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Background: The prognostic factors, including gastric variceal bleeding itself, in patients with gastric varices (GV) after endoscopic treatment remain unclear. The aim of this study was to analyze prognostic factors in patients with GV after endoscopic treatment as well as to evaluate safety and efficacy of our endoscopic treatment. Patients and Methods: This study enrolled 115 patients who underwent endoscopic treatment for GV between October 1988 and December 2003 using cyanoacrylate and 5% ethanolamine oleate. Successful hemostasis, recurrence rates, rebleeding rates, survival rates, complications and prognostic factors after the treatment were retrospectively reviewed. Results: Treatment sessions for GV were performed 3.4 ± 2.5 times. All cases, including 14 emergency cases, were treated successfully. The cumulative recurrence rates at 1, 3 and 5 years after the treatment were 7.0%, 15.6% and 20.0%, respectively, and the cumulative rebleeding rates at 1, 3 and 5 years were 3.5%, 8.7% and 14.8%, respectively. The overall survival rates were 78.3%, 63.7% and 51.5% at 1, 3 and 5 years, respectively. Grade B or C in Child–Pugh classification, emergency or elective cases, and association with hepatocellular carcinoma were identified as significant negative prognostic factors after endoscopic treatment by multivariate analysis. Although several complications were observed, there was no mortality. Conclusions: Grade B or C in Child–Pugh classification, emergency or elective situation, and association with hepatocellular carcinoma are negative prognostic factors after endoscopic treatment.

Background: In patients with portal hypertension, EUS reveals the presence of collateral vessels within and outside the esophageal wall such as esophageal varices, periesophageal collateral veins (peri-ECVs), paraesophageal collateral veins (para-ECVs), and perforating veins. This study retrospectively compared radial EUS images of these collateral vessels with histopathologic findings. Methods: Four patients with esophageal varices treated by endoscopic injection sclerotherapy were studied. EUS was performed to evaluate the effects of endoscopic injection sclerotherapy. After endoscopic injection sclerotherapy, the segment of the esophagus from the esophagogastric junction to a point 5 cm proximal to junction was imaged with a 20-MHz radial scanning catheter US probe. Esophageal collateral veins outside the esophageal wall were identified as peri-ECVs (veins lateral to muscularis propria or within adventitia) and para-ECVs (veins lateral and separate from muscularis propria) along with perforating veins (veins connecting extramural collateral veins to submucosal varices). At autopsy, the esophagus with surrounding tissue was removed and cross-sectioned at 1-cm intervals from the esophagogastric junction to a point 5 cm proximal to the junction. Radial EUS images were correlated with histopathologic findings. Results: Radial EUS after endoscopic injection sclerotherapy demonstrated peri-ECVs and perforating veins in all cases and para-ECVs in 3 cases. Based on histopathologic findings, veins associated with the esophageal wall were divided into 3 groups: those adjacent to the muscularis propria, veins separated from the wall without contact with the muscularis propria, and veins perforating the muscularis propria. All 3 groups of veins were observed in all cases. These 3 types of veins identified by histopathologic examination corresponded, respectively, to the peri-ECVs, para-ECVs, and perforating veins observed by EUS. Conclusion: Collateral esophageal veins demonstrated by radial EUS in patients with portal hypertension correspond to collateral veins identified histopathologically. In patients with portal hypertension, EUS is useful for assessment of vascular anatomy around the esophageal wall. (Gastrointest Endosc 2002;56:249-53.)

A 38-year-old woman visited our hospital with edema on her face and conjunctivae. The underlying disease was not clarified, and she did not visit the hospital afterwards. She suffered from diarrhea, polyarthralgia, Raynaud's phenomenon, malar rash and hair loss in the subsequent two years, and was hospitalized because of hypoproteinemia. Her urine, liver and heart test results did not account for her hypoproteinemia. She was diagnosed as having protein-losing enteropathy (PLE) associated with SLE based on the 99mtechnetium-labeled human serum albumin scintigraphy findings, clinical findings and laboratory results of antinuclear and anti-Sm antibodies. This case report demonstrates a strong association between PLE and SLE because PLE was aggravated along with the appearance of SLE symptoms and PLE subsided with prednisolone treatment along with improvement of SLE.(Internal Medicine 40: 449-453, 2001)

A 30-year-old woman with primary antiphospholipid syndrome (PAPS) presented with cerebral ischemia, thrombocytopenia, anemia and proteinuria. Administration of warfarin potassium, without concomitant corticosteroid administration, significantly improved all of these symptoms along with a decrease in the titers of antiCL-beta2-GP-I antibodies and a shortening of prolonged APTT. Therefore, the antiphospholipid antibodies in this patient could have been evoked by vitamin-K-dependent coagulation factors or plasma proteins which are assumed to undergo conformational changes exposing cryptic epitopes. This case report provides clues to the mechanisms underlying the production of antiphospholipid antibodies in patients with PAPS.

