Recruiting "Friends of Medical Progress": Evolving Tactics in the Defense of Animal Experimentation, 1910s and 1920s.

In 1923, Thomas Barbour of Harvard announced the creation of a national lay organization, the Society of Friends of Medical Progress (FMP), to defend animal research in the United States against a resurgent antivivisection movement. After decades of successful behind-the-scenes lobbying and avoiding the public spotlight, medical scientists significantly altered their tactics and sought public engagement, at least by proxy. Although the authority of scientific medicine was rising, women's suffrage, the advent of the ballot initiative, and a growing alliance of antivivisectionists and other groups in opposition to allopathic medicine so altered the political landscape that medical scientists reconsidered formerly rejected ideas such partnering with laymen. Medical scientists, Walter B. Cannon and Simon Flexner chief among them, hoped that the FMP would relieve the scientists of a time-consuming burden and defend against government regulation of medical institutions without the charge of material self-interest. However, financial problems and the frequent conflicts that arose between the lay leadership and Flexner eventually undermined the FMP's value as a defender of animal experimentation and reveal the distrust of reformers like Flexner who did not believe that laymen could speak for scientific medicine.

Exercise training does not correct abnormal cardiac glycogen accumulation in the db/db mouse model of type 2 diabetes.

Substrate imbalance is a well-recognized feature of diabetic cardiomyopathy. Insulin resistance effectively limits carbohydrate oxidation, resulting in abnormal cardiac glycogen accumulation. Aims of the present study were to 1) characterize the role of glycogen-associated proteins involved in excessive glycogen accumulation in type 2 diabetic hearts and 2) determine if exercise training can attenuate abnormal cardiac glycogen accumulation. Control (db(+)) and genetically diabetic (db/db) C57BL/KsJ-lepr(db)/lepr(db) mice were subjected to sedentary or treadmill exercise regimens. Exercise training consisted of high-intensity/short-duration (10 days) and low-intensity/long-duration (6 wk) protocols. Glycogen levels were elevated by 35-50% in db/db hearts. Exercise training further increased (2- to 3-fold) glycogen levels in db/db hearts. Analysis of soluble and insoluble glycogen pools revealed no differential accumulation of one glycogen subspecies. Phosphorylation (Ser(640)) of glycogen synthase, an indicator of enzymatic fractional activity, was greater in db/db mice subjected to sedentary and exercise regimens. Elevated glycogen levels were accompanied by decreased phosphorylation (Thr(172)) of 5'-AMP-activated kinase and phosphorylation (Ser(79)) of its downstream substrate acetyl-CoA carboxylase. Glycogen concentration was not associated with increases in other glycogen-associated proteins, including malin and laforin. Novel observations show that exercise training does not correct diabetes-induced elevations in cardiac glycogen but, rather, precipitates further accumulation.

Fiber atrophy and hypertrophy in skeletal muscles of late middle-aged Fischer 344 x Brown Norway F1-hybrid rats.

We examined young adult and late middle-aged male rats to test the hypothesis that gastrocnemius (a locomotor muscle) demonstrates reduced fiber size with aging, whereas soleus (a postural muscle) demonstrates atrophy of some fibers and compensatory hypertrophy in other fibers. Although body mass was greater in late middle-aged animals, mass was reduced in gastrocnemius but not soleus muscle. In another group of animals, physical activity was reduced by 34% in late middle-aged animals. Whereas mean fiber size was lower in gastrocnemius of late middle-aged animals, it was not different in soleus. Histograms revealed atrophied fibers (/=8000 micro m(2)) in soleus with aging. Atrophied fibers often demonstrated no subsarcolemmal mitochondrial staining, suggesting denervation, whereas hypertrophied fibers often demonstrated cytochrome oxidase deficiency, suggesting mitochondrial dysfunction. These results underscore the divergent influences (e.g., physical inactivity, denervation, mitochondrial dysfunction) affecting fiber size with aging.