SRNT Newsletter, Vol. 4 No. 3, August 1998
Letting the Sunshine In
As research findings become news, the need for high standards is as important as ever
Janet Brigham, Ph.D.
SRNT Newsletter Editor
From The Daily Telegraph in London: "Teenage girls smoke because of an obsession with their weight."
From The Washington Star in Washington, D.C.: "Talk of new drug to render nicotine useless."
From the San Francisco Examiner: "Players finally coming to grips with chaw’s health hazards."
We have come to expect headlines about tobacco policies and litigation, but we are unaccustomed to science news seeing much daylight outside of the peer-reviewed academic venues where it is published. Only recently has the public interest in findings about tobacco-use behaviors and health risks resulted in increased media coverage of the illuminating, ongoing work of nicotine and tobacco scientists.
As tobacco legislation, legal maneuvering, and document disclosures highlight the news, research findings provide an increasingly visible backdrop of scientific information. It is difficult to assess the impact of this heightened exposure on such crucial matters as funding, faculty appointments, and publication opportunities — issues that affect the feasibility of building and maintaining a career in research.
Interest in nicotine and tobacco as topics is evident far beyond the United States, where legal and legislative battles have captured headlines and broadcasts for many months. News outlets in Canada, Australia, Africa, and Great Britain are also among those reporting research findings as breaking news.
One reason for this upsurge in attention — a cause invisible to the public at large and even to many scientists — is assertive news marketing by some scientific journals. It is not a coincidence that findings reported in The New England Journal of Medicine and The Journal of the American Medical Association show up in news articles before the first copies reach subscribers. These publications provide the news media with rapid, timely news releases about each issue, spotlighting stories of interest to a wide audience. Such news generation goes far beyond merely publishing the contents of a current issue on a World Wide Web page and issuing news releases.
Many publications use news dissemination venues such as EurekAlert!, an online news service produced by the American Association for the Advancement of Science, which provides a comprehensive Web listing of current research advances in science, medicine, health, and technology.
At this writing, EurekAlert! is accessed by 1,814 reporters representing 846 news organizations worldwide, from The Sydney Herald in Australia to the Swedish Broadcasting Corp., and including many major U.S. news providers. The approximately 20 news releases posted daily on EurekAlert! come primarily from the 878 public information officers registered with the service, SRNT’s public information officer among them.
This increased production of news combines with the spillover effect of news about tobacco legislation and lawsuits to provide an unprecedented forum for reaching readers, viewers, and listeners worldwide.
The following are examples of nicotine and tobacco research news articles that were published in newspapers, broadcast on television and radio, and made available on Internet news sites during late July and early August.
July 27: A survey from the Ontario Tobacco Research Unit in Canada reports that 13-year-olds use cigarette smoking to cope with stress, depression, and low self-esteem. A report by the Associated Press quotes study author Linda Pederson (also a corresponding editor of the SRNT Newsletter), now of Morehouse University School of Medicine in Atlanta, Georgia.
July 27 and several days following: Reports from the Addicted to Nicotine research forum are made public both inside and outside the U.S. August 4: A British-Canadian study funded by the Cancer Research Campaign indicates that teenage girls smoke because of an obsession with weight, not because of peer pressure. The article reporting this study was carried on both sides of the Atlantic Ocean, with interviews of Arthur Crisp of St. George’s Hospital Medical School in London, England.
August 7: An Australian study finds that 6 of every 10 employers believe smokers should be required to make up time lost for taking smoking breaks. The survey of 3,600 employers reports that time lost to smoking breaks costs Australian businesses some $1.6 billion (Australian) per year.
August 11: The generic antidepressant nortriptyline could help smokers quit, according to a report in the August issue of the Archives of General Psychiatry. A team led by Sharon M. Hall of the University of California at San Francisco, notes that nortriptyline helps curb post-cessation depression.
August 11: Major-league baseball players in the United States are coming to grips with the health hazards of smokeless tobacco. The article quotes John Greene, dean emeritus of the University of California at San Francisco School of Dentistry, who has studied smokeless tobacco use among baseball players for more than a decade.
August 14: The CDC announces that white high school students are more likely than other groups to be hurt by tobacco or drugs. The article, citing results of a 1997 survey of more than 16,000 teenagers, is carried by major news agencies; local media use statewide statistics from the CDC report.
Of course, other tobacco-related events also are reported. For example, on August 9 comes a report from the South African Sunday Times: "Chimpanzees at a zoo in KwaZulu-Natal are astounding visitors by begging for cigarettes and puffing away at lighted smokes." The chimps beg for cigarettes by extending their arms toward smoking visitors "and pulling sorrowful faces if they are denied."
Orangutans also beg for cigarettes but prefer unlit ones; they unwrap them, pinch the tobacco out, and chew it. Zoo-medicine specialist Mark Penning says that the animals, who are intelligent, learn the behavior from humans and also teach each other. He blames "the idiotic members of the public who throw them...cigarettes."
Not all news about nicotine and tobacco research is welcome news.
An August 4 report from the Associated Press brought home the need for maintaining high ethical standards. According to documents made public as a result of a lawsuit, the tobacco industry paid 13 scientists more than $156,000 to write letters and manuscripts discrediting a U.S. government report about environmental tobacco smoke (ETS). Although editors of the journals where those letters and articles were published apparently did know that at least some of the authors had ties to the tobacco industry, editors were unaware that the authors had been paid many thousands of dollars specifically to write the manuscripts.
The documents disclosing the situation were among tobacco industry papers made public as a result of a suit brought by the state of Minnesota against cigarette manufacturers. Letters and manuscripts submitted to scientific journals took issue with findings in a U.S. Environmental Protection Agency report linking ETS to lung cancer. The letters were printed in such forums as The Journal of the American Medical Association, and an article was published in the journal Risk Analysis.
The policy of SRNT on disclosure of funding sources is clear and unequivocal and can be expressed in one word: "Sunshine." SRNT President Jack Henningfield explained SRNT’s policy:
"The key principle is that...people indicate their sources of support for their research that is presented in any SRNT venue." This means that abstracts submitted for posters or oral presentations require full disclosure of the sources of all funding. A similar requirement is necessary for articles submitted to the new SRNT journal, Nicotine & Tobacco Research, which will publish its first issue at the end of 1998.
