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A similar inverse relation was also found in the vitamin D2treated group r 0.681, P 0.003; Figure 2 ; . For the vitamin D3treated group, the regression equation between the change in 25 OH ; change ; and the baseline value baseline ; was as follows: change 0.418 baseline ; + 40.6; for the vitamin D2treated group: change 0.440 baseline ; + 33.0. On the basis of the subjects baseline 25 OH ; D concentrations, data from the vitamin D3treated group was divided into tertiles to test for the effect of prior vitamin D nutrition on the response to vitamin D supplementation. The first lowest ; tertile had the largest increase in 25 OH ; concentration whereas the third tertile showed less than one-half of that increase Table 2 ; . Oneway ANOVA and Tukey's HSD test indicated that the increase in 25 OH ; the third tertile was smaller than the increase seen in the first or second tertile. Because the increase in 25 OH ; after dosing was affected by baseline concentration, the baseline concentration was used as a covariate in the ANCOVA to adjust for the slight differences between the 2 vitamin Dtreated groups. After accounting for the slight differences in baseline concentrations between the vitamin D3 and D2supplemented groups, the increase in 25 OH ; with vitamin D3 supplementation remained significantly greater than that for vitamin D2 P 0.03 ; . DISCUSSION As expected, vitamin D2 and vitamin D3 both elevated serum 25 OH ; D concentrations. With vitamin D3, the increase in 25 OH ; was 70% greater 1.70 times ; than the increase obtained with vitamin D2. At first glance, this difference in the 25 OH ; D response may seem modest. However, in studies in which the same form of vitamin D was given at doses that differed by 2- to 5-fold, the differences in 25 OH ; response have been even smaller and more difficult to measure. Van Der Klis et al 15 ; found no difference in the final serum 25 OH ; D concentration achieved after 1 mo of 400 or 800 IU vitamin D3. Davie et al 16 ; treated subjects with 400 or 1000 IU vitamin D3 d and reported that the higher and propecia.

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Recommendation 1. Informational request Council direct staff how to proceed. 2. Approve attached Ordinance extending the moratorium for an additional 10 months and 15 days, the legal maximum to 12: 00 am, July 31, 2005 ; . Fiscal Impact This report is provided for informational purposes and therefore does not result in any immediate fiscal impact. However, the issues presented in this report may lead to future Council action with potentially minor major fiscal impact. Background and Analysis The voters of the State of California approved Proposition 215, codified as Health and Safety Code section 11362.5 et seq. and entitled "The Compassionate Use Act of 1996" the "Compassionate Use Act" ; . The purpose of this Act was to allow patients suffering from a number of serious illnesses an opportunity to find relief through the use of doctor recommended marijuana. Additionally, in January 2004 the State enacted SB 420 to clarify the scope of the Compassionate Use Act and allows cities to adopt and enforce rules and regulations consistent with SB 420. This includes controlling sites where medical marijuana is dispensed to primary caregivers and patients. Other provisions of SB 420 include: Recognizes the right of patients and caregivers to associate collectively or cooperatively to cultivate medical marijuana. Requires the State Department of Health, working with county health departments, to set up a voluntary statewide identification program to protect qualified patients and their primary caregiver from arrest and prosecution of certain marijuana related crimes. Disallows marijuana smoking in no smoking zones, within 1000 feet of a school or youth center except in private residences, on school buses, in a motor vehicle that is being operated, or while operating a boat and sonata.
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This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education through the sponsorship of the Massachusetts Medical Society and Boston University School of Medicine. The Massachusetts Medical Society is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians and testosterone.

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Sulfate has few indoor sources Sarnat et al. 2002 ; . Table 2 also shows personal-to-outdoor ratios P: O ; for PM2.5 and SO4 2, as well as differences between these ratios [P: O 2 PM2.5 ; P: O SO4 ; ]. During winter 1 and winter 2, the difference between P: O PM2.5 ; 2 and P: O SO was approximately 0.35 Table 2, next to last row ; . In contrast, during winter 3, summer 1, and summer 2, this difference was much larger, ranging from 0.75 to 1.55. The larger difference indicates that indoor sources were making a larger contribution to personal PM2.5 concentrations during these final three monitoring periods than during the first two monitoring periods. It is unlikely that this was due to recognized Wallace et al. 2006 ; indoor sources of PM2.5 such as cooking, cleaning, and personal care because these sources should not be significantly stronger during milder weather. Nor is the larger difference due to more time indoors during the final three periods; the seniors were indoors 97% of the time in the winter and 93% of the time in the summer time in transit included ; . Instead, the larger difference may be due to greater amounts of indoor ozone generated SOAs during winter 3, summer 1, and summer 2 than during winter 1 and winter 2 [personal ozone concentrations Table 2, last row ; were 2.5, 5.1, and 4.8 ppb during the former periods and 0.1 and 0.8 ppb during the latter periods]. Additional data in Sarnat et al. 2005 ; lend further support to this interpretation. Regression results for measurements made during the summer months indicate a slope of 0.35 0.220.47 ; for personal sulfate regressed on personal ozone, compared with a slope of 0.72 0.421.01 ; for personal PM2.5 regressed personal ozone [see table 3 of Sarnat et al. 2005 ; ]. The much larger slope for the latter pairing is consistent with contributions to personal PM2.5 from SOAs generated by ozoneinitiated indoor chemistry. Health effects of ozone reaction products. Certain ozone reaction products are known to have adverse health effects. For example, formaldehyde has been designated a Group 1 carcinogen in a 2004 International Agency for.

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