Suppressive effects of Sairei-to on monoclonal antibody 1–22–3-induced glomerulonephritis: Analysis of effective components

The effects of treditional Chinese medlclne (Salrel-to) on experimental glomerulonephritls Induced In rats by monodonal antibody (mAb) 1–22–3 lnjectlon was examined. The level of proteinuria in the Sairel-to-treated group was significantly lower than that In the PBS treated group. This suppressive effect was caused by the major component of Sealer-to, Syo-salko-to but not by another component, Gorel-san. The suppressive effect of Syo-salko-to was Identified In Its components ( Bupleuri radix, Pindilae tuber and Zingibers rhizoma ), but not In the other combined components ( Ginseng radix and Zizyphl fructus ). Further study weeled that the suppressive effects of the combined components were mainly derived from Bupleuri radix . It was demonstrated that the actual active Ingredient is probably Salkosaponin-d. Light microscopy revealed that Sairel-to and Its effective components suppressed the proliferation of mesanglal cells and mesanglal matrix expansion. Semi quantitative morphological studies of glomerular lesions on the eighth day showed that Syo-salko-to and Its combined components ( Bupleuri radix, Zinglberis rhizoma and Pinelliae tuber ) suppressed mesanglal matrix expansion significantly compared with phosphate-buffered saline control groups (matrix score: 28.0±19.1 vs 102.3±14.1; 30.9±30.1 vs 102.3±14.1, p<0.005, respectively). It was concluded that Salkosaponln-d, as well as Bupleuri radix , Syo-salko-to and Sairel-to can suppress proteinurla and morphological changes In the rat glomerulonephritls model Induced by mAb 1–22–3.     

Precise mapping of the EGF receptor gene on the human chromosome 7p12 using an improved fish technique

Summary The gene for epidermal growth factor receptor (EGFR) has been localized to the p14-p12 region of human chromosome 7 by somatic cell hybridization and radioisotopein situ hybridization techniques. In this paper, we report the precise mapping of the EGFR gene to the band p12 of chromosome 7 using a novel method in which fluorescence images fromin situ hybridization and Q-banding are computer graphically merged. The novel procedure is described in detail.     

Interaction between Sendai virus and the cell membrane II. The role of Sendai virus neuraminidase in haemolysis

When chicken erythrocytes (CRBC) were pretreated with non-haemolytic Sendai virions or isolated HANA spikes, they acquired a resistance to the haemolytic action of "second challenge" viruses. This resistance was dependent on the quantity of N-acetylneuraminic acid liberated from the surface of the CRBC by the initial virus, and not on the use of different viral sources. When exposed to Sendai virus, CRBC were more difficult to be lysed and easier liberated N-acetylneuraminic acid than human 0 erythrocytes. The restricted number of virions able to fuse CRBC was explained by such neuraminidase function of the HANA spike of the virion.     

Cloning of TPA-inducible early (TIE) genes by differential hybridization using TPA-Nonresponsive variant of mouse 3T3-L1 cells

The tumor promoter 12-O -tetradecanoylphorbol-13-acetate (TPA) induces DNA synthesis in quiescent 3T3-L1 cells but not in its variant VT-1 cells. A gt10 cDNA library was constructed using poly(A)⁺ RNA from 3T3-L1 cells that were stimulated by TPA for 20 min. Radioactive cDNA probes were prepared from mRNAs of TPA-treated 3 T3-L1 and VT-1 cells and used for screening of the 3T3-L1 cDNA library by differential hybridization. Nine of 6000 phage plaques hybridized only to the 3T3-L1 cDNA probe. Analysis of the nucleotide sequence of five of these clones indicated a high degree of homology with human or mouse type I and type III collagen genes. Three other independent clones showed no homology with any known DNA sequences. These isolated clones of TPA-inducible early (TIE) genes may be useful to study the signal transduction pathway of phorbol esters.     

An autopsy case of interlobar arterial dissection of the kidney following long-term hemodialysis

An autopsy case of massive renal hemorrhage in a 49-year-old male who had undergone maintenance hemodialysis for 8 years, is reported. No bleeding tendency had been noticed, and blood pressure had been reduced to within the normal range. Histological investigation with semiserial sections revealed that hemorrhage had occurred in four arteries, corresponding to the interlobar, arcuate, and interlobular levels, which existed in the same ruptured cyst wall. Acute dissection had occurred in two of the four arteries, leading to rupture of the cyst; this led to destruction of the remaining arteries. Both kidneys, which were markedly shrunken and had numerous cysts in the cortex and medulla, fell into the category of acquired cystic renal disease of long-term hemodialysis. It was suspected that renal vascular change during hemodialysis, mechanical factors compressing the protruding artery in the cyst with scanty renal interstitium, and relatively radical hemodynamic changes during dialysis had contributed to the hemorrhage.     

Convergence of hepatoportal glucose-sensitive afferent signals to glucose-sensitive units within the nucleus of the solitary tract

Units which are activated by ascending impulses from the liver within the nucleus of the solitary tract (NTS) were identified by electrical stimulation delivered to the hepatic branch of the vagus. Responses of descending units were eliminated by a collision test. The units which showed decreased firing rates during portal infusion of isotonic glucose solution were also glucose-sensitive so that they showed decreased firing rates during topical application of glucose by means of micro-electro-osmotic techniques. It is concluded that glucose-sensitive neurons exist within the NTS and also that they are functionally linked with hepatoportal glucose-sensitive afferent units.     

Mechanoenergetics characterizing oxygen wasting effect of caffeine in canine left ventricle

Caffeine causes a considerable O(2) waste for positive inotropism in myocardium by complex pharmacological mechanisms. However, no quantitative study has yet characterized the mechanoenergetics of caffeine, particularly its O(2) cost of contractility in the E(max)-PVA-VO(2) framework. Here, E(max) is an index of ventricular contractility, PVA is a measure of total mechanical energy generated by ventricular contraction, and VO(2) is O(2) consumption of ventricular contraction. The E(max)-PVA-VO(2) framework proved to be powerful in cardiac mechanoenergetics. We therefore studied the effects of intracoronary caffeine at concentrations lower than 1 mmol/l on left ventricular (LV) E(max) and VO(2) for excitation-contraction (E-C) coupling in the excised cross-circulated canine heart. We enhanced LV E(max) by intracoronary infusion of caffeine after beta-blockade with propranolol and compared this effect with that of calcium. We obtained the relation between LV VO(2) and PVA with E(max) as a parameter. We then calculated the VO(2) for the E-C coupling by subtracting VO(2) under KCl arrest from the PVA-independent (or zero-PVA) VO(2) and the O(2) cost of E(max) as the slope of the E-C coupling VO(2)-E(max) relation. We found that this cost was 40% greater on average for caffeine than for calcium. This result, for the first time, characterized integratively cardiac mechanoenergetics of the O(2) wasting effect of the complex inotropic mechanisms of intracoronary caffeine at concentrations lower than 1 mmol/l in a beating whole heart.