Henningfield explained that this disclosure is necessary not only regarding support from tobacco industries, but also for those whose funding from developers of treatments for tobacco-caused diseases might present some conflict of interest. Such disclosure is similar to the practice by grant reviewers of not critiquing proposals for which they might have any conflict of interest, e.g., a proposal from their home institution, a proposal from a relative, or a proposal in which they have a financial interest. It is also considered ethical for reviewers to decline to review articles against which they might have a negative bias, or proposals or papers whose publication might prove detrimental to their own careers or points of view.
Excusing oneself from such review is not an indication that a scientist cannot be fair, but instead indicates the need to avoid the appearance of a conflict of interest, even if no actual conflict exists. Reviewers of SRNT abstracts and manuscripts similarly are required to be free of conflict of interest regarding submissions they evaluate. The Society does not require that authors have funding sources outside the tobacco industry, but it expects all sources of funding to be disclosed, whatever those sources are.
Nicotine & Tobacco Research authors must the following statement of ethical standards, included in the submission guidelines: " Submissions must be accompanied by a signed statement from all authors saying that: (a) the material has not been published in whole or in part elsewhere; (b) the paper is not currently being considered for publication elsewhere; (c) all authors have been personally and actively involved in substantive work leading to the report and will hold themselves jointly and individually responsible for its content; (d) all relevant ethical safeguards have been met in relation to patient or subject protection, or animal experimentation. This statement must also declare sources of funding, direct or indirect, and any connection with the tobacco or pharmaceutical industries" [emphasis added].
A New Day for SRNT
By Jack E. Henningfield, Ph.D.
SRNT President, 1998-1999
To establish SRNT as a stronger organization that is better able to serve its mission of fostering scientific exchange and research, we are in the process of obtaining a new management organization to replace Phoenix Partnerships. A new management organization should be in place on January 1, 1999.
In the meantime, there is much to be done to ensure that our spring meeting in San Diego provides another outstanding forum for scientific exchange. I encourage those of you who have ideas and/or are willing to assist our Program Chair, Joy Schmitz, with the meeting to contact her directly (see back page for contact information).
This is also a time that it is extremely important not to lose any members in the renewal process and to further build our organization through new member recruitment. We will keep you posted on any changes in address, telephone, or fax, but for the next few weeks or months, you should continue to direct correspondence as in the past. We believe that through automated forwarding services, we will not have to change contact information until our new management service takes over.
We do appreciate the efforts of Phoenix to establish the SRNT, but we also believe that the Society will be best served by making as expeditious a transition as possible to a new management organization. The Executive Committee and Board of Directors believe that our Society will have increasing opportunities to foster scientific research and contribute to public health (we have had input to the U.S. Congress, the White House, the Food and Drug Administration, the Federal Trade Commission, various National Institutes of Health institutes, and much more in the past six months alone, and our journal is soon to be launched).
Thus, it is more important than ever before to ensure that the administration and management of SRNT meet the same standards of excellence as the science of our members. We believe we are on the right course. We ask you to be patient during the next few months of transition, and we appreciate your advice at this time of opportunity to make our Society stronger than ever.
John Hughes, M.D.
Chair, SRNT Public Policy Committee
Many tobacco control advocates are very disappointed at the failure of the McCain comprehensive tobacco legislation in the U.S. Senate and the abandonment of a negotiated national settlement with the industry. Many tied the failure of the legislation to a "no new taxes/no big government telling little people what to do" ad campaign by the industry, and attributed the failure of the settlement to advocates’ just getting too greedy.
Originally, we thought the Republicans would introduce a very weak bill against tobacco into the House so that in the November elections they could say they did something. Instead, perhaps bolstered by recent polls that indicate Americans do not list tobacco control among their top five agenda items, the Republicans have decided not to introduce a bill in the House. There are at least two Democratic bills, but they probably do not have serious chance of passage.
On other stages, the states of Minnesota, Florida, Mississippi, and Texas have settled, and at least one (Minnesota) and perhaps more of these states will use some of the money for local tobacco research. Negotiations between California, Washington, North Carolina, New York and Massachusetts and the industry are currently under way, but I do not know whether research is included in these provisions.
So, here’s my optimistic (or naive) take on all this. Legislation rarely is passed the first year it is proposed. Overall, the industry is in no better and, in many ways, in a worse position than before. In my opinion, the two events that will shape whether we have legislation considered next fall are whether Democrats find that chiding the Republicans for "sacrificing our children to big tobacco" sways voters and whether the industry loses more trials. You can help by bringing up tobacco in your local elections via call-ins, editorials, and requests for positions in writing, etc., of both Republican and Democratic candidates.
The focus of the SRNT Public Policy Committee will probably turn to nonlegislative ways to increase nicotine and tobacco research, such as meeting with top National Institutes of Health officials and pushing for an active trans-NIH committee to recommend increased funding.
The recent derailing of federal tobacco legislation is not the end of the government’s efforts to control tobacco, U.S. Vice President Al Gore declared recently. Gore told hundreds attending the Addicted to Nicotine research forum at Bethesda, Maryland, in July that the Administration will continue to fight for legislation to control tobacco use by youths.
Gore also announced that the National Cancer Institute will fund $38 million (U.S.) in the next two years for tobacco research, an $18 million increase. He noted, "For too long, taking on the tobacco companies was considered virtually impossible in Washington." He cited state and federal measures that brought tobacco companies to the bargaining table, listing the five points the Clinton Administration has determined are imperative in legislation (see SRNT Newsletter, Vol. 3 No. 4, pp. 4-5.)
"I promise you, this is not the end of this fight, by any means. It is just the beginning, and we’re going to keep pushing the fight again and again and again, until we win this victory for America’s children," Gore said. "At the same time, we need to do more to find out why children smoke and how we can help them stop. Government can provide the resources, but you must provide the answers."
Gore challenged the nicotine and tobacco research community to explore these questions: ·
Is It Present in Schizophrenia?
Sherry Leonard, Ph.D.,
and Robert Freedman, M.D.
University of Colorado Health Sciences Center and Denver Veterans
Affairs Medical Center
The role of nicotine in psychopathology is a new and interesting topic to contemplate. However, it may not be so new to those in our population who suffer from mental illness, many of whom are heavy users of tobacco products. In subjects suffering from the most common mental illnesses, schizophrenia, bipolar disorder, and major depression, the incidence of smoking is greater than 50% [1-3]; in schizophrenics, levels of smoking approach 80% of those affected. These patients often smoke high-tar cigarettes and sometimes use multiple forms of tobacco [2]. They have also been found to extract more nicotine from cigarettes than do nonaffected smokers [4]. The role of nicotine has been most fully characterized in schizophrenia [5, 6].
