In Japan, a large U.S. export market, there has been growing public opposition against genetically modified (GM) foods. Using a dichotomous choice contingent valuation method, findings show the discount needed for Japanese Seikyou consumers to purchase GM food products is positively affected (i.e., a greater discount is required) by higher levels of self-reported risk perceptions toward GM food, higher levels of concern about food safety and the environment, higher self-reported knowledge about biotechnology, education levels, and income. Interestingly, gender does not significantly affect the discount needed for GM food. Further, it can be inferred from the results that a transformation of Japanese consumers’ perceptions and attitudes is needed for GM food products to successfully enter the Japanese market.

The discovery of bovine spongiform encephalopathy (BSE), commonly known as 'mad cow disease', in Japan caused anxiety about consuming beef and beef products. As a result, there was a sudden fall in sales of beef that hurt the Japanese beef industry as well as major beef exporters to Japan. We analyse factors that affect Japanese consumers' willingness to pay (WTP) price premiums for BSE-tested beef and estimate the mean WTP for BSE-tested beef using data obtained from a consumer survey in Japan. A single-bounded dichotomous choice contingent valuation model is used to recover the premium amount. We find that attitudes to food safety, reduction in beef consumption following the BSE outbreak, and being female all have a statistically significant positive effect on the WTP for BSE-tested beef. Interestingly, demographic variables such as age and income do not affect the WTP, possibly indicating that the BSE scare similarly affected multiple segments of the population. In our sample, consumers are willing to pay a premium on average of greater than 50 per cent for BSE-tested beef.

In this article, we review and repropose our hypothesis of the endogenous appearance of anticholinergic activity (AA) in Alzheimer's disease (AD). First, we introduce our previous articles and speculate that, because acetylcholine (ACh) regulates both cognitive function and inflammation, downregulation of this neurotransmitter causes upregulation of the inflammatory system. AA then appears endogenously with the production of cytokines and the downregulation of ACh in AD. To support our hypothesis, we present a female AD patient whose AA was considered to occur endogenously through her AD pathology. Her serum anticholinergic activity (SAA) was positive at her first visit to our memory clinic, was negative at the 1-year and 2-year follow-up visits, and had become positive again by 3 years. We speculate that the initial positive SAA was related to her AD pathology plus mental stress, and that her SAA at 3 years was related to her AD pathology only. Consequently, we believe that 2 patterns of SAA positivity (and therefore AA) exist. One occurs when the downregulation of ACh reaches a critical level, and the other occurs with the addition of some other factor such as medication, induced illness or mental stress that causes AA to affect AD pathology. Finally, we consider the pharmacotherapy of AD based on the proposed hypothesis and conclude that cholinesterase inhibitors can be used to prevent rapid disease progression, whereas N-methyl-D-aspartate receptor antagonists should be reserved for the treatment of AD that is already in a stage of rapid progression. We also propose a staging schema for patients with AD.

We previously proposed the hypothesis of endogenous anticholinergic activity (AA) in Alzheimer's disease (AD). According to this hypothesis, the downregulation of acetylcholine seen in AD is associated with upregulation/hyperactivity of N-methyl-D-aspartate receptor (NMDAR). The hyperactivation of NMDAR then induces inflammation, which, in turn, causes AA to appear endogenously. Based on this hypothesis, we commented that cholinesterase inhibitors (ChEIs) are ‘preventative' therapy for AD and NMDAR antagonists are the true ‘treatment' for AD. We also noted that ChEIs, such as donepezil, could treat delirium. Moreover, we proposed measuring serum anticholinergic activity in patients, particularly AD patients, in out-of-hospital pharmacies to monitor the anticholinergic burden for targeted treatment.

We examined barrier size (pore size) and charge selectivity (anionic sites) of the glomerular basement membrane (GBM) in experimental diabetes. For estimation of the pore size we employed a new method, tissue negative staining. In diabetic rats, enlarged pores and decreased numbers of anionic sites of GBM were observed. Both insulin treatment and angiotensin-converting enzyme inhibitors prevented these changes. The renoprotective effect of the two drugs is discussed in the article.