Role of CD4+ T lymphocytes and interleukin-5 in antigen-induced eosinophil recruitment into the site of cutaneous late-phase reaction in mice.

Previous studies suggested that the eosinophil recruitment into the site of cutaneous late-phase reaction (LPR) was dependent on IgE antibody and mast cells. In this study, we determined the role of CD4+ T cells and CD8+ T cells in causing antigen-induced eosinophil recruitment of LPR in mouse skin. Eosinophil infiltration into the subcutaneous tissue of ovalbumin (OVA)-sensitized BALB/c mice was biphasic, reaching the first peak at 6 h after the subcutaneous challenge with OVA and the second peak at 24 to 48 h. The in vivo depletion of CD4+ T cells by pretreatment with anti-L3T4 monoclonal antibody (mAb) significantly decreased the second peak (at 24 h and 48 h), but not the first peak (at 6 h), of OVA-induced eosinophil infiltration into the skin of OVA-sensitized mice. However, the depletion of CD8+ T cells by pretreatment with anti-Lyt-2 mAb had no significant effect on either the first peak or second peak of OVA-induced cutaneous eosinophilia. Pretreatment with anti-murine interleukin-5 (IL-5) mAb also decreased the second peak, but not the first peak, of OVA-induced cutaneous eosinophilia. In contrast to the inhibitory effects of depletion of CD4+ T cells and of anti-IL-5 mAb on the second peak of antigen-induced cutaneous eosinophilia, disodium cromoglycate and a selective antagonist for platelet activating factor (PAF) CV-6209 decreased the first peak of OVA-induced cutaneous eosinophilia in the mouse. These results indicate that CD4+ T cells, but not CD8+ T cells, cause the second peak of antigen-induced eosinophil recruitment of cutaneous LPR and that IL-5 mediates this eosinophil recruitment. In contrast, the first peak of antigen-induced eosinophil recruitment of cutaneous LPR is mediated by mast cells and PAF.     

Reduction in QSART and vasoactive intestinal polypeptide expression in the skin of Parkinson's disease patients and its relation to dyshidrosis

Background:  With regards to dyshidrosis in Parkinson's disease (PD), there is no established and consistent view on the occurrence sites, frequency and etiology, although there have been several reports on hypohidrosis of the limbs and sudoresis on the face/cervical region.
Methods:  Hydrosis in the forearms of PD patients and healthy individuals were compared by quantitative sudomotor axon reflex test (QSART). The expression of various neuropeptides and α-synuclein was examined with immunohistochemical staining.
Results:  There was a significant reduction in QSART of PD patients but not of healthy controls. Reduced expression of vasoactive intestinal polypeptide (VIP) was also detected in the sweat glands of PD patients.
Conclusion:  Reduction in QSART and VIP expression in the sweat glands might be involved in the dyshidrosis of PD patients.     

HBV- and HCV- infected workers in the Japanese workplace

Around three million Japanese are persistently infected with HBV or HCV. Though most of them work in various industries, little is known about the actual conditions in their workplaces. To clarify the workplace conditions of workers with hepatitis, three kinds of questionnaire surveys, answered by occupational health physicians and workers with hepatitis, were carried out. The rates of workers recognized as workers with hepatitis B or C by occupational health physicians were 0.82% and 0.48% of 130,092 workers, respectively. About 30% of workers with hepatitis were engaged in "hazardous work". The percentage of workers engaged in various types of hazardous work among workers with hepatitis was nearly the same as that among all Japanese workers. About 30% of occupational health physicians witnessed exacerbation of hepatitis in the workers at their workplaces, and 22% of workers with hepatitis experienced exacerbation of hepatitis. The rate of workers with hepatitis who had experienced exacerbation was not significantly different between workers with and without hazardous work. Workers with hepatitis have strong concerns about the relationship between work and exacerbation. As causes of exacerbation, occupational health physicians cited "unknown", "drinking" and "quit treatment" while workers with hepatitis answered "work-related causes", besides "unknown" and "drinking."     

International comparison of sensitizing chemical substances

Some occupational and environmental chemicals cause allergic diseases. To prevent chemical allergies, it is essential to identify the chemical substances that cause sensitization and to eliminate such sensitizers from daily life. As an occupational countermeasure, information for evaluating sensitization of chemical substances is needed. The aims of this article are to compare the criteria for sensitizers among national organizations in various countries and international organizations, and to make out a list of these chemical substances. The definition of sensitizing chemicals and the designation of respective sensitizers according to the PRTR law, Japan Society for Occupational Health (JSHO), American Conference of Governmental Industrial Hygienists (ACGIH), European Union (EU), Deutsche Forschungsgemeinshaft (DFG) and Japanese Society of Occupational and Environmental Allergy were studied. There are 1,389 chemical substances which are designated as sensitizers by any of the laws and five organizations. We specify each chemical substance in the list.     

Nutritional and hormonal regulation of uncoupling protein gene expression in rat adipocytes

Nutritional and hormonal regulation of the expression of uncoupling protein (UCP)-1, -2, and -3 mRNA and protein was investigated in primary cultured adipocytes of rats. The UCP-1, -2, -3 mRNA and protein induction in the adipocytes reached maximal levels at 4 h in the presence of glucose with or without insulin. Moreover, the UCP induction was accelerated by triiodothyronine (T3) or epinephrine, and reached a maximum at 2 h. It appeared that the induction of UCP mRNA and protein was rapid. UCP-1 mRNA expression was stimulated by the presence of T3 or epinephrine in the culture medium. UCP-2 mRNA expression was more markedly increased by glucose, unsaturated fatty acids, insulin and T3 than UCP-1 or -3 mRNA expression. UCP-3 expression was more markedly increased by epinephrine than by T3. The protein expression of the UCPs was induced by glucose and the hormones nearly parallel to the UCP mRNA expression. Thus, UCP-2 expression appears to be stimulated by energy sources such as glucose and fat, and by regulators of thermogenesis and basal metabolic rate such as T3 and insulin, in contrast to UCP-1 and -3 expression.     

