 0.008-0.038). CONCLUSION: Radiation dose can be markedly reduced for contrast-enhanced CT imaging of the pancreas without compromising image quality using a 320-MDCT with AIDR, compared with 64-section helical CT.

Change in carrier type in high-k gate carbon nanotube field-effect transistors by interface fixed charges.

We study the phenomenon of change in carrier type in carbon nanotube field-effect transistors (CNFETs) caused by the atomic layer deposition (ALD) of a HfO(2) gate insulator. When a HfO(2) layer is deposited on a CNFET, the type of carrier changes from p-type to n-type. The so-obtained n-type device has good performance and stability in air. The conductivity of such a device with a channel length of 0.7 microm is 11% of the quantum conductance 4e(2)/h. The contact resistance for electron current is estimated to be 14 kOmega. The n-type conduction of this CNFET is maintained for more than 100 days. The change in carrier type is attributed to positive fixed charges introduced at the interface between the HfO(2) and SiO(2) layers. We also propose a novel technique to control the type of conduction by utilizing interface fixed charges; this technique is compatible with Si CMOS process technology.

ADAMTS-1: a metalloproteinase-disintegrin essential for normal growth, fertility, and organ morphology and function.

A disintegrin and metalloproteinase (ADAM) represents a protein family possessing both metalloproteinase and disintegrin domains. ADAMTS-1, an ADAM family member cloned from cachexigenic colon adenocarcinoma, is unusual in that it contains thrombospondin type I motifs and anchors to the extracellular matrix. To elucidate the biological role of ADAMTS-1, we developed ADAMTS-1-null mice by gene targeting. Targeted disruption of the mouse ADAMTS-1 gene resulted in growth retardation with adipose tissue malformation. Impaired female fertilization accompanied by histological changes in the uterus and ovaries also resulted. Furthermore, ADAMTS-1(-/-) mice demonstrated enlarged renal calices with fibrotic changes from the ureteropelvic junction through the ureter, and abnormal adrenal medullary architecture without capillary formation. ADAMTS-1 thus appears necessary for normal growth, fertility, and organ morphology and function. Moreover, the resemblance of the renal phenotype to human ureteropelvic junction obstruction may provide a clue to the pathogenesis of this common congenital disease.

Molecular basis of ocular abnormalities associated with proximal renal tubular acidosis.

Proximal renal tubular acidosis associated with ocular abnormalities such as band keratopathy, glaucoma, and cataracts is caused by mutations in the Na(+)-HCO(3)(-) cotransporter (NBC-1). However, the mechanism by which NBC-1 inactivation leads to such ocular abnormalities remains to be elucidated. By immunological analysis of human and rat eyes, we demonstrate that both kidney type (kNBC-1) and pancreatic type (pNBC-1) transporters are present in the corneal endothelium, trabecular meshwork, ciliary epithelium, and lens epithelium. In the human lens epithelial (HLE) cells, RT-PCR detected mRNAs of both kNBC-1 and pNBC-1. Although a Na(+)-HCO(3)-cotransport activity has not been detected in mammalian lens epithelia, cell pH (pH(i)) measurements revealed the presence of Cl(-)-independent, electrogenic Na(+)-HCO(3)-cotransport activity in HLE cells. In addition, up to 80% of amiloride-insensitive pH(i) recovery from acid load in the presence of HCO(3)(-)/CO(2) was inhibited by adenovirus-mediated transfer of a specific hammerhead ribozyme against NBC-1, consistent with a major role of NBC-1 in overall HCO(3)-transport by the lens epithelium. These results indicate that the normal transport activity of NBC-1 is indispensable not only for the maintenance of corneal and lenticular transparency but also for the regulation of aqueous humor outflow.

Sentinel node biopsy in primary breast cancer: radioactive detection and metastatic disease.

