Exercise training alters endothelium-dependent vasoreactivity of rat abdominal aorta

We tested the hypothesis that adaptations in peripheral arterial vasoreactivity are induced by exercise training. Male rats were trained to run on a treadmill at 30 m/min (15 degrees incline) for 1 h/day 5 days/wk for 10-12 wk. Efficacy was indicated by a 51% increase (P < 0.05) in citrate synthase activity in soleus muscle of exercise-trained (ET) rats compared with that of sedentary (SED) control rats. Responses to vasoactive compounds were examined in vitro using rings of abdominal aorta. Maximal isometric contractile tension evoked by KCl, norepinephrine (NE), and phenylephrine were not different between groups; sensitivity to phenylephrine was also not different between groups. However, sensitivity was lower for both KCl and NE in vessels from ET animals. Endothelium removal did not influence KCl sensitivity but did abolish the difference in NE sensitivity of vessel segments between ET and SED animals. Maximal vasodilator responses induced by acetylcholine (ACh; NE or prostaglandin F2 alpha preconstriction) were greater in vessel rings from ET rats. However, dilatory responses by sodium nitroprusside (NE or prostaglandin F2 alpha preconstriction) and forskolin (NE preconstriction) were not different between groups, indicating that the augmented ACh-induced dilatory response resulted from an adaptation of the endothelium. Blockade of nitric oxide synthase activity diminished ACh-induced vasodilation by 79 and 100% in SED and ET rats, respectively. These results indicate that training alters vasomotor function in rat abdominal aortas through adaptations of both endothelium and smooth muscle.     

Maxillary sinus augmentation in the non-human primate: a comparative radiographic and histologic study between recombinant human osteogenic protein-1 and natural bone mineral

The posterior maxilla has traditionally been one of the most difficult areas to successfully place dental implants due to poor bone quality and close approximation to the maxillary sinus. Sinus augmentation procedures have become a viable means of assuring adequate bone for the placement of dental implants in this area. However, with the techniques currently employed, a considerable variation in the quality of bone attained with the sinus augmentation procedure exists. The purpose of this in vivo study was to evaluate the healing response and bone formation stimulated by 3 doses of recombinant human osteogenic protein-1 (rhOP-1), 0.25, 0.6, and 2.5 mg OP-1 per gram of collagen matrix; natural bone mineral; or collagen matrix alone (control) placed in the maxillary sinus of adult chimpanzees. Results were assessed using clinical, histologic, and radiographic techniques. Radiographic analysis of the computed tomography scans taken at 1 week, and 2.5, 4.5, and 6.5 months revealed a more rapid mineralization with the 2.5 mg OP-1/g collagen matrix and natural bone mineral treatment groups. The incremental bone mineral density (BMD) increase for these 2 treatments from 1 week to 2.5 months was over 2.5 times the increase found with the collagen matrix alone; these 2 treatments also had a higher BMD at the most superior slices evaluated when compared to the other 3 groups. Biopsy specimens were taken at 3.5, 5.5, and 7.5 months and for all 5 treatment groups bone formation was observed at all time points in the majority of the specimens. At 7.5 months the 2.5 and 0.6 mg OP-1/g collagen matrix treatment groups had an increase in the percent bone area when compared to the matrix alone control. In conclusion, these results demonstrate that sinus augmentation with natural bone mineral or 2.5 mg OP-1/g collagen matrix induce comparable radiographic and histologic evidence of bone formation and that both of these treatments performed superior to the control group of collagen matrix alone based upon all methods of evaluation.     

DNA methylation and developmental genes in lymphomagenesis--more questions than answers?

There is now considerable evidence suggesting that alterations in the DNA methylating machinery play an important role in tumorigenesis and tumour progression. For example, focal hypermethylation and generalised genomic demethylation are features of many different types of neoplasms. It is thought that tumorigenesis and tumour progression may be caused by hypermethylation induced mutational events and silencing of genes which control cellular proliferation and/or demethylation induced reactivation of genes which may only be required during embryological development. Consequently, we have begun to investigate the role of DNA methylation and developmental genes in malignant lymphoproliferative diseases. Previously, in all cases of non-Hodgkins lymphoma and leukemia studied, we have shown that the myogenic developmental gene Myf-3 is abnormally hypermethylated. In this review we discuss the possible significance of these findings since in vitro studies suggest that Myf-3 may play an important role in control of the cell cycle and therefore lymphomagenesis. In vitro and in vivo evidence suggests that PAX genes may also have oncogenic potential. The PAX family of developmental genes are involved in cellular differentiation, proliferation and cell migration. Expression of PAX3 in particular is associated with cellular mobility. Our previous studies have indicated that alternate regional expression of PAX genes may be controlled by DNA methylation. Therefore, we have proposed that abnormal methylation profiles of PAX3 may be associated with neoplastic transformation and/or metastatic potential. Results thus far reveal that the paired box of PAX3 is abnormally hypermethylated and the homeobox abnormally hypomethylated in lymphomas and leukemias. These new findings are consistent with our postulate and support the idea that inappropriate methylation induced activation or inactivation of developmental genes such as Myf-3 and PAX3 play an important role in lymphomagenesis and disease progression and that inspection of the methylation status of other developmental genes is warranted.     

Effects of four maintenance programs on the long-term management of obesity.

This study evaluated the effectiveness of four posttreatment programs designed to enhance the long-term maintenance of weight loss. Mildly and moderately obese adults (N?=?123) were randomly assigned to one of the following five conditions: (a) behavior therapy only; (b) behavior therapy plus a posttreatment therapist-contact maintenance program; (c) behavior therapy plus posttreatment therapist contact plus a social influence maintenance program; (d) behavior therapy plus posttreatment therapist contact plus an aerobic exercise maintenance program; or (e) behavior therapy plus posttreatment therapist contact plus both the aerobic exercise and social influence maintenance programs. All posttreatment programs were conducted in 26 biweekly sessions during the year following behavioral treatment for obesity. At an 18-month follow-up evaluation, all four conditions that combined behavior therapy with a posttreatment maintenance program yielded significantly greater long-term weight losses than behavior therapy alone. (PsycINFO Database Record (c) 2010 APA, all rights reserved)