The world is in the midst of a huge fundamental shift in fibre supply, demand balances, and policy changes. Governments around the world are introducing policy changes which influence the supply demand balance as the politicians' thoughts are uttered. Government agencies and their bureaucrats are imposing changes on industry even before the legislation is passed by the government in question.
This ad hoc change process will continue for a time to come until the countries in question show a tough-mindedness with regard to their land use policies. Policies affecting forest areas such as protection areas, Native land claims, the protection of biodiversity and a true goal of sustainable development ; which addresses the combined issues of cultural, environmental, social and economic matters.
Eventually all of these difficult issues will reach essential closure. Then there will be great new opportunities for investment to meet the growing demand for forest products ; leading to a strengthening competitive position in the more traditional producing areas such as Canada.

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1) P. aeruginosa has been consistently isolated from 26.5 to 42.4% of the patients with urinary tract infections in the urological ward of Okayama University Hospital for the past years. 232 (.3%) out of 1042 hospitalized patients were with urinary tract infections with P. aeruginosa for past 4 years. Of these, 149 (64.2%) were thought to be the catheter induced urinary tract infections. The mode of spreading of this organism was epidemiologically investigated.
2) The following three laboratory assays were used for identification of P. aeruginosa isolated from clinical and environmental strains; serological typing, antibiotic sensitivity and protease and elastase production. Serological typing with 13 immunodiagnostic sera (Toshiba Chemical Industry) was performed by slide agglutination method. Protease and elastase production were detected by the method described by Goto et al.
In combination with serological typing and antibiograms, protease and elastase production offers the finest means of differentiating the strains of P. aeruginosa.
3) Of 136 clinical strains of P. aeruginosa, .% were serotypable strains. Serotype K was the most prevalent (36.%), followed by serotype (28.%), F (10.3%) and A (.4%). Most of serotype F and which were concurrently isolated from patients in 1976 had the same patterns of antibiogram and production of protease and elastase. It was strongly suggested that these patients were nosocomially cross-infected with the P. aeruginosa from the catheterization or through instrumentation.
4) Of 354 environmental specimens, 78 P. aeruginosa (.8%) were isolated, which were frequently isolated from floor mops and sink-drains. Of these strains, 87.2% were serotypable strains. Serotype was the most prevalent (42.3%), followed by serotype K (24.4%) and (12.8%). The same strains were seldom detected at the same sources successively, but different types of P. aeruginosa were usually detected. Among the serotypes , F and K, 18 strains (23.1%) were identical with the clinical strains. All of these were found during or after the clinical outbreaks of P. aeruginosa infections. There was no environmental strains that caused clinical infections. The other 60 strains (76.%) were different from the clinical strains, and present only transiently in the hospital environments.
5) Both clinical and environmental strains similary produced protease and elastase at 70 to %, hemolysin at 100%. Only 10 out of 37 environmental strains (27.%) were found to produced exotoxin.

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Seven hundred fifty mg of cholesterol were fed daily to 32 patients of the ischemic heart disease (IHD) for 2 weeks. Cholesterol amounts in VLDL, LDL, HDL, HDL₂ and HDL₃ were estimated on the th, th and 14th days of cholesterol load. Plasma apoprotein A-I, A-II, , C-II, levels were also measured in 16 from 32 IHD subjects. Apoprotein levels were estimated by a method of single radial immunodiffusion (SRID). Before cholesterol administration, cholesterol amounts in VLDL, LDL, HDL, HDL₂ and HDL₃ were 15.±.5mg/dl (mean±SD), 150.±58.1mg/dl 43.8±.6mg/dl, 16.4±5.8mg/dl and 24.±6.3mg/dl respectively. Plasma apoprotein A-I, A-II, , C-II and levels were 81.±. mg/dl, 15.1±5.4mg/dl, 93.±36.mg/dl, 3.83±1.00mg/dl and 4.29±1.36mg/dl respectively. After 2 weeks' cholesterol feeding, all plasma lipoprotein cholesterol and apoprotein levels did not change significantly. Correlation coefficients between plasma apoprotein and lipoprotein cholesterol levels were calculated. Apoprotein A-I and A-II correlated with HDL-C (r=.348), HDL₂-C (r=.612) and HDL₃ (r=.569). Apoprotein correlated with total cholesterol (TC) (r=.610), VLDL-C (r=.341), LDL-C (r=.726), HDL-C (r=.432) and HDL₂-C (r=.465). Apoprotein C-II correlated with TC (r=.765), TG (r=.679), VLDL-C (r=.651), LDL-C (r=.461) and HDL₂-C (r=.326). Apoprotein correlated with TC (r=.580), TG (r=.575) and VLDL-C (r=.666). Interapoprotein's correlations were also calculated. Apoprotein A-I correlated with apoprotein A-II (r=.468). Apoprotein correlated with apoprotein C-II (r=.393). Apoprotein C-II correlated with apoprotein (r=.393) and (r=.549). Apoprotein only correlated with apoprotein C-II (r=.549).

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