Schizophrenics have deficits in inhibitory mechanisms regulating the processing of both visual and auditory sensory information. Several of these deficits can be assayed in both humans and laboratory animals. Two measures that have been used to characterize these deficits are smooth-pursuit eye movement [7-10] and gating of auditory evoked potentials [11-13]. For both of these measures, most schizophrenic subjects have uniformly abnormal responses. Deficits in both smooth-pursuit eye movement [14] and gating of the P50 auditory evoked potential [15, 16] are normalized by nicotine, suggesting that nicotinic receptors may play a role in neuronal pathways regulating the function of these sensorimotor processing mechanisms in the brain.
Rodents also have the capacity to filter out extraneous auditory information, measured by gating of a similar wave, the N40 [17]. The effects of cholinergic agonists and antagonists on gating of auditory stimuli in both anesthetized and awake-behaving rat paradigms [17-19] have shown that antagonists of the a7 nicotinic receptor (a-bungarotoxin, methyllycaconitine, and antisense oligonucleotides complementary to the a7 translation start site) efficiently block the capacity to gate or filter auditory information [20, 21]. Neither mecamylamine nor dihydro-b-erythroidin, antagonists of the high-affinity and ganglionic types of nicotinic receptors, had any effect [20]. Scopolamine, a muscarinic blocker, likewise had no effect on auditory gating in the rat. This pharmacological evidence suggests that the a7 neuronal nicotinic receptor may function in the processing of auditory information.
A mouse model for the auditory gating deficit, the DBA/2 line, also supports this hypothesis. These mice have a schizophrenia-like deficit in the inhibition of auditory evoked potentials, compared to other mouse strains such as C3H [22], that is normalized by nicotine and also by a partial agonist of the a7 nicotinic receptor, GTS-21 [23]. Interestingly, the DBA/2 mouse line also exhibits a 40% decrease in levels of a-bungarotoxin binding receptors in the brain, compared to other strains [24, 25]. Regional localization of a7-containing receptors indicates a wide, but relatively low-level, distribution in both rat and human brains. A recent study comparing a7 mRNA and a-bungarotoxin binding at the cellular level in human brain showed that a7 is most highly expressed in both cell somata and dendrites of nuclei involved in processing of sensory information, such as the hippocampus, lateral and medial geniculates, and the reticular nucleus of the thalamus [26]. The a7-containing receptor is also found in the periphery in ganglionic tissue from the chick [27] and in lung tumor cells [28], and a recent study in tissues of neural crest origin shows that a7 receptors are expressed in almost all cells derived from these progenitors [29]. The latter results suggest that a7 may have non-synaptic roles in the periphery, possibly involving peptide secretion.
Expression of both high- and low-affinity nicotinic receptors has been studied in postmortem brain from chizophrenics and control subjects. We have previously reported that a-bungarotoxin binding was decreased by about 40% in the brains of subjects who were schizophrenic in life compared to subjects, matched for age, sex, postmortem interval, and smoking history, who were not mentally ill [30].
High-affinity nicotinic receptors appear to be affected in schizophrenia as well. In normal subjects, the number of high-affinity nicotinic receptors in both hippocampus and thalamus was correlated with the number of cigarettes smoked per day [31]. In smokers who had quit for varying periods before death, we found receptor levels in the non-smoking range. However, when we examined the effect of smoking history on high-affinity receptor levels in postmortem brain of schizophrenics, we found that the schizophrenics had fewer receptors, at every smoking level, than comparable normal smokers [29]. A study of the effects of typical neuroleptics on regulation of nicotinic receptor numbers in rats treated chronically with nicotine or with nicotine and haloperidol suggests that haloperidol does not appear to affect the normal up-regulation of nicotinic receptor numbers seen with nicotine dosing (manuscript in preparation). Since the postmortem brain tissue used in our experiments was from subjects who had taken only typical neuroleptics in life, our results suggest that regulation of receptor levels in schizophrenics may, indeed, be aberrant. Additionally, since nicotine addiction is thought to be partially characterized by nicotinic receptor number, the low levels of receptors in schizophrenics who are heavy smokers may mean that their addiction level and/or need for nicotine may be different than those in nonaffected smoking subjects.
Genetic studies in schizophrenic pedigrees also support an involvement of the a7 nicotinic receptor in schizophrenia. The chromosomal site of the a7 nicotinic receptor subunit at 15q13-q14 (and a marker nearby, D15S1360) has been genetically linked to the P50 deficit in nine schizophrenic pedigrees with a lod of 5.3, q=0, p<0.001 [32]. This means there are ~200,000-to-1 odds that the chromosomal locus of the a7 gene is genetically linked to the P50 deficit in schizophrenia. We have recently repeated linkage analysis in a second schizophrenic cohort ascertained through the National Institute of Mental Health Schizophrenia Genetics Initiative. We also found linkage of schizophrenia to the a7 marker D15S1360, with p < 0.005 [33].
We have isolated genomic clones for the human a7 receptor subunit. The gene is similar in structure to that of the chick [34], having 10 exons and exon/intron borders in the same locations. However, we have found that human exons 5 to 10 have been duplicated, with intervening introns, and lie proximal to the full-length a7 gene at chromosome 15q13-q14 [35]. Additionally, there are novel exons located 5‘ of the duplicated exon 5 that are expressed with the duplicated sequences (exons 5-10) as mRNA. The function of these duplicated and expressed a7 sequences is not yet known, but alternative transcripts in at least two other mammalian nicotinic receptor subunits have been shown to have a regulatory function [36, 37].
The body of data summarized here provides support for the role of nicotinic receptors in schizophrenia. At the present time, evidence is strongest for involvement of a7 subunit-containing receptors. However, the finding that schizophrenics do not increase receptor numbers of either the low- or high-affinity nicotine-binding subtypes, with nicotine dose suggests that the regulation and function of nicotinic receptors in the human brain may be more complicated than previously thought and, further, that nicotinic receptor neuropathology may play a role in the incidence of smoking in schizophrenia.
Sherry Leonard, Ph.D., is with the Departments of Psychiatry and Pharmacology, Box C-268-71, University of Colorado Health Sciences Center, 4200 East 9th Ave., Denver, Colorado 80262; telephone 303-315-8412; fax 303-315-5347; e-mail <Sherry.Leonard@UCHSC.edu>.
