Objective To assess the patient effective dose during SPECT/CT imaging.Methods A total of 157 patients (85 males,72 females;mean age:(60.46±13.44) years,range:24-88 years) who underwent SPECT/CT from April 2013 to September 2014 were retrospectively analyzed.They were divided into 3 groups:99Tcm-MDP bone scan group (n=113),99Tcm-MIBI parathyroid imaging group (n=23) and 99Tcm-MAA pulmonary perfusion imaging group (n=21).The injection dose (MBq) was recorded and the effective dose (mSv) was estimated according to the International Commission on Radiological Protection (ICRP) guideline.The volume-weighted computed tomography dose index (CTDIvol) and dose length product (DLP) of CT were also recorded and the effective dose (mSv) due to CT was calculated.The effective doses among different groups were statistically compared by Kruskal-Wallis rank sum test and Wilcoxon rank sum test.Results The effective dose from radiopharmaceuticals were (4.02±0.35) mSv for 99Tcm-MDP bone scan,(6.13±0.53) mSv for 99Tcm-MIBI parathyroid imaging and (1.66±0.13) mSv for 99Tcm-MAA pulmonary perfusion imaging (x2=96.853;Z =7.533,7.262 and 5.676;all P＜ 0.05).The effective dose due to CT were (3.84±1.98),(1.04±0.19),(4.05±0.47) mSv respectively (x2 =41.225,P＜0.05),and there were significant differences between 99Tcm-MIBI parathyroid imaging group and 99Tcm-MDP bone scan group,99Tcm-MAA pulmonary perfusion imaging group(Z=6.046 and 5.672,both P＜0.05).The total effective dose during SPECT/CT imaging were (7.86± 1.98),(7.21±0.81) and (5.71±0.45) mSv (x2 =28.988,P＜ 0.05).There were significant differences between 99Tcm-MAA pulmonary perfusion imaging group and 99Tcm-MDP bone scan group,99Tcm-MIBI parathyroid imaging group(Z=4.967 and 4.994,both P＜0.05).Conclusions The increase in effective dose due to spiral CT during SPECT/CT examination should be concerned.Appropriate utilization and optimization of SPECT/CT is needed.

Objective To investigate clinical features, outcomes and laboratory findings of thrombotic thrombocytopenic purpura (TTP).Methods Patients with TTP admitted between April 2006 and January 2013 were identified by a retrospective review of records.Totally 21 patients were available,15 females and 6 males,with a median age of 46 years (ranged 18-66).The diagnostic criteria were defined by:(1)thrombocytopenia (<100 ×9 L-1)without other identifiable causes;(2)a negative Coombs'test and hemolytic anemia with schistocytes on the peripheral blood smear;and only those patients meeting the criteria for TTP,both on clinical presentation and their clinical course,were included in this study. Exclusion criteria were:(1)patients discharged or dead within 24 hours after admission;(2)patients treated with plasma exchange therapy in other hospitals;(3)medical data were incomplete;(4)cannot be followed up;and (5 )other causes of thrombotic microangiopathies.General condition of patients,etiology, clinical features,treatment and prognosis were analyzed by using the SPSS 20.0 software.P value of <0.05 was considered as significant.Results Hemolytic anemia and thrombocytopenia appeared in all of the patients. Twelve patients (57.2%) had the classical pentad manifestations of TTP (fever, thrombocytopenia,microangiopathic hemolytic anemia,symptoms of nervous system,renal injury),seven patients (33.3%)had tetrad of TTP clinical manifestations (thrombocytopenia,microangiopathic hemolytic anemia,symptoms of nervous system,fever or renal injury),and only two patients showed the triad manifestations of TTP (thrombocytopenia, microangiopathic hemolytic anemia, symptoms of nervous system).In our studies,seven patients accepted plasmapheresis,and five of them (71.4%)achieved remission.Conclusions TTP progresses quickly.Plasmapheresis is still the treatment of choice for TTP patients.Etiological treatment can help to control the conditions of patients with TTP.