AIM: To examine the relationship between the intensity of the radioactive counts and the presence of tumor metastasis in sentinel lymph nodes (SLNs) in order to correctly identify the number of SLNs to be removed. PATIENTS AND METHODS: Five hundred three breast cancer patients with successful radioisotope localization of SLNs using the combined blue dye and radioisotope method were analyzed. SLN biopsy was continued until all the blue-stained and radioactive nodes were removed. RESULTS: The mean number of harvested SLNs was 1.7+/-0.9, and the number of radioactive SLNs among the harvested nodes was 1.6+/-0.8. SLN metastasis was found in 123 of the 503 cases. The metastasis was detected in the SLN with the highest radioactive count (the hottest SLN) in 94 of the 123 cases with positive SLNs. The positive rate in the hottest SLN was 89% in 61 cases with a single radioactive SLN, and 65% in 62 cases with multiple radioactive SLNs. Of the 29 cases with positivity in other than the hottest SLNs, the metastasis was detected in the second hottest SLN in 16 cases, in the third hottest SLN in one case, in a mixture of negative radioactive SLNs and blue-dye-stained in four cases, and in the negative SLNs and positive non-SLNs (false-negative) in eight cases. Of 123 node-positive cases, 111 cases had metastasis that was detected within the first three hottest SLNs. CONCLUSIONS: These data suggest that lymph node metastasis may not always be detected in the hottest SLN. Thus, in practice, all radioactive and/or blue-dye-stained nodes should be removed for further examination.

Adrenomedullin induces endothelium-dependent vasorelaxation via the phosphatidylinositol 3-kinase/Akt-dependent pathway in rat aorta.

To study the mechanisms by which adrenomedullin (AM) induces endothelium-dependent vasorelaxation, we examined whether AM-induced endothelium-dependent vasodilation was mediated by the phosphatidylinositol 3-kinase (PI3K)/Akt-dependent pathway in rat aorta, because it was recently reported that PI3K/Akt was implicated in the activation of endothelial NO synthase. AM-induced vasorelaxation in thoracic aorta with intact endothelium was inhibited by pretreatment with PI3K inhibitors to the same level as that in endothelium-denuded aorta. AM elicited Akt phosphorylation in a time- and dose-dependent manner. AM-induced Akt phosphorylation was inhibited by pretreatment with a calmodulin-dependent protein kinase inhibitor as well as with PI3K inhibitors. When an adenovirus construct expressing a dominant-negative Akt mutant (Ad/dnAkt) was injected into abdominal aortas so that the mutant was expressed predominantly in the endothelium layer, AM-induced vasodilation was diminished to the same level as that in endothelium-denuded aortas. Finally, AM-induced cGMP production, which was used as an indicator for NO production, was suppressed by PI3K inhibition or by Ad/dnAkt infection into the endothelium. These results suggested that AM induced Akt activation in the endothelium via the Ca(2+)/calmodulin-dependent pathway and that this was implicated in the production of NO, which in turn induced endothelium-dependent vasodilation in rat aorta.

Vascular abnormalities and elevated blood pressure in mice lacking adrenomedullin gene.

BACKGROUND: Adrenomedullin (AM) is a vasodilating peptide involved in the regulation of circulatory homeostasis and in the pathophysiology of certain cardiovascular diseases. Levels of AM are markedly increased in the fetoplacental circulation during pregnancy, although its function there remains unknown. To clarify the physiological functions of AM, we chose a gene-targeting strategy in mice. METHODS AND RESULTS: Targeted null mutation of the AM gene is lethal in utero: the mortality rate among AM(-/-) embryos was >80% at E13.5. The most apparent abnormality in surviving AM(-/-) embryos at E13.5 to E14.0 was severe hemorrhage, readily observable under the skin and in visceral organs. Hemorrhage was not detectable at E12.5 to E13.0, although the yolk sac lacked well-developed vessels. Electron microscopic examination showed endothelial cells to be partially detached from the basement structure at E12.5 in vitelline vessels and hepatic capillaries, which allowed efflux of protoerythrocytes through the disrupted barrier. The basement membrane was not clearly recognizable in the aorta and cervical artery, and the endothelial cells stood out from the wall of the lumen, only partially adhering to the basement structure. AM(+/-) mice survived to adulthood but exhibited elevated blood pressures with diminished nitric oxide production. CONCLUSIONS: AM is indispensable for the vascular morphogenesis during embryonic development and for postnatal regulation of blood pressure by stimulating nitric oxide production.

