K. Ohshima

A case of histiocytic necrotizing lymphadenitis with bone marrow and skin involvement

We report a case of histiocytic necrotizing lymphadenitis (HNL) with bone marrow extension in a 29-year-old male in which many large mononuclear cells infiltrated the bone marrow and mimicked malignant lymphoma. A lymph node biopsy confirmed the diagnosis of HNL. Immunohistologically, the infiltrating cells in the bone marrow were positive for lysozyme, LeuM1, Kp-1 and T-cell markers. The cells did not show haemophagocytosis. A skin biopsy from an accompanying facial skin rash revealed a proliferation of large cells similar to those observed in affected foci of the lymph node in subcutaneous tissue. The infiltrating cells were mainly lysozyme and Kp-1-positive histiocytes, some with phagocytosis of nuclear debris but none characteristic of haemophagocytosis. Transformed T-cells were also infiltrating.

Alpha-interferon in Kikuchi's disease

SummaryIn Japan, histiocytic necrotizing lymphadenitis (Kikuchi’s disease) is a relatively common reactive lesion affecting lymph nodes, but the histogenesis and pathogenesis of the disease have not been clarified. Alpha-interferon has a role in the body’s defense against, viral infections. Using a polyclonal antibody to human alpha-interferon, we found numerous cells, mainly histiocytes, containing alpha-interferon in affected foci in the lymph nodes from 24 patients with Kikuchi’s disease. Tubuloreticular structures, thought by some authors to be associated with the production of interferon, were detected by electron microscopy in histiocytes, activated lymphocytes and vascular endothelial cells in the affected foci. These results suggested that the formation of tubuloreticular structures is a secondary phenomenon following stimulation by alpha-interferon. Further, the activity of 2′–5′ oligoadenylate synthetase, which is induced by alpha-interferon and enhanced during the early or active stage of viral infection, showed increased levels of activity in the active stage of Kikuchi’s disease and decreased to normal levels in the convalescent stage 2 weeks later. These results suggested the possibility of a viral etiology for Kikuchi’s disease.

Clinicopathological study of Ki-1-positive lymphomas.

We examined an antibody against Ki-1 antigen in 161 cases of malignant lymphoma, four of histiocytic sarcoma, and six of nonspecific lymphadenitis, using monoclonal antibody Ki-1, which is known to react selectively with activated lymphocytes, Reed-Sternberg cells, and Hodgkins cells. Among them, 12 cases of malignant lymphoma demonstrated a diffuse positive cell membrane and/or cytoplasmic reaction of tumor cells and were categorized as Ki-1-positive lymphoma. Nine of these cases exhibited large cells with indented nuclei, distinct nucleoli, and abundant basophilic or amphophilic cytoplasm. Of the remaining three cases, two were of medium-sized and one of small-cell type. Immunologically, the 12 cases of malignant lymphoma demonstrated T-helper/inducer phenotype in six cases, B-cell in two case, and non-T, non-B in four cases. Tac and HLADR were positive in 9/12 and 4/5, respectively, and markers for histiocytes (lysozyme, alpha-1 anti-chymotrypsin, and OK-M1) were usually negative. Clinically, T-cell Ki-1-positive lymphoma was most likely to occur in the elderly, at extranodal sites, and had a rather poor prognosis (mean survival 35.5 months) as compared with B-cell and non-T, non-B lymphoma (7-52 months survival).

Analysis of herpesvirus genomes in Kikuchi's disease

We examined the cervical lymph nodes of 30 patients with Kikuchis disease and 15 patients with nonspecific lymphadenitis, using Southern blot analysis and polymerase chain reaction (PCR) to identify human herpesviruses such as Epstein-Barr virus (EBV), cytomegalovirus, herpes simplex virus, and varicella-zoster virus. By Southern blot analysis, no virus DNA was recognized, but 16 of the 30 nodes from patients with Kikuchis disease and 8 of the 15 nodes from patients with non-specific lymphadenitis showed amplified EBV DNA by PCR.

Processor with 4.9-μs break-even time in power gating using crystalline In-Ga-Zn-oxide transistor

A processor having a power management unit (PMU) and an 8-bit CPU including flip-flops with shadow memories is fabricated by 0.5-μm Si and 0.8-μm c-axis-aligned crystalline In-Ga-Zn-oxide (CAAC-IGZO) technology. The shadow memories hold data without power supply utilizing low off-state current of CAAC-IGZO FETs. A break-even time (BET) of 4.9μs has been obtained. Good scalability of the processor in writing data to shadow memories and in area (5.7% overhead or less) is also confirmed through simulation and layout, based on flip-flops using 30-nm Si FETs combined with 0.3-μm CAAC-IGZO FETs which show good electronic characteristics and no overhead in area.