Objective To explore the risk factors influencing the prognosis of patients with acute poisoning by analysis of clinical data of 356 patients in order to provide the scientific evidence for planning therapeutic strategies in ICU.Methods The clinical data of 356 patients with acute poisoning were collected during the period from January 1,2005 through December 30,2009,and the clinical findings from close observation were filled into the tables of specially designed “ Clinical observation of acute poisoning patients”.Some risk factors of 356 cases with complete clinical data were studied by single-factor analysis and Logistic multiple regression,such as gender,age,mode and cause of poisoning,kind of poison agents,time elapsed from poisoning to admission into the hospital,time elapsed from poisoning to admission into ICU,length of hospital stay,cardiopulmonary resuscitation,mechanical ventilation,APACHE Ⅱ score.Results Three hundred fifty-six patients with complete data were divided into survival group (n =260) and death group (n =96).Univariate analysis showed the length of hospital stay (5.72 ± 4.37) d,APACHE Ⅱ score (10.27 ±7.77),time elapsed from poisoning to admission into ICU (17.16 ± 31.22)h in the survival group,and the length of hospital stay (3.53 ± 5.79) d,APACHE Ⅱ score (18.78 ±8.66),time elapsed from poisoning to admission into the ICU (37.21 ±67.35) h in the death group (P ＜0.05 or P ＜ 0.01).The differences in rates of CPR,mechanical ventilation and kind of poison agents between the two groups were statistically significant (P ＜ 0.05).Multivariate Logistic regression analysis revealed that the length of hospital stay,APACHE Ⅱ score,rates of cardiopulmonary resuscitation,mechanical ventilation and kind of poison agents were positively correlated with prognosis of patients with acute poisoning (P ＜ 0.05).Model to predict mortality was established:Y =-0.817-0.137X1 +0.140X3 + 2.133X4 + 1.039X5-0.291X6.Conclusions Hospital stay,APACHE Ⅱ score,cardiopulmonary resuscitation,mechanical ventilation and kind of poison agents were independent risk factors for predicting prognosis.APACHE Ⅱ score system and Logistic regression analysis can be used to evaluate the severity and prognosis of patients with acute poisoning.

Objective The aim of the study was to investigate the expression of P-glycoprotein (P-gp)and nuclear factor κB (NF-κB) in the cerebral cortex of rat with chronic fluorosis,and to reveal the mechanisms of damaged nervous system resulted from the toxicity of fluoride.Methods Sixty SD rats were randomly divided into three groups.The rats in each group were given drinking water containing different levels of fluoride:control group less than 0.5 mg/L,small amount of fluoride exposure group 10.0 mg/L and large amount of fluoride exposure group 50.0 mg/L.The animals were examined at the sixth month after initiating the experiment.Protein levels of P-gp and NF-κB in brain tissues were detected by immunocytochemistry and Western blotting,and the P-gp protein and mRNA level by quantitative real time PCR method.Results As compared to the control group(28.21 ±6.13),the numbers of positive staining cells by P-gp antibody in the cortex of rat brains were significantly increased in both the small and the large amount of fluoride exposure groups[(48.46 ± 8.00),(53.72 ± 9.15),respectively,all P ＜ 0.05] ; the protein levels in the control group(100.00 ± 3.86)％ detected by Western blotting were significantly increased in the cortex of rat brains treated with fluoride in both the small and the large amount of fluoride exposure groups[(189.47 ± 3.14)％,(191.36 ± 11.09)％,respectively,all P ＜ 0.05].The significantly increased expression of NF-κB at the protein level was observed in the cortex of rat brains of the small and the large amount of fluoride exposure groups[(365.97 ± 6.04)％ and (417.15 ± 10.89)％,respectively] as compared with the control group[(100.00 ± 10.07)％,all P ＜ 0.05].The mRMA level of P-gp in the cortex of rat brains of the small and the large amount of fluoride exposure groups(2396 ± 427,3479 ± 371,respectively) were higher than that of the control group(260 ± 106,all P ＜ 0.05).Conclusion The increased expressions of P-gp and NF-κB in the cortex of rat brains are induced by chronic fluorosis,which might be connected with the mechanism of brain damages.

Objective To observe the expression of mitochondrial fission protein locus Fis1 and ultrastructural changes in the renal cells of rats with chronic fluorosis,and to reveal the mechanism in mitochondrial damage of the renal cells.Methods Sixty SD rats were randomly divided into 3 groups according to sex and body mass(20 in each group):control group,lower fluoride group and higher fluoride group.All the rats were fed with different doses of sodium fluoride in drinking water(0,10 and 50 mg/L,respectively).Six-month later,the expression of Fisl in renal cells was determined by real-time fluorenscence quantitative PCR and immunohistochemistry technology,the mitochondrial morphology of renal cells was observed under transmission electron microscopy (TEM).Results As compared with the control group(28.70 ± 12.41),Fis1 mRNA levels(91.48 + 34.83 and 582.09 ± 184.69) in renal cells of the lower fluoride and the higher fluoride groups were increased(all P ＜ 0.05).As compared with the control group(10.49 ± 7.66),Fisl protein levels(16.33 ± 10.26 and 21.50 ± 5.24) in renal cells of the lower fluoride and the higher fluoride groups showed a trend of increasing,the higher fluoride group was higher than that of the control group(P ＜ 0.05).By TEM,mitochondrial crest in renal cells of the lower fluoride and the higher fluoride groups was vague or disappeared,mitochondrial division section appeared.Conclusions Fluoride is a kind of toxicant that can cause damage to mitochondrion of renal cells,induce the expression of Fis1 in transcriptional and protein level,and lead to the obstacles of mitochondrial fusion-fission and ultrastructural abnormality of mitochondrion,which may play an important role in mechanism of mitochondrial damage in the renal cells of rats with chronic fluorosis.

