The basic formulation of Al2O3- C slide plates was65%（ in mass,the same hereinafter） white fused corundum particles,25% white fused corundum fines,6% active α-Al2O3 micropowder,4% carbon black and flake graphite, a...The basic formulation of Al2O3- C slide plates was65%（ in mass,the same hereinafter） white fused corundum particles,25% white fused corundum fines,6% active α-Al2O3 micropowder,4% carbon black and flake graphite, and additional 4% phenolic resin.Based on this formulation,3% Al powder,3% Si powder,and 3% Al ＋ 3% Si powder were used to substitute equivalent white corundum fines to improve the hot mechanical properties of Al2O3- C slide plates. The specimens with dimensions of 140 mm × 25 mm × 25 mm were pressed at 150 MPa,dried at 200 ℃ for 24 h,and hot treated at 1 400 ℃ for 3 h in carbon embedded condition. Then hot modulus of rupture and thermal shock resistance of the specimens were tested and the phase compositions and microstructure were analyzed. The results show that specimen with 3% Al powder has the higher hot modulus of rupture but lower residual modulus of rupture after thermal shock than the specimen with3% Si powder; the specimen with 3% Al ＋ 3% Si powders exhibits the highest hot modulus of rupture and the best thermal shock resistance; the change of mechanical property is closely related with the in-situ formed nonoxides： AlN in the form of bars is formed in specimens with Al powder; fibrous SiC whiskers are formed in specimens with Si powder; in the specimens with both Al and Sipowders,besides AlN and SiC whiskers,hexagonal tabular SiAlON is in-situ synthesized,which interlocks with each other.展开更多
Pain is a sensation related to potential or actual damage in some tissue of the body. The mainstay of medical pain therapy remains drugs that have been around for decades, like non-steroidal anti-inflammatory drugs （...Pain is a sensation related to potential or actual damage in some tissue of the body. The mainstay of medical pain therapy remains drugs that have been around for decades, like non-steroidal anti-inflammatory drugs （NSAIDs）, or opiates. However, adverse effects of opiates, particularly tolerance, limit their clinical use. Several lines of investigations have shown that systemic （intraperitoneal） administration of NSAIDs induces antinociception with some effects of tolerance. In this review, we report that repeated microinjection of NSAIDs analgin, clodifen, ketorolac and xefocam into the central nucleus of amygdala, the midbrain periaqueductal grey matter and nucleus raphe magnus in the following 4 days result in progressively less antinociception compared to the saline control testing in the tail-flick reflex and hot plate latency tests. Hence, tolerance develops to these drugs and cross-tolerance to morphine in male rats. These findings strongly support the suggestion of endogenous opioid involvement in NSAIDs antinociception and tolerance in the descending pain-control system. Moreover, the periaqueductal grey-rostral ventro-medial part of medulla circuit should be viewed as a pain-modulation system. These data are important for human medicine. In particular, cross-tolerance between non-opioid and opioid analgesics should be important in the clinical setting.展开更多
Corticotropin-releasing factor (CRF) is a peptide that is released from the hypothalamus into widespread areas of the brain. Evidence has suggested that CRF is involved as a neuromodulator outside of the hypothalamic-...Corticotropin-releasing factor (CRF) is a peptide that is released from the hypothalamus into widespread areas of the brain. Evidence has suggested that CRF is involved as a neuromodulator outside of the hypothalamic-pituitary-adrenal axis, playing an important role in fear, anxiety, depression and pain modulation. Our previous report demonstrated that CRF receptor activation in basolateral (BLA) or central nuclei of the amygdala (CeA) produces innate fear in guinea pigs. Inhibition of these receptors via administration of α-helical CRF9-41 (a nonspecific antagonist) into the CeA or BLA decreased innate fear behavior [1]. Additionally, there is strong evidence that emotional behavior and nociception can be modulated simultaneously. The present study was conducted to investigate the involvement of the CRF receptors of the BLA or CeA in nociception in guinea pigs. Guinea pigs were treated with CRF and α-helical CRF>9-41> in three different doses or injected with α-helical CRF9-41 preceded by CRF into the BLA or CeA, and they were evaluated using the hot plate test. Our findings indicated that activation of CRF receptors in the BLA and in the CeA promoted antinociception, and this effect was reversed by preadministration of α-helical CRF9-41 in the same area. The treatment with α-helical CRF>9-41> per se into the BLA and CeA did not alter nociception. Thus, nociception modulation occurs in a phasic manner, whereas defensive behavior can occur tonically because the α-helical CRF9-41 did not cause any modification on the index of analgesia in the hot plate test but did reduce innate fear behavior [1].展开更多
