Near-infrared spectral results of asteroid Itokawa from the Hayabusa spacecraft.

The near-infrared spectrometer on board the Japanese Hayabusa spacecraft found a variation of more than 10% in albedo and absorption band depth in the surface reflectance of asteroid 25143 Itokawa. Spectral shape over the 1-micrometer absorption band indicates that the surface of this body has an olivine-rich mineral assemblage potentially similar to that of LL5 or LL6 chondrites. Diversity in the physical condition of Itokawa's surface appears to be larger than for other S-type asteroids previously explored by spacecraft, such as 433 Eros.

Amyloid A-type renal amyloidosis in a patient with sarcoidosis: report of a case and review of the literature.

A 53-year-old man developed chronic renal failure during a protracted course of sarcoidosis. A renal biopsy showed Congo red-positive homogenous deposits in the subendothelial space of glomerular capillary walls and arterial walls. On electron microscopy, amyloid fibrils were observed in the deposits. Immunohistochemistry showed positive staining for amyloid A (AA) protein. Treatment with prednisolone resulted in poor response, followed by progressive deterioration of renal function requiring hemodialysis. To our knowledge, there are 5 cases with histologically proven renal amyloidosis accompanied by sarcoidosis. Prognosis in these patients is extremely poor. AA-type amyloidosis should be considered as a rare renal complication in the setting of long-standing sarcoidosis.

Endocapillary proliferative glomerulonephritis in a patient with parvovirus B19 infection.

A 45-year-old woman developed acute nephritic syndrome after erythema infectiosum. Laboratory data on admission showed decreased serum C3, C4, and CH50 levels and the presence of both immunoglobulin (Ig) M and IgG antibodies to human parvovirus B19 (HPV). A renal biopsy showed diffuse endocapillary proliferative glomerulonephritis. Immunofluorescence microscopy indicated 2+ granular staining for IgG, IgM, and C3 over the mesangial area and along glomerular capillary walls. HPV antigen was also detected in glomeruli by immunohistochemistry. Electron microscopy showed electron-dense deposits in the subendothelial space and the paramesangial area. These findings suggest that immune complex-type glomerulonephritis is caused by glomerular deposition of HPV antigen-antibody complexes in some patients with HPV infection.

[Pulmonary complications after allogeneic hematopoietic stem cell transplantation].

We investigated the occurrence of pulmonary complications in patients who underwent allogeneic hematopoietic stem cell transplantation at our institution. Pulmonary complications were observed in 12 out of 60 patients. Interstitial pneumonia developed in 12 cases: 7 idiopathic, 2 cytomegalovirus-associated, 1 P. carinii, 1 HSV, and 1 HHV-6-associated. HSV- and HHV-6-associated pneumonias were exhibited 100 days after transplantation. PCR analysis was diagnostically useful for detection of viral DNA in bronchial alveolar lavage fluid. Respiratory disease with airway obstruction was observed in 4 patients with chronic graft-versus-host disease, and all 4 had a history of interstitial pneumonia. Three patients died of respiratory failure. Mycobacicrium avium complex was detected in 2. Exacerbation of respiratory failure may be associated with mycobacterial infection.

Extensive intraglomerular thrombi of monoclonal IgM-kappa in a patient with malignant lymphoma.

We describe an 80-year-old man who developed malignant lymphoma (ML) complicated by extensive intraglomerular thrombi of immunoglobulin M (IgM)-kappa monoclonal immunoglobulin. The clinical picture was characterized by nephrotic syndrome and systemic lymphadenopathy. Laboratory examination showed mild anemia and a small amount of monoclonal IgM-kappa in the blood. The histopathologic findings and surface immunoglobulin analysis of the lymph node biopsy specimen were consistent with CD5-positive diffuse large B-cell (type, IgM-kappa) lymphoma. The subsequent renal biopsy showed a massive deposition of amorphous material in the glomerular capillary lumens, subendothelial areas, and mesangium. Nodular glomerulosclerosis was not found. An immunofluorescent study showed that the deposits consisted of IgM-kappa monoclonal immunoglobulin. Ultrastructurally, the deposits were composed of granular electron-dense material. Chemotherapy was effective for both the ML and nephrotic syndrome, and the patient's urine analysis results returned to normal. The histopathologic manifestations of this case are rare, and the pathogenesis of these glomerular lesions was obviously associated with ML.