Renal damage and salt-dependent hypertension in aged transgenic mice overexpressing endothelin-1.

The recent development of endothelin-1 (ET-1) antagonists and their potential use in the treatment of human disease raises questions as to the role of ET-1 in the pathophysiology of such cardiovascular ailments as hypertension, heart failure, renal failure and atherosclerosis. It is still unclear, for example, whether activation of an endogenous ET-1 system is itself the primary cause of any of these ailments. In that context, the phenotypic manifestations of chronic ET-1 overproduction may provide clues about the tissues and systems affected by ET-1. We therefore established two lines of transgenic mice overexpressing the ET-1 gene under the direction of its own promoter. These mice exhibited low body weight, diminished fur density and two- to fourfold increases in the ET-1 levels measured in plasma, heart, kidney and aorta. There were no apparent histological abnormalities in the visceral organs of young (8 weeks old) transgenic mice, nor was their blood pressure elevated. In aged (12 months old) transgenic mice, however, renal manifestations, including prominent interstitial fibrosis, renal cysts, glomerulosclerosis and narrowing of arterioles, were detected. These pathological changes were accompanied by decreased creatinine clearance, elevated urinary protein excretion and salt-dependent hypertension. It thus appears that mild, chronic overproduction of ET-1 does not primarily cause hypertension but triggers damaging changes in the kidney which lead to the susceptibility to salt-induced hypertension.

Murine interleukin 4 transgenic heart allograft survival prolonged with down-regulation of the Th1 cytokine mRNA in grafts.

BACKGROUND: Data supporting the differential activation of T helper (Th) 2 cells in transplantation acceptance/tolerance in rodents have been presented by several investigators. However, the differential activation of Th2 cells may be simply the result of allograft acceptance/tolerance induction instead of a contribution to the maintenance of grafts. METHODS: Therefore, we established interleukin (IL)-4 transgenic mice under the control of a cardiac alpha-myosin heavy chain promotor and transplanted IL-4-expressing heart allografts into unmodified recipients to determine the actual contribution of the Th2 bias to allograft acceptance. RESULTS: Among 16 newborn C57BL/6J (B6) mice, three were positive for the IL-4 transgene. Serum IL-4 levels of transgenic versus control B6xC3H F1 mice were not statistically different. Reverse-transcriptase polymerase chain reaction showed that the transgenic B6xC3H F1 mice expressed IL-4 mRNA in the heart and in the lung, whereas control mice did not express IL-4 in any organ. IL-4 mRNA expression in the transgenic but not in the control heart was also confirmed by RNAse protection assay and fluorescence in situ hybridization. The survival of IL-4 transgenic B6xC3H heart grafts heterotopically placed in C3H recipients was prolonged compared with that of nontransgenic grafts (19.0+/-9.1 vs. 6.8+/-2.2 days, P=0.003). Interferon-gamma mRNA expression in IL-4 transgenic heart grafts on the fifth posttransplant day as assessed by Northern blotting was suppressed compared with that in control grafts. Reverse-transcriptase polymerase chain reaction analysis showed that IL-2 mRNA was suppressed in the IL-4 transgenic grafts compared with that in control grafts, while IL-4 mRNA was observed only in IL-4 transgenic grafts. IL-10 mRNA was detected at similar levels in both transgenic and control grafts. CONCLUSIONS: A Th2 bias may contribute to allograft acceptance in part by inducing the down-regulation of Th1-cytokine mRNAs, but it may not be sufficient to induce indefinite graft survival.