Nearly all mucosal surfaces participate in a common mucosal immune system, and application of an antigen to one mucosal surface elicits local as well as distant mucosal immune responses. However, whether the gastric mucosa is a part of this network has not been examined directly. We show here that the injection of plasmid DNA encoding β-galactosidase into the gastric wall caused transfection of gastric mucosal epithelial cells, induced systemic and mucosal antibody responses at both local (digestive tract) and distant (genital and respiratory tracts) sites, and induced cytotoxic T lymphocyte responses in the spleen and the mesenteric and iliac lymph nodes.

Background: The relation between esophageal varices and venous collaterals outside the esophageal wall in patients with portal hypertension remains unclear. We investigated this relationship with endoscopy and endoscopic ultrasound (US). Methods: Twenty-two patients with untreated varices were examined. The collaterals were studied with a 20 MHz US catheter probe. Collaterals were divided into two groups: (1) periesophageal collateral veins adjacent to the muscularis externa of the esophagus and (2) paraesophageal collateral veins external to the esophageal wall but without contact with the muscularis externa. Periesophageal and paraesophageal collateral veins were scored as mild or severe according to stage of development. Results: Varix form as defined endoscopically was significantly larger in the severe periesophageal collateral veins group than in the mild periesophageal collateral veins group (p < 0.01). In contrast, varix form did not differ significantly between the mild and severe paraesophageal collateral veins groups. Perforating veins were detected in the distal esophagus in 18 of 22 patients (81.8%) by means of US. The prevalence of perforating veins increased in relation to varix form. Two types of perforating veins were found on the basis of connection with periesophageal and paraesophageal collateral veins. The frequency with which perforating veins were connected to periesophageal collateral veins was 81.8%; the frequency of connection to paraesophageal collateral veins was 27.3%. Conclusion: Periesophageal collateral veins play a more important role in the formation of esophageal varices than do paraesophageal collateral veins. (Gastrointest Endosc 1999;50: 374-80.)

The concentrations of interleukin-5 (IL-5), granulocyte-macrophage colony-stimulating factor GM-CSF, and interleukin-3 (IL-3) in serum and in IL-2-stimulated lymphocyte culture medium (L-IL2-CM) prepared from patients with reactive eosinophilia were measured by enzyme-linked immunosorbent assay (ELISA). Serum IL-5 levels were increased in 16 out of 42 cases. GM-CSF and IL-3 were below the detectable levels in all sera examined. The concentrations of IL-5 and GM-CSF in L-IL2-CM were increased in 10 out of 29 patients. IL-3 was below the detectable levels in all L-IL2-CM.

Summary. Chromosomal translocations involving band 3q27 are recently described common specific cytogenetic abnormalities in B-cell neoplasms, and the BCL-6 gene, identified on 3q27, was shown to be disrupted and over-expressed in lymphoma cells having these chromosomal translocations. In the present study we found rearrangements within the BCL-6 gene in seven out of 3 5 cases with B-cell non-Hodgkin's lymphoma (NHL). Further analysis revealed that three of these patients with BCL-6 abnormality had multiple rearranged bands hybridized with probes from a single restriction fragment within the major translocation cluster (MTC). suggesting that independent DNA rearrangements would occur on both alleles. Additionally, Southern blot analysis indicated that three patients carry deletions encompassing the area containing the first exon of the BCL-6 gene. Our results suggest that biallelic DNA rearrangements and deletions would occasionally occur in NHL patients with BCL-6 abnormality.

Blood lymphocytes from patients with eosinophilia are known to produce interleukin-5 (IL-5) with appropriate stimulation in vitro. To determine whether blood lymphocytes from these patients produce IL-5 in vivo, we tested the IL-5 mRNA expression in blood lymphocytes immediately after separation by reverse-transcriptase polymerase chain reaction (RT-PCR) method. We found that lymphocytes from eosinophilic patients expressed IL-5 mRNA, but lymphocytes from normal volunteers did not express the lymphokine. These findings suggest that in patients with eosinophilia, peripheral blood lymphocytes produce IL-5 in vivo. © 1994 Wiley-Liss, Inc.