[Dissecting aneurysm of the middle cerebral artery: case report].

We present a surgical case of a dissecting aneurysm of the right middle cerebral artery associated with subarachnoid hemorrhage and intracranial hemorrhage. A 61-year-old woman with consciousness disturbance and left hemiplegia was referred to our hospital. She had suffered severe headache for a week. CT scan showed a subarachnoid hemorrhage in the right Sylvian fissure and intracranial hemorrhage in the right putamen. The right carotid angiogram revealed string sign in M1 portion and occlusion at M2 lower branch of the right middle cerebral artery. On the 12th day, we undertook surgery to confirm whether it was a dissecting aneurysm or not. In the operation, it was reddish in the M1 portion corresponding to the "string sign" and dark-purplish in the lower M2 portion corresponding to an "aneurysm-like lesion". To prevent bleeding, the arterial wall in the M1 portion was coated using muscle. Though the left hemiplegia was unchanged, the postoperative course was uneventful. The patient was transferred to another hospital and underwent rehabilitation. There has been no reccurrence during the four years since surgery. The middle cerebral artery dissecting aneurysm is extremely rare. We presented this case with review of the literature.

A new variant translocation of t(15;17) in a patient with acute promyelocytic leukemia (M3): t(15;19;17)(q22;p13;q12).

The reciprocal translocation (15;17) is specifically associated with acute promyelocytic leukemia [APL; M3 subtype according to French-American-British (FAB) classification]. A few patients with this disease have complex variant translocations. We describe a patient with M3 carrying t(15;19;17)(q22;p13;q12), which is a new type of variant translocation. The karyotypic interpretation was confirmed by Southern blot analysis with the use of RAR alpha and by fluorescence in situ hybridization (FISH) with the use of painting probes of chromosomes 15, 17, and 19 and a (15;17) translocation DNA probe. The results support the idea that the key event in APL is the formation of fusion gene PML/RAR alpha on the der(15).

Rearrangements of the BCL6 gene and chromosome aberrations affecting 3q27 in 54 patients with non-Hodgkin's lymphoma.

Chromosome aberrations affecting 3q27 are among the most frequent non-random abnormalities in non-Hodgkin's lymphomas (NHL), especially the diffuse, large cell type. Recently, an association between BCL6 rearrangement and frequent extranodal lesions, rare bone marrow infiltration and a favorable clinical outcome was reported. We performed molecular studies of the BCL6 gene in 54 patients with NHL. Twelve patients (22%) with rearranged BCL6 genes were selected for histological, clinical, molecular, and cytogenetic studies. Ten of these cases were diffuse, large cell type lymphoma, one a follicular lymphoma, and one a mantle cell lymphoma (MCL). All cases were of the B-cell type and this is the first time a rearranged BCL6 gene has been found in an MCL. Cytogenetic data for 10 cases were available and the partner sites of the 3q27 translocation were determined in 7 of 10 patients. These locations were variable, including 6p21.3, 9p22, and 14q11 in addition to the immunoglobulin loci 14q32 (IGH), 2p12 (IGK), and 22q11 (IGL). The heterogeneity in partner sites is distinct from other lymphoma subgroups and may suggest that the genetic events are not uniform among patients with BCL6 rearrangements.

[Autologous peripheral blood stem cell transplantation for CHOP-resistant mediastinal diffuse large B-cell lymphoma].

