Objective:To observe any effect of combining ultrasound-guided drug injection into the subacromial bursa, coracoid bursa and shoulder joint cavity with hydraulic dilation of the glenohumeral joint in the treatment of frozen shoulder (FS).Methods:A total of 116 persons diagnosed with FS were randomly divided into an injection treatment group and a combined treatment group, each of 58. On the first day, both groups received ultrasound-guided steroid injections into the subacromial bursa, coracoid bursa and shoulder joint cavity. The combined treatment group was also injected with 30ml of normal saline into the glenohumeral joint for hydraulic dilation. All then followed a family-based program of shoulder function training for 15 days. Shoulder pain assessment (VAS) and shoulder function assessment (PROM) were performed for both groups before the treatment, after the injections and after the shoulder function training.Results:The average VAS and PROM scores of both groups were significantly different after the treatment, with those of the combined treatment group significantly better than the injection group′s averages at each time point.Conclusion:Combining ultrasound-guided drug injection with hydraulic dilation of the subacromial bursa, the coracoid bursa and the shoulder joint cavity can significantly relieve pain of FS and improve shoulder mobility. It is more effective than drug injection alone.

OBJECTIVE: To investigate the clinical significance of early troponin I (TnI) level in the prognosis of severe heat stroke. METHODS: Clinical data of 131 patients with severe heat stroke in the intensive care unit (ICU) of the Affiliated Changzhou NO.2 People's Hospital of Nanjing Medical University (study dataset) and ICU 67 patients with severe heat stroke in Jintan First People's Hospital of Changzhou (validation dataset) were retrospectively analyzed from June 2013 to September 2022. The patients were divided into survival group and death group according to 30-day outcomes. TnI was collected within 24 hours after admission to the emergency department. Cox regression analysis was performed to analyze the risk factors of severe heat stroke death. Spearman correlation test was used to analyze the correlation between TnI and heart rate, and peripheral systolic blood pressure. The receiver operator characteristic curve (ROC curve) was drawn to evaluate the predictive value of TnI for death in patients with severe heat stroke. Decision curve analysis (DCA) was conducted to assess the clinical net benefit rate of TnI prediction. Grouping by TnI cut-off value, Kaplan-Meier survival curve was used to analyze 30-day cumulative survival. Sensitivity analysis included modified Possion regression, E-value, and subgroup forest map was used to evaluate the mortality risk of TnI in different populations. External dataset was used to verify the predictive value of TnI. RESULTS: The death group had significantly higher TnI compared to the survival group [μg/L: 0.623 (0.196, 1.510) vs. 0.084 (0.019, 0.285), P < 0.01]. Multivariate Cox regression analysis after adjusting for confounding factors showed that TnI was an independent risk factor for death [hazard ratio (HR) = 1.885, 95% confidence interval (95%CI) was 1.528-2.325,P < 0.001]. Spearman correlation test showed that TnI was positively correlated with heart rate (r = 0.537, P < 0.001) and negatively correlated with peripheral systolic blood pressure (r = -0.611, P < 0.001). ROC curve showed that the area under the curve (AUC) of the TnI (0.817) was better than that of the acute physiology and chronic health evaluation II (APACHE II, 0.756). The DCA curve showed that the range of clinical net benefit rate of TnI (6.21%-20.00%) was higher than that of APACHE II score (5.14%-20.00%). Kaplan-Meier survival curve showed that patients in the low-risk group (TnI ≤ 0.106) had a significantly higher 30-day survival rate than that in the high-risk group (TnI > 0.106) group (Log-Rank test: χ² = 17.350, P < 0.001). Modified Possion regression with adjustment for confounding factors showed that TnI was still an independent risk factor for death in patients with severe heat stroke [relative risk (RR) = 1.425, 95%CI was 1.284-1.583, P < 0.001]. The E-value was 2.215. The subgroup forest plot showed that the risk factors of TnI were obvious in male patients and patients ≤ 60 years old (male: HR = 1.731, 95%CI was 1.402-2.138, P < 0.001; ≤ 60 years old: HR = 1.651, 95%CI was 1.362-2.012, P < 0.001). In the validation dataset, ROC curve analysis showed that the AUC (0.836) of TnI predicting the prognosis of severe heat stroke was still higher than the APACHE II score (0.763). CONCLUSIONS Early elevation of TnI is a high-risk factor for death in patients with severe heat stroke, and it has a good predictive value for death.
Humans ; Male ; Middle Aged ; Troponin I ; Retrospective Studies ; Clinical Relevance ; ROC Curve ; Prognosis ; Intensive Care Units ; Heat Stroke/diagnosis* ; Sepsis