Effects of leukemic cells (LC) on bone marrow stromal cells and myeloid progenitor cells (CFU-C) were studied in vitro, using LC lines with different lineage characteristics. LC and/or LC-conditioned medium (LC-CM) inhibited the growth of a stromal cell line, KM-101, and adherent cells of a long-term bone marrow culture (LTBMC) established from normal bone marrow. The inhibition was more prominent when LC were cocultured directly with KM-101 cells than when LC were cultured separate from the KM-101 cell layer via membrane filtration, or when LC-CM was added to KM-101 cells or LTBMC. LC-CM also exerted an inhibitory effect on the ability of LTBMC adherent cells to bind CFU-C. Furthermore, LC-CM inhibited the growth and survival of early and late CFU-C, but not the growth of LC. All these inhibitory effects were seen irrespective of the lineage characteristics of LC, but not seen with CM prepared from normal bone marrow immature granulocytes or peripheral blood lymphocytes. Neither tumor necrosis factor-alpha nor interferon-alpha was detected in these LC-CM. These findings suggest that LC suppress normal hematopoiesis through the release of undefined substance(s) inhibiting the growth and/or survival of stromal cells and hemopoietic progenitor cells as well as the function of stromal cells.

We describe a patient with common acute lymphoblastic leukemia associated with blood and cerebrospinal fluid (CSF) eosinophilia. Serum obtained at onset and conditioned medium prepared from T cells obtained at remission stimulated with interleukin-2 contained eosinophil colony stimulating activity (Eo-CSA), which was confirmed to be predominantly GM-CSF. Leukemic cell conditioned medium and serum obtained at remission contained no Eo-CSA. The CSF contained increased eosinophil chemotactic activity, however, this factor was not identified.

A 17 years old male who had been receiving growth hormone treatment for pituitary dwarfism for 20 months developed malignant histiocytosis (MH). He had had a history of severe hypersensitivity to mosquito bites since the age of 4. Before and upon admission he had 5 episodes of high fever which occurred cyclically about 4 weeks apart. The febrile phase was associated with hepatosplenomegaly, pancytopenia, marked elevation of serum LDH activity and ferritin level, all of which almost subsided or became normal during the afebrile phase. Accordingly, it was difficult to diagnose him as having MH. During the fifth episode of fever, hepatosplenomegaly increased markedly, atypical, immature monocytoid cells appeared in the bone marrow, and serum ferritin and LDH activity were extraordinarily elevated, strongly suggesting a diagnosis of MH. Combination chemotherapy resulted in a marked decrease in hepatosplenomegaly. However, MH was complicated with cerebral hemorrhage, and he died 3 months after admission. Immunohistochemical results showing positivity for lysozyme and α1 antichymotrypsin and negativity for pan T antigen confirmed the diagnosis of MH. Of several serum cytokines assayed, M-CSF and IFN γ showed increase during the febrile phase and normalization during the afebrile phase.

Autologous or allogeneic peripheral blood T cells can stimulate the human megakaryocyte progenitor cell (CFU-Meg)-derived colony formation in a dose-dependent fashion in agar cultures of nonadherent (NA), T cell-depleted (NT) bone marrow (BM) cells. Low concentrations of monocytes and T cells can collaborate in the stimulation of CFU-Meg colony formation or in the production of megakaryocyte colony stimulating factor (Meg-CSF) by T cells in the presence of mitogens or IL-2. Monocytes alone can produce only negligible Meg-CSF under any conditions. When monocyte conditioned medium (CM) was added to T cell-stimulated NA, NT BM cell cultures, CFU-Meg colony growth was appreciably increased compared with that stimulated by T cells alone. Dose-dependent increase in CFU-Meg colony growth was noted when varying concentrations of IL-1 were added to T cell-stimulated NA, NT cell cultures, although IL-1 itself could support no CFU-Meg colony growth in the absence of T cells. These data suggest that a synergistic interaction between T cells and monocytes during the production of Meg-CSF by T cells could be partly mediated by IL-1. IL-2 was found to stimulate Meg-CSF production by T cells in the presence or absence of mitogens. IL-2-stimulated Meg-CSF production by T cells was augmented by the addition of monocytes. Although IL-2 itself had no stimulatory effect on CFU-Meg colony growth, dramatic augmentation in the CFU-Meg colony number was noted when IL-2 was added to T cell-stimulated NA, NT cell cultures. High concentrations of monocytes and prostaglandin E (PGE) inhibited the CFU-Meg colony formation. These results suggest that IL-1 and IL-2 may play a stimulatory role on the normal human in vitro megakaryocytopoiesis, and may be involved in the development of reactive thrombocytosis and bone marrow megakaryocytic hyperplasia in various inflammatory diseases.

Sera from 10 patients with eosinophilia contained eosinophil colony stimulating factor (Eo-CSF) activity. Using anti murine (m) interleukin-5 (IL-5) antibody, we demonstrated that this activity was mainly derived from IL-5. Administration of prednisolone to patients decreased both Eo-CSF activity in sera and the number of eosinophils in blood. These results extend our recent study demonstrating that T cells from eosinophilic patients produce IL-5 with IL-2 stimulation and may support the speculation that IL-5 is an important factor which induces eosinophilia.

