Temporal changes in the physical properties of healing fractures in rabbits

Temporal changes in the physical properties of healing fractures in rabbits were studied. The mechanical environment at the fracture site was measured and monitored during healing. Animals were sacrificed after 3 to 8 weeks. The results of healing were quantified by whole bone dynamic torsional strength tests. Torque-angle curves were recorded by computer. At maximum torque four parameters were calculated: torque, angle, energy absorbed and stiffness. Torque and stiffness increased while energy remained constant and angle decreased with time. However, values calculated by a constant deformation criteria showed the three strength parameters to increase with time. The rate of increase was highest for stiffness followed by torque and energy.     

Prostaglandin release by spinal cord injury mediates production of hydroxyl radical, malondialdehyde and cell death: a site of the neuroprotective action of methylprednisolone

The present study explores in vivo whether and how prostaglandin F(2alpha) (PGF(2alpha)), a membrane phospholipid hydrolysis product, causes neuronal death. The concentration of PGF(2alpha) measured by microdialysis sampling increased threefold immediately following impact injury to the rat spinal cord. Administration of PGF(2alpha) into the cord through a dialysis fiber caused significant cell loss, increased extracellular levels of hydroxyl radicals and malondialdehyde - an end product of membrane lipid peroxidation - to 3.3 and 2.3 times basal levels, respectively. This suggests that PGF(2alpha)-induced cell death is partly due to hydroxyl radical-triggered peroxidation. Generating hydroxyl radical by administering Fenton's reagents into the cord through the fibers significantly increased malondialdehyde production - the first direct in vivo evidence that hydroxyl radical triggers membrane lipid peroxidation. Methylprednisolone significantly reduced the release of PGF(2alpha) upon spinal cord injury and blocked PGF(2alpha)-induced hydroxyl radical and malondialdehyde production, but did not significantly reduce Fenton's reagent-induced malondialdehyde production, despite the production of more malondialdehyde by PGF(2alpha). This suggests that methylprednisolone may not directly scavenge hydroxyl radical, and that its 'antioxidant' effect is a consequence of blocking the pathways for producing toxic PGF(2alpha) and for PGF(2alpha)-induced hydroxyl radical formation, thereby reducing membrane lipid peroxidation.     

Perfusion of hearts with triglyceride-rich particles reproduces the metabolic abnormalities in lipotoxic cardiomyopathy

Hearts with overexpression of anchored lipoprotein lipase (LpL) by cardiomyocytes (hLpL(GPI) mice) develop a lipotoxic cardiomyopathy. To characterize cardiac fatty acid (FA) and triglyceride (TG) metabolism in these mice and to determine whether changes in lipid metabolism precede cardiac dysfunction, hearts from young mice were perfused in Langendorff mode with [14C]palmitate. In hLpL(GPI) hearts, FA uptake and oxidation were decreased by 59 and 82%, respectively. This suggests reliance on an alternative energy source, such as TG. Indeed, these hearts oxidized 88% more TG. Hearts from young hLpL(GPI) mice also had greater uptake of intravenously injected cholesteryl ester-labeled Intralipid and VLDL. To determine whether perfusion of normal hearts would mimic the metabolic alterations found in hLpL(GPI) mouse hearts, wild-type hearts were perfused with [14C]palmitate and either human VLDL or Intralipid (0.4 mM TG). Both sources of TG reduced [14C]palmitate uptake (48% with VLDL and 45% with Intralipid) and FA oxidation (71% with VLDL and 65% with Intralipid). Addition of either heparin or LpL inhibitor P407 to Intralipid-containing perfusate restored [14C]palmitate uptake and confirmed that Intralipid inhibition requires local LpL. Our data demonstrate that reduced FA uptake and oxidation occur before mechanical dysfunction in hLpL(GPI) lipotoxicity. This physiology is reproduced with perfusion of hearts with TG-containing particles. Together, the results demonstrate that cardiac uptake of TG-derived FA reduces utilization of albumin-FA.     

Reproductive life history of South African cheetahs (Acynonyx jubatus jubatus) at the San Diego Zoo Wild Animal Park, 1970–2005

We analyzed 35 years of data from a captive breeding program of cheetahs to determine basic reproductive life history characteristics of females. Breeding females ranged in age from 2.7–10.5 years. Sixteen females and over 13 males produced 129 cubs in 36 litters, with an average litter size of 3.6. Older females produced significantly fewer cubs per litter than younger females, but cub survivorship was comparable across female ages. Sex ratio was balanced at birth and 71% of infants survived the weaning period. Given that the reproductive output of captive cheetahs in our study is similar to that in other zoologic institutions and to cheetahs in the wild, we suggest that reproductive deficits in captive cheetahs arise from the inability of some pairs to breed, due to a lack of mating preference, rather than from a species‐wide problem. Zoo Biol 0:1–8, 2006. © 2006 Wiley‐Liss, Inc.     

MYASTHENIA GRAVIS—Problems in Diagnosis

The possibility of myasthenia gravis must be considered in patients persistently complaining of weakness and fatigue. There may be many difficulties and pitfalls in differentiating myasthenia gravis from other disorders in which muscular weakness is a common complaint.Observation of a group of 36 patients with myasthenia gravis, and another group of 30 cases involving the differential diagnosis of myasthenia gravis, led to a conclusion that a physician should apply criteria carefully before arriving at a diagnosis of myasthenia gravis and instituting drug therapy, since nonmyasthenics may frequently respond with subjective improvement temporarily following administration of cholinergic drugs.Myasthenia gravis may be a more common disorder than was suspected in the past.