The effect of Rhizoma curcumae oil on the learning and memory in rats exposed to chronic hypoxia and the possible mechanisms were investigated. The rats were divided randomly into 5 groups (14 animals in each group): control, chronic hypoxia, chronic hypoxia with low (5 mg/kg body weight), middle (10 mg/kg body weight) and high (20 mg/kg body weight) concentrations of Rhizoma curcumae oil injection. The animals undergoing chronic hypoxia were exposed to hypoxia in a hypoxic chamber containing 10% O(2) and 5% CO(2) for 10 h/d, lasting 28 d. Morris water maze (MWM) test was used to obtain the scores of leaning and memory. The superoxide dismutase (SOD) activity and malonaldehyde (MDA) content were determined in the serum and hippocampus as well as [Ca(2+)](i) in the hippocampus. The expression of phosphorylated Ca(2+)/calmodulin-dependent protein kinase II (p-CaMKII) in the hippocampus was evaluated by using immunohistochemistry and Western blot. Compared with the control group, the chronic hypoxia group showed the following changes: (1) The escape latency to the hidden platform was remarkably prolonged (P<0.05); (2) The content of MDA and [Ca(2+)](i) were obviously higher, but the activity of SOD and the expression of p-CaMKII were significantly lower (P<0.05, P<0.01). Compared with the chronic hypoxia group, groups with Rhizoma curcumae oil injection had the following changes: (1) The escape latency to the hidden platform was remarkably shorter in 10, 20 mg/kg body weight groups (P<0.05); (2) The content of MDA and [Ca(2+)](i) were markedly decreased in 5, 10, 20 mg/kg body weight groups (P<0.05, P<0.01), but the activity of SOD in the serum and the expression of p-CaMKII were significantly higher in 10, 20 mg/kg body weight groups (P<0.05, P<0.01). The results showed that the capacity of learning and memory was degraded following chronic hypoxia. The decrease in MDA content and [Ca(2+)](i) and (or) the increase in SOD activity and p-CaMKII expression might participate in the enhancing effect on learning and memory induced by Rhizoma curcumae oil.
Animals ; Calcium ; metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; metabolism ; Curcuma ; chemistry ; Hippocampus ; metabolism ; Hypoxia ; physiopathology ; Learning ; drug effects ; Malondialdehyde ; metabolism ; Memory ; drug effects ; Plant Oils ; pharmacology ; Rats ; Rhizome ; chemistry ; Superoxide Dismutase ; metabolism

Background The effect of chronic stress on cognitive functions has been one of the hot topic in neuroscience. But there has been much controversy over its mechanism. Such single stressor applied in the past could not simulate complicated living circumstances that people confronted with. The aim of this study was to investigate the effects of chronic multiple-stress on learning and memory as well as on the levels of calcium/calmodulin-dependent protein kinase II (CaMKII), calmodulin (CaM) mRNA, and cAMP-response element binding protein (CREB) mRNA in the hippocampus of rats. Methods The rats were divided randomly into stressed and control groups. The stressed group was given chronic multiple-stress for 6 weeks to set up a chronic multiple-stressed model. The rats' performance of spatial learning and memory was tested using Morris Water Maze (MWM) and Y-maze. Meanwhile, the expressions of CaMKII, CaM mRNA and CREB mRNA of rats' hippocampus were detected by immunohistochemistry, Western blot and reverse transcription-polymerase chain reaction (RT-PCR), respectively. In addition, the width of synaptic cleft and the thickness of post-synaptic densities (PSD) were observed in the hippocampal CA3 region of rats by electron microscopy. Results After exposure to chronic multiple-stress for 6 weeks, the ability of learning and memory of the stressed group was higher than that of the control group (P<0.05, P<0.01). The width of synaptic cleft was smaller and the thickness of PSD was larger in the hippocampal CA3 region of the stressed group than in that of the control group (P<0.01). The CaMKII immunostaining of the stressed group was stronger than that of the control group in the stratum radiatum and oriens of the hippocampal CA1 and CA3, especially in the stratum oriens. Quantitative analysis indicated that the expression of CaMKII, CaM mRNA, and CREB mRNA in the hippocampus of the stressed group was higher than that of the control group (P<0.05, P<0.01). Conclusions The capacity of learning and memory can be enhanced after chronic multiple-stress. The increased levels of CaMKII, CaM mRNA, and CREB mRNA may contribute to the enhancing effect of chronic multiple-stress on learning and memory.