We report two cases of CHOP-resistant mediastinal diffuse large B-cell lymphoma (MDLCL) treated by autologous peripheral blood stem cell transplantation (auto-PBSCT). The patients were 17 and 28 year old female, and they had anterior mediastinal bulky masses at presentation. The clinical stage was IV in both patients. They were initially treated with 6 courses of bi-weekly CHOP therapy following by irradiation of the mediastinal tumors. During the last few cycles of CHOP therapy, their disease had become progressive. They underwent auto-PBSCT after high-dose chemotherapy consisting of busulfan, cyclophosphamide and etoposide, but failed to achieve remission. They died within one year after the auto-PBSCT because of the disease progression. Our experience suggests that this conditioning regimen is not effective for CHOP-resistant MDLCL, and it is necessary to develop new conditioning regimens.

Translocation (8;12;21)(q22.1;q24.1;q22.1): a new masked type of t(8;21)(q22;q22) in a patient with acute myeloid leukemia.

The translocation t(8;21)(q22;q22) is found in 40% of cases of acute myeloid leukemia (AML) designated as the subtype M2 in the French-American-British (FAB) classification. The 8;21 translocation is clinically of interest because patients with this subtype have a good prognosis. We describe a masked type of the translocation, t(8;12;21)(q22.1;q24.1;q22.1). The translocation was first interpreted as t(8;12)(q22;q24) based on cytogenetics, but was reevaluated as a result of Southern blot and fluorescence in situ hybridization (FISH) analyses.

Prediction of delayed ischemic injury with diffusion-weighted MRI following temporary middle cerebral artery occlusion in rats.

Early reductions in the apparent diffusion coefficient of water (ADC) during focal cerebral ischemia are often reversible with reperfusion. With sustained ischemia, the magnitude of the ADC reduction generally increases with time, which could reflect increased severity of ischemic damage. Thus, a threshold in ADC reduction may exist beyond which damage can not be reversed with reperfusion. The goal of this study was to determine if such a threshold exists that is independent of the duration of ischemia in a rat model. Rats were subjected to either 30, 60, or 90 min of temporary middle cerebral artery occlusion. ADC maps acquired just before and 30 min after reperfusion were compared to histology performed after a 72 h survival period to determine the relationship between ADC reduction and final ischemic injury. Significant variability in tissue recovery was observed for the 30 min group. Regions with ADC reductions of up to 45% often recovered, while some regions not exhibiting any change in ADC during occlusion showed ischemic injury at 72 h. Similar observations were made in cortical regions of the 60 min group. In the caudate-putamen, reduced ADC was often associated with ischemic injury. For the 90 min group, results for the caudate-putamen were similar to those for the 60 min group, while reduced ADC was a much better predictor of final ischemic injury in cortical regions than it was in both the 30 and 60 min groups. Thus, no single threshold of ADC reduction that was independent of the duration of ischemia was associated with irreversible injury.

BCL6 rearrangement in a patient with mantle cell lymphoma.

We describe a patient with mantle cell lymphoma (MCL) associated with BCL6 gene rearrangement. MCL is a distinct subtype of non-Hodgkin's lymphoma characterized by CD5+, CD10-, CD20+, t(11;14)(q13;q32) and PRAD1/cyclin D1 overexpression. Although rearrangement of the BCL6 gene is the most frequent genetic change among diffuse lymphomas and some follicular lymphomas this is the first report of a patient with MCL associated with BCL6 rearrangement.

11q23 aberration is an additional chromosomal change in de novo acute leukemia after treatment with etoposide and mitoxantrone.

We report on 2 patients with acute leukemia who had an 11q23 chromosomal aberration as an additional change after treatment with etoposide and mitoxantrone, agents that affect topoisomerase II (Topo II). One patient with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (L2) received chemotherapy, including 1,000 mg of etoposide and 75 mg of mitoxantrone. She relapsed 10 months later. Analysis at time of relapse showed a chromosomal aberration of del(11)(q23) as an additional cytogenetic change. The other patient was diagnosed with acute monoblastic leukemia (M5a) and received two autologous peripheral blood stem-cell transplantations. Her cumulative doses of etoposide and mitoxantrone were 6,000 mg and 42 mg, respectively. She also relapsed, and analysis at that time revealed del(11)(q23) as an additional chromosomal aberration. The mixed lineage leukemia/myeloid-lymphoid leukemia (MLL) gene was not rearranged in either case, making these cases distinct from previously described therapy-related leukemias caused by Topo II inhibitors. Based on these two cases, it may be that Topo II inhibitors can cause clonal evolution affecting chromosome band 11q23.

