Effects of swimming exercise at two different water temperature on hepatic lipid and lipoprotein levels in experimental fatty liver rats

The present study was aimed at demonstrating the effects of exercising in water at two different temperatures on lipid-lipoprotein metabolism in experimental fatty liver rats. The rats were fed a high fat, high cholesterol (CHL) diet for 6 weeks, then returned to standard chow. The fatty liver rats were then divided at random into three groups, two for swimming in 20 degrees C (20SWG) and 30 degrees C (30SWG) water, 5 days/week, 30 min/day for 6 weeks, and a sedentary control group (SG). The concentrations of serum triglyceride (TG) and CHL were significantly lower (p less than 0.01) in both the 20SWG and 30SWG than in the SG. The serum concentration of very low density lipoprotein (VLDL)-CHL was clearly less in the 20SWG than in the SG (p less than 0.05) or the 30SWG (p less than 0.01). Compared to the SG, the two swimming groups had significantly lower levels (p less than 0.01) of low density lipoprotein (LDL)-CHL. The LDL-CHL in the 30SWG was significantly lower (p less than 0.01) than that in the 20SWG. There were no significant differences among the three groups in high density lipoprotein (HDL)/CHL. However, the ratio of HDL to CHL was over 10% greater in the two swimming groups than in the SG. Hepatic CHL ester and TG were significantly lower (p less than 0.05) in the 20SWG than in the SG. These results indicate that swimming in water at the lower temperature was more stimulating to lipid-lipoprotein metabolism in fatty liver than swimming in the higher temperature water.     

Effect of lafutidine on CGRP release from cultured rat dorsal root ganglion cells

Lafutidine increased capsaicin-stimulated CGRP release from isolated rat stomach without changing basal CGRP levels. In order to clarify the mechanism of this effect, we used cultured rat DRG cells and measured CGRP release. (1) DRG cells were treated with each drug, and the CGRP content of the supernatant was determined by EIA. (2) RGM-1 cells were co-cultured with DRG cells through a cell culture insert, and capsaicin-evoked CGRP release from the DRG cells was determined when lafutidine or PGE₂ was added to the RGM-1 cells. (3) The supernatant of isolated rat stomach incubated with lafutidine was added to cultured DRG cells, and capsaicin-evoked CGRP release was determined. PGE2, but not lafutidine, augmented capsaicin-evoked CGRP release from DRG cells. Lafutidine did not modulate CGRP release from DRG cells, even though it sensitized CGRP-containing afferent nerves in the rat stomach. Lafutidne and PGE₂ may have different mechanisms of sensitization.     

Studies on detection of serum IgA and IgG antibodies specific for Chlamydia trachomatis in latent infections in males

We determined the serum concentrations of IgA and IgG antibodies specific for Chlamydia trachomatis (C. trachomatis) by an indirect immunoperoxidase assay (IPAzyme kit, Savyon Diagnostics, Ltd., Bee, Shova, Israel) to evaluate their diagnostic significance in latent infections in males. Forty-five asymptomatic males whose wife or partner was suspected to be infected with C. trachomatis were studied and the incidence of serum IgA (titer greater than or equal to 16) and IgG (titer greater than or equal to 64) antibodies for C. trachomatis was compared with that in a healthy group, a group with non-gonococcal urethritis (NGU) patients. Changes in IgA titer during treatment were also examined. The incidence of IgA and IgG antibodies in the healthy group was found to be 2.4% and 11.9% in males, and 4.8% and 18.1% in females, respectively. In patients whose wife or partner who was positive to C. trachomatis, the incidence of IgA and IgG antibodies was 42.2% and 75.6%, respectively. In the NGU patients the incidence of IgA and IgG antibodies was 56.3% and 62.5%, respectively. The incidence of IgA and IgG antibodies in patients whose wife or partner was antibody-positive were significantly higher (p less than 0.01) than the corresponding value in healthy men and women, but there was no significant difference from NGU patients or the elderly group. The IgA antibody titer during treatment of C. trachomatis infection showed no reduction in some cases. This study revealed frequent latent incidence of C. trachomatis infection in male patients. Determination of C. trachomatis IgA and IgG antibodies is considered to be supplemental for diagnosis of chlamydial latent infections.     

