Objective:To evaluate the efficacy and safety of palonosetron in preventing chemotherapy-induced vomiting. Meth-ods:A multi-center, randomized, double-blind, and self-cross-over positively controlled clinical trial design was used. All patients were randomized into two groups, as follows:Regiment A (61 cases) and Regiment B (64 cases). Regimen A with palonosetron hydrochlo-ride injection (test agent) was used in the treatment cycle A, whereas granisetron hydrochloride injection (control drug) was used in the cycle B. Treatments were randomly administered on the patients of the two groups. Regimen B was on the contrary, the control drug was used in the cycle A, and the test agent was used in the treatment cycle B. All patients treated with the test agent were classified as the test group, whereas those treated with the control drug were classified as the control group. Complete control rate and adverse reac-tion of acute and delayed vomiting in the two groups during the two cycles of chemotherapy regimen were compared. Results: In Group One, the complete control rate of delayed vomiting was significantly higher in the palonosetron administration cycles than in the granisetron cycles (76.92%vs. 55.38%, P=0.0110). In the same group, the frequency of vomiting was significantly less in palonosetron cycles than in the granisetron cycles during day 1 to day 5 (1.32±3.42 vs. 1.94±3.03, P=0.0096). The incidences of adverse effects were low in both groups. No grades 3 and 4 adverse effects were observed. Conclusion: Palonosetron showed efficacy in preventing the acute and delayed chemotherapy-induced vomiting. The drug is superior to granisetron, specifically in delaying vomiting in Group One. Palonosetron hydrochloride showed slight adverse effects. Hence, this drug can be used in clinic.

Aim Toinvestigatetheanalgesiceffectsof epidural osthole application on the mechanical allodyn-ia and the ERK/MAPK signaling pathway and the expression of COX-2 mRNA in the spinal dorsal horn.Methods 125adultmaleSDratswererandomizedin-to five groups( n=25 each) :Blank, Sham, NP, Ost and vehicle. At postoperative day 6, 1mg/rat osthole 50 μl was injected epidurally into group Ost and the same volume of vehicle was given into group vehicle. The mechanical pain threshold was measured by 50%MWT at 1 day before operation and the 3 rd,6 th,7 th, 14 th,21 st day after operation. After the measurement of pain threshold on postoperative day 14 , the L4-6 segment of spinal dorsal horn was removed for determi-nation of the expression of ERK, pERK and COX-2 mRNAbyWesternblotandRT-PCR.Results Com-pared with blank group, the mechanical pain threshold was only down-regulated at day 1 after operation in sham group, the expression of pERK and COX-2 mR-NA in sham group showed no significant difference ( P>0. 05 ); the mechanical pain threshold was signifi-cantly down-regulated after operation in NP, Ost and vehicle groups( P<0. 05 ) and the expression of pERK and COX-2 mRNA was significantly increased ( P <0. 05). Compared with vehicle group, the pain thresh-old in Ost group was significantly increased after drug administration( P<0. 05 ) and the expression of pERK and COX-2 mRNA was significantly reduced ( P <0. 05 ) . The expression of ERK showed no significant difference among each group(P>0. 05). The correla-tion analysis on pERK1/2 and COX-2 mRNA revealed the Pearson correlation coefficient was 0 . 878 and 0 . 910 , suggesting a strong positive correlation between pERKandCOX-2mRNA.Conclusions Ostholead-ministrated in the early stage after surgery can alleviate the nucleus pulposus-induced radicular inflammatory pain probably by inhibiting the expression of pERK and COX-2 mRNA in spinal dorsal horn.

Objective To examine the expression of tight junction protein claudin-5 in blood-spinal cord barrier (BSCB) after spinal cord injury about rat. Methods One hundred-twenty adult male SD rats were randomly divided into blank group (60) and injured group (60). The animal model of spinal cord injury was established using modified Allen method. The expression of claudin-5 in BSCB was examined at 6 h, 12 h, 1 d, 3 d, 5 d and 7 d (five rats per time point). Western blot and RT_PCR were used to detect protein and mRNA expression levels of claudin-5, respectively. Results The success rate of spinal cord injury molding was 81.7%. In injured group, EB content increased gradually over time, reached the peak at the third day(0.9435 ± 0.0813)μg/g and then reduced gradually (P<0.05), EB content was signifi-cantly higher in injured group than in blank group. Claudin-5 mRNA expression in injured group reduced gradually over time and reached the lowest point at the third day(2.871 ± 0.527)and then increased gradually(P<0.05). Claudin-5 mRNA expression was significantly lower in injured group than in blank group(P<0.05). Claudin-5 protein expression in injured group reduced gradually over time, reached the lowest at the third day(0.072 ±0.008)and then increased gradually (P<0.05). Claudin- 5 protein expression was significantly lower in injured group than in blank group(P<0.05). Con-clusions The alteration of claudin-5 expression after SCI may lead to the permeability of BSCB, which may in turn con-tribute to the secondary spinal cord injury.