Objective:To investigate the value of neutrophil-to-lymphocyte ratio (NLR) in predicting the prognosis of patients with severe heat stroke.Methods:A retrospective analysis was performed on patients with severe heat stroke hospitalized in the ICU of Changzhou No. 2 People's Hospital from June 2013 to September 2019. The patients were divided into the survival group and death group according to their 30-day survival. The basic data of the patients were recorded. Blood routine, liver and kidney function parameters, troponin, brain natriuretic peptide, myocardial enzyme spectrum, blood coagulation routine, and acute physiology and chronic health evaluation (APACHE)Ⅱ were analyzed within 24 h after admission. Multivariate COX regression analysis was used to screen the risk factors of 30-day death. Spearman correlation test was used to analyze the correlation between NLR and APACHEII score. Receiver operating characteristic (ROC) curves were drawn to assess the predictive value of NLR for the 30-day death in patients with severe heat stroke. Kaplan-Meier survival curve was used to analyze 30-day cumulative survival of high-risk patients.Results:A total of 115 patients with severe heat stroke were included in this study, and they were divided into the survival group ( n=92) and the death group ( n=23) according to the prognosis. NLR in the death group was significantly higher than that in the survival group ( P<0.05). Multivariate COX regression analysis showed that NLR was an independent risk factor for death after adjusting confounders ( HR=1.091, 95% CI: 1.049-1.136, P<0.001). Spearman correlation test showed a correlation between NLR and APACHEII score ( r=0.655, P<0.001). ROC curve analysis showed that NLR had the greatest predictive value for 30-day death, with an area under ROC curve (AUC) of 0.787, a sensitivity of 82.6%, a specificity of 67.4%, and the cut-off value of 7.35. Kaplan-Meier survival analysis curve shows that patients in the below NLR cut-off value group had a significantly higher 30-day survival rate than those in the above NLR cut-off value group ( P<0.001). Conclusions:The increased NLR is a high risk factor for death in patients with severe heat stroke, and helps predict the prognosis of patients with severe heat stroke.

Frontopsylla spadix is one of important transmission vectors of plague in the wild rat foci in Yunnan Province.In the classification,it belongs to Leptopsyllidae and Frontopsylla,with agile activities and a wide range of hosts.Based on domestic and international literatures,this paper reviews the taxonomic position and identifies features of Frontopsylla spadix,together with its distribution,life cycle,disease transmission,artificial rearing,isozyme and some other aspects.The paper is an attempt to provide more data for the surveillance and control of Frontopsylla spadix and its related flea-borne diseases.

Aim To investigate the role of TNF-αin propofol-induced neuronal apoptosis and long-term cog-nitive impairment in neonatal rats .Methods Seven-day-old SD rats were randomly divided into 3 groups:Control group ( n =12 ) , P ( single ) group ( n =6 ):propofol 50 mg · kg -1 was injected intraperitoneally (ip.)once;P(repeated) group(n=6):propofol 50 mg · kg -1 was injected ip.once daily, and for seven times. Hippocampal TNF-αlevel was measured 2 hours after propofol anesthesia , there were two time points(n=6) in Control group as control levels (post-natal day 7 for P ( single ) group and postnatal day 13 for P ( repeated ) group ) .In another experiment , 7-day-old rats were randomly divided into 5 groups:Con-trol group; P ( single ) group; P ( repeated ) group; P ( single ) +ETN group: ETN ( etanercept ) 0.4 mg · kg -1 was injected intracerebroventricularly 30 min be-fore propofol administration; P ( repeated ) +ETN group:ETN 0.4 mg· kg -1 was injected intracerebrov-entricularly 30 min before the 1st and 4th administration of propofol , which was injected ip .for seven times , once daily .Hippocampal neuronal apoptosis was detec-ted at postnatal day 7 [ P ( repeated ) and P ( repeated )+ETN groups not involved at this time point ] , 13, 21 and 35 , cognitive function was measured at postnatal day 36 to 41 using Morris water maze test .Results Propofol with different exposure times could increase hippocampal TNF-αlevels(P<0.05,P<0.01);in P ( single ) group, active caspase-3 positive neurons in hippocampal pyramidal cell layer were much greater than control level only at postnatal day 7 ( P<0.05 ) , there were no changes of escape latency or platform crossing times compared with control ( P>0.05 );in P ( repeated ) group, active caspase-3 positive neurons were more significantly increased at postnatal day 13, 21 and 35 than those in control group ( P<0.01 ) , es-cape latency was increased or platform crossing times were decreased more significantly than control in Morris water maze test ( P <0.01 ); after etanercept was ad-ministered intracerebroventricularly , there were no sig-nificant changes of active caspase-3 positive neurons , escape latency and platform crossing times after propo-fol anesthesia compared with control ( P>0.05 ) .Con-clusion TNF-αmediates hippocampal neuronal apop-tosis and long-term cognitive impairment induced by propofol in neonatal rats , and long-term cognitive im-pairment may be related with persistent neuronal apop-tosis.

