Basic fibroblast growth factor and epidermal growth factor reverse impaired ulcer healing of the rabbit oral mucosa

BACKGROUND: The therapies for refractory ulcers on the oral mucosa are symptomatic and very unsatisfactory. We hypothesized that application of growth factors might be able to achieve successful remission of the lesion. We evaluated the effects of systemic administration and topical application of epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) on impaired wound healing of ulcers in the rabbit gingiva. METHODS: Almost uniform round ulcers could be created on the gingiva of the rabbits by chemical injury with acetic acid. When the submandibular glands were removed or i.v. injection of cisplatin (CDDP) and peplomycin sulfate was performed before ulcer formation, healing of the ulcers took longer than in untreated rabbits. To ascertain whether or not human EGF and bFGF affect rabbit cells, we first examined the effects of EGF and bFGF on the proliferation of the cells derived from rabbit gingiva. We then applied EGF or bFGF in these impaired healing models. RESULTS: EGF and bFGF promoted proliferation of the fibroblasts, and EGF also promoted proliferation of the keratinocytes isolated from gingival tissue of rabbits in vitro. Systemic injections of EGF and bFGF in rabbits, which had their submandibular glands removed, and topical application of bFGF accelerated healing of ulcers created in rabbits injected with CDDP and peplomycin sulfate. The ability of bFGF to promote the healing of ulcers was much greater than that of EGF. CONCLUSION: Basic FGF may be effective for refractory oral mucosal lesions.     

Intramuscular hypoperfusion, adrenergic receptors, and chronic muscle pain.

Despite a high prevalence of chronic muscle pain disorders such as fibromyalgia and regional myofascial pain, there is still limited knowledge about the factors that initiate and perpetuate these pain states. Although there are also likely to be downstream neuropathic changes in the central nervous system and spinal cord that sustain and exacerbate the pain states known as fibromyalgia, the focus of this critical review is on studies that examined the connection between both fibromyalgia and regional myofascial pain and sympathetic function. Specifically, we looked at studies that described Raynaud-like symptoms, cardiovascular dysfunction and altered intramuscular perfusion in chronic muscle pain. Our analysis showed that although the first 2 phenomena were intermittently present, a prominent and consistent feature for regional myofascial pain and to a lesser degree for fibromyalgia was intramuscular hypoperfusion. Several hypotheses can be offered why this hypoperfusion exists, and additional studies comparing and contrasting these theories are needed. This review focuses on one of these theories, namely, agonist-induced beta-adrenergic receptor desensitization as an explanatory model for hypoperfusion. What cannot be done at this time and is needed in the future is to compare and contrast to what degree the regional muscle pain disorder (myofascial) is similar or different from the more generalized disorder (fibromyalgia).     

Dopamine D-1 receptor-mediated inhibition of nucleus accumbens neurons from the ventral tegmental area.

1. Spike generation by stimulation of the parafascicular nucleus of thalamus was extracellularly recorded in the nucleus accumbens of chloral hydrate-anesthetized adult Wistar rats using a silver-wire microelectrode attached along a seven-barreled micropipette, each of which was filled with dopamine, SKF 38393 (D-1 agonist), bromocriptine (D-2 agonist), haloperidol, SCH 23390 (D-1 antagonist) and domperidone (D-2 antagonist). The drugs were microiontophoretically applied to the target neurons recorded. 2. Effects of dopamine receptor antagonists on the inhibition of the spike generation by conditioning stimuli applied to the ventral tegmental area preceding the test stimulus to the parafascicular nucleus and those of dopamine agonists on the test stimulus-induced spikes were examined. 3. The parafascicular nucleus stimulation-induced spikes were inhibited by dopamine as well as D-1 and D-2 agonists and by the conditioning stimulation of the ventral tegmental area. The conditioning stimulation-induced inhibition was antagonized by haloperidol and SCH 23390, but not by domperidone. 4. Activation of D-1 receptors, which make probably synaptic contact with dopaminergic nerve terminals from the ventral tegmental area, is considered to result in inhibition of the neuronal activity of the nucleus accumbens neurons receiving input from the parafascicular nucleus of the thalamus. In addition, D-2 receptors located extrajunctionally may be involved in the inhibition of the same neurons in the nucleus accumbens.     