The ultrastructural localization of RNA in myeloma cells was studied by the RNase-gold method. Gold particles indicating the presence of RNA were observed in large numbers, particularly in the granular component of the nucleolus and periphery of the rough endoplasmic reticulum, but not in the Golgi area, mitochondria, intranuclear inclusion bodies, cytoplasmic inclusion bodies, dense bodies, or cisternae of the rough endoplasmic reticulum. In the nuclear chromatin and nucleolus, gold particles were more numerous as these structures were less mature. They were found in larger numbers also in the cytoplasm of immature cells. In plasma cells from patients with macroglobulinemia, gold particles were fewer than in myeloma cells of multiple myeloma, but there was no difference in their distribution pattern.

A 20 year-old male with congenital afibrinogenemia was admitted to our hospital because of chronic subdural hematoma of the right temporal area. He had had several episodes of hypersensitivity reactions to fibrinogen administration, including hypotension, bronchospasm and cutaneous rash. An intradermal test for fibrinogen was positive without precipitating antifibrinogen antibodies.Because subdural hemorrhage progressed despite of cerebral decompression by medication, fresh frozen plasma was administered usng a method of rapid desensitization after pretreatment with adrenocorticosteroid, bronchodilator, antiallergic drug and H1-antihistamine, resulting in arise of a plasma fibrinogen level to 100mg/dl without occurrence of any hypersensitivity reactions. Immediately after this procedure he received surgical therapy for the hematoma. Fresh frozen plasma could be uneventfully administered without pretreatment or rapid desensitization to maintain a plasma fibrinogen level more than 50mg/dl during 2 weeks after the operation. He is in good condition 9 months after this episode.

The concentrations of interleukin-5 (IL-5) in serum and in IL-2-stimulated lymphocyte culture medium (L-IL2-CM) prepared from patients with reactive eosinophilia were measured by enzyme-linked immunosorbent assay. The serum IL-5 concentration was increased in 16 of 34 cases. The concentrations of IL-5 in L-IL2-CM were increased in 8 of 21 patients.

Background and Aims: Para-esophageal collateral veins (para-ECV) are observed by endoscopic ultrasonography (EUS) in patients with portal hypertension. However, the role of para-ECV in the portal venous system is not clear. To verify the role of para-ECV in the portal venous system, we investigated the relationship between the development of para-ECV as determined by EUS, and the portal blood flow ratio (PBFR) as determined by liver scintigraphy using 99mTc-phytate. Methods: Eighteen patients who did not have fundal gastric varices were studied before the start of and after the completion of all endoscopic sclerotherapy sessions for esophageal varices. EUS was performed to observe veins around the esophagus, para-ECV and perforating veins. To quantify the degree of development of para-ECV, the cross-sectional area of each para-ECV observed by EUS was measured. The sum total of these areas was used as an index of development of para-ECV. The PBFR was calculated by liver scintigraphy using 99mTc-phytate. The correlation between the sum total cross-sectional area of para-ECV and PBFR was examined. Results: After all endoscopic injection sclerotherapy sessions, the total cross-sectional area of para-ECV was 29.32 (26.72) mm2 (mean (SD)) and the PBFR was 48.47 (17.87)% (mean (SD)). A significant correlation between them was noted after treatment (r = − 0.70, P

We report a case of rectal varices that developed after endoscopic injection sclerotherapy (EIS) and Hassab's operation for esophageal varices with extrahepatic portal obstruction. A 54-year-old woman was admitted to our hospital in September 1997 for treatment of hematochezia. Emergent colonoscopy revealed tortuous rectal varices with a white plug. Angiography revealed that rectal varices were provided with backward blood flow by the inferior mesenteric vein due to extrahepatic portal obstruction. In this case, previous treatment, EIS and Hassab's operation, for esophago-gastric varices might have inhibited the development of collaterals apart from surface of gastrointestinal tract, such as para-esophageal collateral veins or spleno-renal shunt. Since the thrombus in the extrahepatic portal vein causes strong pressure on inferior mesenteric vein which is connected to the inferior vena cava via the inferior rectal vein, rectal varices might be developed. In this case, it was considered that rectal varices were not treated enough by endoscopic therapy because of regurgitant hyper blood flow against portal venous pressure. Therefore, rectal transection was performed. After the treatment, the patient suffered no further episodes of bleeding from rectal varices.

