Evaluation of treatment of lung cancer combined with the disease which has needed a semi-emergency operation

Six cases of lung cancer combined with the disease which has needed semi-emergency operation, two cases of unstable angina, two of ileus due to colon cancer, one of impending rupture of abdominal aortic aneurysm and one of purulent cholecystitis with cholelithiasis, were discussed. Mean age was 62.0 years (range, 36 to 73); four were male and two were female. Case 1 and 2 were admitted with anterior chest pain, Case 3 with lumbago and abdominal pain, Case 4 and 5 with an abnormal shadow on chest x-ray film and Case 6 with abdominal pain. Of the two with unstable angina, one was operated on with right upper lobectomy during the first months after aorto-coronary bypass. Of the two with colon cancer, one was operated on with right upper lobectomy during about 5 weeks after right hemi-colectomy. Case 3 with abdominal aortic aneurysm operated on with left upper lobectomy during 4 weeks after replacement of abdominal aorta. Case 4 with cholecystitis was operated on with left pneumonectomy during about 3 weeks after cholecystectomy. The postoperative course of 4 cases and the post-chemotherapy condition of 2 cases were uneventful.     

Campylobacter jejuni strains from patients with guillain-barré syndrome belong mostly to penner serogrpup 19 and contain β-N-acetylglucosamine residues

Campylobactor jejuni was isolacted from stool cultures from 14(30%) of 46 partients with Guillain-Barré syndrome and from 6(1.2%) of healthy persons, and the difference was highly significant (P<0.0001). In addition, serological evidence of recent. C. Jejuni infection. Ten of 12(83%) isolated from partients with Guillain-Barré syndrome belonged to Penner serogroup 19, which is a rare serogroup in sporadic patients with C. Jejuni enterties. In the lection typing stude, all serogroup 19 strains from patients with Guillain-Barré syndrome patients with Guillain-Barré syndrome were shown to contain terminal b?-N-acetylglucosamine residues on their cell surface, bur serogroup 19 strains from patients with enteritis were not.     

Central nervous system lesions in rats infected with Friend murine leukemia virus-related PVC441: ultrastructural and immunohistochemical studies

Newborn F344 rats were injected intraperitoneally with PVC441 virus, a neuropathogenic variant of Friend murine leukemia virus, and developed paraparesis of hind limbs 35–40 days after infection. Immunohistochemical study using monoclonal anti-PVC441 antibody revealed that in the central nervous system endothelial cells but not neuronal or glial cells were infected with PVC441 virus. The major pathological changes were myelin vacuolation and oligodendrocyte degeneration in the white matter at the white-gray border zone. Anterior and lateral funiculi and intercalated myelin of anterior horns were dominantly affected in the spinal cord from the sacral to cervical level. The midbrain was also vacuolated. An ultrastructural study demonstrated that many viral particles were present outside the endothelial cells but only sparsely inside endothelial cells and pericytes. Endothelial cell membranes and tight junctions were also disrupted. Immunohistochemical studies with antibodies against major histocompatibility complex class Ia, intercellular adhesion molecule-I, glial fibrillary acidic protein, neurofilament protein, CD3 and OX42 revealed the presence of abundant microglia but not of lymphocytes or polymorphonuclear cells in the lesions. Axonal degeneration and astrogliosis were mild in degree. These pathological changes explain the observed spastic paraparesis in the rats, and represent a good model of spongiform diseases of the human central nervous system of retroviral origin, such as human T cell leukemia virus-associated myelopathy and AIDS. Received: 4 March 1996 / Revised, accepted: 8 October 1996     

Human and simian glial cells infected by human T-lymphotropic virus type I in culture

