No abstract

Recent research indicates that areas of the primary somatosensory (SI) and primary motor cortex show massive cortical reorganization after amputation of the upper arm, forearm or fingers. Most of these studies were carried out months or several years after amputation. In the present study, we describe cortical reorganization of areas in the SI of a patient who underwent amputation of the traumatized middle and ring fingers of his right hand 10 days before cortical magnetic source imaging data were obtained. Somatosensory-evoked magnetic fields (SEF) to mechanical stimuli to the finger tips were recorded and single moving dipoles were calculated using a realistic volume conductor model. Results reveal that the dipoles representing the second and fifth fingers of the affected hand were closer together than the comparable dipoles of the unaffected hand. Our findings demonstrate that neural cell assemblies in SI which formerly represented the right middle and ring fingers of this amputee became reorganized and invaded by neighbouring cell assemblies of the index and little finger of the same hand. These results indicate that functional plasticity occurs within a period of 10 days after amputation.

The effects of GH and PTH on cancellous histomorphometry were determined in the proximal tibial metaphysis of hypophysectomized (HYPOX) sexually mature female rats. HYPOX resulted in uterine atrophy and a loss in body weight. Longitudinal bone growth ceased and bone formation was greatly reduced. There were decreases in cancellous bone area, trabecular number, and trabecular thickness. Intermittent treatment with GH did not influence uterine weight in HYPOX rats. However, GH resulted in resumption of whole body weight gain, as well as maintenance of normal longitudinal bone growth. Additionally, GH partially maintained bone formation in HY POX rats and did not have a significant effect on steady state messenger RNA levels for osteocalcin. Intermittent treatment with PTH had no effect on whole body weight gain, uterine weight, or longitudinal bone growth. In contrast, PTH increased bone formation compared with the baseline, HYPOX, and GH-treated HYPOX rats, and dramatically increased osteocalcin messenger RNA levels compared with the latter two groups. The increased bone formation was primarily due to an increase in osteoblast number; the mineral apposition rate, an index of osteoblast activity, was increased compared with control and GH-treated rats but not compared with baseline values. Interestingly, neither treatment influenced indices of bone resorption.

No abstract

The present study was performed to evaluate possible interactions between estrogen and progesterone on peak cancellous bone mass. Ovariectomized (OVX) growing rats were treated with 17beta-estradiol (4.8 microg/day), progesterone (4.8 mg/day), a combination of the two sex steroids, or with vehicle for 14 days beginning 7 days after OVX. The tibiae were removed for histomorphometric analysis of the proximal metaphysis. OVX and growth each resulted in net resorption of cancellous bone at a sampling site adjusted for longitudinal bone growth. Estradiol and progesterone treatment each antagonized bone loss by inhibiting the decrease in trabecular number. Estradiol increased but progesterone had no effect on trabecular thickness. Progesterone did not influence either osteoclast number or the resorption of the pretreatment fluorochrome label. Estradiol reduced osteoclast number and inhibited label resorption, the latter change being accentuated by combination treatment. Estradiol reduced and progesterone enhanced the mineral apposition and bone formation rates. The results indicate that estradiol and progesterone have independent activities on cancellous bone turnover during growth. Whereas estradiol reduced bone turnover, progesterone had a stimulatory effect on bone formation. These findings suggest that progesterone has a role in establishing and maintaining peak cancellous bone volume during growth.