The correlation of between the endoscopic findings of esophageal varices and endoscopic ultrasound findings of the collaterals outside the esophageal wall in patients with portal hypertension remains unclear. We investigated the relationship between esophageal varices and the collaterals by endoscopy and endoscopic ultrasound. Moreover, we investigated the correlation between the collaterals around the esophagus and recurrence of esophageal varices in patients with portal hypertension who had undergone endoscopic injection sclerotherapy. The collaterals were divided into two groups: 1; those with peri-esophageal collateral veins (peri-ECVs) adjacent to the muscularis externa of the esophagus, and 2; those with para-esophageal collateral veins (para-ECVs) distal to the esophageal wall without contact with the muscularis externa. Peri- and para-ECVs were scored as mild or severe according to the stage of development. According to endoscopy, the varix form was significantly larger in severe peri-ECVs group than in mild peri-ECVs group. In contrast, the varix form did not differ significantly between the mild and severe para-ECVs group. The prevalence of perforating veins increased according to the varix form. With regard to variceal recurrence, in patients with variceal recurrences, EUS findings included a significantly higher incidence of severe-type peri-ECVs, a significantly larger number of perforating veins, and a significantly larger diameter of perforating veins compared with patients without recurrence. Moreover, when EUS found the abnormalities when no endoscopic recurrence was found, the results were the almost same as the findings when EUS was performed at the same time when endoscopic recurrence was found. In conclusion, the presence of severe peri-ECVs and large perforating veins in the esophageal wall strongly correlates with occurrence and recurrence of esophageal varices in patients with portal hypertension. An understanding of these EUS abnormalities on the basis of hemodynamics around the esophagus is thought to be important for management of esophageal varices in patients with portal hypertension.

Endoscopic ultrasonography (EUS) with a 20 MHz ultrasound (US) catheter probe can clearly demonstrate esophageal collateral veins. The presence of large periesophageal collateral veins has been correlated with large esophageal varices in patients with portal hypertension. The correlation between the size of esophageal collateral veins and endoscopic recurrence of esophageal varices in patients with portal hypertension who had undergone endoscopic injection sclerotherapy was investigated. Furthermore, whether EUS findings could predict the variceal recurrence was retrospectively studied.Thirty-eight patients who had undergone endoscopic injection sclerotherapy were examined every 3 to 4 months with endoscopy and US catheter probe for a period of 2 years. Recurrence of esophageal varices was determined by endoscopic findings of either new varix formation or appearance of red color sign. Esophageal collateral veins were identified by US catheter probe as peri-esophageal collateral veins (adjacent to the esophageal wall) and para-esophageal collateral veins (separated from the esophageal wall) along with perforating veins; and they were graded as severe and mild type by US catheter probe.Ten of the 38 patients (26.3%) had endoscopic recurrence at a mean of 10.9 months after endoscopic injection sclerotherapy. In patients with endoscopic recurrences, EUS findings included a significantly (p0.001) higher incidence of severe type peri-esophageal collateral veins, a significantly larger number of perforating veins (p0.001) and a significantly larger diameter of perforating veins (p0.001) compared with patients without recurrence (8 of 10, 80% vs. 2 of 28, 7.1%; 1.30 vs. 0.21; 2.00 vs. 0.32 mm, respectively). The presence of veins at the esophagogastric junction did not correlate with recurrence.Severe type peri-esophageal collateral veins and large perforating veins of the esophagus detected by EUS in patients treated by endoscopic injection sclerotherapy signify recurrence of esophageal varices and predict endoscopic recurrence of varices in subsequent months.

Macrolide antibiotics have unique immunomodulatory actions apart from their antimicrobial properties. We examined the effect of erythromycin (EM), a 14-member macrolide, on the immune response to a DNA vaccine that induces a T-helper-1 (Th1)-biased immune response through a Th1-promoting adjuvant effect of unmethylated CpG motifs within plasmid DNA. EM enhanced Th1 responses in plasmid DNA-immunized mice as measured by antigen-specific IgG2a antibody production, interferon-γ production by antigen-specific CD4 + T cells, and cytotoxic T lymphocyte responses. EM augmented the accessory cell activity of unmethylated CpG DNA-stimulated antigen-presenting cells (APCs), suggesting that EM enhances Th1 responses to a DNA vaccine, possibly through augmentation of accessory cell activity of APCs stimulated with CpG motifs within plasmid DNA.

We describe calcium oxalate and amyloid arthropathy with cutaneous calcinosis without vitamin C supplement. A 34-year-old woman developed glomerulonephritis requiring chronic hemodialysis. Seven years after beginning hemodialysis, multiple crystal deposits appeared in her skin; she also presented with arthralgia and gait disturbance. A skin biopsy was performed, which disclosed calcium oxalate deposition. In addition, a right femoral neck prosthetic replacement was performed. Pathologic examination of the hip synovia revealed diffuse calcium oxalate, amyloid, and iron deposition. Calcium oxalate and amyloid arthropathy with synovial hemosiderosis was diagnosed, and therapy with desferal and high-flux membrane dialysis was started. Clinical improvement occurred after 6 months.

Normal lymphocytes produce IL-5 with PHA and PMA stimulation. In this system, IL-5 production was enhanced by IL-4 and was inhibited by IFN alpha, TGF beta and IL-6.