ObjectiveTo investigate the transcriptional changes of nitochondria fission and fusion gene loci and reactive oxygen species (ROS) level in cortical neurons of rats with chronic fluorosis,and to reveal their roles in mitochondria damage due to chronic fluorosis.MethodsSD rats were fed with different doses of fluoride through drinking water[＜ 0.5(control),10,50 mg/L,respectively] for 3 and 6 months.The level of ROS and mRNA contents of mitochondria fission gene loci Drp1/Fis1 and fusion gene locus Mfn1 in the cortical neurons of rat brains were detected with ROS fluorescent probe and real-time PCR,respectively.ResultsAs compared with control group [10.43 ± 5.98,(3.4 ± 0.6) × 103,(8.8 ± 1.4) × 10,(1.2 ± 0.2) × 102] at the experiment period of 3 months,the level of ROS and mRNA contents of mitochondria fusion gene locus Mfn1 and fission gene loci Drp1/Fis1 in the cortical neurons were obviously increased in the rats fed with 50 mg/L fluoride through drinking water[25.48 ± 6.09,(1.0 ± 0.2) × 1011,(3.0 ± 1.6) × 103,(8.9 ± 3.6) × 102,all P ＜ 0.05],whereas no significant changes were found in the rats fed with 10 mg/L fluoride[11.67 ± 3.49,(3.1 ± 0.3) × 104,(6.7 ± 2.7) × 10,(5.0 ± 0.9) × 10,all P ＞0.05].Furthermore,at 6 months of the experiment the increases in ROS level(63.02 ± 8.15,65.60 ± 7.40) and mRNA contents of mitochondria fission gene loci Drp1/Fis1 [(2.0 ± 0.8) × 106,(4.0 ± 0.6) × 105,(3.8 ± 1.3) × 103,(1.3 ± 0.2) × 103] and the decrease in mitochondrial fusion gene locus Mfn1[(3.0 ± 0.4) × 106、(4.0 ± 0.9) × 104]were observed in the cortical neurons of the rats fed with 10 mg/L and 50 mg/L fluoride as compared with the control group[25.26 ± 6.41,(3.0 ± 0.8) × 109,(5.1 ± 0.8) × 103,(2.8 ± 0.7) × 102,all P ＜ 0.05].Conclusions Excessive intake of fluorine leads to elevated ROS levels,and decreased transcription of mitochondrial fusion gene loci Mfn1,which is positively correlated with the time and dose-exposed to fluoride.The changes of mitochondrial fission and fusion gene loci in the cortical neurons may be related to high level of oxidative stress induced by chronic fluorosis.

Objective To investigate the deletion pattern of 4.8 kb mitochondrial DNA(mito-DNA) in liver,kidney,and brain of rats with chronic fluorosis and to explore the significance of mitochondria in the pathogenesis of chronic fluorosis.Methods Sixty SD rats were randomly divided into 3 groups according to body mass (20 in each group):control,low-fluoride and high-fluoride groups,and they were fed with different concentrations of fluoride in drinking water (0,10,50 mg/L,respectively) for 6 months.Mito-DNA in liver,kidney and brain was detected by real-time PCR.Results The amounts of 4.8 kb mito-DNA in liver(2.1 × 10-3,1.6 × 10-3),kidney (1.7 × 10-3,1.4 × 10-4) and brain cortex (1.5 × 10-5,1.3 × 10-5) in low-and high-fluoride groups were significantly reduced,as compared with that of control group (2.9 × 10-3,2.0 × 10-3,1.1 × 10-4,all P ＜ 0.05).The amount of 4.8 kb mito-DNA in kidney in high-fluoride group was lower than that in low-fluoride group (P ＜ 0.05).Conclusions Excessive fluoride intake can result in missing of 4.8 kb mito-DNA in liver,kidney and brain cortex.The abnormal of mito-DNA might be related to the dysfunction of mitochondrial respiratory chain.