References
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4. Olincy, A., Young, D.A., Freedman, R. (1997). Increased levels of the nicotine metabolite cotinine in schizophrenic smokers compared to other smokers. Biological Psychiatry, 42, 1-5.
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14. Olincy, A., Ross, R.G., Young, D.A., Roath, M., Freedman, R. (1998). Improvement in smooth pursuit eye movements after cigarette smoking in schizophrenic patients. Neuropsychopharmacology, 18, 175-185.
15. Adler, L.E., Hoffer, L.D., Wiser, A., Freedman, R. (1993). Normalization of auditory physiology by cigarette smoking in schizophrenic patients. American Journal of Psychiatry, 150, 1856-1861.
16. Adler, L.E., Hoffer, L.J., Griffith, J., Waldo, M.C., Freedman, R. (1992). Normalization by nicotine of deficient auditory sensory gating in the relatives of schizophrenics. Biological Psychiatry, 32, 607-616.
17. Adler, L.E., Rose, G.M., Freedman, R. (1986). Neurophysiological studies of sensory gating in rats: Effects of amphetamine, phencyclidine, and haloperidol. Biological Psychiatry, 21, 787-798.
18. Adler, L.E., Pang, K., Gerhardt, G., Rose, G.M. (1988). Modulation of the gating of auditory evoked potentials by norepinephrine: Pharmacological evidence obtained using a selective neurotoxin. Biological Psychiatry, 24, 179-190.
19. Bickford-Wimer, P.C., Nagamoto, H., Johnson, R., Adler, L., Egan, M., Rose, G.M., Freedman, R. (1990). Auditory sensory gating in hippocampal neurons: A model system in the rat. Biological Psychiatry, 27, 183-192.
20. Luntz-Leybman, V., Bickford, P.C., Freedman, R. (1992): Cholinergic gating of response to auditory stimuli in rat hippocampus. Brain Research, 587, 130-136.
21. Rollins, Y.D., Stevens, K.E., Harris, K.R., Hall, M.E., Rose, G.M., Leonard, S. (1993). Reduction in auditory gating following intra-cerebroventricular application of a-bungarotoxin binding site ligands and a7 antisense oligonucleotides. Society for Neuroscience Abstracts, 19, 837-837.
22. Stevens, K.E., Freedman, R., Collins, A.C., Hall, M., Leonard, S., Marks, M.J., Rose, G.M. (1996). Genetic correlation of inhibitory gating of hippocampal auditory evoked response and alpha-bungarotoxin-binding nicotinic cholinergic receptors in inbred mouse strains. Brain Research, 15, 152-162.
23. Stevens, K.E., Kem, W.R., Mahnir, V.M., Freedman, R. (1998). Selective a7-nicotinic agonists normalize inhibition of auditory response in DBA mice. Psychopharmacology, 136, 320-7.
24. Marks, M.J., Romm, E., Gaffney, D.K., Collins, A.C. (1986). Nicotine-induced tolerance and receptor changes in four mouse strains. Journal of Pharmacology and Experimental Therapeutics, 237, 809-819.
25. Marks, M.J., Romm, E., Campbell, S.M., Collins, A.C. (1989). Variation of nicotinic binding sites among inbred strains. Pharmacology, Biochemistry and Behavior, 33, 679-689.
26. Breese, C.R., Adams, C., Logel, J., Drebing, C., Rollins, Y., Barnhart, M., Sullivan, B., DeMasters, B.K., Freedman, R., Leonard, S. (1997). Comparison of the regional expression of nicotinic acetylcholine receptor a7 mRNA and [125I]-a-bungarotoxin binding in human postmortem brain. Journal of Comparative Neurology, 387, 385-398.
27. McGehee, D.S., Role, L.W. (1995). Physiological diversity of nicotinic acetylcholine receptors expressed by vertebrate neurons. Annual Review of Physiology, 57, 521-546.
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29. Logel, J., Breese, C., Gillen, K.M., Adams, C.E., Leonard, S. (1997). Expression of high and low affinity neuronal nicotinic receptors in tissues of neural crest origin. Society for Neuroscience Abstracts, 23, 382.
30. Freedman, R., Hall, M., Adler, L.E., Leonard, S. (1995). Evidence in postmortem brain tissue for decreased numbers of hippocampal nicotinic receptors in schizophrenia. Biological Psychiatry, 38, 22-33.
31. Breese, C.R., Marks, M.J., Logel, J., Adams, C.E., Sullivan, B., Collins, A.C., Leonard, S. (1997). Effect of smoking history on [3H]nicotine binding in human postmortem brain. Journal of Pharmacology and Experimental Therapeutics, 282, 7-13.
32. Freedman, R., Coon, H., Myles-Worsley, M., Orr-Urtreger, A., Olincy, A., Davis, A., Polymeropoulos, M., Holik, J., Hopkins, J., Hoff, M., Rosenthal, J., Waldo, M.C., Reimherr, R., Wender, P., Yaw, J., Young, D.A., Breese, C.R., Adams, C., Patterson, D., Adler, L.E., Kruglyak, L., Leonard, S., Byerley, W. (1996). Linkage of a neurophysiological deficit in schizophrenia to a chromosome 15 locus. Proceedings of the National Academy of Sciences, 94, 587-592.
33. Leonard, S., Moore, T., Gault, J., Hopkins, J., Robinson, M., Olincy, A., Adler, L.E., Cloninger, C.R., Kaufmann, C.A., Tsuang, M.T., Faraone, S.V., Malaspina, D., Svrakic, D.M., Freedman, R. (1998). Further investigation of a chromosome 15 locus in schizophrenia: Analysis of affected sibpairs from the NIMH Genetics Initiative. American Journal of Medical Genetics, 81, 308-312.
34. Couturier, S., Bertrand, D., Matter, J.-M., Hernandez, M.-C., Bertrand, S., Millar, N., Valera, S., Barkas, T., Ballivet, M. (1990). A neuronal nicotinic acetylcholine receptor subunit a7 is developmentally regulated and forms a homo-oligomeric channel blocked by a-BTX. Neuron, 5, 847-856.
35. Gault, J., Robinson, M., Berger, R., Drebing, C., Logel, J., Hopkins, J., Moore, T., Jacobs, S., Meriwether, J., Choi, M.J., Kim, E.J., Walton, K., Buiting, K., Davis, A., Breese, C.R., Freedman, R., Leonard, S. (in press). Genomic organization and partial duplication of the human a7 neuronal nicotinic acetylcholine receptor gene. Genomics.