Background: In a previous study, we demonstrated the collaterals around the esophageal wall observed by endoscopic ultrasound (EUS) in patients with portal hypertension can be divided into two groups, peri-esophageal collateral veins (peri-ECVs) and para-esophageal collateral veins (para- ECVs), and that the peri-ECVs and the perforating veins play an important role in the development of esophageal varices (Gastrointestinal Endosc 1999;50). Aim: To compare EUS imaging with microscopic findings in the peri- and para-ECVs and the perforating veins. Patients and Methods: Four patients with esophageal varices treated by endoscopic injection sclerotherapy were studied. After the therapy, the esophago-gastric junction (EGJ) to the upper 5 cm was scanned by EUS. In autopsy, the esophagus with surrounding tissue was removed, and 1 cm cross sections of the EGJ to the upper 5 cm were cut. EUS imaging and microscopic findings were compared. Results: EUS showed that peri-ECVs were developed in all cases and that para-ECVs were developed in 3 cases. Perforating veins were visualized in all cases. On the basis of microscopic findings in autopsy, the collaterals around the esophageal wall were divided into two groups: collaterals adjacent to the muscularis externa of the esophagus, and collaterals distal to the esophageal wall without contact with the muscularis externa. These collaterals were observed in all cases and were considered to correspond to the peri- and para-ECVs observed by EUS. Veins connecting vessels in the submucosal layer and veins around the esophageal wall were observed in all cases. These veins were considered to correspond to the perforating veins observed by EUS. Conclusion: The veins corresponding to peri-ECVs, para-ECVs and perforating veins observed by EUS were identified in autopsy. EUS has shown to be useful for an understanding of vascular structure around the esophageal wall.

Background: In patients with portal hypertension, many collaterals develop around the esophageal wall. Endoscopic ultrasonography (EUS) can reveal the para-esophageal collateral veins (para-ECVs) around the esophageal wall (Gastrointestinal Endosc 1999;50). Liver scintigraphy using 99mTc-phytate enables quantitative grading of the ratio of portal venous to total hepatic blood flow. Collaterals that have developed around the esophageal wall are thought to cause a reduction in the portal blood flow ratio (PBFR). To verify the role of para-ECVs on portal venous blood flow, we investigated the relationship between the development of para- ECVs and the PBRF by EUS and liver scintigraphy. Patients and Method: Twenty patients who did not associate with fundal gastric varices were studied before and after endoscopic injection screlotherapy (EIS). To quantify the degree of development of blood vessels outside the esophageal wall, the cross-sectional area of each para-ECVs observed by EUS was calculated, and the sum total of the areas was used as an index of development of para-ECVs. Portal blood flow was calculated by liver scintigraphy using 99mTc-phytate. Results: The correlation between PBRF and the total cross sectional area of the para-ECVs before and after treatment was examined. Before EIS, the PBRF was 53.42±12.34 % (mean±SD), and the total crosssectional area of the para-ECVs was 34.15±22.39 mm2 (mean±SD). The correlation between the PBRF and the total cross sectional area of para- ECVs before EIS was not significant. On the other hand, the PBFR was 53.42±12.34 % (mean±SD) and the total cross-sectional area of the para- ECVs was 34.15±22.39 mm2 (mean±SD) after EIS. After treatment, the correlation between these two parameters was significant (r=0.70, p

Summary. Normal human peripheral blood T cells and T-cell subsets defined by monoclonal antibodies of the OKT series were pretreated with pokeweed mitogen (PWM). Their effects on the haematopoietic precursors, erythroid (BFU-E, CFU-E), granulocyte-macrophage (CFU-GM) and megakaryocyte (CFU-M) colony forming cells were evaluated by coculture. While unstimulated T cells and T-cell subsets enhanced growth of autologous blood BFU-E, PWM-stimulated T and OKT4+ cells suppressed it, also inhibiting proliferation of both autologous and allogeneic bone marrow BFU-E, CFU-E, CFU-GM and CFU-M. PWM-stimulated OKT8+ cells had little effect on the growth of any of the precursors at the cell concentration at which growth was completely inhibited by PWM-stimulated OKT4+ cells. Irradiation of T or OKT4+ cells with 3000 rad before PWM stimulation completely abrogated the inhibition. These observations might be related to the mechanism of pancytopenia in some cases of immune-mediated aplastic anaemia.

Summary. NK cell activity was studied in 28 cases of acute leukaemia in remission. It was found that patients in long-term remission for 5 years or more had normal NK cell activity but those in remission for less than 5 years had significantly lowered activity. This suggests that patients with acute leukaemia had not been constitutionally deficient in NK cell activity. Low activity was augmented but not fully restored by interferon pretreatment in vitro. Therefore, the low NK cell activity observed during remission is not solely attributable to inadequate secretion of interferon in the host. It is suggested that the production of NK cells in bone marrow is impaired, or the function of NK cells is suppressed, by the leukaemia itself or by chemotherapeutic agents. Increased consumption of NK cells is also a possibility.

