Associations between venous thromboembolism onset,D-dimer,and soluble fibrin monomer complex after total knee arthroplasty

Growth factors such as nerve growth factor (NGF) and insulin-like growth factor-1 (IGF-1) have been shown to play a role in the healing process of nerve injury. Recent researches have also shown that oxytocin administration activates these growth factors of importance for the healing of nerve tissue. The objective of the present study was to evaluate the effects of oxytocin on peripheral nerve regeneration in rats. Twenty-four male Sprague-Dawley rats were underwent transection damage model on the right sciatic nerve and defective damage model on the left sciatic nerve. The animals were assigned to one of two groups: control group or treatment group (received 80 mg/kg oxytocin intraperitoneally for 12 weeks). The sciatic nerve was examined, both functionally (on the basis of climbing platform test) and histologically (on the basis of axon count), 3, 6, 9, and 12 weeks after the injury. Also, stereomicroscopic and electrophysiological evaluations were carried out. Significantly greater improvements in electrophysiological recordings and improved functional outcome measures were presented in the treatment group at 12-week follow-up. Stereomicroscopic examinations disclosed prominent increases in vascularization on proximal cut edges in the oxytocin group in comparison with the control group. Higher axon counts were also found in this group. Intraperitoneal oxytocin administration resulted in accelerated functional, histological, and electrophysiological recovery after different sciatic injury models in rats.     

D-2 dopamine receptors inhibit release of aspartate and glutamate in rat retina.

Release of endogenous Asp, Glu and gamma-aminobutyric acid (GABA) has been investigated using synaptosomes prepared from rat retina. Exposure in superfusion to a depolarizing concentration of KCl (30 mM) evoked overflow of Asp and Glu, which were almost entirely Ca-dependent. However, 70% of the GABA release was Ca-independent. Dopamine (DA) almost completely inhibited the K(+)-evoked release of Asp and Glu in a concentration-dependent manner, but the release of GABA was only partly inhibited. The potencies of DA (IC50) to Asp and Glu release were 12 and 30 nM, respectively. A selective D-2 receptor antagonist, S-sulpiride, counteracted the DA-induced inhibition of Asp and Glu release, but a selective D-1 antagonist, SCH 23390, showed no effect. The data suggest that D-2 dopamine receptors located on the Asp and Glu neurons in rat retina may inhibit the release of these excitatory amino acids.     

Clonidine inhibition of potassium-evoked release of glutamate and aspartate from rat cortical synaptosomes

Release of endogenous glutamic acid (Glu), aspartic acid (Asp) and gamma-aminobutyric acid (GABA) has been investigated using synaptosomes prepared from rat cerebral cortex. Exposure in superfusion to a depolarizing concentration of KCl (30 mM) evoked 3-, 2- and 2-fold increases in Glu, Asp and GABA release, respectively. More than 70% of Glu and Asp overflow were calcium-dependent, although 67% of the GABA overflow was calcium-independent. Clonidine inhibited the K(+)-evoked overflow of Glu and Asp in a concentration-dependent manner, but the GABA overflow was not inhibited. Clonidine inhibited K(+)-evoked Glu and Asp overflow to 40 and 30% of the control with a potency (IC50) of 11 and 36 nM, respectively. Similarly, norepinephrine inhibited the K(+)-evoked overflow of Glu and Asp, although phenylephrine and isoproterenol showed no effect. Rauwolscine, yohimbine and idazoxan counteracted the effects of clonidine on Glu and Asp overflow. The data suggest that the depolarization-evoked overflow of excitatory amino acids is regulated in an inhibitory fashion by alpha 2 adrenoceptors, which are located on the nerve terminals of Glu and Asp neurons in rat cortex.     

Presynaptic inhibition by clonidine of neurotransmitter amino acid release in various brain regions.

The release of endogenous aspartic acid (Asp), glutamic acid (Glu) and gamma-aminobutyric acid (GABA) was investigated in synaptosomes prepared from various regions of the rat brain. The basal release of Asp, Glu and GABA from various regions was 12-35, 24-107 and 15-43 pmol/min per mg protein, respectively. Exposure to a depolarizing concentration of KCl (30 mM) resulted in 1.7 to 3.6-fold increases in Asp, Glu and GABA release. When clonidine (10(-4) M) was added to the perfusion medium, the K(+)-evoked overflow of both Asp and Glu was inhibited by 50-90% in the anterior cortex, thalamus and hypothalamus. Clonidine inhibited the K(+)-evoked Glu overflow by 30-40% in the posterior cortex and hippocampus. No significant effects were observed in the other brain regions (olfactory bulb, striatum, midbrain, cerebellum, pons, medulla oblongata). The inhibitory effects of clonidine were counteracted by an alpha 2-adrenoceptor antagonist, rauwolscine. The data suggest that the basal and K(+)-evoked release of Asp, Glu and GABA from nerve terminals is different in rat brain regions and that the presynaptic alpha 2-adrenoceptors which regulate the release of excitatory amino acids are mainly distributed in the anterior cerebral cortex, thalamus and hypothalamus of the rat brain.     

Studies of the humoral factors produced by layered chondrocyte sheets

The authors aimed to repair and regenerate articular cartilage with layered chondrocyte sheets, produced using temperature‐responsive culture dishes. The purpose of this study was to investigate the humoral factors produced by layered chondrocyte sheets. Articular chondrocytes and synovial cells were harvested during total knee arthroplasty. After co‐culture, the samples were divided into three groups: a monolayer, 7 day culture sheet group (group M); a triple‐layered, 7 day culture sheet group (group L); and a monolayer culture group with a cell count identical to that of group L (group C). The secretion of collagen type 1 (COL1), collagen type 2 (COL2), matrix metalloproteinase‐13 (MMP13), transforming growth factor‐β (TGFβ), melanoma inhibitory activity (MIA) and prostaglandin E2 (PGE2) were measured by enzyme‐linked immunosorbent assay (ELISA). Layered chondrocyte sheets produced the most humoral factors. PGE2 expression declined over time in group C but was significantly higher in groups M and L. TGFβ expression was low in group C but was significantly higher in groups M and L (p < 0.05). Our results suggest that the humoral factors produced by layered chondrocyte sheets may contribute to cartilaginous tissue repair and regeneration. Copyright © 2012 John Wiley & Sons, Ltd.