36. Garcia-Guzman, M., Sala, F., Sala, S., Campos-Caro, A., Stuhmer, W., Gutierrez, L.M., Criado, M. (1995). Alpha-Bungarotoxin-sensitive nicotinic receptors on bovine chromaffin cells: Molecular cloning, functional expression and alternative splicing of the alpha 7 subunit. European Journal of Neuroscience, 7, 647-655.
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University of Minnesota researcher Dorothy K. Hatsukami has been elected president of SRNT for the 1999-2000 term.
Hatsukami is professor of psychiatry at the University of Minnesota Medical School. Born in Hiroshima, Japan, she earned an undergraduate degree in psychology from the University of California at Berkeley in 1973 and a Ph.D. in clinical psychology at the University of Minnesota in 1980.
She was awarded the Ove Fernö Award for contributions to understanding tobacco dependence. As director of the Tobacco Research Laboratory and Treatment Programs at the University of Minnesota, she has been involved in a variety of significant areas of research. She is one of the world’s leading authorities on nicotine dependence and smokeless tobacco use. At present, she is principal investigator of National Institute on Drug Abuse grants to study medication development for treating drugs of abuse and smokeless tobacco cessation treatment. She is co-principal investigator of a NIDA study of tobacco cessation in postmenopausal women.
A member of the board of directors of the College on Problems of Drug Dependence, she is also chair of the CPDD Publications Committee. She has served on the SRNT executive committee and has been a member-delegate. She also has been as director of the Minnesota Consortium for Addiction Studies at the University of Minnesota.
She has served as co-editor of Behavioral Approaches to Addiction and is on the editorial board of Drug and Alcohol Dependence. She has co-authored a nicotine withdrawal scale widely used in various forms throughout nicotine and tobacco research.
Elected member-delegate for a term covering the years 1998 to 2002 was Judith K. Ockene, professor of medicine and director of the Division of Preventive and Behavioral Medicine at the University of Massachusetts Medical School. She replaces Murray E. Jarvik, who served a 1995-1998 term.
Ockene has been involved in smoking research, education, and clinical practice for the last 20 years. Her major research focus has been the development and application of a patient-centered counseling model for brief physician-based interventions for smoking, alcohol abuse, and diet. She also has developed clinical and community-based interventions for smoking prevention and control, and has explored factors that affect lifestyle behavior changes, the relationship of smoking to disease, and women’s health.
She and her research team are currently working on a potential certification process for smoking cessation counselors. She teaches medical students, residents in training, community physicians, and a variety of other health-care providers and students.
The deadline for abstract submissions for the Fifth Annual Meeting of the Society for Research on Nicotine and Tobacco is October 9, 1998. The meeting will be held March 5-7, 1999, at the Sheraton Hotel, San Diego, California, in conjunction with the 20th Annual Meeting of the Society of Behavioral Medicine, and several co-sponsored sessions are being planned.
The goal of the annual scientific meeting is to present and disseminate information about ongoing nicotine research from a variety of perspectives. The program will include invited addresses by leaders in the field, state-of-the-art symposia, roundtable discussions, oral presentations, and a new-investigator paper session. A vital component of the program will be poster sessions presenting the most recent research findings in the field of nicotine and tobacco use.
SRNT invites submissions for organized symposia as well as individual paper and poster presentations. Because of limited time and space on the program, preference will be given to symposia that span a range of disciplines, such as studies that explore a research area from molecular/animal levels through human clinical approaches.
The Call for Abstracts is being mailed in August. Abstract submissions should be returned to 1999 SRNT Program Chair Joy Schmitz, Ph.D., 1300 Moursund Avenue, Houston, TX 77030.
An Update and Call for Integration
Karen S. Hudmon, Dr.P.H., R.Ph.,
and Gary E. Swan, Ph.D.
SRI International
Results from family, twin, and molecular genetic studies provide compelling evidence supporting a role for genetic factors in smoking behavior.
Recent findings (Carmelli et al., 1992; Cheng et al., 1997; Wang et al., 1997; Pianezza et al., 1998; Lerman et al., 1998; Picciotto et al., 1998; Spitz et al., 1998) indicate that genetic variation gives rise to alterations in dopamine receptors and/or the liver enzymes that metabolize nicotine, and thus some persons appear to be at an elevated risk for tobacco use and nicotine addiction.
One line of research in the study of genetic susceptibility for tobacco use stems from knowledge of nicotine’s actions on the dopamine reward pathway of the central nervous system. One of the ways that nicotine exerts its effects is by facilitating the release and inhibiting the reuptake of the neurotransmitter dopamine; this increased level of dopamine is associated with self-reinforcing behavior and the establishment of drug dependence for a variety of drugs of abuse, including nicotine.
In this context, variation in the DNA that codes for the D2 dopamine receptor alters the number of the dopamine binding sites (Noble et al., 1991), thereby mediating the effects of nicotine. It has been hypothesized that persons with genetic polymorphisms in the dopamine receptor gene have a deficit in their reward system, experience an enhanced reward when exposed to dopaminergic agents, and may be more vulnerable to nicotine addiction (Noble et al., 1994).
A study conducted at the M.D. Anderson Cancer Center in Houston, Texas, lends support to this hypothesis; persons who exhibited certain D2 alleles were more likely to have (1) smoked 100 or more cigarettes in their lifetime, (2) started smoking at an earlier age, and (3) reported fewer quit attempts, compared with persons without the polymorphism (Spitz et al., 1998).
In a separate study examining predictors of smoking to obtain stimulatory effects and smoking to reduce negative affect, researchers found a significant interaction between depression and genotype status for a polymorphism on the D4 dopamine receptor gene (Lerman et al., 1998). In other words, the nature of the relationship between smoking and D4 is a function of whether a person is depressed. Collectively, these studies suggest that genetically-induced variation in the functional properties of the dopamine reward system is an important factor contributing to smoking behavior. In fact, researchers recently have identified a specific subunit (b2) of the nicotinic receptor that appears to be associated with nicotine’s reinforcing effects on dopaminergic neurons in the mesolimbic system of the brain (Picciotto et al., 1998).
