Comparison of genomic structures and antigenic reactivities of orthologous 29-kilodalton outer membrane proteins of Helicobacter pylori.

We purified a 29-kDa Helicobacter pylori outer membrane protein (Omp29 protein) and cloned the gene encoding the protein from H. pylori strain ATCC 43504. The Omp29 gene corresponded to the reported JHP73 and the HP78-79 genes of H. pylori strains. A corresponding nucleotide fragment was detected in all 150 tested H. pylori clinical isolates by PCR or Southern blotting. The amplified Omp29-corresponding fragments were categorized into a ca. 770-bp-long group and a larger-fragment group. Sequence analysis indicated that the larger fragments were likely synthesized from the 770-bp fragments by insertion of an irrelevant fragment via 17-bp-long repeat sequences. Immunoblot analysis implies that the ca. 770-bp fragment is responsible for the protein homologous to Omp29, whereas the larger fragments are not responsible for those proteins or encoding antigenically distinct proteins. We postulate that the H. pylori outer membrane protein Omp29 can alter its antigenicity through gene modifications mediated by nucleotide transfer.

Hepatitis B virus harboring nucleotide deletions in the core promoter region and genotype B correlate with low viral replication activity in anti-HBe positive carriers.

BACKGROUND: Emergence of anti-HBe following seroconversion of HBe antigen indicates reduced hepatitis B virus (HBV) replication in the liver and low infectivity in the natural course of infection. However, some patients show continued replication or reactivation even in the presence of anti-HBe. OBJECTIVE: To clarify the cause of HBV replication, we investigated genotype differences and mutations in the core promoter and precore region in relation to virus titer. STUDY DESIGN: Using quantification of HBV DNA, nucleotide sequencing of the core promoter and precore region, and genotyping with the S gene by restriction fragment length polymorphism (RFLP), we analyzed sera of 26 anti-HBe positive carriers (28 serum samples). RESULTS: Various mutations were detected including C to T point mutation at nt 1653, A to T and G to A contiguous point mutations at nt 1762 and 1764 in the core promoter region, and G to A point mutation at nt 1896 in the precore region, but no common mutations were detected that were directly related to the virus titer from earlier reported mutations. In contrast, the mean titer of genotype B virus was 1.5 x 10(5) copies per ml and that of mutant HBV of genotype C having 8 base pairs (8-bp) deletion (nt 1768-1775) in the core promoter region was 7.9 x 10(4) copies per ml (mean titer). These titers showed commonly lower than that of genotype C virus without 8-bp deletion (median titer 5.0 x 10(6) copies per ml). Transition of genotype from C to B after viral reactivation and reduction of proportion of 8-bp deletion mutant at reactivation period was observed in a patient who demonstrated exacerbation of liver dysfunction due to immunosuppressive therapy and increased viral replication. CONCLUSIONS: These results confirm those of our earlier study describing low replication ability of 8-bp deletion mutant HBV in vitro, and also indicate that the presence of genotype B correlates with reduced titer of HBV.

Nasal CD56 positive small round cell tumors. Differential diagnosis of hematological, neurogenic, and myogenic neoplasms.

CD56-positive nasal and nasal-type natural killer (NK)/T-cell lymphoma is now a well-defined disease entity. Rare cases of blastic NK-cell lymphoma positive for CD56 have been recently reported. However, CD56 expression is also identified in several types of non-hematopoietic small round cell tumors in which lymphoma is included as a differential consideration. Here, we present nine cases of CD56+ small round cell tumors of histological origin unrelated to nasal NK/T-cell lymphoma. Eight of the nine cases presented as solid tumors of the sinonasal region. Clinical, histological, ultrastructural, and immunohistochemical examination and gene analysis for T-cell receptor (TcR) and immunoglobulin heavy chain (IgH) genes and in situ hybridization (ISH) for Epstein-Barr virus (EBV) were performed. Two cases presented with features consistent with blastic NK-cell lymphoma or lymphoblastic lymphoma of NK-cell phenotype. These cases showed features of lymphoblastic lymphoma, phenotypes of sCD3-, cCD3+, CD45+, CD56+, TdT+, and human leukocyte antigen (HLA)-DR+, germline of IgH and TcR genes, and EBV negative reactivity. One case had myeloid/NK-precursor acute leukemia/lymphoma with a phenotype of CD13+, CD33+, CD34+, CD56+, and MPO-. Three cases were neurogenic, including one case of olfactory neuroblastoma and two of primitive neuroectodermal tumors (PNET). It was difficult to differentiate CD56+ PNET from blastic NK-cell lymphoma, especially when only paraffin-embedded sections were available. Myogenic markers, such as HHF35, alpha-sarcomeric actin, and desmin, were positive in three cases of rhabdomyosarcomas. Our findings suggest that as CD56 is used more routinely as a marker in immunohistochemical staining, the differential diagnosis of extranodal lymphohematological malignancies and small round cell tumors will become more complicated.

A case of ovarian carcinoma with production of granulocyte colony-stimulating factor.

A 60-year-old female with ovarian carcinoma showed marked leucocytosis. After exploratory laparotomy she had received carboplatin-based chemotherapy, but she died of respiratory failure. In this case the immunohistochemical examination of the tumour cells showed partial-positive staining for anti-G-CSF monoclonal antibody in addition to the elevation of the serum G-CSF concentration. This case is the first report of an ovarian carcinoma producing G-CSF.

Significance of urinary fibrin/fibrinogen degradation products in renal diseases measured by a highly sensitive ELISA.