Quantification and distribution of alpha 1-adrenoceptor subtype mRNAs in human prostate: comparison of benign hypertrophied tissue and non-hypertrophied tissue.

1. There are at least three alpha 1-adrenoceptor subtypes, alpha 1a, alpha 1b and alpha 1d, in human tissues. Using an RNase protection assay, we have now determined the amount of each subtype mRNA in human prostatic tissue, for both benign prostatic hypertrophy (BPH) and non-BPH. In all tissue samples examined, the predominant subtype mRNA was alpha 1a. The total abundance of alpha 1-adrenoceptor mRNA in BPH samples was over six times that in non-BPH samples. This increase was mostly accounted for by alpha 1a, which was almost nine times as abundant in BPH samples as in non-BPH samples. The abundance of alpha 1b was almost the same between BPH and non-BPH samples, and the abundance of alpha 1d in BPH samples was about three times that in non-BPH samples. The ratio of the numbers of the subtype mRNAs, alpha 1a: alpha 1b: alpha 1d, was 85:1:14 in BPH samples and 63:6:31 in non-BPH samples. 2. In situ hybridization studies showed no significant differences in the tissue localization of alpha 1-adrenoceptor subtype mRNAs between BPH and non-BPH samples. alpha 1a and alpha 1d were clearly detected in the interstitium of the prostate, where alpha 1a was stained more intensely than alpha 1d, and the positive sites were primarily smooth muscle cells. In contrast, alpha 1b staining was very faint. 3. This increase in mRNA abundance may be directly related to the contraction of prostatic tissue that leads to obstruction of the urinary tract in BPH patients. Specifically, our data suggest that increased expression of the alpha 1a subtype may be primarily responsible for the contraction of the prostate.

Quantification and distribution of alpha1-adrenoceptor subtype mRNAs in human proximal urethra.

1. We performed RNase protection assays and in situ hybridization to investigate the ratio of the three alpha1-adrenoceptor subtype mRNAs, alpha1a, alpha1b and alpha1d, in human proximal urethra, and their localization in urethral cross-sections. As revealed by the RNase protection assays, alpha1a was the predominant subtype mRNA in both male and female urethral samples. Alpha1d mRNA was detected only in the female sample, and alpha1b mRNA was not detected in any of the samples tested. The ratio of the abundance of the subtype mRNAs, alpha1a:alpha1b:alpha1d, was 100:0:0 in the male urethra and 90:0:10 in the female urethra. 2. In situ hybridization studies showed no significant differences in the cross-sectional distribution of alpha1-adrenoceptor subtype mRNAs between male and female urethras. Intense alpha1a staining was observed in the smooth muscle of the urethra, but alpha1b and alpha1d staining was much less intense. 3. Of the three cloned alpha1 subtypes, alpha1a is the most likely to be responsible for the contraction of the human urethra. Owing to the side effects of nonselective alpha1 drugs, alpha1-selective drugs may be clinically superior to nonselective drugs for the treatment of urethral disorders.

Alpha 1a-adrenoceptor polymorphism: pharmacological characterization and association with benign prostatic hypertrophy.