Although human T-lymphotropic virus type I (HTLV-I) has been implicated in the etiology of tropical spastic paraparesis (TSP) and HTLV-I associated myelopathy (HAM), the direct infectivity of the virus against constituent cells in the central nervous system remains undetermined. To investigate the neurotropism of HTLV-I, we exposed cultured human and simian glial cells to HTLV-I. Primary mixed glial cell cultures of astrocytes and oligodendrocytes were obtained from adult human and cynomolgus monkey (Macaca fascicularis) brains by an enzyme digestion-Percoll gradient method. After two weeks in vitro, the cells were co-cultured with irradiated MT-2 cells, an HTLV-I-producing T-cell line. Cultures were double stained with antibodies against cell-type specific markers and anti-HTLV-I p19 (gag) monoclonal antibody. The HTLV-I antigen was demonstrated in small numbers of glial fibrillary acidic protein-positive cells (astrocytes) and galactocerebroside-positive cells (oligodendrocytes) in both the human and simian cultures. Electron microscopy demonstrated the presence of type C virus-like particles in the cytoplasm of astrocytes. These results indicate that HTLV-I is capable of infecting human and simian glial cells in vitro.     

Gene locus for autosomal recessive distal myopathy with rimmed vacuoles maps to chromosome 9

Distal myopathy with rimmed vacuoles is an autosomal recessive muscular disorder, characterized clinically by weakness of the distal muscles in the lower limbs in early adulthood. Recently, the gene locus for familial vacuolar myopathy with autosomal recessive inheritance (hereditary inclusion body myopathy) was mapped to chromosome 9 by genome-wide linkage analysis of nine Persian-Jewish families. Since both disease conditions share similar clinical, genetic, and histopathological features, we analyzed seven families with distal myopathy with rimmed vacuoles using ten microsatellite markers within the region of the hereditary inclusion body myopathy locus. Significantly high cumulative pairwise lod scores were obtained with three markers: D9S248 (Z_max = 5.90 at Θ = 0), D9S43 (Z_max = 5.25 at Θ = 0), and D9S50 (Z_max = 4.23 at Θ = 0). Detection of obligate recombination events as well as multipoint linkage analysis revealed that the most likely location of the distal myopathy with rimmed vacuoles gene is in a 23.3-cM interval defined by D9S319 and D9S276 on chromosome 9. The results raise the possibility that distal myopathy with rimmed vacuoles and hereditary inclusio body myopathy in Persian Jews are allelic diseases.     

Genetic contribution of the tumor necrosis factor region in guillain-barré syndrome

We studied genetic polymorphisms in the tumor necrosis factor (TNF) region in 81 Japanese patients with Guillain-Barré syndrome (GBS) and 85 controls. A significantly higher frequency of the 100–base pair (bp) (TNFa2) allele of the TNFa microsatellite marker, which is associated with high TNFα production, existed in Campylobacter jejuni-positive (Cj⁺) GBS patients than in controls, suggesting the involvement of a genetic predisposition to high TNFα secretion in the development of c. jejuni-related GBS.     

Time-Course Alterations of Monoamine Levels and Cerebral Blood Flow in Brain Regions after Subarachnoid Hemorrhage in Rats

To investigate the possible correlation between changes in monoaminergic neuronal activity and cerebral blood flow (CBF) in the same brain regions after subarachnoid hemorrhage (SAH), monoamine levels were analyzed by both HPLC-ECD and fluorohistochemistry techniques, and CBF was measured by using colored microspheres. At the second day of SAH, significant and nonsignificant reductions in blood flow were seen in the examined brain regions with a marked increase in CBF appearing in the telencephalon and hypothalamus on the third day. Significant reductions of monoamine levels in most brain regions were also observed on the second day after SAH, whereas norepinephrine (NE) levels in midbrain increased to 1.5 times compared to the normal level. These reductions were sustained until the fourth day of SAH, although at the third day, serotonin (5-HT) and dopamine levels in the hippocampus and 5-HT levels in the cerebellum were significantly elevated. In fluorohistochemical studies, the fluoro-intensities of monoamines, particularly catecholamines, in the midbrain dorsal NE bundle were enhanced at the second day after SAH. These NE neurons originated from the A6 cell group close to the area where homologous blood was applied through the cisterna magna. The results obtained after SAH show an apparent correlation between changes in monoamine levels and CBF in norepinephrine (NE)-rich areas. These results suggest that SAH-induced neuronal dysfunctions, particularly with NE neurons, are caused not only by reductions of blood flow but also by hemorrhage.