The urinary fibrin/fibrinogen degradation products (FDP), as sensitive indicators of various renal disorders, have been measured by several methods. For their determination, a new and highly sensitive enzyme-linked immunosorbent assay not requiring the urine concentration has been developed. The study comprised 42 patients with nonnephrotic chronic glomerulonephritis (CGN), 23 patients with primary nephrotic syndrome (NS), and 29 healthy adults. The results were as follows: (1) the content of urinary FDP in normal subjects was 10.30 +/- 9.08 ng/ml; (2) the mean level of urinary FDP in both CGN and NS groups was significantly higher than in normal subjects; (3) in the CGN group itself there was a tendency for an increase of urinary FDP during more active forms of the disease, and (4) there was a significant correlation between urinary FDP and urinary protein in the CGN group, whereas no correlation was observed in the NS group. These results suggest that the major part of urinary FDP in the CGN group derives from the increased filtration, while its origin in the NS group is not related to increased filtration only, but may also have involved intraglomerular coagulation abnormalities. The newly developed enzyme-linked immunosorbent assay can detect urinary FDP levels lower than 3.9 ng/ml. Therefore, this method can be of great value in determining the degree of abnormalities of intraglomerular coagulation and fibrinolysis in renal diseases.

A case of nephrotic syndrome associated with traumatic chronic osteomyelitis.

A 19-year-old male developed nephrotic syndrome during the course of chronic osteomyelitis complicating a traumatic suppurative arthritis of the knee. Renal biopsy revealed severe mesangial proliferative glomerulonephritis, and immunofluorescent microscopy demonstrated the presence of IgA. Nephrotic syndrome remitted during the treatment for chronic osteomyelitis, suggesting a close association of the two conditions.

[Significance of urinary fibrin/fibrinogen degradation product (FDP) D-dimer measured by highly sensitive ELISA method with a new monoclonal antibody (D-D E72) in various renal diseases].

In order to clarify the abnormalities of the coagulation and fibrinolysis system in patients with various renal diseases, we produced a new monoclonal antibody for FDP (fibrin/fibrinogen degradation product) D-dimer (D-D E72). We also established a new highly sensitive method of enzyme-linked immunosorbent assay (ELISA) for urinary FDP D-dimer using this monoclonal antibody. The urine from 110, patients with various renal diseases was investigated for the FDP D-dimer. The results are summarized as follows: 1) Urinary FDP D-dimer in normal subjects was 0.69 +/- 0.60 ng/ml. 2) The level of urinary FDP D-dimer in patients with primary nephrotic syndrome and in patients with chronic renal failure was significantly higher than that of normal subjects, whereas the urinary FDP D-dimer levels in patients with diabetes mellitus were higher than those of normal subjects. 3) In the CGN and NS groups there was a tendency for an increase in the level of urinary FDP D-dimer in more active forms of the disease. 4) A significant correlation between urinary FDP D-dimer and urinary protein in the CGN and NS groups was demonstrated. 5) In all of the renal diseases investigated in this study, the ratio of urinary FDP D-dimer to total FDP was less than 4%.

[Significance of urinary fibrin/fibrinogen degradation products (FDP) measured by highly sensitive ELISA method in various renal diseases].

In order to clarify the abnormalities of intra-glomerular coagulation and fibrinolysis in patients with various renal diseases, urinary fibrin/fibrinogen degradation products (FDP) have been examined by several methods. We established a highly sensitive new method of enzyme-linked immunosorbent assay for urinary FDP. The results were as follow: 1) The mean +/- SD of urinary FDP in normal subjects was 10.30 +/- 9.08ng/ml. 2) The urinary FDP levels in chronic glomerulonephritis, nephrotic syndrome and chronic renal failure patients were significantly higher than normal subjects, and the levels in SLE, Alport's syndrome patients were higher than normal subjects. 3) The urinary FDP levels were a little bit higher in the patients with proliferative glomerulonephritis than in chronic glomerulonephritis patients with minor lesion or membranous nephropathy. 4) There was significant correlation between urinary FDP and urinary protein in chronic glomerulonephritis, while there was no correlation in nephrotic syndrome. 5) There was no correlation between urinary FDP and intra-glomerular fibrin deposits examined by immunofluorescent study in chronic glomerulonephritis, while in nephrotic syndrome, there were high levels of urinary FDP in the positive fibrin deposits cases. These results suggested that the most of the part of excretion of the urinary FDP in chronic glomerulonephritis is associated with the filtration of blood FDP to urine through the glomerular basement membrane, while in the nephrotic syndrome cases the origin of urinary FDP is related to the filtration and/or the intra-glomerular coagulation abnormalities.

A case report of allergic granulomatosis and angiitis (Churg-Strauss syndrome) with a review of the literature.

We report the case of a 67-year-old man with allergic granulomatosis and angiitis (AGA; Churg-Strauss syndrome) who developed nephrotic syndrome during his clinical course and demonstrated membranous nephropathy on renal necropsy by electron microscopy. Following the development of symptoms of bronchial asthma accompanied by eosinophilia and mononeuritis multiplex, transbronchial lung biopsy confirmed a diagnosis of AGA. The patient died of pneumonia and disseminated intravascular coagulopathy, but necropsy revealed severe tubulo-interstitial damage with neutrophilic infiltration and, in half of the glomeruli, mesangial proliferation with subepithelial dense deposits. This paper thus describes a rare case of AGA complicated by a secondary type of stage I membranous nephropathy.