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SHA officers will start pounding the pavement in October under the National Emphasis Program (NEP) on Warehousing and Distribution Center Operations. State-plan states have six months to launch their own [...]

Many OSHA standards require employers to develop an emergency action plan (EAP) that meets the requirements of 29 CFR 1910.38. For example, if fire extinguishers are required or provided at [...]

Discusses how American Telephone & Telegraph Co. Chairman Robert E. Allen is attempting to inject a new aggressiveness into AT&T's corporate culture, cut costs, and replace old-guard bureaucrats with militants. Explores the magnitude of Allen's challenge to totally restructure the company and how AT&T's new aggressiveness could backfire.

Discusses how, from the US to Europe to the Far East, telecommunications companies are joining forces, buying into fledgling businesses, or hitching a ride on one another's hot strategy. They want to limit the risk in attacking new markets by spreading the investment load.

Background & Aims: There is limited data on the spectrum and risk for cancer associated with germline serine/threonine protein kinase 11 (STK11) mutations that cause Peutz-Jeghers syndrome (PJS). Methods: We analyzed the incidence of cancer in 240 individuals with PJS possessing germline mutations in STK11. Results: Fifty-four cancers were found among carriers. Overall, the risk for developing cancer at ages 20, 30, 40, 50, 60, and 70 years was 1%, 3%, 19%, 32%, 63%, and 81%, respectively. Kaplan-Meier analysis showed similar cancer risks between missense and truncating mutation carriers (log-rank @g^2 = 2.48; P = 0.12). There was some evidence that mutations in exon 3 of STK11 were associated with a higher cancer risk than mutations within other regions of the gene. We found no difference in overall cancer risk between male and female carriers (log-rank @g^2 = 1.31; P = 0.25) or between familial and sporadic cases (log-rank @g^2 = 1.16, with 1 df; P = 0.28). The most common cancers represented were gastrointestinal in origin-gastroesophageal, small bowel, colorectal, and pancreatic-and the risk for these cancers at ages 30, 40, 50, and 60 years was 1%, 10%, 18%, and 42%, respectively. In women, the risk for breast cancer was substantially increased, being 32% by age 60 years. Conclusions: These results quantitatively show the spectrum of cancer risk associated with STK11 germline mutations in the context of PJS and provide a valuable reference for defining surveillance regimens.

Aim--To investigate whether mutations in the STK11/LKB1 gene and genes implicated in the colorectal adenoma-carcinoma sequence are involved in Peutz-Jeghers syndrome (PJS) related tumorigenesis.Methods--Thirty nine polyps and five carcinomas from 17 patients (from 13 families) with PJS were analysed for loss of heterozygosity (LOH) at 19p13.3 (STK11/LKB1 gene locus), 5q21 (APC gene locus), 18q21-22 (Smad4 and Smad2 gene locus), and 17p13 (p53 gene locus), and evaluated for immunohistochemical staining of p53. In addition, mutational analysis of K-ras codon 12, APC, and p53 and immunohistochemistry for Smad4 expression were performed on all carcinomas.Results--LOH at 19p was seen in 15 of the 39 polyps and in all carcinomas (n = 5). Interestingly, six of the seven polyps from patients with cancer had LOH, compared with nine of the 31 polyps from the remaining patients (p = 0.01). In one polyp from a patient without a germline STK11/LKB1 mutation, no LOH at 19p or at three alternative PJS candidate loci (19q, 6p, and 6q) was found. No LOH at 5q was observed. However, mutational analysis revealed an APC mutation in four of the five carcinomas. LOH at 17p was not seen in polyps or carcinomas; immunohistochemistry showed expression of p53 in one carcinoma and focal expression in three polyps. At subsequent sequence analysis, no p53 mutation was found. One carcinoma had an activating K-ras codon 12 mutation and another carcinoma showed 18q LOH; however, no loss of Smad4 expression was seen.Conclusions--These results provide further evidence that STK11/LKB1 acts as a tumour suppressor gene, and may be involved in the early stages of PJS tumorigenesis. Further research is needed to see whether LOH in PJS polyps could be used as a biomarker to predict cancer. Differences in molecular genetic alterations noted between the adenoma-carcinoma sequence and PJS related tumours suggest the presence of a distinct pathway of carcinogenesis.

As president of American Telephone & Telegraph's Data Systems Group, Robert M. Kavner took over a corporation that had lost more than $2 billion in four years and had failed to give AT&T a significant role in the computer market. Discusses how Kavner, 44, plans to revive AT&T's computer business.

Discusses how American Telephone & Telegraph Co.'s Data Systems Group, a rocky performer over the past few years, may grow 30 percent to 35 percent in 1989, far faster than the overall computer industry.

Under the guidance of President Paolo L. Guidi, Telenet Communications Corp., the subsidiary of US Sprint Communications Co., has evolved from a struggling pioneer into a $450 million world leader in private data communications networks. Telenet's business should produce profits this year of $45 million, a big help for Sprint, the only national long-distance carrier that's losing money.

On July 18, US Sprint Communications Co.'s parents, GTE and United Telecommunications, called their business relationship off with GTE selling 30.1 percent of Sprint to United for $600 million while retaining a 19.9 percent stake. Discusses how United Telecom's buyout of GTE may end an uneasy relationship and benefit Sprint in the long run.