1. Two restriction fragment length polymorphisms of the human alpha 1a-adrenoceptor gene digested with PstI restriction enzyme exist; the nucleotide change causes the substitution of C residue for T at nucleotide 1441, thereby Arg492 to Cys492 transition, which might confer an additional putative palmitoylation site in the carboxy-terminal segment of the alpha 1a-adrenoceptor. In the present study, we compared their pharmacological properties and examined whether this alpha 1a-adrenoceptor polymorphism is associated with benign prostatic hypertrophy (BPH). 2. The frequency of alpha 1a-adrenoceptor polymorphism was not differently distributed between patients with benign prostatic hypertrophy (BPH) and normal subjects in Japan; thus, the relative frequencies of the C and T alleles were 0.90 : 0.10 in normal male subjects (n = 45) and 0.87 : 0.13 in BPH patients (n = 222), respectively. However, the frequency distribution of this polymorphism was significantly different between the Japanese and U.S. populations; thus, C and T alleles were 0.34 and 0.66 in U.S. populations. 3. Utilizing Chinese hamster ovary (CHO) cells stably expressing the two polymorphic alpha 1a-adrenoceptors (Arg492 and Cys492), we compared their binding affinity and signal transduction. Radioligand binding studies with 2-[beta-(4-hydroxy-3[125I]-iodophenyl) ethylamino-methyl]tetralone ([125I]-HEAT) showed no marked difference in the antagonist or agonist binding affinities between the two receptors. Also, both receptors were found to be coupled to the calcium signaling, and the concentration-cytosolic Ca2+ concentrations ([Ca2+]i) response relationships for noradrenaline were similar for the two polymorphic receptors. Furthermore, the receptor-mediated [Ca2+]i response was markedly desensitized after a 2 h exposure of phenylephrine (10 microM), and the extent of the desensitization was not significantly different between the two receptors. 4. In summary, the results showed that the two alpha 1a-adrenoceptors generated by genetic polymorphism have similar pharmacological characteristics, and the receptor-mediated [Ca2+]i response can be desensitized in a similar manner. The study did not provide any evidence to support the hypothesis that alpha 1a-adrenoceptor gene polymorphism is associated with BPH.

Quantification and distribution of alpha 1-adrenoceptor subtype mRNAs in human vas deferens: comparison with those of epididymal and pelvic portions.

1. This study was intended to quantify the amounts of the alpha 1-adrenoceptor subtype mRNAs in human vas deferens, and demonstrate the receptor subtype responsible for the vas contraction. 2. The RNase protection assay showed that the mean total amount of alpha 1a mRNA was 7.4 +/- 2.2 pg/5 micrograms of poly (A)+ RNA (97.0% of the total alpha 1 mRNA) in the epididymal portion (E-vas) and 4.9 +/- 0.8 pg/5 micrograms of poly (A)+ RNA (96.3% of the total) in the pelvic portion (P-vas). The E-vas showed a tendency to have a greater alpha 1a mRNA abundance than the P-vas (P = 0.11). The alpha 1b and alpha 1d mRNAs were absent or of extremely low abundance. 3. By an in situ hybridization, the alpha 1a and alpha 1d mRNAs were recognized in the smooth muscle cells of the E-vas and the P-vas, and the distribution pattern the same in both tissue. The alpha 1b mRNA positive site was scarcely detectable in both vas portions. 4. In a functional study, l-phenylephrine produced concentration-dependent contraction in the E-vas (Emax = 2.24 +/- 0.70 g; pD2 = 5.32 +/- 0.09) and the P-vas (Emax = 2.46 +/- 0.46 g; pD2 = 5.07 +/- 0.12). KMD-3213, a novel alpha 1A-adrenoceptor-selective antagonist, caused parallel rightward shifts of the concentration-response curves for l-phenylephrine. Apparent pKB values were 9.90 +/- 0.16 for the E-vas and 9.71 +/- 0.17 for the P-vas. There was no significant difference in Emax, pD2 or pKB estimates between the two portions. 5. We have found that alpha 1a mRNA is predominant in the human vas deferens, and confirmed that contraction of this organ is mediated by the alpha 1A-adrenoceptor.

Engineered IGF-I expression induces glandular enlargement in the murine prostate.