Primary sclerosing cholangitis with marked eosinophilic infiltration in the liver

A 16-year-old boy was diagnosed as having primary sclerosing cholangitis (PSC), based on retrograde cholangiography showing mixed features of narrowing and dilatation of the common hepatic and intrahepatic bile ducts. However, periductal fibrosis was not observed in the needle biopsy liver specimen. The liver biopsy specimen obtained 11 years previously, at the onset of the disease had disclosed a marked infiltration of eosinophils in the portal tract with eosinophilic catinonic protein immunostaining, with marked eosinophilia (54%) being noted. In Japanese reports, eosinophilia of more than 7% was reported in 13 of 32 (40.6%) PSC patients. However, the early stage of PSC, with marked eosinophilia and eosinophilic infiltration in the liver, such as in the present case, has rarely been reported. The findings in this case suggest that eosinocytes are related to the pathogenesis of PSC.     

Electrophysiology of a gap created on the canine atrium

Objective It is crucial to detect the unablated regions (=“gap”) in the radiofrequency linear ablation of atrial tachyarrhythmias. The purpose of this study was to examine the relationship between the electropysiological properties of the gap created in the canine atrium and its anatomicohistologic findings. Methods and Results In 17 dogs, a linear epicardial radiofrequency ablation lesion was created on the right atrial wall with a gap of surviving tissue in the mid-portion of the lesion. For each gap, the local electrogram (LE) from the gap and conduction pattern through the gap were recorded using an electrode catheter and a plaque electrode during pacing from each side of the gap and the gap size was measured. The gaps >5 mm exhibited a conductive property and the gaps <3 mm had no conduction property according to 3-D mapping. The size of the conductive gaps was larger than that of the non-conductive gaps (7.1 ± 2.6 vs. 2.6 ± 2.5 mm, p < 0.0001). The LE configurations were categorized into single, double and continuous potentials and single potentials were demonstrated only in wide gaps >7 mm. There was a significant inversed correlation between the duration of the LE and gap size and also between the LE duration and the conduction velocity. Histological examination showed that the conduction properties through the gap depended mainly on its size. Conclusions The conductivity through the gap, which was affected by the size of the gap, may be evaluated by the duration and configuration of the local electrogram recorded from the gap.     

Identification of minimal regions of deletion at 8p23.1-22 associated with metastasis of hepatocellular carcinoma.

AIMS/BACKGROUND: Loss of heterozygosity (LOH) at 8p is the most frequent chromosomal alteration in tumorigenesis of human cancers. However, the genetic change in metastasis of hepatocellular carcinoma (HCC) still has to be investigated. METHODS: We used 16 microsatellite markers informative in Japanese patients, selected from among 61 published microsatellite markers at 8p23.2-21 to compare the frequency of LOH in primary tumours (Tps) and metastatic tumours (Tms) in a PCR-based analysis. Sixty-three informative cancerous lesions (26 were Tps, 37 were Tms) from 23 cases of HCC were used. RESULTS: The frequency of LOH at 8p23.2-21 with at least one marker was 19% in Tps and 68% in Tms. Allelic loss at 8p23.2-21 was significantly more frequent in Tms than in Tps (P=0.0003). More specifically, the frequency of LOH at D8S262, D8S1819, D8S503, D8S1130, D8S552, D8S1109, and D8S261 in Tms was 36-60% respectively. CONCLUSIONS: In contrast, allelic loss at the same markers in Tp was only detected in 0-17% of the tumour respectively. The significant difference in the frequency of LOH at 8p between primary cancer and metastatic cancer in individual cases of HCC suggests LOH at 8p to be involved in the enhancement of tumour aggressiveness, especially during metastasis.     

Degradation of the cardiac sarcoplasmic reticulum in acute myocardial ischemia

The degradation of the sarcoplasmic reticulum (SR) in acute myocardial ischemia was studied with references to the regional irreversibility and to the mechanism of ischemic degradation by the measurements of Ca++-stimulated ATPase activity and composition of the major ATPase protein of the SR and activity of cathepsin B of the SR and lysosome (Ly) fractions. Ca++-stimulated ATPase activity decreased to 66% of that of the nonischemic portion at 20 min after coronary ligation in the subendocardium (Endo) and to 44% at 30 min in the subepicardium (Epi). Composition of the major ATPase protein decreased to 55% and 73% at 30 min in Endo and Epi, respectively. In both SR and Ly fractions cathepsin B exhibited the maximal activity at 6.0-6.5, and pH dependent. And incubation of the SR at pH 6.0 induced the degradation of the ATPase protein quite similarly to that in vivo ischemia. These results suggest that the degradation of the SR membrane of ischemic myocardial cells begins earlier in Endo 20 to 30 min after the cease of the coronary blood flow, and extends to Epi later. Cathepsin B is strongly conceivable to play an initial role of necrotic process of the ischemic myocardial cells by activation inside of the SR in ischemic acidic state.