A new non-random chromosomal translocation t(3;6)(q27;p21.3) associated with BCL6 rearrangement in two patients with non-Hodgkin's lymphoma.

We describe two cases of non-Hodgkin's lymphoma associated with t(3;6)(q27;p21.3) and BCL6 rearrangement. The first case was in a 78-year old woman, whose performance status (PS) was 1, the serum lactate dehydrogenase (LDH) level was elevated, and the Ann Arbor stage was IIIA with no extra nodal lymphomatous site. The pathological diagnosis from a biopsy of the inguinal lymph node was 'malignant lymphoma (ML), follicular, small cleaved' according to the Working Formulation. Complete remission was achieved. Although she had relapse in 1992, remission was obtained again. The second case was in a 62-year old man, whose PS was 1, the serum LDH was normal, and Ann Arbor stage was IVA with the involvement of the small intestine. Histological diagnosis of the cervical lymph node was 'ML, diffuse, large cell'. Complete remission was obtained without relapse. The 3q27 translocations, found in 20-30% of non-Hodgkin's lymphoma, are unique in having multiple chromosomal translocation partners. Chromosome band 6p21.3 is one of these partner sites that may be the site of a novel gene. The two cases presented here show that this translocation is a non-random chromosomal change involving 3q27 and BCL6. Since t(3;6) was the sole karyotypic abnormality in one case, this translocation may play a role in lymphomagenesis.

Translocation (3;14)(q27;q11): a new variant translocation in a patient with non-Hodgkin's lymphoma of B-cell type with BCL6 rearrangement.

We report a 65-year-old woman with non-Hodgkin's lymphoma (NHL) carrying a t(3;14)(q27;q11) and BCL6 rearrangement in the affected cells. She had generalized lymphadenopathy and the bone marrow was infiltrated by lymphoma cells at presentation. Histological diagnosis was "malignant lymphoma, diffuse, large cell" type according to an International Working Formulation. Chromosome analysis revealed a t(3;14)(q27;q11), which is a new variant translocation of t(3;14) (q27;q32). Southern blot analysis showed rearrangement of BCL6, JH, and TCR beta but not of TCR delta. Cosmid probe of BCL6 hybridized to 14q11 and 3q27 by fluorescence in situ hybridization (FISH). Although the band 14q11 is a locus of T-cell receptor alpha- and delta-chains (TCR alpha/delta), lymphoma cells expressed B-cell, IgGk phenotype. The findings suggest that a novel proto-oncogene in the vicinity of TCR alpha/delta is involved in this translocation.

Duplication of chromosome 9 carrying a BCR/ABL chimeric gene in Philadelphia chromosome negative chronic myeloid leukemia.

We investigated a patient with Philadelphia chromosome (Ph) negative but BCR positive chronic myeloid leukemia (CML) by fluorescence in situ hybridization (FISH). In the chronic phase one chromosome 9 contained a BCR/ABL fusion gene instead of chromosome 22. Although in blast crisis, both chromosomes 9 had BCR/ABL fusion genes. This could be caused by duplication of the rearranged chromosome 9, which may have a significance similar to a double Ph chromosome. This may suggest that the critical event in CML is the formation of a BCR/ABL chimeric gene regardless of its locus in the genome.

Translocation (9;11;22)(p22;q23;q11). A new type of complex variant translocation of t(9;11)(p22;q23) with MLL rearrangement.