IGF-I has been implicated as a factor that may predispose one to prostate cancer and to benign prostatic hypertrophy (BPH). We established murine IGF-I transgenic mice under the control of rat probasin promoter and analysed the histology of the murine IGF-I-overexpressing prostate. Immunohistochemically, IGF-I was expressed in prostatic epithelial cells or basement membranes of the ventral, dorsal and lateral lobes in a line of IGF-I transgenic mice, but not in their control littermates. The anterior lobe did not express IGF-I. IGF-binding protein-3 (IGFBP-3), inhibitory to the mitogenic action of IGF-I, was detected in epithelial cells of prostatic ventral lobes, but not in those of the dorsal, lateral or anterior lobes of IGF-I transgenic mice. In controls, IGFBP-3 was not detected in epithelial cells of any prostatic lobe. Macroscopic prostatic size and the appearance of IGF-I transgenic mice were comparable with those of their control littermates of the same age. With a computed morphometric analysis, epithelial glands and intraglandular lumens in the prostatic lobes except the ventral lobe were smaller at 17 Months of age than at 14 Months both in IGF-I transgenic mice and controls. Glands and intraglandular lumens in the ventral prostatic lobes of IGF-I transgenic mice expressing more IGF-I protein in the prostate than controls were dense and enlarged similar to cysts compared with those of non-transgenic littermates without showing epithelial growth. Glands and lumens in the dorsal and lateral lobes of the IGF-I transgenic mice were also larger than controls at 14 and/or 17 Months of age. Glands in the anterior prostatic lobe of the IGF-I transgenic mice were not morphologically or morphometrically different from those of non-transgenic littermates. In conclusion, IGF-I transgenic mice under the control of rat probasin promoter showed more dense and enlarged epithelial glands in their prostatic ventral, dorsal and lateral lobes.

Optimal injection protocol for CT evaluation during hepatic arterial infusion chemotherapy.

OBJECTIVE: As an imaging modality for follow-up during continuous or repeated hepatic arterial infusion chemotherapy using a hepatic intra-arterial indwelling catheter, the usefulness of CT while infusing contrast through the indwelling catheter (reservoir port) was examined. METHODS: Using reservoir ports implanted in eight patients with hepatic metastasis from colon cancer, radioisotope perfusion scintigraphy (RI), CT (three rates of infusion of contrast were used), and digital subtraction angiography (AG) were performed to compare the modalities' ability to visualize the intrahepatic and abnormal extrahepatic distributions. RESULTS: CT (infusion rate 0.1 mL/sec) was superior to AG and RI in terms of the ability to visualize intrahepatic distribution, particularly in small areas, and facilitated 3D delineation of the distribution. In evaluating extrahepatic distribution, CT also outperformed the other modalities. CONCLUSIONS: For imaging study follow-up during hepatic arterial infusion chemotherapy, CT proved to be more useful than conventional RI and AG.

Computer-aided diagnosis in full digital mammography.

RATIONALE AND OBJECTIVES: The authors clarify the detection rates for breast cancerous tumors and clustered microcalcifications with computer-aided diagnosis (CAD) based on Fuji Computed Radiography. The authors also determine whether mammographic reading with CAD contributes to the discovery of breast cancer. METHODS: Data acquired by Fuji Computed Radiography 9000, which consisted of 4148 digital mammograms including 267 cases of breast cancer, was transferred directly to an analysis workstation where an original software program determined extraction rates for breast tumors and clustered microcalcifications. Furthermore, using another 344 mammograms from 86 women, observer performance studies were conducted on five doctors for receiver operating characteristic (ROC) analysis. RESULTS: Sensitivity to breast cancerous tumors and clustered microcalcifications were 89.9% and 92.8%, respectively false-positive rates were 1.35 and 0.40 per image, respectively. The observer performance studies indicate that an average Az value for the five doctors was greater with the CAD system than with a film-only reading without CAD, and that a reading with CAD was significantly superior at P < 0.022. CONCLUSIONS: It has been shown that CAD based on Fuji Computed Radiography offers good detection rates for both breast cancerous tumors and clustered microcalcifications, and that the reading of mammograms with this CAD system would provide potential improvement in diagnostic accuracy for breast cancer.

Prognostic significance of grading (MIB-1 system) in patients with myxoid liposarcoma.