ObjectiveTo explore the effects and underlying mechanisms of acid sensing ion channels (ASICs) on pain behavior in a rat model of post-incision pain.MethodsFifty-eight adult male Sprague Dawley rats were used in this study,four rats were used for immunofluorescence test,thirty rats were employed for pain behavior test,and twenty-four rats were used for Western blot.Rats used for pain behavior test and Western blot were randomly divided into 3 groups:control group ( C group),incision pain model group ( I group) and amiloride group (A group).Plantar skin of rats in A group were infiltrated with 20 μl(200 μg)amiloride solution.Paw withdrawal mechanical threshold(PWMT) and paw withdrawal thermal latency(PWTL) of all rats in pain behavior test was tested at 24 h preoperative,2 h,4 h,8 h,12 h,24 h postoperative.Western blot was tested at 4 h postoperative.ResultsImmunofluorescence test displayed ASIC3 was expressed in plantar skin of all rats.The basal level of PWMT and PWTL of all rats in three groups was C group( (23.15 ± 5.10) g,( 11.32 ± 1.21 ) s),I group ( (23.26 ± 5.69) g,( 11.75 ± 2.01 ) s),A group ( (23.63 ± 4.96 ) g,( 11.47 ± 1.96) s) respectively,which was no significantly difference (P ＞ 0.05 ).PWMT and PWTL of I group and A group was significantly lower than that of C group at all time points postoperative (P ＜ 0.05) ; PWMT and PWTL of A group was at 2 h( ( 13.75 ±3.25)g,(9.96±1.32)s),4h((14.05±3.75)g,(9.17±2.11)s),8 h((9.75 ±2.74)g,(8.11 ±1.22)s)postoperative,which was significantly higher than that of I group (P ＜ 0.05 ).Compared with that of C group,the level of pERK1/2 expression was significantly increased in I group at 4 h postoperative (P ＜ 0.05 ),which could be inhibited by amiloride local infiltration (P ＜ 0.05 ).ConclusionASIC3 can mediate incision pain in a rat model of post-incision pain,through pERK1/2 signaling pathway,which can be inhibited by amiloride.

Objective To investigate the role of neurokinin-1 receptor (NK-1R) in the anti-nociceptive effect of enflurane, isoflurane and sevoflurane in mice. Methods Three hundred and twenty Kunming mice of both sexes weighing 20-25 g were randomly divided into4 groups (n =80 each): group normal saline (group NS);group enflurane (group E); group isoflurane (group I) and group sevoflurane (group S). Normal saline (NS) 1.0ml/kg, erflurane 0.5 ml/kg, isoflurane 0.4 ml/kg and sevoflurane 2.0 ml/kg were injected intraperitoneally in NS,E,I and S groups respectively. Each group was further divided into 4 subgroups receiving intrathecal NS 5 μl and Sar-SP (NK-IR agonist) 20, 40 and 80 ng respectively at 5 min after intraperitoneal injection of inhalation anesthetics. The anti-nociceptive effect of the inhalation anesthetics was assessed by tail flick latency (TFL) (the latency for removal of the tail from the path of heat source) and paw-licking time (PLT) after intraplantar formalin injection. Results lntraperitoneal enflurane, isoflurane and sevoflurane significantly prolonged TFL and shortened PLT. Intrathecal Sar-SP 20, 40 and 80 ng significantly shortened TFL dose-dependently but had no significant effeet on PLT as compared with control subgroup. Conclusion NK-1R is involved in the anti-nociceptive effect of enflurane, isoflurane and sevofluran on thermal pain but not chemical and inflammatory pain.

Aim To observe the effects of promethazine on the analgesia,hypnosis,amnesia and therapeutic index of isoflurane.Methods The experiments were designed to study promethazine on the analgesic effect of isoflurane by hot-plate test and writhing test,and to study the effect of promethazine on the sleeping time of isoflurane by the method of righting reflex,and the amnesia of isoflurane by Morris water maze,and the ED_(50),LD_(50) by sequential method in mice.Results The result of hot-plate test and writhing test indicated that promethazine could enhance the analgesic effect of isoflurane(P＜0.05 or P＜0.01);through the experiment of righting reflex, sleeping time of isoflurane in mice was extended by promethazine(P＜0.01);in Morris water maze experiment, the average latency in the combination of promethazine and isoflurane was longer than that of the promethazine group or isoflurane group(P＜0.05 or P＜0.01), while aiming to the residence time, the combination of the two was shorter than that in the third quadrant(P＜0.01 or P＜0.05),the TCPP of the group of isoflurance was more than that of the combination group;promethazine could decrease the ED_(50) of isoflurance(P＜0.01),but it did not obviously affect its LD_(50)(P＞0.05).Conclusion Promethazine can not only reinforce the effect of isoflurance on analgesia,hypnosis and amnesia, but also boost the therapeutic index of isoflurance.