Objective To construct MIA3 psicheck2 wild-type and mutant vectors targeting miR-374b,and provide the previous guarantee for the dual luciferase reporter assay.Methods The amplification primer was firstly designed according to mice MIA3-3'UTR sequence information,mice whole blood genomic DNA was taken as the template for PCR amplification of MIA3-3'UTR sequence,and the PCR product was cloned into psicheck2 dual luciferase reporter vector.Then,mutant primer was designed to mutate the MiR-374b seed sequence target TATTATA into AAATTAT so as to construct mutant vector.At last,the vector enzyme digestion evaluation and sequencing method was used to evaluate the constructed vectors.Results It could be seen from the analysis of agarose electrophoresis that the PCR amplification size of vector was consistent with the theoretical size.DNA sequencing evaluation showed that the MIA3-3'UTR-WT vector had been constructed successfully.The construction of mutant vector has successfully mutated the MiR-374b seed sequence target TATTATA into AAATTAT.Conclusion The successful construction of the vector will lay a foundation for the further evaluation on whether there is an actual binding site between the miR-374b and the chondrogenic differentiation-related target gene MIA3.

Objective To analyze changes in lactic acid level in patients with late-onset intracranial hematoma after craniocerebral injury and investigate their relativity.Methods Forty-eight patients with late-onset intracranial hematoma after craniocerebral injury treated in our hospital between May 2009 and December 2012 were enrolled as observation group.There were 32 males and 16 females.Moreover,50 cases checked up in our hospital during the same period were studied as health population controls,including 35 males and 15 females.Level of lactic acid was measured on admission,at the time of definite diagnosis as well as at days 7 and 14 after treatment and compared between groups.Results Level of lactic acid was (1.77 ±0.21) mmol/L in control group and (1.82 ± 0.25) mmol/L in observation group respectively on admission (t =1.070,P ＞ 0.05) ; Level of lactic acid was (3.32 ± 0.89) mmol/L in observation group at the time of definite diagnosis,which increased to (3.74 ± 1.16) mmol/L at days 7 after treatment and decreased to (1.89 ±0.75) mmol/L at days 14 after treatment.When diagnosed and treated for 7 days,level of lactic acid differed significantly between the two groups (P ＜ 0.05).Level of lactic acid related to craniocerebral injury at each time point,but higher correlation coefficient was observed at the time of definite diagnosis and 7 days after treatment with 0.986 and 0.989 respectively.Conclusion Level of lactic acid relates to late-onset intracranial hematoma after craniocerebral injury,which can be used as reference for progression of the disease.

Objective To study the effects of methylprednisolone on the permeability of blood-spinal cord barrier (BSCB) and claudin-5 expression after spinal cord injury in rats. Methods The rat model of spinal cord injury was estab?lished using modified Allen method. SD rats were randomly divided into sham-operated group, spinal cord injury group and methylprednisolone pretreatment group. The permeability of BSCB and expression of claudin–5 were assessed at 12 h, 1, 3, 5, and 7 d after the onset of spinal cord injury (five animals per each time point). RT-PCR and Western blot were used to detect the expression of claudin-5. Results The success rate of the model was 84.0%. EB content was sig?nificantly higher in spinal cord injury group than in sham-operated group at each time point (F value 27.732,P<0.05). EB content was lower in methylprednisolone pretreatment group than in spinal cord injury group (F value 48.149,P<0.05). The mRNA expression of claudin-5 was lower in spinal cord injury group than sham-operated group at each time point (F value 12.248,P<0.05). The mRNA expression of claudin–5 was higher in methylprednisolone pretreatment group than in spinal cord injury group at each time point (Fvalue 15.316,P<0.05). The protein expression of claudin-5 was lower in spinal cord injury group than in sham operated group at each time point (Fvalue 18.108,P<0.05). The pro?tein expression of Claudin-5 was higher in methylprednisolone pretreatment group than spinal cord injury group at each time point (F value 20.247,P<0.05). Conclusions Methylprednisolone improves permeability of BSCB after spinal cord injury probably through enhancing claudin-5 expression in rats.
was lower in spinal cord injury group than in sham operated group at each time point (Fvalue 18.108,P<0.05). The pro?tein expression of Claudin-5 was higher in methylprednisolone pretreatment group than spinal cord injury group at each time point (F value 20.247,P<0.05). Conclusions Methylprednisolone improves permeability of BSCB after spinal cord injury probably through enhancing claudin-5 expression in rats.