目的观察丙泊酚在vlPAG对大鼠伤害性感受的影响及GABAA受体在其中可能的作用。方法Sprague-Daw ley(SD)♀大鼠随机分组,丙泊酚(Propofol,Pro)和荷包牡丹碱(B icucu lline,B ic)采用中脑导水管周围灰质腹外侧区(ven-trolateral portion o...目的观察丙泊酚在vlPAG对大鼠伤害性感受的影响及GABAA受体在其中可能的作用。方法Sprague-Daw ley(SD)♀大鼠随机分组,丙泊酚(Propofol,Pro)和荷包牡丹碱(B icucu lline,B ic)采用中脑导水管周围灰质腹外侧区(ven-trolateral portion of the PAG,vlPAG)注射。行为学实验采用热板法和福尔马林实验,分别以舔后爪潜伏时间(Hot-p latelatency,HPL)和疼痛(累计)评分为指标。免疫组化方法观察丙泊酚在vlPAG对福尔马林单侧足底皮下注射诱发的脊髓背角Fos蛋白表达的影响。结果行为学部分:两种疼痛模型中丙泊酚(10 g.L-1)vlPAG注射引起痛敏(P<0.01)。热板法实验中,丙泊酚vlPAG微量注射的痛敏作用可被相同部位预先注射25 mg.L-1B ic在10和20 m in时间点分别拮抗70%和71%(均P<0.01),在30和40 m in完全拮抗。在福尔马林实验中,丙泊酚vlPAG微量注射使福尔马林疼痛评分增加,此作用可被B ic(25 mg.L-1)在60 m in拮抗57%(P<0.05)。免疫组化部分中,丙泊酚vlPAG微量注射使福尔马林引起的脊髓背角各层FLI阳性细胞数明显增多(P<0.01),B ic vlPAG微量注射(25 mg.L-1)可部分拮抗丙泊酚vlPAG微量注射的作用(P<0.01)。结论在大鼠vlPAG微量注射丙泊酚能产生痛敏作用;GABAA受体部分介导了丙泊酚的以上作用。展开更多
目的观察不同剂量咪达唑仑对氯胺酮镇痛效应的影响,为临床合理配伍使用药物提供依据。方法腹腔注射25 mg/kg氯胺酮建立镇痛模型,150只小鼠均分为NS组、M组、K组、M1K组和M2K组,采用甩尾法、热板法和扭体法(n=10)分别观察腹腔注射1、2 mg...目的观察不同剂量咪达唑仑对氯胺酮镇痛效应的影响,为临床合理配伍使用药物提供依据。方法腹腔注射25 mg/kg氯胺酮建立镇痛模型,150只小鼠均分为NS组、M组、K组、M1K组和M2K组,采用甩尾法、热板法和扭体法(n=10)分别观察腹腔注射1、2 mg/kg咪达唑仑对氯胺酮镇痛小鼠甩尾潜伏期(TFL)、热板法痛阈(HPPT)和扭体次数(WTs)的影响。结果给药后5、10、15、20 min K组TEL、HPPT延长(P<0.05);各时点M组小鼠TFL、HPPT均无明显变化;M1K组和M2K组给药后10、15、20 min TFL、HPPT延长,给药后15 min M1K组和M2K组TEL、HPPT明显长于K组(P<0.05或P<0.01)。给药后15 min内K、M1K和M2K组小鼠WTs明显少于NS组(P<0.01)。但K、M1K和M2K组间差异无统计学意义(P<0.05或P<0.01)。结论一定剂量的咪达唑仑可以增强氯胺酮的体表镇痛作用。展开更多
文摘The basic formulation of Al2O3- C slide plates was65%（ in mass,the same hereinafter） white fused corundum particles,25% white fused corundum fines,6% active α-Al2O3 micropowder,4% carbon black and flake graphite, and additional 4% phenolic resin.Based on this formulation,3% Al powder,3% Si powder,and 3% Al ＋ 3% Si powder were used to substitute equivalent white corundum fines to improve the hot mechanical properties of Al2O3- C slide plates. The specimens with dimensions of 140 mm × 25 mm × 25 mm were pressed at 150 MPa,dried at 200 ℃ for 24 h,and hot treated at 1 400 ℃ for 3 h in carbon embedded condition. Then hot modulus of rupture and thermal shock resistance of the specimens were tested and the phase compositions and microstructure were analyzed. The results show that specimen with 3% Al powder has the higher hot modulus of rupture but lower residual modulus of rupture after thermal shock than the specimen with3% Si powder; the specimen with 3% Al ＋ 3% Si powders exhibits the highest hot modulus of rupture and the best thermal shock resistance; the change of mechanical property is closely related with the in-situ formed nonoxides： AlN in the form of bars is formed in specimens with Al powder; fibrous SiC whiskers are formed in specimens with Si powder; in the specimens with both Al and Sipowders,besides AlN and SiC whiskers,hexagonal tabular SiAlON is in-situ synthesized,which interlocks with each other.
基金supported by the grant from Georgian National Science Foundation,No.GNSF/ST07/6-234
文摘Pain is a sensation related to potential or actual damage in some tissue of the body. The mainstay of medical pain therapy remains drugs that have been around for decades, like non-steroidal anti-inflammatory drugs （NSAIDs）, or opiates. However, adverse effects of opiates, particularly tolerance, limit their clinical use. Several lines of investigations have shown that systemic （intraperitoneal） administration of NSAIDs induces antinociception with some effects of tolerance. In this review, we report that repeated microinjection of NSAIDs analgin, clodifen, ketorolac and xefocam into the central nucleus of amygdala, the midbrain periaqueductal grey matter and nucleus raphe magnus in the following 4 days result in progressively less antinociception compared to the saline control testing in the tail-flick reflex and hot plate latency tests. Hence, tolerance develops to these drugs and cross-tolerance to morphine in male rats. These findings strongly support the suggestion of endogenous opioid involvement in NSAIDs antinociception and tolerance in the descending pain-control system. Moreover, the periaqueductal grey-rostral ventro-medial part of medulla circuit should be viewed as a pain-modulation system. These data are important for human medicine. In particular, cross-tolerance between non-opioid and opioid analgesics should be important in the clinical setting.
