A report in 1984 on the success of zinc gluconate against common cold symptoms could not be confirmed in three subsequent studies, which are now known to have used formulations that inactivated zinc. A non-chelating formulation including glycine, which releases 93% of contained zinc into saliva, was tested in a randomized, placebo-controlled, double-blind trial in 73 young adults. Efficacy was recorded in symptom diaries using a symptom severity rating. Patients' symptoms first appeared 1.34 days prior to entry to the study in both groups. Disappearance of symptoms occurred after an additional 4.9 days for zinc-treated patients versus 6.1 days for placebo-treated patients. A difference was noted in the efficacy of treatment if it was started 1 day after symptom onset: cold duration was an additional 4.3 days in zinc-treated patients compared with 9.2 days for placebo-treated patients. Cough, nasal drainage and congestion were the symptoms most affected, and only mild side-effects were noted.

Four microsatellite loci have been characterised in Eucalyptus nitens Maiden and in six other eucalypt species. The dinucleotide repeats were identified by screening a Sau3AI genomic DNA library from E. nitens with (CA)n and (GA)n oligonucleotide probes and sequencing the positive clones. Genetic analysis of 20 unrelated individuals from five populations of E. nitens showed all loci to be highly polymorphic with an average of 9.5 alleles per locus and an average heterozygosity of 0.575. Analysis of four individuals from each of six species from three subgenera showed complete conservation of microsatellite loci between species within the same subgenus, Symphyomyrtus, and conservation of 50% of loci across species between the two main subgenera, Symphyomyrtus and Monocalyptus. None of the primers amplified microsatellite loci in Eucalyptus maculata from the subgenus Corymbia. All microsatellite loci that were detected were polymorphic. Highly polymorphic microsatellite loci that are conserved across species will be useful for mapping quantitative traits, fingerprinting breeding lines, and for within-population studies requiring fine-scale analysis of genetic variation.

Zinc is a trace metal with in vitro activity against rhinovirus, the major etiologic agent in acute upper respiratory tract infections (URIs). A previous trial of zinc gluconate supported its efficacy in treating URIs, but the effectiveness of blinding was uncertain. We conducted a prospective randomized trial of zinc gluconate versus a taste-matched placebo of sucrose octaacetate. Lozenges containing either 23 mg of elemental zinc or placebo were taken every 2 h. Eleven URI symptoms were rated daily on a scale of 0 (not present) to 3 (severe). Duration of illness, reflected in the proportion of subjects remaining symptomatic on each day, was not significantly reduced (maximum difference of 12.6% on day 7, P = 0.09; 95% confidence interval, -6 to 31%) by either treatment. Severity of illness, assessed by using a summed severity score, was reduced incrementally by 7 to 8% on days 5 to 7 (P = 0.02) in subjects taking zinc. Adverse effects, mostly nausea and altered taste, were reported by 50% of subjects taking zinc. We conclude that while zinc gluconate may produce a small reduction in overall severity of symptoms, this is not clinically significant. Given the additional high incidence of adverse effects, zinc gluconate cannot be recommended for use in the treatment of acute URIs.

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Diabetic gastroparesis is a common and debilitating condition affecting millions of patients with diabetes mellitus worldwide. Although gastroparesis in diabetes has been known clinically for more than 50 years, treatment options remain very limited. Until recently, the scientific literature has offered few clues regarding the precise aetiology of gastric dysfunction in diabetes.Up to 50% of patients with diabetes may experience postprandial abdominal pain, nausea, vomiting and bloating secondary to gastric dysfunction. There is no clear association between length of disease and the onset of delayed gastric emptying. Gastroparesis affects both type 1 (insulin dependent) and type 2 (non- insulin dependent) forms of diabetes. Diagnosis requires identifying the proper symptom complex, while excluding other entities (peptic ulcer disease, rheumatological diseases, medication effects). The diagnosis of gastroparesis may be confirmed by demonstrating gastric emptying delay during a 4-hour scintigraphic study. Treatment options are limited and rely on dietary modifications, judicious use of available pharmacological agents, and occasionally surgical or endoscopic placement of gastrostomies or jejunostomies. Gastric pacing offers promise for patients with medically refractory gastroparesis but awaits further investigation. Current pharmacological agents for treating gastroparesis include metoclopramide, erythromycin, cisapride (only available via a company-sponsored programme) and domperidone (not US FDA approved). All of these drugs act as promotility agents that increase the number or the intensity of gastric contractions. These medications are not uniformly effective and all have adverse effects that limit their use. Cisapride has been removed from the open market as a result of over 200 reported cases of cardiac toxicity attributed to its use. Unfortunately, there is a paucity of clinical studies that clearly define the efficacy of these agents in diabetic gastroparesis and there are no studies that compare these drugs to each other. The molecular pathophysiology of diabetic gastroparesis is unknown, limiting the development of rational therapies. New studies, primarily in animals, point to a defect in the enteric nervous system as a major molecular cause of abnormal gastric motility in diabetes. This defect is characterised by a loss of nitric oxide signals from nerves to muscles in the gut resulting in delayed gastric emptying. Novel therapies designed to augment nitric oxide signalling are being studied.

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We have proposed that tissue metabolic failure during hypoxia or ischemia is related to the microheterogeneous distribution of tissue oxygen and not to failure of the creatine kinase equilibrium. This theory is based on the concept that sharp oxygen gradients exist in rapidly metabolizing tissue and that shifts in these gradients can place specific cells at risk for metabolic death while relatively adjacent cells escape unharmed; cells that are unharmed meet the steady-state requirements (V less than Vmax), those at risk do not (V greater than Vmax). Though it would seem that confirmation of such a hypothesis would require metabolic delineation at a high resolution, we have shown how 31P MRS provides information supporting this hypothesis. This possible use of MR spectroscopy to define microheterogeneous events suggests further clinical possibilities for this instrument in defining the rate of cell loss and the response to therapeutic interventions.