Several published articles have examined the question of whether screening HBsAg-positive carriers for early detection of liver cancer is beneficial and prolongs survival rate. [5][6][7][8][9][10][11][12][13][14][15] However, HBsAg-positive carriers involved in these studies have not been followed up long enough to determine whether prolonged survival time is truly a benefit of early detection or is a result of lead time bias from detection of tumors when they were smaller in size. In addition, these previous studies include in their survival analysis only cases that are detected early and do not include control patients who had not been screened before diagnosis of HCC for comparison. Natives of Alaska have been shown to have a high rate of HBV infection and HCC. 16,17 Serologic surveys of Alaska natives in the 1970s identified several hundred carriers of HBsAg. A retrospective study of stored serum samples in carriers who were diagnosed with HCC showed that alpha-fetoprotein (AFP) levels were elevated as long as 3 years before clinical presentation of HCC in several patients. 18 Between November 1982 and December 1987, over 53,000 Alaska natives were screened for HBV seromarkers and a hepatitis B vaccine was administered to all seronegative persons and all newborns. 19 In addition, we began a program to follow-up all HBsAg-positive carriers, including those identified previously, with semiannual determinations of AFP levels to determine if HCC could be detected at an early, potentially resectable, stage. In a preliminary report written 3 years after the start of this program, 4 patients were detected at a potentially resectable stage. 20 However, this report could not address any benefits of screening in regard to long-term survival. This article presents the 16-year longitudinal follow-up of 1,487 identified HBsAg-positive carriers tested semiannually with AFP determinations. PATIENTS AND METHODSPatients. A total of 1,487 patients chronically infected with HBV (HBsAg-positive for 12 months or longer) were identified. These carriers resided in 126 communities; most are isolated villages without road access. All carriers identified were contacted by mail, informed that they were at increased risk of developing HCC, and urged to have blood drawn every 6 months by their local Community Health Aide at the village clinic or at the nearest hospital. Every 6 months a reminder letter was sent to all carriers, to the Community

We reviewed records of all food-borne outbreaks of botulism in Alaska from 1947 through 1985. Fifty-nine confirmed or suspected outbreaks with 156 cases were reported. All outbreaks occurred in Alaska Natives and were associated with eating traditional Alaska Native foods. Forty-four (75%) of the outbreaks were laboratory confirmed and involved 133 persons. The overall annual incidence of confirmed or suspected botulism was 8.6 cases per 100,000 population. Seventeen persons died, an overall case-fatality rate of 11%. Type E toxin accounted for 32 (73%) laboratory-confirmed outbreaks; type A, six (14%); and type B, five (11%). Forty-one cases demonstrated botulinal toxin in one or more specimens (serum, gastric contents, or stool). Of the 41 botulinal toxin-positive persons, 38 (93%) had at least three of the commonly recognized pentad of signs or symptoms--nausea and vomiting, dysphagia, diplopia, dilated and fixed pupils, or dry mouth and throat--and 20 (49%) required respiratory assistance.