Selective anticancer effects of 3',5'-dioctanoyl-5-fluoro-2'-deoxyuridine, a lipophilic prodrug of 5-fluoro-2'-deoxyuridine, dissolved in an oily lymphographic agent on hepatic cancer of rabbits bearing VX-2 tumor

3',5'-Dioctanoyl-5-fluoro-2'-deoxyuridine (FdUrd-C8), one of the lipophilic prodrugs of 5-fluoro-2'-deoxyuridine (FdUrd) was dissolved in an oily lymphographic agent (Lipiodol Ultra-Fluid), which had been studied as a carrier of the anticancer drug for hepatic cancer. The prodrug was administered into the left proper hepatic artery of rabbits bearing VX-2 tumor in the liver in order to examine the anticancer effects and possible adverse effects on nontumorous hepatic cells. Lipiodol or FdUrd-C8*Lipiodol selectively remained in the hepatic cancer area but disappeared from nontumorous parts of the liver 7 days after injection. Tumor growth rates in 1 week of the untreated group, a group given injections of 0.2 ml of Lipiodol alone, and groups given injections of 0.2 ml of Lipiodol containing 30, 50, 70, and 100 mg of FdUrd-C8 were 636, 436, 34.8, 14.9, -2.4, and -10.4% of the size at the time of treatment, respectively. Pathological observation also showed that FdUrd-C8 had a strong anticancer effect on VX-2 tumor growing in the liver of the rabbits. In contrast to the effect on the cancerous cells, that on nontumorous hepatic cells was very slight. In pathological observation, necrosis or degeneration of nontumorous hepatic cells was hardly observed. Plasma glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase levels temporarily rose 1 day after injection but returned to the initial levels within 7 days in all groups.     

Ca2+/calmodulin-dependent protein kinase II immunoreactivity in Lewy bodies

Summary Ca²⁺/calmodulin-dependent protein kinase II (CaM kinase II) is one of the predominant protein kinases in the brain. We found that CaM kinase II immunoreactivity was concentrated in the peripheral halos of Lewy bodies (LBs) in Parkinson's disease and Lewy body-like hyaline inclusions (LBHIs) in amyotrophic lateral sclerosis. An immunoelectron microscopic examination of LBs revealed that the filaments at the periphery of LBs were decorated with immunopositive deposits. Since CaM kinase II has a broad substrate specificity and can phosphorylate neurofilaments and other cytoskeletal proteins, it may play some role in the formation of LBs and LBHIs through the aberrant phosphorylation of the cytoskeletal elements in these inclusions.Supported by a Grant-in-Aid for Scientific Research on Priority Areas, No. 02240104, from the Ministry of Education, Science and Culture, Japan     

Experimental evaluation of myocardial protective effect of prostacyclin analog (OP-41483) as an adjunct to cardioplegic solution

A stable prostacyclin analog (OP-41483) was evaluated for myocardial protective effect against global ischemia with the use of cardioplegia. Isolated canine hearts (n = 25) were exposed to 60 minutes of warm (37 degrees C) global ischemia after the arrest by crystalloid cardioplegia. Prostaglandin analog was given in three different ways: preadministration (700 ng/kg body weight per minute) before ischemia for 30 minutes (group I, n = 5), given as a component of cardioplegic solution (600 ng/ml, group II, n, = 6), and post-administration (25 ng/kg body weight per minute) during reperfusion for 30 minutes (group III, n = 7). During reperfusion, coronary sinus blood flow, 6-keto-prostaglandin F1 alpha in coronary sinus blood, and myocardial oxygen consumption were measured during reperfusion. As a result, groups II and III showed significantly better global left ventricular function (developed pressure, maximum dP/dt, and diastolic compliance) than the control group (without prostaglandin analog, n = 7) and group I. Myocardial oxygen consumption at reperfusion (1 minute) was significantly larger in group II than in the control group. 6-keto-prostaglandin F1 alpha flux was significantly larger in group II than in the other three groups during reperfusion. The results indicated that prostaglandin analog has a beneficial effect on myocardial protection under global ischemia with cardioplegia, particularly when used as a component of cardioplegic solution and also during reperfusion. The mechanism may relate to the cytoprotective effect (including protection of endothelium with enhanced endogenous prostacyclin production at reperfusion and also to the modulation of reperfusion per se.