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At least 235 records · Page 13Linked to original sources
PubMed1994

[Clinical features and morbidity of group B diffuse interstitial pneumonia, atypical subtype, compared with group A, typical idiopathic subtype].

Diffuse interstitial pneumonia of unknown etiology has been subclassified into two groups on the patho-histological basis by the study group under the sponsorship of the Japanese Ministry of Health and Welfare. One is Group A, typical idiopathic subtype, fundamentally corresponding to UIP (usual interstitial pneumonia, Liebow) and the other is Group B, closely similar to Group A but possibly modified by respiratory infection. As the clinical features of Group B have not been clarified so far, we investigated them in 8 cases of Group B (M:F = 7:1, 56.7 years at first visit) and 5 cases of Group A (M:F = 4:1, 54.4 years), all of which were pathologically diagnosed by open lung biopsy and/or autopsy. Only in Group B, there were 3 cases with occupations related to dust exposure, and 7 cases with intermittent but persistent mucus expectoration. The duration of symptoms before the first presentation to hospital was longer in Group B than in Group A (1.6 years vs. 0.6 years). Clubbed fingers were more frequently observed in Group B (n = 6 vs. n = 1), but induration in the tuberculin test was less frequent in Group B (n = 1 vs. n = 5). In the chest X-ray findings, pleural thickening was frequent in Group B (n = 6 vs. n = 0), but elevation of the diaphragm was unusual in Group B (n = 2 vs. n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Molecular basis for subtypic differences of the "a" subunit of coagulation factor XIII with description of the genesis of the subtypes.

The "a" subunit of human coagulation factor XIII (F13A) exhibits genetic polymorphism defined by four common alleles, F13A*1A, *1B, *2A, and *2B. We have previously suggested on the basis of the isoelectric focusing patterns of the four allele products that point mutations at two separate sites and one intragenic crossing over might be involved in the genes of F13A polymorphism. Here, we report nucleotide substitutions associated with F13A polymorphism. A C/T transition of the second nucleotide of codon 564 in exon 12 is responsible for the difference between F13A*1A and *1B and that between F13A*2A and *2B, and a set of two base changes in codons 650 and 651 in exon 14 leads to the differences between F13A*1A and *2A and those between F13A*1B and *2B. The four combinations of the point mutations at the two exons thus correspond to the four alleles, two of which were generated by the point mutations from ancestral monomorphic gene. The results suggest strongly that intragenic crossing over must be involved in the genesis of the fourth allele. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods discriminating these base changes in exons 12 and 14 are also presented.

Alleles↗
PubMed2005

Bilateral enhancement of excitation via up-regulation of vesicular glutamate transporter subtype 1, not subtype 2, immunoreactivity in the unilateral hypoxic epilepsy model.

In the present study, the change of vesicular glutamate transporter (VGLUT) immunoreactivity on long-term impaired excitability in the hippocampus after recovery from unilateral hypoxic-ischemic insult was investigated in order to extend our understanding of the mechanism of epileptogenesis using unilateral hypoxic epilepsy models. Both the lesioned (submitted to ischemia) and the unlesioned hippocampi exhibited the frequent occurrence of interictal spikes and occasionally the sustained ictal discharges. However, paired-pulse inhibition was significantly reduced in the unlesioned dentate gyrus, not in the lesioned dentate gyrus. VGLUT1 immunoreactivity was significantly elevated in both hippocampi following hypoxic ischemia, although VGLUT2 immunodensity was unaltered. These findings suggest that the enhancement of VGLUT1 immunoreactivity in both hippocampi after unilateral hypoxic ischemia may contribute to the hyperexcitability, which may play an important role in the epileptogenesis (presumably accompanied by altered inhibitory transmission) after neurodegeneration.

Animals↗
PubMed2005

A DNA HIV-1 vaccine based on a fusion gene expressing non-structural and structural genes of consensus sequence of the A-C subtypes and the ancestor sequence of the F-H subtypes. Preclinical and clinical studies.

A potent DNA vaccine against HIV, combining a vector that takes advantage of the segregation and compartmentalization effect of bovine papilloma virus E2 protein with MultiHIV insert, expressing a fusion gene coding for the non-structural and structural proteins was developed and tested for immunogenicity in mice and humans.

AIDS Vaccines↗
PubMed2003

Synthetic studies on himbacine, a potent antagonist of the muscarinic M2 subtype receptor. Part 2: synthesis and muscarinic M2 subtype antagonistic activity of the novel himbacine congeners modified at the C-3 position of lactone moiety.