AIMS: To determine the relation between clinical outcome and tumour grade defined by a MIB-1 (Ki-67) score based grading system. METHOD: The clinical and pathological features of 50 patients with myxoid liposarcoma were evaluated, and MIB-1 immunostaining was performed to grade these patients' tumours. Univariate and multivariate analyses were conducted to evaluate survival. Clinical follow up details were available for all patients (median, 46.5 months; range, 9-408). RESULTS: Univariate analysis revealed that the tumour site (p < 0.05), round cell component content (p < 0.01), necrosis (p < 0.01), mitosis (p < 0.01), MIB-1 labelling index (p < 0.001), and tumour grade (p < 0.001) had a significant impact on overall survival. Multivariate analysis showed that, of the variables evaluated, the tumour grade defined by a MIB-1 score based grading system was the most significant adverse prognostic factor. CONCLUSION: Tumour grade determined by the grading system using the MIB-1 score (MIB-1 system) is a very strong prognostic factor in patients with myxoid liposarcoma.

A hepatoblastoma originating in the caudate lobe radically resected with the inferior vena cava.

Complete resection of a rare hepatoblastoma in the caudate lobe, involving the inferior vena cava (IVC), is reported. After systemic chemotherapy, a 5-year-old child underwent exploratory laparotomy at another hospital, but resection was not attempted because the tumor in the caudate lobe had extensively invaded the retrohepatic IVC. However, because not only the lack of distant metastases but also the establishment of extrahepatic collaterals were confirmed by imaging, we thought it was possible to radically resect the tumor. We successfully performed an extended left hepatic lobectomy including total excision of the caudate lobe and the involved portion of the IVC. Although we did not reconstruct the IVC, no clinical manifestations arising from caval congestion were seen. The serum alpha-fetoprotein value declined below the normal limit. Our experience with this case has introduced a radical resectability for hepatic malignancy in the caudate lobe, even if it has extended into the IVC.

Blood supply to the pancreatic head, bile duct, and duodenum: evaluation by computed tomography during arteriography.

HYPOTHESIS: Blood supply to the peripancreatic region is derived from the celiac and superior mesenteric arteries, complementary to each other. DESIGN: Cohort analytic study. SETTING: Tertiary care public hospital. PATIENTS AND METHODS: Computed tomography (CT) during superior mesenteric artery arteriography (SMAA-CT) and during celiac artery arteriography (CEAA-CT), in which a catheter tip was inserted into the common hepatic or gastroduodenal artery, was performed in 25 patients. MAIN OUTCOME MEASURE: Distribution and correlation of these areas of marked enhancement on SMAA-CT and CEAA-CT were analyzed. RESULTS: The right cephalic part of the pancreatic head that is derived from the dorsal bud was enhanced on CEAA-CT, and the left caudal part of the pancreatic head that is derived from the ventral bud was enhanced on SMAA-CT. Blood supply to the intrapancreatic bile duct, including the ampulla of Vater, is derived from the CEA. The boundary between the areas of the duodenum supplied from the CEA and SMA was in the second or third portion. CONCLUSION: The pancreatic head can be separated into 2 segments by the arterial supply, and each segment may be removed separately.

Growth inhibitory effects of somatostatin on human leukemia cell lines mediated by somatostatin receptor subtype 1.

Reverse transcription polymerase chain reaction analysis revealed that only somatostatin receptor (SSTR) 1 mRNA was expressed in Ball-1 B-, Jurkat T-, and HL60 leukemia cell lines. In contrast, human normal mononuclear cells expressed the mRNA of all five subtypes of SSTR, although the expression level of SSTR1 was the highest. A binding study, revealed that [125I]-somatostatin bound specifically to HL60 cells and this binding was inhibited concentration-dependently by unlabeled somatostatin (SS). A [3H]thymidine incorporation study showed that SS significantly and concentration-dependently inhibited HL60 and BALL-1 leukemia cell growth. Furthermore, this inhibition of leukemia cell growth was associated with reduces c-fos gene expression. These data indicate that leukemia cells express SSTR1 and SS reduce c-fos gene expression with resultant suppression of leukemia cell growth, possibly mediated by the SSTRI.