Objective To investigate the effects of propofol on P2X7 receptor activition and IL-1β production induced by endotoxin in murine RAW264.7 macrophages. Methods RAW264.7 macruphages were treated with LPS (1 μg/ml) for 4 h to induce the production and release of IL-1β, and pretreated with BBG (specific P2X7 receptor antagonist) 1 μmol/L or propofol 1-100 μmol/L for 20 min before LPS stimulation, and IL-1β release was measured using ELISA kit. Whole-cell patch clamp technique was used to record the P2X7-gated currents induced by 1 mmol/L ATP, the cells were exposed to propofol with 1-1 000 -μmol/L for 4 min, and the IC_(50) level of propofol was achieved. Western blot technique was used to measure the production of pro-lL-1β protein and IL-1β protein intracellularly after LPS treatment for 4 h under different concentrations of propofol. Results IL-1β was released from RAW264.7 macrophages after LPS stimulation, which was decreased by propofol, and the IC_(50) level of propefol was (24±3) μmol/L. P2XT-gated currents were inhibited by propofol, and the IC_(50) level was (33±5) μmol/L. Pro-IL-1β protein intracellularly was up-regulated after LPS stimulation, and propofol with 3-100 μmol/L decreased the up-regulation of pro-IL-1β intracellularly induced by LPS. Conclusion Propefol could inhibit IL-1β release from RAW264.7 macrophages treated by LPS, which is mediated by inhibiting P2X7 receptor activition and decreasing the production of pro-IL-1β intracellularly.

BACKGROUND: Quantitative pharmaco-electroencephalography (QPEEG) can reflect cerebral cortical function, which can be certainly affected by general anesthetics. Anesthesia depth has good correlation with the anesthetic dosage, so if we can find out the areas of brain and band of QPEEG which is relative to the anesthetic dosage, the band may be taken as the index to reflect the depth of anesthesia. OBJECTIVE: To observe the effects of propofol on the alpha2-band (α2- band) of QPEEG in rabbits. DESIGN: A randomized control animal experiment. SETTING: Jiangsu Provincial Key Laboratory of Anesthesiology, Xuzhou Medical College. MATERIALS: The experiment was carried out in the animal laboratory of Xuzhou Medical College from October 2004 to August 2005. Thirtysix healthy adult rabbits were randomly divided into propofol 2.5, 5 and 10 mg/kg groups with 12 rabbits in each, including 6 were used to observe the change of percentage of each band power of QPEEG, and the other 6 were used to observe the latency and duration for the disappearance of righting reflex in the rabbits. METHODS: The experiment was performed between 14:00-17:00 every day. Rabbits in the three groups were treated with intravenous injection of propofol of 2.5, 5 and 10 mg/kg respectively within 30 seconds. ① The conscious rabbits were fixed onto the platform in a prone osition, and the QPEEG was recorded with the method of power spectrum analysis before administration and at 20, 30, 40, 50, 60, 70, 80, 90, 100 and 110 s and 2, 5, 10, 15, 20 and 30 minutes after administration respectively. The sampling time for each time point was 5 s. ② The latency and duration for the disappearance of righting reflex in the rabbits were recorded. RESULTS: ll the 36 rabbits were involved in the analysis of esults. ① After the intravenous injection of propofol, the righting reflexes all disappeared within 1 minute. The greater the dosage, the shorter the latency and the longer the duration r=0.79, P ＜ 0.01). ② Compared with before administration, propofol of 2.5 mg/kg had no obvious influence on the percentage of α2-band power (P ＞ 0.05); The percentages of α2-band power in the brain areas were increased after administration in the propofol 5 mg/kg group (P ＜ 0.05); Except that there were no significant differences in the left and right parietal regions between the propofol 10 mg/kg group and the propofol 5 mg/kg group, the percentages of α2-band power in the other brain areas in the propofol 10 mg/kg group were decreased as compared with those before administration and those in the other two groups (P ＜ 0.05), and the changes above were more obvious in the frontal and temporal regions.CONCLUSION: The influence of propofol on the percentage of α2-band power of QPEEG is biphasic, it is suggested that α2-band would be an index to reflect the anesthesia depth of propofol.