A total of 179 samples of meat and 35 samples of egg from Japan and China were examined for the
pollution of Escherichia coli, Salmonella enterica serovar Enteritidis and Staphylococcus aureus using the identical assay
methods. The results showed that the pollution rates of E. coli, S. Enteritidis and S. aureus were 46.4 % , 4.4 % and
36.2 % in Japan and were 37.9 % , 5.5 % and 44.1 % in China, respectively. The pollution rate of E. coli in Japan (46.4 %)
was higher than that in China (37.9 %). In contrast, the pollution rate of S. aureus in China (44.1 %) was higher than
that in Japan (36.2 %). For the bacterial numbers in the contaminant meats, 4 of 69 samples in Japan and 4 of 145
samples in China were over 10⁴ colony-forming units (CFU)/g for E. coli, and 2 of 69 samples in Japan and 7 of
145 samples in China were over 10⁴ CFU/g for S. aureus. These results suggest that more thorough temperature
control and hygiene management are necessary in the processing, safekeeping, circulation and sales of meats.
230-kD bullous pemphigoid antigen (BPAG1) is known as an autoantigen in bullous pemphigoid and is
expressed exclusively in proliferating basal keratinocytes. TGF-β is a growth factor that has pleiotropic effects on
a wide range of target cells and induces differentiation of basal keratinocytes. Therefore, TGF-β is postulated to
inhibit BPAG1 expression. However, previous report conversely demonstrated an increase of BPAG1 expression
by TGF-β. In this study, to understand regulatory role of TGF-β on BPAG1 functions, we examined the effect
of TGF-β on BPAG1 gene expression using cultured keratinocytes. This study showed that BPAG1 mRNA
expression was inhibited by TGF-β1 in concentration higher than 1.0 ng/ml. Furthermore, incubation of the
cells with TGF-β1 in the presence of cycloheximide demonstrated that newly synthesized protein was required
for BPAG1 regulation. To understand the detailed mechanisms of BPAG1 modulation by TGF-β, we preformed
transient transfection assay with a BPAG1 promoter-CAT construct to know the detailed mechanisms of BPAG1
modulation by TGF-β. The results revealed that calcium and IFN-γ inhibited BPAG1 expression at transcriptional
level, but TGF-β1 is not responsible for that transcriptional inhibition, suggesting that TGF-β may have differential
molecular mechanism for down-regulation of BPAG1 gene expression from the events induced by IFN-γ.
Dystrophic epidermolysis bullosa (DEB) is caused by mutations in the COL7A1 gene encoding type
VII collagen. DEB is clinically characterized by mucocutaneous blistering in response to minor trauma, followed
by scarring and nail dystrophy. DEB is inherited in either an autosomal dominant (DDEB) or recessive (RDEB)
fashion. DDEB basically results from a glycine substitution mutation within the collagenous domain on one COL7A1
allele, while a combination of mutations such as premature termination codon, missense, splice-site mutations on both
alleles causes RDEB. In this study, we examined a Japanese EB boy with generalized blistering and scar formation,
and made a diagnosis of the Hallopeau-Siemens type RDEB (HS-RDEB), the most severe form of RDEB. Mutational
analysis of the COL7A1 gene revealed a novel missense mutation A80P and a novel nonsense mutation Q1211X. In
general, HS-RDEB is caused by combination of premature termination codon mutations, but 3 HS-RDEB cases have
been reported to have combination of premature termination codon and missense mutations one of which was S48P.
This study suggests that even missense mutation, which leads to substitution for proline in amino terminal end of
type VII collagen, can cause HS-RDEB.
Purpose: To investigate the effects of anthocyanins in black currant on retinal blood flow circulation of patients
with normal tension glaucoma (NTG). Methods: Thirty consecutive patients with NTG were included in this study. They were orally administrated anthocyanins
extracted from black currant in tablet form once a day for a 6-month period. Systemic blood pressures. intraocular
pressures (IOPs), concentrations of the plasma endothelin-1 (ET-1), blood flows at the neuroretinal rim of the optic nerve
head and peripapillary retina, and visual field defects were measured before and just after the administration period. Results: Our study demonstrated that oral administration of anthocyanins tablets significantly increased the blood flows
at both neuroretinal rim of the optic nerve head and peripapillary retina (p < 0.05), with no significant changes in
mean blood pressures or IOPs. Furthermore, none of the subjects showed progression of their visual field defects. We
also demonstrated that the oral administration of anthocyanins tablets significantly increased, and thus normalized the
concentrations of plasma ET-1 (p < 0.05). Conclusion: These results suggest that anthocyanins orally administrated might be a safe and valuable choice for
neuroprotective treatment of patients with NTG.
Dystrophic epidermolysis bullosa (DEB) is a heritable mechanobullous skin disease derived from
mutations in the type VII collagen gene (COL7A1). DEB cases are divided into dominant dystrophic EB (DDEB)
and recessive dystrophic EB (RDEB). Most of the DDEB cases are induced by glycine substitution (GS) mutation
because of its dominant negative effect, although there are silent GS which are not pathogenic without combination
of other mutation in COL7A1. To know the relations between clinical features and COL7A1 mutations, we examined
COL7A1 gene mutation in two Japanese families with DEB, one is dominantly inherited and another is sporadic.
We identified three mutations; 8068del17ins2 in case 1, G2395D/152delG in case 2. Case 1 is DDEB, which does not result
from GS but from insertion/deletion mutation. In case 2, GS does not result in DDEB but causes recessive DEB (RDEB)
with the combination of premature termination codon (PTC) in non-collagenous amino-terminal region (NC-1). This
study demonstrates novel COL7A1 mutations for DEB and furthers our understanding of genotype-phenotype correlation
displayed in DEB patients.
AIM: Intravesical Bacillus Calmette-Guérin (BCG) therapy is an effective treatment for superficial bladder
cancer. However, its frequent and severe side-effects were major obstacles for clinical setting. In this study, BCG was fractionized with simple methods to find an active component. METHODS: Sonicated or autoclaved Tokyo
172 BCG strain was fractionated to supernatant and precipitate. These fractions were co-cultured with 5637 human bladder cancer cell line (5637 cell). The growth inhibitory effect on 5637 cell was analyzed by dye exclusion test.
³H-thymidine incorporation, cytologic examination with Giemsa staining, and cell cycle analysis using flowcytometry. RESULTS: Live BCG and supernatant fractions obtained by sonication or autoclave suppressed the growth of 5637
cell. The dark-stained spots suggesting early phase apoptosis were found in nuclei of 5637 cells by co-cultured with live BCG or supernatant fractions. In these cells, the ratios of apoptotic cells were increased compared with non treated cells. CONCLUSION: These results suggest that BCG has a direct anti-tumor effect to induce apoptosis on
5637 cell. Supernatant fractions obtained by sonication or autoclave maintained the direct anti-tumor effects as well as live BCG. Further purification of these fractions may provide a new BCG derivatives which has higher efficacy with reduced toxicity.