We describe a patient with acute monocytic leukemia (M5a, FAB classification) associated with a new type of variant translocation (9;11). Southern blot analysis showed the rearrangement of the MLL (ALL-1/HRX) gene at 11q23. Fluorescence in situ hybridization (FISH) with painting probes of chromosomes 9, 11, and 22 revealed the translocation as t(9;11;22) (p22;q23;q11). This is more evidence that the production of chimeric mRNA following the translocation of the LTG9 (MLLT3/AF9) gene at 9p22 to 11q is a critical event in this leukemia subtype.

Heme oxygenase-1 (HO-1) protein induction in rat brain following focal ischemia.

The induction of the heme oxygenase-1 (HO-1) protein, also called HSP32, was compared to HSP70 heat shock protein induction following focal ischemia. Adult Sprague-Dawley male rats (n = 14) were subjected to either 30 min or 2 h of focal cerebral ischemia using the suture, middle-cerebral-artery (MCA) occlusion model. Controls (n = 4) had sham surgery. Following 24 h of reperfusion, subjects were killed and their brains stained immunocytochemically for HO-1 and the HSP70 heat shock proteins. One day following 30 min of ischemia, HO-1 and HSP70 staining in striatum occurred mainly in endothelial cells in infarcts and in glial cells surrounding the areas of infarction. Following the 30 min ischemia HO-1 was not induced in cortex whereas HSP70 was induced in cortical neurons in the MCA distribution. One day following 2 h of MCA ischemia, both HO-1 and HSP70 were induced in neurons in cortex in the MCA distribution. HO-1, however, was induced in glial cells throughout ipsilateral cortex, inside as well as outside the MCA distribution. This suggests that translation and/or transcription of the HO-1 and HSP70 genes are blocked in neurons and glia destined to die within infarcts, whereas translation of these stress genes continues in the endothelial cells. The duration of ischemia required to induce HSP70 in cortical neurons appears to be less than that required to induce HO-1 in cortical glia. Prolonged spreading depression and/or diffuse hemispheric ischemia may induce HO-1 in glia throughout the ipsilateral cortex via immediate early gene activation of the AP-1 site in the HO-1 promoter. Since HO-1 degrades heme, a pro-oxidant, to antioxidant molecules, the induction of HO-1 may augment oxidative defense mechanisms compromised by cerebral ischemia.

Bone and brain involvement in a case of diffuse large B cell lymphoma associated with t(2;3)(p12;q27).

We report a 57-year-old male with non-Hodgkin's lymphoma (NHL) associated with t(2;3)(p12;q27). The patient showed bone lesions at presentation and brain involvement at relapse in addition to systemic lymph node swelling. Histological diagnosis was malignant lymphoma, diffuse, large cell, immunoblastic, plasmacytoid. Chromosome analysis revealed t(2;3) which is a variant type of t(3;14)(q27;q32). Fluorescence in situ hybridization (FISH) analysis disclosed splits of signals of BCL-6 gene. Among the cases reported in the literature, the common feature of t(2;3)(p11 or p12;q27) was diffuse, large cell lymphoma of B cell, kappa phenotype and four patients immunosuppressive state before lymphoma.

Risk factors for hepatosplenic abscesses in patients with acute leukemia receiving empiric azole treatment.

The authors retrospectively evaluated 63 febrile neutropenic episodes in 33 consecutive patients with leukemia who received empiric azole treatment for refractory or relapsing fever that occurred despite broad-spectrum antibiotics. In 8 patients (24%), hepatosplenic abscesses (HSA) developed. To identify the risk factors for the development of HSA, the authors compared various characteristics of febrile episodes in those with and without HSA. The risk factors included relapsed status of leukemia (P = 0.04) and Candida colonization of surveillance cultures from the throat (P = 0.03) and stool (P = 0.03). However, the duration of neutropenia, gastrointestinal symptoms, types of chemotherapy, and leukemia subtypes were not correlated with the development of HSA. Based on these results, the authors identified the high risk group for the development for HSA as patients with relapsed leukemia with fungal colonization of gastrointestinal tract during neutropenia despite empiric antifungal treatment with azoles.