Using data from nearly 500 three-generation families, investigators (Cheng et al., 1997) at SRI International in Menlo Park, California, used segregation analyses to determine if a genetic mode of inheritance for smoking explains clustering of smoking behavior among families. This study identified a significant major gene effect that controls for smoking behavior. The probability of becoming a smoker among persons who carry the gene is estimated at 65%; however, this value varies as a function of spousal and parental smoking status. Forty-nine members, distributed in 11 pedigrees, were identified as having a probability of 70% or greater of being gene carriers. These results are perhaps the first to provide evidence of a major gene for smoking behavior. Although there appears to be an identifiable genetic mode of inheritance for smoking, results of this study also suggest that the best model requires the inclusion of a factor to explain additional familial influences, such as the effect of other small contributing gene effects, environment, or gene-environment interactions.
By applying knowledge gained through pharmacokinetic studies, investigators are examining genetic influences on the mechanism and speed at which smokers and non-smokers metabolize nicotine. In an article recently published in Nature, investigators at the University of Toronto reported that genetic variation may be responsible for inter-individual differences in the rate of nicotine metabolism by the liver’s CYP2A6 enzyme system (Pianezza et al., 1998). Specifically, nicotine-dependent smokers who lacked full CYP2A6 capacity (i.e., slow nicotine metabolizers) smoked fewer cigarettes per day than the more rapid metabolizers; slow metabolizers were less common among tobacco-dependent smokers than among control group subjects who had tried smoking but had never been nicotine dependent. Considering these results along with the observation that reduced activity of the CYP2A6 enzymes also reduces the rate of conversion of tobacco nitrosamines to carcinogens (Yamazaki et al., 1992), one could hypothesize that smokers with the genetic variant for CYP2A6 would be significantly protected from tobacco-related cancers.
Although genetics appear to play an important role in predicting tobacco use and the development of nicotine addiction, it is not likely that knowledge of genetic risk alone can result in effective tobacco prevention strategies. Current thinking remains that nicotine addiction also arises from a host of environmental and psychological factors. To further scientific knowledge regarding the predictors of tobacco use, it is imperative that future research efforts use an integrative approach that incorporates psychosocial, cultural, behavioral, and genetic influences, as well as the interactions between these factors (Swan, in press).
We propose that tobacco researchers consider the following research aims:
To successfully approach the problem of tobacco use and nicotine addiction, it is important to recognize that, in all likelihood, genes and environment do not work independently of each other.
Karen Hudmon, Dr. P.H., R.Ph., is with the Center for Health Sciences, SRI International, 333 Ravenswood Ave., Menlo Park, CA 94025; telephone 650-859-5110; fax 650-850-5099; e-mail khudmon@unix.sri.com.
References
Carmelli, D., Swan, G.E., Robinette, D., Fabsitz, R. (1992). Genetic influence on smoking—A study of male twins. New England Journal of Medicine, 327, 829-833.
Cheng, L.S., Swan, G.E., Carmelli, D. (1997). A genetic analysis of smoking behavior in 1480 families. Genetic Epidemiology, 14, 521 (abstract).
Lerman, C., Caporaso, N., Main, D., Audrain, J., Boyd, N.R., Bowman, E.D., Shields, P.G. (1998). Depression and self-medication with nicotine: The modifying influence of the dopamine D4 receptor gene. Health Psychology, 17, 56-62.
Noble, E.P., Blum, K., Ritchie, T., Montgomery, A., Sheridan, P.J. (1991). Allelic association of the D2 dopamine receptor gene with receptor-binding characteristics in alcoholism. Archives of General Psychiatry, 48, 648-654.
Noble, E.P., St. Jeor, S.T., Ritchie, T., Syndulko, K., St. Jeor, S.C., Fitch, R.J., Brunner, R.L., Sparkes, R.S. (1994). D2 dopamine receptor gene and cigarette smoking: A reward gene? Medical Hypotheses, 42, 57-260.
Pianezza, M.L., Sellers, E.M., Tyndale, R.F. (1998). Nicotine metabolism defect reduces smoking. Nature, 393, 750.
Picciotto, M.R., Zoli, M., Rimondini, R., Lena, C., Marubio, L.M., Pich, E.M., Fuze, K., & Changeaux, J. (1998). Acetylcholine receptors containing the b2 subunit are involved in the reinforcing properties of nicotine. Nature, 391, 173-177.
Spitz, M.R., Shi, H., Yang, F., Hudmon, K.S., Jiang, H., Chamberlain, R.M., Amos, C.I., Wan, Y., Cinciripini, P., Hong, W.K., Wu, X. (1998). Case-control study of the D2 dopamine receptor gene and smoking status in lung cancer patients. Journal of the National Cancer Institute, 90, 358-363.
Swan, G.E. (in press). Implications of genetic epidemiology for the prevention of tobacco use. Nicotine and Tobacco Research.
Wang, Y.F., Wang, S., Sun, C., Gillanders, E., Freas-Lutz, D., Schenkein, H.A., & Diehl, S.R. (1997). Linkage analysis of smoking behavior and IgG2 levels in early onset periodontitis. Genetic Epidemiology, 14, 542 (abstract).
Yamazaki, H., Inui, Y., Yun, C.H., Guengerich, F.P., Shimada, T. (1992). Cytochrome P450 2E1 and 2A6 enzymes as major catalysts for metabolic activation of N-nitrosodialkylamines and tobacco-related nitrosamines in human liver microsomes. Carcinogenesis, 13, 1789-1794.
Try MEDLINE and the World beyond MEDLINE
Editor’s Note: This is one in a series of articles featuring sources of information that might be useful to nicotine and tobacco researchers. Suggestions of other periodicals or sources are encouraged.
A welcome change in citation access was last year’s inauguration of free online MEDLINE. Many researchers are not only unaware of the ease of accessing MEDLINE now, but are unaware of the wealth of nonindexed journals and other materials that are also valuable sources.
"For more than 25 years, MEDLINE has been one way in which health professionals have attempted to keep up with what's new in their field," according to the National Library of Medicine. Since free MEDLINE searching on the Internet became available last year, the number of searches on the service has increased dramatically. About 7 million searches took place annually before the first free MEDLINE search. About 120 million searches have been performed in the year since MEDLINE became free.
This is as it should be — MEDLINE is an invaluable, rich tool. But it would be impossible for MEDLINE to reference all sources of information that might be useful and necessary. One example of how it may be helpful to broaden the scope of inquiry beyond MEDLINE journals is the monthly journal American Demographics, subtitled Consumer Trends for Business Leaders. This colorful and timely periodical, which is available in print form by subscription and online, offers full-text search and archive retrieval of articles. The most current issues are available online only to subscribers, but past issues are fully accessible.
American Demographics often focuses on health behaviors, and consequently often reports on trends in tobacco sales. It also provides demographic information that can be instrumental in planning and carrying out research studies.