With an aim to disclose the convergency and flexibility of our previously explored synthetic route to natural himbacine 1, and moreover, to clarify some novel aspects of the structure-activity relationships of 1, we prepared various structural types of novel himbacine congeners, 3-demethylhimbacine (3-norhimbacine) 2 and 4-epi-3-demethylhimbacine (4-epi-3-norhimbacine) 4-epi-2 and their enantiomers (ent-2 and ent-4-epi-2), 11-methylhimbacine 3, and 3-epihimbacine 4 in optically pure forms by employing our methodology. All of the synthesized congeners correspond to the compounds modified at the C-3 position of gamma-lactone moiety involved in 1. Among these congeners, 3-demethylhimbacine (3-norhimbacine) 2 was found to exhibit more potent muscarinic M(2) receptor binding affinity than natural 1.

Alkaloids↗
PubMed1994

Identification of endothelin receptor subtype (ETB) in human cerebral cortex using subtype-selective ligands.

Specific endothelin (ET) binding sites were characterized in membranes prepared from human cerebral cortices using binding assay and cross-linking analysis. The presence of immunoreactive (IR) ET-1 was studied by radioimmunoassay. Saturation binding experiments revealed that the KD and Bmax for 125I-ET-1 and 125I-ET-3 to membranes from gray matter were 25 +/- 6 pM and 115 +/- 15 fmol/mg of protein and 24 +/- 5 pM and 108 +/- 13 fmol/mg of protein, respectively. Similar results were obtained for white matter. In the presence of 10 nM sarafotoxin-6c, which is selective for ETB receptors, 125I-ET-1 and 125I-ET-3 binding was totally abolished. However, in the presence of 1 microM BQ123, which is selective for ETA receptors, both bindings were not affected. These results suggest that the human cerebral cortex contains only ETB receptors. Cross-linking of 125I-ET-1 and 125I-ET-3 to membranes with disuccinimidyl suberate resulted in the labeling of two bands of 48 and 31 kDa. Concentrations of IR-ET-1 in the gray and white matter were 7.0 +/- 3.2 and 2.5 +/- 1.7 fmol/g wet weight, respectively. The demonstration of high-affinity ETB receptors and the presence of IR-ET-1 suggest that the peptide may act as a neurotransmitter or neuromodulator in the human cerebral cortex.

Binding, Competitive↗
PubMed2001

Angiotensin subtype-2 receptor (AT2 ) negatively regulates subtype-1 receptor (AT1 ) in signal transduction pathways in cultured porcine adrenal medullary chromaffin cells.

BACKGROUND: Two distinct types of angiotensin II (AngII) receptors, AT1 and AT2, have been cloned. We have shown previously that stimulation of AT2 reduces intracellular cyclic guanosine monophosphate (cGMP) levels in cultured porcine chromaffin cells in which AT2 is the predominantly expressed receptor. However, it has not been determined whether AT1 or AT2 affects signal transduction pathways involving mitogen-activated protein kinases (MAPKs) and signal transducers and activators of transcription (STATs) in chromaffin cells. Also, it is unclear whether cGMP/protein kinase G (PKG) is involved in the regulation of MAPKs and STATs in these cells. DESIGN: Chromaffin cells were derived from porcine adrenal medulla. The effects of AngII alone (representing physiological conditions), AngII plus CV-11974 (an AT1 antagonist, which simulates specific AT2 stimulation), AngII plus PD 123319 (an AT2 antagonist, which simulates specific AT1 stimulation), and 8-Br-cGMP (a membrane-permeable cGMP analogue) alone on MAPKs (ERKs, JNK, p-38 MAPK) and STATs (STATs 1, 3 and 5) activity were measured. METHODS: Phosphorylated MAPKs (extracellular signal-related kinases (ERKs), c-jun N-terminal kinase (JNK) and p38 MAPK) and STATs (STATs 1, 3 and 5) were measured by immunoprecipitation-Western blot analysis (IP-Western blot). RESULTS: AT1 stimulation markedly increased expression of ERKs, JNK, p38 MAPK via Ca2+-dependent protein kinase C (PKC) isoforms (cPKC), as well as STATs 1, 3 and 5 in cultured porcine chromaffin cells. In contrast, AT2 stimulation markedly decreased the expression of these signaling molecules. Also, 8-Br-cGMP alone induced increases in ERKs, JNK, p38 MAPK, and STATs 1, 3 and 5. Because AT2 inhibits cGMP production, we speculate that AT2 may act to suppress cGMP production, which in turn reduces the activity of both MAPKs and STATs in chromaffin cells. CONCLUSION: AT2 negatively regulates AT1 in signal transduction pathways in chromaffin cells.

Angiotensin II↗