Objective To investigate the correlation of angiotensin Ⅱ type 1 receptor (AT1R) gene polymorphism with AT1R expression levels and brain edema after hypertensive intracerebral hemorrhage .Methods 45 operative patients with hypertensive intracerebral hemorrhage in the Affiliated Yongchuan Hospital of Chongqing Medical Univercity from December 2011 to August 2012 were collected as the experimental group and 45 operative patients with refractory epilepsy weres selected as the control group .The venous blood in the two groups were collected for detecting the AT 1R gene polymorphism ;The brain tissue was taken from lesions in operation ,then AT1R mRNA concentration was determined by RT-PCR and the AT1R protein level was determined by Western blot ;Head CT was performed on postoperative 1 ,3 ,5 d;the degree of cerebral edema was reflected by CT value . Results The levels of two kinds of genotype AT1R mRNA in the experimental group had no statistically significant difference(P>0 .05);the operative area CT value of AC genotype was significantly lower than that of AA genotype with statistical difference (P<0 .05);the ATIRmRNA of various genotypes ,protein level and cerebral edema in the control group had no statistical differences . Conclusion The AT 1R gene polymorphism has no obvious correlation with the concentration expression of AT 1R mRNA in the brain tis-sue;there is correlation between AT 1R protein level and AT 1R protein level and the cerebral edema degree in the brain tissue .

Objective To investigate the effect of neutrophil elastase (NE) inhibitor on the blood-brain barrier(BBB) permeabili-ty and hydrocephalus in rats with traumatic brain injury (TBI) .Methods 99 SD rats were randomly divided into the control group , the TBI group and the intervention group(dividing into 5 sub-groups:6 ,24 ,48 ,72 ,168 h) .The hydraulic impact model of rats was duplicated .Sivelestat sodium was given in the intervention group .The NE concentration in the brain tissue ,BBB permeability and brain water content were detected in each group and performed the comparative analysis .Results The NE concentration in the brain tissue ,BBB permeability and brain water content at each timepoint in the TBI group and the intervention groups were higher than those in the control group .The NE concentration at 24 ,48 ,72 ,168 h in the intervention group was lower than that in the TBI group .The BBB permeability and the brain water content at 48 ,72 ,168 h in the intervention group were lower than those in the TBI group(P<0 .05) .Conclusion Sivelestat sodium can inhibit the NE release in TBI rat brain tissue ,reduce the BBB permeability and the occurrence of hydrocephalus ,which indicating that sivelestat sodium has the protective effect on TBI secondary lesion in rat .

Objective To investigate relationship of immunoglobulin concentrations (IgG,IgA,and IgM)and decrease of serum Mg2+ concentration in patients with severe traumatic brain injury (sTBI).Methods Sixty patients with sTBI were randomly divided into control group and study group.Intravenous injection of MgSO4 was given to study group.Levels of Mg2+ in serum and immunoglobulin (IgG,IgA,and IgM) in both groups were measured at 1,3,7,and 14 days after injury so as to analyze correlations of serum Mg2+ concentration with each humoral immune indices.Results IgG concentration at days 3 and 7 in study group were (10.79 ± 2.65) g/L and (10.2 1 ± 2.54) g/L respectively,higher than that in control group (P ＜ 0.05).IgM at days 3 and 7 in study group were (1.27 ± 0.32) g/Land (1.31 ± 0.25) g/L respectively,higher than that in control group (P ＜ 0.05).Difference of IgA level between the two groups was not significant.Level of Mg2 + was positively related to levels of IgM and IgG,but not to level of IgA.Pathological amelioration at day 14 between the two groups showed insignificant difference.Conclusion Intravenous replenishment of MgSO4 for patients with sTBI at acute phase can improve humoral immunosuppressive state,but can not ameliorate prognosis.