The relationship between jaw deformity and scoliosis

Objectives To analyze the relationship between lateral displacement of the mandible and scoliosis. Methods From April 2002 through July 2003, we examined posteroanterior cephalometric radiographs and chest X-rays from 85 patients with jaw deformities and a control group of 20 patients with no jaw deformities. To measure the lateral shift of the mandible, we drew a horizontal baseline (X axis) on the cephalogram connecting the intersection of the external margins of the orbits and the most lateral points of the greater wings of the sphenoid. A vertical baseline (Y axis) was then marked perpendicular to the X axis, intersecting the ethmoid crista galli. Then, we measured the lateral displacement of the mandibular mentum from the Y axis. Displacement to the right was designated positive; that to the left was designated negative. Cobb's method was used to measure scoliosis curves on chest X-rays; the direction of the curve was designated similarly. Results Of the 85 patients with jaw deformity, 23 (27.1%) had a Cobb angle exceeding 10°. None of the control group had scoliosis exceeding 10°. No correlation was found between the direction of mandibular displacement and the direction of scoliosis. Conclusion This study suggests a relationship between jaw deformities and scoliosis, as scoliosis was found in 27.1% of the patients with a main complaint of jaw deformity.     

Minocycline attenuates hyperlocomotion and prepulse inhibition deficits in mice after administration of the NMDA receptor antagonist dizocilpine.

The present study was undertaken to examine whether the second generation antibiotic drug minocycline attenuates behavioral changes (eg, acute hyperlocomotion and prepulse inhibition (PPI) deficits) in mice after the administration of the N-methyl-D-aspartate (NMDA) receptor antagonist (+)-MK-801 (dizocilpine). Dizocilpine (0.1 mg/kg)-induced hyperlocomotion was significantly attenuated by pretreatment with minocycline (40 mg/kg). Furthermore, the PPI deficits after a single administration of dizocilpine (0.1 mg/kg) were attenuated by pretreatment with minocycline (10, 20, or 40 mg/kg), in a dose-dependent manner. Moreover, in vivo microdialysis study in the free-moving mice revealed that pretreatment with minocycline (40 mg/kg, i.p.) significantly attenuated the increase of extracellular dopamine (DA) levels in the frontal cortex and striatum after administration of dizocilpine (0.1 mg/kg), suggesting that the inhibition of dizocilpine-induced DA release by minocycline may, at least in part, be implicated in the mechanism of action of minocycline with respect to dizocilpine-induced behavioral changes in mice. These findings suggest that minocycline could attenuate behavioral changes in mice after the administration of the NMDA receptor antagonist dizocilpine. Therefore, it is possible that minocycline would be a potential therapeutic drug for schizophrenia.     

Urological emergency in neonates with congenital hydronephrosis

OBJECTIVE: It is well described that unilateral pelviureteric junction obstruction (PUJO) is a benign condition, because the dilatation resolves spontaneously and the function does not decrease in most of the kidneys. However, there is exceptional PUJO that requires emergent treatment in neonatal periods. The aim of this article is to report the urological emergency and management in neonates with PUJO. MATERIALS AND METHODS: Nine children (seven boys and two girls) with PUJO who underwent neonatal emergent treatment during the last 13 years were reviewed. Renal function was evaluated according to decay curve of serum creatinine (SCr) levels corresponding to gestational age (GA) at delivery. Physical examination, ultrasonographic monitoring, and chest and abdominal plain radiographs were repeated in each neonate. RESULTS: Eight patients were detected prenatally. In five patients, multicystic dysplastic kidney (MCDK) was demonstrated on the contralateral side. Three patients underwent percutaneous puncture of fetal hydronephrosis. Decrease of amniotic fluid was evident in three fetuses. Indications for emergent treatment included mass effect from hydronephrosis in three patients, renal dysfunction in five, and severe urinary tract infection in one. During neonatal periods, a percutaneous nephrostomy tube was placed in seven, and open nephrostomy in one with anorectal malformation. Repeated punctures of the dilated renal pelvis were done in one patient. Renal function after pyeloplasty was stable in eight patients, while it was moderately decreased in one who was associated with oligohydramnios in utero. CONCLUSION: Indications for emergent treatment in neonates with PUJO included mass effect from giant hydronephrosis, renal dysfunction and severe urinary tract infection. At birth, respiratory and circulatory conditions must first be stabilized. In neonates with hydronephrosis of the solitary kidney or severe bilateral PUJO, serial SCr should be monitored to evaluate renal function. Decrease of amniotic fluid suggested renal functional compromise that would not recover after urological management.