For example, a researcher might write a grant application proposing administering computerized questionnaires to a sample of young-adult Native Americans who use smokeless tobacco. Peer reviewers, perhaps unfamiliar with the population, might argue that Native Americans in that age group are unlikely to be adept at using computers. The researcher, however, could anticipate such criticism by citing statistics from the August 1998 issue of American Demographics indicating that Native Americans have the highest rate of time spent on home computers of any U.S. group, with an average of 8.4 hours per week. They lead white, African American, Hispanic, and Asian groups. And young adults ages 18-24 are second only to the 55-64 age group (many of whom are widowed) in hours of at-home computer usage.
Another example: A scientist might not be aware of such sources as the California Tobacco Use Survey or the U.S. Department of Agriculture’s Economic Research Service — but American Demographics was aware of them and used them extensively in a July 1998 article titled "The Cocktail Nation." The article started: "Cigars. Steaks. Cocktails. This jazzy trio of former American favorites came roaring back in the 1990s." A table showed the inverse relationship between cigar smoking and cigarette smoking among income groups. The article also noted that the circulation of Cigar Aficionado magazine rose from 141,000 in 1994 to nearly 400,000 in 1996. Such markers can be valuable indications of public-health needs and attitudes, and can suggest research directions.
American Demographics also lists addresses, telephone numbers, and Internet contact information for sources of information included in the articles — information typically not available in peer- reviewed scientific journals.
On occasion, American Demographics becomes a vehicle for taking scientific information to the business community, as it did with an August 1997 article titled "People Behaving Badly," which used statistics from the Centers for Disease Control’s 1995 Behavioral Risk Factor Surveillance System report.
Don’t count on finding an anti-tobacco bias in periodicals such as American Demographics — just count on finding a timely, fresh perspective.
MEDLINE: <www.nlm.nih.gov/databases/freemedl.html>
American Demographics: <www.demographics.com>
Editor’s Note: Full texts and summaries of many documents useful to researchers are now available online. Readers aware of full-text sites not listed here are encouraged to contribute them to the Newsletter for future listing.
Addiction Research Foundation (Canada): statistics, publications, cessation information, and full texts of reports: <www.arf.org>.
Agency for Health Care Policy and Research (U.S.): clinical practice guidelines, 1996 Smoking Cessation documents available online: <www.ahcpr.gov/clinic/>.
American Medical Association: online versions of key journals, including The Journal of the American Medical Association, and Archives titles: <www.ama-assn.org/scipub.htm>.
California Environmental Protection Agency: Office of Environmental Health Hazard Assessment (OEHHA) comprehensive health assessment on environmental tobacco smoke, final draft: <www.calepa.cahwnet.gov/oehha/docs/ets/ets-main.htm>.
Centers for Disease Control (U.S.): Tobacco Information and Prevention Sources (TIPS), includes U.S. Surgeon General report summaries, links to the full text of 1998 report, Tobacco Use among U.S. Racial/Ethnic Minority Groups <www.cdc.gov/nccdphp/osh/sgrpage.htm>, texts of research reports on a broad scope of topics, cessation helps, recent citations of published research reports, educational materials, publications, and useful links to tobacco-related sites: <www.cdc.gov/ nccdphp/osh/index.htm>.
Environmental Protection Agency (U.S.): fact sheet on 1992 report on environmental tobacco smoke: <www.epa.gov/iaq/pubs/etsfs.html>.
Food and Drug Administration (U.S.): Children and Tobacco Web site, information about the new regulations, health effects of tobacco on children and adolescents, and what retailers and consumers can do to help reduce tobacco use by young people: <www.fda.gov/opacom/ campaigns/tobacco.html>.
Morbidity and Mortality Weekly Report (U.S.): can be accessed through CDC site <www.cdc.gov>; online version of current and past issues: <http://www.cdc.gov/epo/mmwr/mmwr.html> and <ftp://ftp.cdc.gov/pub/mmwr>.
National Cancer Institute (U.S.): Cigars: Health Effects and Trends, recent monograph, most comprehensive description of cigar use: <http://rex.nci.nih.gov/NCI_MONOGRAPHS/ INDEX.HTM>.
National Institute on Drug Abuse (U.S.): full video of presentations at recent Addicted to Nicotine: A National Research Forum (requires RealPlayer software, has link for free downloading), links to publications, other NIDA programs and information: <www.nida.nih.gov/>.
New England Journal of Medicine: online version: <www.nejm.org/content/index.asp>.
Health Department of Western Australia: information about smoking, written for professionals, parents, and children; information about national health: <www.public.health.wa.gov.au>.
Quit Victoria (Australia): Tobacco in Australia: Facts and Issues includes many statistics and reports <www.peg.apc.org/~vshp>.
World Health Organization: documents on Tobacco or Health program topics: <www.who.int> <www.who.org/psa/docs/index.htm> .
The Society’s recently renovated Web site now has several new enhancements.
A bulletin board feature allows visitors to post questions and invite answers. This also provides a forum for immediate dissemination of SRNT news. A new feature of the Resources section is an extensive listing of training opportunities, with tables listing numbers and types, duration, salary, and application deadlines for training positions at several dozen universities and other institutions.
Richard Brown of Brown University, and Webmaster Michelle Ricci developed and maintain the site. They welcome members’ input and suggestions through the Contact section of the site.
Editor’s Note: When a book about tobacco becomes popular, it also becomes a primary vehicle for educating the public. In reviewing books that speak not to the research community but to the public at large, we consider whether they convey scientifically accurate information, and what they can teach us about public perceptions.
The Runaway Jury. John Grisham. New York: Island Books, 1996. ISBN
0-440-22147-1, 550 pp.,
$7.99 U.S.
By Raine Riggs
University of Vermont
Even your most creative fantasies about the bad guys at the tobacco companies probably won’t come close to the portrait of tobacco CEOs that John Grisham has painted in his novel The Runaway Jury.
The villains of this novel are four middle-aged tobacco CEOs and their band of devious thugs. The story unfolds in Biloxi, Mississippi, as the widow of Jacob Wood brings a civil suit against the tobacco company that she believes is responsible for her husband’s death. What ensues includes mystery, legal maneuvering, behind-the-scenes views of a trial, and jury tampering. There’s even some compelling testimony by tobacco researchers.
