used as the source materials, triethyl Sb (TESb) was used as the Sb source, and hydrogen was used as the carrier gas. The flow rates of DMSe, DMZn, and TESb were 15-30, 15, and 0-1.0 µmol/min., respectively. The growth temprature was 550oC and the growth time is 2.5h. Photoluminescence (PL) measurement was done at the temperature range between 6 and 300K using a He-Cd laser. Four-crystals X-ray rocking curves were obtained by X-ray diffractometer. The concentration of Sb was measured by secondary ion mass spectrometry (SIMS). Net acceptor concentration was obtained from capacitance-voltage characteristicsat room temperature.
We investigated the expression of adhesion molecules including LFA‐1α (CD11a), Mac‐1 (CD11b), LFA‐1β (CD18), VLA‐β 1 , (CD29), H‐CAM (CD44), VLA‐4 (CD49d), VLA‐5 (CD49e), ICAM‐1 (CD54), N‐CAM (CD56), LFA‐3 (CD58), VNR‐β (CD61), and LECAM‐1 (CD62L) on fresh myeloma cells and human myeloma cell lines. By two‐color flow cytometric analysis with anti‐CD38 antibody, we demonstrated that myeloma cells were located in the strongly CD38‐positive (CD38 ++ ) fractions. Fresh myeloma cells were obtained from 28 patients with multiple myeloma (MM) and 3 patients with plasma cell leukemia (PCL). All myeloma cells expressed VLA‐4 on their surface. Most of the myeloma cells also expressed VLA‐5, ICAM‐1, and LFA‐3. H‐CAM was strongly expressed in 3 cases of PCL and 2 cases of aggressive myeloma, and moderately expressed in other MMs. N‐CAM was expressed in 68% of MMs, but none of the 3 PCLs. LFA‐1 was expressed in two cases of aggressive myeloma, but not expressed in other non‐aggressive myelomas. Most of the myeloma cells did not express Mac‐1, VNR‐β, or LECAM‐1. These results suggest that VLA‐4, VLA‐5, ICAM‐1, LFA‐3, and H‐CAM are involved in cellular interaction and migration in MM, and that the expression of N‐CAM and LFA‐1 varies with disease activity in MM.
Commercial yeast RNA was extremely highly purified. The DNP-derivatives of such RNA (DNP-RNA) liberated several kinds of DNP-amino acids by alkali treatment and also by acid hydrolysis of the remainder of the alkali treatment. It seems likely that at least some parts of the amino acids liberated have originally been bound to the RNA in a more stable form, in which the NH2-groups of the amino acids are not involved. Ultraviolet absorption spectra and infrared absorption spectra were compared between RNA and DNP-RNA before and after alkali treatment. Quantitative determination of DNP-group introduced into RNA molecule was also made. These data indicated that practically no dinitrophenylation had occurred in purines and pyrimidines. A peptide fraction was separated as DNP-derivatives from DNP-RNA or from a mixture obtained after dinitrophenylation of the alkali digest of RNA. Acid hydrolysis of the peptide fraction yielded DNP-derivatives of histidine, serine, alanine and aspertic acid, indicating the occurrence in the RNA of not less than four different peptides having these amino acids as terminus.
To the Editor: Schwachman's syndrome, a familial disease transmitted as an autosomal-recessive trait, is characterized by moderate chronic neutropenia, marked marrow hypocellularity, occasional thrombocytopenia and anemia, metaphyseal dysostosis of tubular bones, pancreatic fatty infiltration, and accompanying pancreatic insufficiency with absence of pulmonary and sweat elecrolyte pathology.Steatorrhea and growth failure are prominent.Pancreatic enzyme replacement may compensate for pancreatic insufficiency, but no therapy has been fully effective on the hematologic abnor-Fig.1.The case and the fatty infiltration of the pancreas. malities.We report on a 6-year-and-9-month-old white male with Schwachman syndrome, admitted with complaints of stunted growth, distended abdomen, and fatty diarrhea.He was Ͻ3rd percentile with a McLaren scoring of 5. His liver extended 1.5 cm below the costal margin; his right iliac-malleol encountered in the present case, as seen in the ill-defined disease of cyclic neutropenia which is characterized with fever and oral ulcers in older length was 2 cm shorter than the left.Roentgenograms revealed right femur neck shortness, acetabular hypoplasia, and infantile vertebrae.children [1].In addition, an immune-deficient state was also disclosed, with a median T4/T8 ratio of 0.40: 12% (low) T-helper and 30% T-suppressor cell Fat globules and fatty acids were positive in stool specimens and tripsin activity, and Giardia trophozoites were absent in repeated duodenal juice counts.There was normal B-lymphocyte count, but also hypoimmunoglobulinemia with median serum immunoglobulin values of IgA, 11 mg/dl; and stool examinations.Repeated sweat test chemistry was found normal (median Na, 30 mEq/l; Cl, 10 mEq/l).History, and physical and radiologic IgM, 17 mg/dl; IgG, 107 mg/dl; and normal IgE our laboratory normal ranges are close to Hong's International Reference Standard Values) [3].examinations, revealed that the child was generally free of pulmonary disease.Following informed parental consent, endoscopic examination of The patient's glomerule filtration rate, acid-loading test, and thyroid functions were normal.Other systemic and routine hematologic and bio-the small intestine disclosed only mucosal edema.An abdominal CT scan [2] showed fatty infiltration of the pancreas (Fig. 1).chemical findings were remarkable.No medication was instituted during his stay in the hospital.During hospitalization, he presented with intermittent neutropenia (median, 1.1 ϫ 10 9 /l) in cycles of 3 weeks, instead of the moderate chronicWe did not come across such disturbances as were seen in the present case in other cases with Schwachman's syndrome reported formerly, except neutropenia characteristic of Schwachman syndrome, and with moderate marrow cellularity during neutropenic periods, with normal maturity and in the case of Brueton et al. [4], presenting with cyclic neutropenia and variability in immunoglobulins.ratio attained before the advent of each neutropenic cycle.However, there was no intense myelopoiesis beginning with the advent of neutropenia, andThe patient returned for a single follow-up examination 3 months after discharge with pancreatic enzyme replacement.His findings suggested a the typically elevated monocytes at the nadir of the neutrophil count were
A 75-year-old female was diagnosed as having multiple myeloma (IgG.lambda type. Stage IIA) with plasmacytoma of the head and back in October, 1989. She obtained partial remission by MCNU and MP therapy, but relapsed with massive ascites in January, 1991. VAD therapy was not effective and she died of multiple organ failure on February 23. Her ascites contained a large number of myeloma cells, and the phenotypic analysis and the response to interleukin-6 (IL-6) of these myeloma cells were examined. The myeloma cells were positive for CD33, CD45, CD45RA, CD63, CD71, plasma cell associated antigens such as CD38, PCA-1, BL3, and various kinds of adhesion molecules: CD11a/CD18 (LFA-1), CD29 (VLA-beta 1), CD44 (H-CAM), CD49d (VLA-4), CD54 (ICAM-1), CD56 (N-CAM), CD58 (LFA-3). IL-6 level in the ascites was increased at 91.0pg/ml. The myeloma cells showed an IL-6 dependent growth, which was inhibited by anti-IL-6 antibody (Ab) and anti-IL-6 receptor Ab in vitro. Myeloma cells appearing in ascites have rarely been reported. Our case suggested that IL-6 was a potent growth factor of myeloma cells through an autocrine mechanism in the ascites, and resulted in an aggressive myeloma.