Analysis of human herpes virus-6 genomes in lymphoid malignancy in Japan.

Ninety cases of malignant lymphoma and 56 cases of reactive lymphadenopathy were studied using Southern blot analysis and the polymerase chain reaction to identify human herpes virus-6 (HHV-6) DNA. This was detected in cases of lymphoid malignancy at a rate which ranged from 50.0% to 68.8%. There were no differences in rates for different types of lymphoid malignancies. Herpes virus-6 DNA was detected by PCR in lymphoid malignancies less frequently than in reactive lymphadenopathies. It was not detected in lymphoid malignancies using Southern blotting. These results suggest that HHV-6 DNA was not related to lymphoid malignancy and was only a latent infection of non-neoplastic cells in tumour tissue.

Genotypic and Immunophenotypic Analysis of Anaplastic Large Cell Lymphoma (Ki-1 Lymphoma)*

Genotypic and immunological analysis was performed in 10 patients with anaplastic large cell lymphoma (Ki-1 lymphoma), 4 were male and 6 female. Immunophenotypically, 9 of these patients expressed some T cell markers; CD 2 in 9, CD 4 in 9, CD 3 in 6, CD 8 in 4, and UCHL-1 in 8. For B cell markers, 4 patients expressed B 1 and one expressed L 26; these patients also expressed T cell markers. In genotypic analysis, 9 of 10 cases displayed some incidence of T cell receptor gene (TCR) rearrangement or deletion, which was found in 3 patients for C beta 1, 7 for C beta 2, 8 for J gamma, 5 for C gamma (Hind III), 5 for C gamma (EcoRI), 3 for J delta 1 (Hind III), 3 for J delta 1 (BamHI), 3 for J delta 2, and 2 for C delta. One patient with rearrangement of TCR also showed rearrangement of immunoglobulin heavy chain. Another patient exhibited rearrangement of both TCR and immunoglobulin chain. These results indicate a common T cell lineage for this type of lymphoma.

Monoclonal B cells and restricted oligoclonal T cells in T-cell-rich S-cell lymphoma

Immunophenotyping of lymphoma using paraffin-embedded lymphoid tissue is useful in identifying the large neoplastic B cells in T-cell-rich B-cell lymphoma (TRBL), but does not succeed in deciding clonality. We studied six cases to determine the clonal population of B and T cells of TRBL. Immunohistochemistry on frozen and paraffin-embedded material showed that the cellular population in all six cases consisted mainly of T cells; fewer than ten percent of the cells stained as B cells. However, in all cases, monoclonality of the immunoglobulin was helpful for diagnosing the B-cell neoplasia. Southern blot-yielded genetic analysis showed monoclonality of B cells in three cases, but no evidence of clonality in the T cells. Moreover, gene monoclonality has been detected in all cases examined by polymerase chain reaction, using the primers for the V and J regions of the immunoglobulin heavy chain gene. For T cells, the D and J regions of the T-cell receptor (TCR) beta chain showed the same patterns of oligoclonal bands in all cells, and the V and J regions of the TCR gamma chain showed the same bands in all. The expression of TCR V beta families was polyclonal but restricted.

Clonality of Benign Lymphoid Hyperplasia in Orbit and Conjunctiva

In order to thoroughly characterize the clonal population of lymphoid hyperplasia of the orbit and conjunctiva, we investigated six cases which were histologically proven to be benign lymphoid hyperplasia. We analyzed the clonal rearrangements of the antigen receptors and bcl-2 gene, Epstein-Barr virus (EBV), and human T-cell leukemia virus type 1 (HTLV-I) by Southern blot and/or polymerase chain reaction (PCR), and performed in situ hybridization for mRNA of kappa and lambda immunoglobulin. Five cases showed rearrangements of immunoglobulin heavy chain gene (JH) and/or light chain gene (J kappa), and the monoclonal V-J recombination of JH in PCR. However, the rearranged bands were much more faint than was the germ-line band. We considered the monoclonal population of B cells small. Two of the five cases recurred locally after four and nine years respectively. Because benign lymphoid hyperplasias frequently contain an occult monoclonal B-cell population, a follow-up should be conducted. The remaining case in our investigation showed a rearrangement of the T-cell-receptor gene and proviral DNA of HTLV-I, and it showed rapid progress to adult T-cell leukemia after the biopsy. EBV and bcl-2 gene rearrangements were not observed in any of the six cases we studied.