Human recombinant (r) IL-5 was shown to have the activity to stimulate eosinophil (Eo) colony formation from human non-T, non-adherent bone marrow cells. The majority of these colonies were found to contain a small number of basophils, macrophages or neutrophils. Human rG-CSF, which alone did not stimulate Eo colony formation, showed an enhancing effect on Eo colony formation when added with IL-5. IL-5 seems to stimulate the proliferation and differentiation of CFU-Eo, while G-CSF acts on the early stage of eosinophilopoiesis.

To elucidate the effects of alcohol on thrombotic diseases we focussed on blood rheology which is one of the most important factors of blood flow. We measured the viscosity of whole blood and plasma of 18 healthy volunteers (11 males and 7 females) before and after drinking at a dinner party. There were significant increases in whole blood viscosity (7.4%, P less than 0.005) and plasma viscosity (3.0%, P less than 0.005) after drinking. Judging from the significant correlations between changes in blood viscosity and changes in variables related to hemoconcentration, the ability of alcohol to increase blood viscosity is considered to be due mainly to hemoconcentration. Alcohol itself did not increase whole blood viscosity in vitro at concentrations of 0.1, 0.2, 0.3 and 0.4% (w/v).

SummaryAgar culture of bone marrow cells from 52 patients with acute nonlymphoblastic leukemia showed the development of higher than normal incidence of eosinophil colonies in 5 patients. Of these, the growth pattern of one patient was of particular interest since the aggregates formed consisted almost exclusively of eosinophilis which matured by 4 weeks of culture. In this patient, the plating efficiency was extraordinarily high and the growth of eosinophil colonies was significantly delayed. In this single patient karyotypic analysis suggested that the eosinophil colonies may have been derived from a leukemic cell line. Further studies are, however, necessary to determine the nature and origin of eosinophil colonies with acute nonlymphoblastic leukemia.We would like to thank Dr. Yasukazu Tanaka, Department of Experimental Pathology, Metropolitan Institute of Gerontrogy, Tokyo, for his assistance in the preparation of the electron micrographs and for his kind comments. We would also like to thank Profess...

Health surveys were made on the bights, weights, blood pressure, electrocardiogram, chest X-ray etc. of about 1400 junior and senior high school boys, 12-17 aged, in Tokyo city, in April 1976. The results were as follows : 1. The frequency distribution of arterial blood pressure showed standard normal distribution curves. 2. The Means and Standard Deviations of systolic blood pressure were 116.41 ±11.20 in junior high school boys, and 128.33±12.48 in senior high school boys. The Means and Standard Deviations of diastolic blood pressure were 67.17±9.77and 72.72±11.03 respectively, and the blood pressure gradually increased with age. 3. According to the modified Minnesota code critetia major electrocardiographic findings were 8.4% right axis deviation, 3.3% PQ prolongation, 2.21 complete or incomplete right bundle bolck, and 1.4% sinus bradycardia. 4. According to the modified classification of essential hypertention of the I WHO Expert Committee, the population were divided into three groups with respect to the Means and Standard Deviations of the respective school age.The normotensive group (under Mean) was 72.1%, boderline hypertensive group (within+1 S. D.) 23.2%, and hypertensive group (above+ 1 S. D.) 4.7% 5. It was shown that the blood pressure correldted with the Rhorer's Index, when overweights were defined above Rhorer's Index 136 (junior hgih school boys), and 146 (senior high school boys), overweights were found more frequently in the hypertensive than in the normotensive groups (p

HLA-A, B, DR, and MT antigens were examined in 50 patients with idiopathic membranous nephropathy (IMN) by the standard microlymphocytotoxicity technique. The frequency of HLA-DR2 was significantly increased in the patients in comparison to the controls. Significant decreases in the frequencies were seen for HLA-DR4, DRw8 and DRw9 in the patients. The linkage disequilibrium between HLA-Bw52 and DR2 was noted in the controls, but it was significantly weaker in the patients. The frequency of MTl was significantly higher, and that of MT3 was significantly lower in the patients as compared with the controls. The findings suggest that an immunological disturbance under the influence of genetic factors may confer a susceptibility to IMN.

