The ACS study, published in the Nov. 8 issue of the Archives of Internal Medicine, analyzed data between 1982 and 1991 from a survey of 121,287 men age 30 and older. Researchers limited their analysis to participants who had never smoked pipes or cigarettes and who had not been diagnosed with heart disease or diabetes at the start of the study. Death rates of current and former cigar smokers were compared with those of nonsmokers. During the nine years examined, a total of 2,508 participants died of coronary heart disease.

Researchers found that current cigar smokers age 30 to 74 faced a 30 percent greater risk of dying from coronary heart disease than nonsmokers. Cigar smokers aged 75 and older and former cigar smokers, however, did not experience an increased risk of CHD death.

Lead author Eric J. Jacobs, Ph.D., explained the inconsistent findings among older smokers. “When you’re talking about men in their 70s, 80s and 90s,” Jacobs explained, “death rates are already so high that it is difficult to detect modest increases in risk.” Jacobs also commented that men who are still smoking at these older ages are likely a healthier group.

Despite a significant decline from 1964 to 1992, cigar use in the United States increased by nearly 50 percent from 1993 to 1996. The past decade has seen the rise of cigar bars, cigar smoking sections in restaurants and cigar sheik led by celebrities, many of whom have posed on the cover of Cigar Aficionado magazine. Adolescents are also picking up the habit with more than 25 percent of high school boys and roughly 10 percent of high school girls reporting that they smoked at least one cigar within the past month.

“Any adverse effect of cigars on coronary heart disease is of particular importance given the recent rise in the prevalence in cigar smoking in the United States,” Jacobs remarked.

The majority of the smokers in the ACS study smoked cigars daily.

“It is quite possible that a lot of people think that because they don’t inhale with cigars as they do with cigarettes, that cigars aren?t as harmful,” Jacobs said. “But, this does not appear to be true.”

The findings from the latest ACS study are consistent with previous reports. A study earlier this year similarly found that cigar smokers had a 27 percent higher risk of heart disease than nonsmokers. This earlier report also found that cigar smokers faced about twice the risk of cancers of the mouth, throat and lung.

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In general, there are two kinds of rotator cuff problems called acute and chronic. Acute injuries are sudden and severe such as in an accident when a person uses his or her arm to cushion a fall, falls on the shoulder, is hit in the shoulder, or lifts something that is too heavy.

Chronic rotator cuff problems are caused by degeneration or inflammation (pain and swelling) of the tendon that comes and goes and gets worse with time. Degeneration of the tendon is caused by aging and by the normal wear and tear that comes with aging or heavy use.

In young, active people, most rotator cuff problems are caused by an injury such as a fall. In older, less active people, rotator cuff problems are caused because the tendon may be weakened and can be injured easily by simple movements such as lifting an object.

For athletes, rotator cuff problems can be caused by over use of the shoulder. Rotator cuff problems can be painful and limit overhead arm movements especially in such sports as baseball, tennis, or swimming.

Rotator cuff problems cause:
Inflammation of a tendon (tendinitis)
Partial or complete tears (ruptures) of a tendon
Calcium deposits in a tendon (calcific tendonitis)

Treatment of rotator cuff problems depends on how bad the injury or loss of strength and movement is, how much shoulder pain the person has, and how much of an injury caused the rotator cuff tear. Treatment also depends upon the person’s age, activity level, and willingness to complete a rehabilitation program.

Most rotator cuff problems are treated without surgery. Treatment may start with a period of rest, first aid steps (including the use of anti-inflammatory drugs), and physical rehabilitation exercises to maintain shoulder motion. In many cases, this approach is enough to decrease pain and restore shoulder strength and movement. In more severe cases, surgery may be done to repair damage within the shoulder, such as a torn tendon. Surgery is done right away if an injury causes a tear of the rotator cuff and sudden weakness

Introduction

The symposium on ?Emerging Therapies for Chronic Viral Hepatitis”, held October 2-4, 1998 in Montreal, Canada was hopefully the first in a series. The main corporate sponsors were Biochem Pharma Inc., OSI Pharmacenticals, GlaxoWellcome and Schering Plough Canada. Other sponsors included the Medical Research Council of Canada. The symposium was chaired by Dr. Lorne Tyrrell (University of Alberta, Canada) and was attended by approximately 205 participants from 17 countries. The meeting was targeted towards both clinicians and basic understanding hepatitis C virus (HCV) and hepatitis B virus (HBV) induced chronic hepatitis.

An important presence at this symposium was provided by pharmaceutical companies which was reflected in the many presentations, in all sessions with an emphasis on new developments in HBV and HCV drug discovery. The scientific program was divided in three major sessions : molecular targets and new therapies, models for the study of HBV and HCV replication and clinical updates on therapies for HBV/HCV infection. In a period of two days, over 40 oral and poster presentations were held plus a keynote symposia given by Dr. Michael Lai. (Howard Hughes Medical Institute, USA). With this extensive scientific program, this short review can only highlight the major report in the HCV and HBV areas.

Review

Molecular targets.

For hepatitis C virus, one major emphasis of the meeting was on the structural studies of the protease and helicase enzymes which are potential targets for small molecule structure-based drug design. Lamarre et al. (Bio-M?ga, Canada) showed that the N-terminal cleavage product DDIVPC-OH of a NS5A/5B protease substrate was a competitive inhibitor of the enzyme. The SAR studies resulted in a lead peptide with a submicromolar potency (Ki = 79uM). The presence of the carboxylic acid group at the C-terminus contributed considerably to binding and imparted specificity to these peptide-based inhibitors. The introduction of activated carbonyl groups does not produce any substantial increase in potency and results in a loss of specificity.

The bound conformation of an hexapeptide inhibitor to the NS3 protease was determined by NMR methods. An extended and well-defined conformation is observed with minor deviations along the backbone chain and the P1, P3 and P4 side chains. Kwong et al. (Vertex Pharmaceuticals, USA) reported the structure of the HCV N-terminal NS3 protease domain complexed with the NS4A activator peptide and the structure of the HCV helicase.

She highlighted the difference between the HCV NS3/4A protease and chymotrypsine which is the presence of the zinc ion in HCV NS3/4A serine protease. This metal is essential for HCV protease activity. While Malcom et al. (Schering Plough Research Institute, USA) reported on newer molecular construct as a single chain NS4A-GSGS-NS3 in which NS4A was tethered to NS3 through a linker.

Cai et al. (OSI Pharmaceuticals, USA) reported on an anti-IRES inhibitor designated as I70, which also showed antiviral activity against HCV in the XTL HCV-Trimera mouse model.