基金supported by CAPES/PROEX,FAPESP(2010/10936-5)A.F.Donatti has a doctorate scholarship from CAPESC.R.A.Leite-Panissi also received grants from the CNPq(Grant No.307383/2012-1).
文摘Corticotropin-releasing factor (CRF) is a peptide that is released from the hypothalamus into widespread areas of the brain. Evidence has suggested that CRF is involved as a neuromodulator outside of the hypothalamic-pituitary-adrenal axis, playing an important role in fear, anxiety, depression and pain modulation. Our previous report demonstrated that CRF receptor activation in basolateral (BLA) or central nuclei of the amygdala (CeA) produces innate fear in guinea pigs. Inhibition of these receptors via administration of α-helical CRF9-41 (a nonspecific antagonist) into the CeA or BLA decreased innate fear behavior [1]. Additionally, there is strong evidence that emotional behavior and nociception can be modulated simultaneously. The present study was conducted to investigate the involvement of the CRF receptors of the BLA or CeA in nociception in guinea pigs. Guinea pigs were treated with CRF and α-helical CRF>9-41> in three different doses or injected with α-helical CRF9-41 preceded by CRF into the BLA or CeA, and they were evaluated using the hot plate test. Our findings indicated that activation of CRF receptors in the BLA and in the CeA promoted antinociception, and this effect was reversed by preadministration of α-helical CRF9-41 in the same area. The treatment with α-helical CRF>9-41> per se into the BLA and CeA did not alter nociception. Thus, nociception modulation occurs in a phasic manner, whereas defensive behavior can occur tonically because the α-helical CRF9-41 did not cause any modification on the index of analgesia in the hot plate test but did reduce innate fear behavior [1].
文摘目的观察丙泊酚在vlPAG对大鼠伤害性感受的影响及GABAA受体在其中可能的作用。方法Sprague-Daw ley(SD)♀大鼠随机分组,丙泊酚(Propofol,Pro)和荷包牡丹碱(B icucu lline,B ic)采用中脑导水管周围灰质腹外侧区(ven-trolateral portion of the PAG,vlPAG)注射。行为学实验采用热板法和福尔马林实验,分别以舔后爪潜伏时间(Hot-p latelatency,HPL)和疼痛(累计)评分为指标。免疫组化方法观察丙泊酚在vlPAG对福尔马林单侧足底皮下注射诱发的脊髓背角Fos蛋白表达的影响。结果行为学部分:两种疼痛模型中丙泊酚(10 g.L-1)vlPAG注射引起痛敏(P<0.01)。热板法实验中,丙泊酚vlPAG微量注射的痛敏作用可被相同部位预先注射25 mg.L-1B ic在10和20 m in时间点分别拮抗70%和71%(均P<0.01),在30和40 m in完全拮抗。在福尔马林实验中,丙泊酚vlPAG微量注射使福尔马林疼痛评分增加,此作用可被B ic(25 mg.L-1)在60 m in拮抗57%(P<0.05)。免疫组化部分中,丙泊酚vlPAG微量注射使福尔马林引起的脊髓背角各层FLI阳性细胞数明显增多(P<0.01),B ic vlPAG微量注射(25 mg.L-1)可部分拮抗丙泊酚vlPAG微量注射的作用(P<0.01)。结论在大鼠vlPAG微量注射丙泊酚能产生痛敏作用;GABAA受体部分介导了丙泊酚的以上作用。
文摘目的观察不同剂量咪达唑仑对氯胺酮镇痛效应的影响,为临床合理配伍使用药物提供依据。方法腹腔注射25 mg/kg氯胺酮建立镇痛模型,150只小鼠均分为NS组、M组、K组、M1K组和M2K组,采用甩尾法、热板法和扭体法(n=10)分别观察腹腔注射1、2 mg/kg咪达唑仑对氯胺酮镇痛小鼠甩尾潜伏期(TFL)、热板法痛阈(HPPT)和扭体次数(WTs)的影响。结果给药后5、10、15、20 min K组TEL、HPPT延长(P<0.05);各时点M组小鼠TFL、HPPT均无明显变化;M1K组和M2K组给药后10、15、20 min TFL、HPPT延长,给药后15 min M1K组和M2K组TEL、HPPT明显长于K组(P<0.05或P<0.01)。给药后15 min内K、M1K和M2K组小鼠WTs明显少于NS组(P<0.01)。但K、M1K和M2K组间差异无统计学意义(P<0.05或P<0.01)。结论一定剂量的咪达唑仑可以增强氯胺酮的体表镇痛作用。