Grisham manages to touch on several areas of nicotine and tobacco research through the testimony of his fictional scientists. Behavioral scientists argue that tobacco companies target children so that they will have a constant supply of lifelong smokers. Addiction experts testify that nicotine is addictive and that tobacco companies routinely spike their cigarettes to make sure that smokers stay addicted. There is testimony from epidemiologists, psychologists, physicians, chemists, and more.
Despite the fact that the book is a work of fiction, many lay readers may believe that the scientific information presented by the experts is accurate. Although much of it is correct, some is not.
For example, a fictional former tobacco company scientist testifies that children become addicted to nicotine much faster than adults — but the reader sees no evidence for this assertion. Any studies designed to test such a hypothesis would be highly unlikely to pass any known human subjects review board, since they could require exposing naive children to nicotine, measuring their dependence and tolerance, and assessing their eventual abstinence symptoms.
Grisham’s experts further mislead the reader by focusing their testimony almost exclusively on lung cancer deaths in smokers. The expert testimony never touches on the greater proportion of smokers who die from cardiovascular problems. This lack of attention to the wide range of health consequences of smoking serves to further perpetuate the common idea that the only risk from smoking is developing lung cancer.
The book also raises several interesting scientific and public policy arguments. First, a significant amount of expert testimony focuses on the definition of addiction. The defense lawyers argue that there is no definitive scientific evidence that cigarettes are addictive and that, in fact, scientists can’t even agree on a definition of addiction. People continue to smoke as a matter of choice, rather than because they are addicted, or so these attorneys claim. Furthermore, the defense calls an expert to testify that only 10 percent of smokers develop lung cancer, while the remaining 90 percent do not. Again, it is argued that there is no definitive evidence that smoking causes lung cancer. Ignoring concepts of risk and vulnerability, they argue that if smoking does cause lung cancer, why do only 10 percent of smokers develop it?
If the scientific arguments don’t hold the reader’s interest, there are plenty of plot twists and turns, as both the plaintiff and the defense attempt to manipulate the jurors into a favorable verdict. The only problem is that the jury seems to have a mind of its own.
Grisham demonstrates considerable insight into the public’s beliefs about smokers and tobacco companies through the conversations that take place in the jury room when no scientists or lawyers are around.
Although little of the plot is legal — and we can only hope it is not completely realistic — the book is entertaining. Grisham has a knack for concealing crucial information and revealing it when you least expect it.
Raine Riggs is a doctoral student in clinical psychology at the University of Vermont <rrigs@zoo.uvm.edu>.
THE INTERNATIONAL HEALTH PROMOTION CONFERENCE, Working Together for Better
Health—New Partners and New Approaches for a New Millennium; 23-25 September 1998, Cardiff, Wales, UK. Contact
Amanda Price or Jon Pontin at Health Promotion Wales, Ffynnon Las, Ty Glas Ave, Llanishen, Cardiff, Wales, UK,
CF4 5DZ. telephone +44 1222 681287/681246/752222; fax +44 1222 756000/755813 e-mail: <Conference.98@hpw.wales.nhs.uk>
<www.hpw.org.uk/conf98/index.htm>.
4TH ANNUAL DUKE NICOTINE RESEARCH CONFERENCE, Nicotinic Actions on Interacting Neural Systems, November 4, Duke University, Durham, North Carolina. For information, telephone (919)416-1515 or fax: (919)286-1388. Conference focus is relationship between nicotinic receptor subtype heterogeneity and differences in response to nicotine and nicotinic drugs. <mmkl@acpub.duke.edu> <www.duke.edu/web/nicotine/ecconf.html>.
AMERICAN SOCIETY OF ADDICTION MEDICINE, 11th National Conference on Nicotine Dependence, November 5-8, Marina Del Rey, California. For information, contact (301) 656-3920. SECOND EUROPEAN CONFERENCE ON TOBACCO OR HEALTH, "Smoke Free 21st Century Conference," 23-27 February 1999, Gran Canaria Island. Abstract application deadline 15 October 1998. Contact: Mrs. Isabel Marcelo, Fundación Canaria de Investigación y Salud, c/o Franchy Roca, nº 1, 35008 Las Palmas de Gran Canaria, Spaine. telephone 00.34.928.49.86.28; fax 00.34.928.27.42.74; <abstract@globalink.org>. Information at <www.rcanaria.es/tobacco99.org>.
SRNT FIFTH ANNUAL MEETING, 5-7 March 1999, at the Sheraton Hotel, San Diego, California. Held in conjunction with the 20th Annual Meeting of the Society of Behavioral Medicine. Abstract submission deadline October 9. Abstract submissions should be returned to Joy Schmitz, Ph.D., 1300 Moursund Avenue, Houston, TX 77030. (Article on p. 9, contact information on p. 16.)
WORKSHOP ON STATE-OF-THE-ART SMOKING CESSATION INTERVENTIONS, 11-12 March 1999, University Place Conference Center, Indianapolis, Indiana. Sponsored by the Indiana University schools of Medicine and Dentistry and the Indiana University Nicotine Dependence Program. Contact (317) 274-8353 or (800) 622-4989.
RENEWALS...AGAIN?? Membership renewal applications will be coming your way in November. "So soon?" you ask. "Didn't I just get one a few months ago?" The answer is yes (although more than a year could have elapsed before continuing members got their last renewal notice). Because of circumstances beyond the control of the Membership Committee, membership renewals for 1998 were sent out much later than anticipated. The committee is putting new procedures in place to ensure that things will run more smoothly in future years. In the meantime, they want to keep renewals on schedule as much as possible. Therefore, they will ask for membership renewals in November 1998. New Membership Chair Lisa Brauer notes: "We realize that paying dues twice in one year might present a hardship for some of you. If this is the case, please contact me and we can make arrangements to ease the burden. We apologize for any inconvenience this may cause, but we feel strongly that keeping to our membership schedule will ease the transition with our new management company and will keep things running smoothly into the next year." (Contact information is on p. 16.)
NEW SRNT MEMBERSHIP DIRECTORIES will be mailed early this fall. The directories, which are being completely updated, will contain names, addresses, telephone and fax numbers, and e-mail addresses of the more than 400 SRNT members. Members will also be listed by state and country. Members whose contact information has recently changed should contact the SRNT Newsletter editor immediately (see publication information box, p. 2) to provide a current listing.
SO SOON? The SRNT Newsletter deadline for the November 1998 issue will be several weeks earlier than usual. Letters to the editor, articles, ideas, photographs, interviews, commentaries, compliments, and complaints are all welcome — by October 1.