Summary. To explore the possibility that an eosinophil colony stimulating factor (EO-CSF) is elaborated independently of neutrophil CSF (N-CSF), we compared the effect on the production of EO-CSF and N-CSF of adding a specific antigen, an aspergillus extract, to peripheral blood leucocytes of an eosinophilic patient with allergic bronchopulmonary aspergillosis. Conditioned media prepared from the patient's mononuclear (MN) and T cells were assayed for EO-CSF and N-CSF activities by agar culture technique, using normal human nonphagocytic MN bone marrow cells as target cells. The addition of the specific antigen to the cultures of the patient's MN or T cells significantly stimulated the production of EO-CSF, but not that of N-CSF, while the patient's non-T cells and normal MN or T cells were not stimulated by the antigen challenge to produce either CSF. These results suggest that EO-CSF is a factor distinct from N-CSF, that its production is dependent on the presence of sensitized T cells with antigen-specific stimulation, and that it might be one of the causes of blood eosinophilia in this patient.

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.

Effects of fish oil rich in eicosapentaenoic acid on serum lipid in hyperlipidemic hemodialysis patients. The incidence of atherosclerosis in hemodialysis (HD) patients is very high. Major risk factors are aging, lipid metabolism disturbances, high blood pressure, and smoking. High blood pressure and hypertriglyceridemia, which is atherogenic in the presence of smoking, are encountered very often in HD patients. The effects of eicosapentaenoic acid (EPA) on plasma lipids and blood pressure were studied for the first time in HD patients by the administration of capsules containing fish oil rich in EPA, which is known to lower serum lipid concentration and blood pressure. We treated 12 hyperlipidemic patients (3 of type IIa, 3 of type IIb, and 6 of type IV; 3 males, 9 females; 31 to 70 years of age; 4 to 90 months on HD) with 24 capsules (1.6 g EPA and 1.0 g docosahexaenoic acid) per day for 13 weeks. Serum triglycerides, total cholesterol, and phospholipid decreased significantly after capsule administration. The ratio of EPA to arachidonic acid in serum increased significantly. There was a small but statistically significant decrease in platelet count. Diastolic blood pressure decreased at the end of the experiment. These effects of fish oil are considered favorable for the prevention of atherosclerosis and its subsequent diseases. Effets d'une huile de poisson riche en acide eicosapentaenoique sur les lipides seriques chez des malades hemodialyses hyperlipidemiques. L'incidence de l'atherosclerose chez les malades hemodialyses (HD) est tres elevee. Les facteurs de risque majeurs d'atherosclerose sont l'âge, les perturbations du metabolisme des lipides, une pression arterielle elevee, et le tabagisme. Une pression arterielle elevee et une hypertriglyceridemie, laquelle est atherogene en presence d'un tabagisme, sont tres souvent rencontrees chez les malades HD. Les effets de l'acide eicosapentaenoique (EPA) sur les lipides plasmatiques et la pression arterielle ont ete etudies pour la premiere fois chez des malades HD en administrant des capsules contenant une huile de poisson riche en EPA, qui est connue pour abaisser la concentration en lipides seriques et la pression arterielle. Douze malades hyperlipidemiques (trois de type IIa, 3 de type IIb, et 6 de type IV; 3 hommes, 9 femmes, 31 a 70 ans; 4 a 90 mois en HD) ont ete traites avec 24 capsules (1,6 g d'EPA et 1,0 g d'acide docosahexenoique) par jour pendant 13 semaines. Les triglycerides, le cholesterol total, et les phospholipides seriques ont significativement diminue apres administration des capsules. Le rapport de l'EPA a l'acide arachidonique dans le serum s'est eleve significativement. Il y a eu une diminution faible mais significative du nombre de plaquettes. La pression arterielle diastolique a baisse a la fin de l'experience. Ces effets de l'huile de poisson sont consideres favorables pour prevenir l'atherosclerose et les maladies qui en resultent.

層流一次元の単純な燃焼場を用いて,微粉炭の燃焼過程とNOx生成特性について,燃焼の進行に伴う現象の経時変化を追跡しつつ詳細な検討を行った.まず,粒子に注目した燃焼履歴,これに及ぼす粒子径の影響を理論的検討も合わせて解明し,そのうえで,炉内でのNOx生成挙動を検討した.ついで,Fuel NからNOxへの転換率に及ぼす,炭種,空気比,温度などの諸因子単独の影響を,炉内現象との関連のうえで明らかにした.

1. ベンゼン及びトルエンを使用している,ビニールのグラビア印刷事業所において,15名の従業員のうち,13名に異常所見を認めた。 2. 夏期(5月s10月)はトルエンを,冬期(11月s4月)は5%のベンゼンを混じたトルエンを使用している。昭和39年6月の調査に際しては,ベンゼンは検出されず,事業所内には150s550ppmのトルエンが検出された。事業所の三階にある居室では,330ppmのトルエンが検出された。 3. 女子従業員4名のうち,3名は,溶剤中毒に起因すると考えられる再生不良性貧血に罹患していた。これらの患者は,日中は9時間以上,高濃度の溶剤蒸気に曝露されつつ作業し,夜間は,溶剤蒸気の充満している事業所の二階,三階に居住し,一日中,溶剤に曝露されていたのであった。