Magnetoacoustic tomography (MAT) has some advantages such as high sensitivity and high spatial resolution. The generating mechanism of acoustic source is the research foundation of forward and inverse problems. A coustic signals were respectively simulated by using monopole and dipole radiation theory in the experimental conditions, then the differences between their acoustic pressures were discussed, and furthermore the contrast and validation were conducted by physical experiments in this study. The physical experimental results showed that acoustic waveform of MAT had a certain directivity and therefore they indicated that dipole model showed higher approximation to the real facts than monopole model. It can be well concluded that this research has cardinal significance for the accurate algorithm of MAT.
Acoustics ; Algorithms ; Tomography ; methods

Objective To evaluate the effects of sevoflurane postconditioning on mitophagy during myocardial ischemia-reperfusion (I/R) in rats.Methods Forty-two pathogen-free adult male SpragueDawley rats, weighing 250-300 g, were randomly divided into 3 groups (n=14 each) using a random number table: sham operation group (group S) , I/R group and sevoflurane postconditioning group (group SP).Myocardial I/R was induced by 30 min ligation of the left anterior descending branch of the coronary artery followed by 2 h of reperfusion.In group SP, 2.4％ sevoflurane was inhaled for 15 min starting from the onset of reperfusion, while 33％ oxygen was inhaled in group I/R.The rats were sacrificed at the end of reperfusion, and the hearts were removed for measurement of myocardial infarct size (by 1％ 2, 3, 5 triphenyltetrazolium chloride) , expression of LC3 Ⅱ/LC3 Ⅰ , Beclin-1, p62 and Parkin (by Western blot) ,and mitochondrial menbrane potential (by using JC-1 probe) , and for examination of the uhrastructure of cardiomyocytes (with transmission electron microscope).Results Compared with group S, the myocardial infarct size was significantly increased, mitochondrial membrane potential was decreased, the expression of LC3 Ⅱ/LC3 Ⅰ , Beclin-1 and Parkin was up-regulated, and the expression of p62 was down-regulated in group I/R.Compared with group I/R, the myocardial infarct size was significantly decreased, the mitochondrial membrane potential was increased, and the expression of LC3 Ⅱ/LC3 Ⅰ , Beclin-1, p62 and Parkin was down-regulated in group SP.Conclusion Sevoflurane postconditioning can mitigate I/R injury in rats, and inhibition of excessive activation of mitophagy may be involved in the nechanism.

Objective To evaluate the effects of sevoflurane postconditioning on the expression of 70 kD aribosomalprotein S6 kinase (p70S6K) during ischemia-reperfusion (I/R) in isolated rat hearts.Methods Pathogen-free male Sprague-Dawley rats,aged 3 months,weighing 270-350 g,were used in the study.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95 ％ O2-5 ％ CO2.Ninety isolated rat hearts with I/R injury were randomly divided into 3 groups (n =30 each):sham operation group (group S),I/R group (group I/R),and sevoflurane postconditioning group (group SP).The hearts were subjected to ischemia for 30 min followed by 2 h reperfusion.In group SP,the hearts were perfused with K-H solution saturated with 3.0％ sevoflurane for 15 min starting from the end of ischemia until 15 min of reperfusion,and then with plain K-H solution for 105 min.At 2 h of reperfusion,myocardial infarct size was measured,the percentage of myocardial infarct size was calculated,and the phosphorylated p70S6K (p-p70S6K)/total p70S6K (tp70S6K) ratio,and cytoplasm,cytochrome C,and caspase-8 expression was measured.Results Compared with group S,the percentage of myocardial infarct size and p-p70S6K/t-p70S6K ratio were significantly increased,the expression of cytochrome C,and caspase-8 was up-regulated,and the expression of cytochrome C was downregulated in I/R group.Compared with I/R group,the percentage of myocardial infarct size was significantly decreased,the ratio of p-p70S6K/t-p70S6K was increased and cytochrome C expression was up-regulated,and the expression of cytochrome C and caspase-8 was down-regulated in SP group.Conclusion Sevoflurane postconditioning can mitigate I/R injury to isolated rat hearts,and up-regulation of p-p70S6K expression,inhibition of transfer of cytochrome C from mitochondria to cytoplasm,and reduced cell apoptosis are involved in the mechanism.

Objective To characterize the clinical manifestations and to evaluate the value of the electrophysio-logical examination in patients with peripheral nerves injuries caused by neurobrucellosis. Methods Electrophysiology examination was conducted in 32 patients with peripheral nerve injuries caused by neurobrucellosis and 32 normal controls who had equivalent age and gender. The results were further statistically analyzed. Results There were sig-nificant difference between patients and healthy control group in distal motor latency (DML), compound motor active potentials (CMAP) amplitude, motor nerve conduction velocity (MCV), sensory nerve action potential latency(SL),senso-ry nerve action potential (SNAP) amplitude and sensory nerve conduction velocity (SCV) ( P﹤0.05). Electrophysiology examination revealed peripheral nerve damage of limbs involving, both sensory nerve and motor nerves, of which sen-sory and motor nerve injuries accounted for 55.47% and 16.80%, respectively. Median and sural nerve injuries were most frequently affected in upper (64) and lower limbs (16). Motor and sensory nerve conduction velocity was delayed in 43 nerves (16.80%) of 256 examined motor nerves and in 142 nerves (55.47%) of 256 examined sensory nerves. The damage of the sensory nerves was more severe than those of the motor nerves and damage of nerves in the upper limbs was more severe than those in the lower limbs. Conclusion Electrophysiologoical examination provides objective basis for the diagnosis of peripheral nerve injuries in neurobrucellosis.

Objective To evaluate the role of nitric oxide in sevoflurane postconditioning-induced mitigation of autophagy and cell apoptosis during ischemia/reperfusion (I/R) in isolated rat hearts.Methods The hearts of male Sprague-Dawley rats,aged 2-3 months,weighing 250-300 g,were excised and retrogradely perfused in a Langendorff apparatus.One hundred and eight isolated rat hearts,which were successfully perfused in a Langendorff apparatus,were equally and randomly divided into 6 groups:control group (C group),sevoflurane group (S group),I/R group,sevoflurane postconditioning group (SSP group),sevoflurane postconditioning + L-NAME (non-selective nitric oxide synthase (NOS) inhibitor group (SSP + L group),and L-NAME group (L group).The hearts were perfused with K-H solution for 150 min in C group.The hearts were continuously perfused for 180 min and perfused with K-H solution containing 3％ sevoflurane for 15 min starting from 60 min of perfusion in S group.After being perfused with K-H solution for 30 min,the hearts were subjected to occlusion for 30 min followed by reperfusion for 120 min in the other groups except C and S groups.After onset of reperfusion,the hearts were perfused with K-H solution containing 3％ sevoflurane for 15 min in SSP group,the hearts were perfused with K-H solution containing 3％ sevoflurane and L-NAME 100 μmol/L for 15 and 60 min,respectively,in SSP + L group,and the hearts were perfused with K-H solution containing L-NAME 100μmol/L for 60 min in L group.Inn ediately before ischemia,and at 30,60,90 and 120 min of reperfusion,each parameter of cardiac function was recorded.At the end of reperfusion,myocardial specimens were obtained at the end of reperfusion for measurement of the infarct size,NOS activity,NO content,and expression of Bcl-2,Beclin 1 and caspase-3,for observation of formation of autophagosomes,and for examination of the pathological changes.Results Compared with C group,LVSP,+ dp/dtmax,-dp/dtmax,NOS activity and NO content were significantly decreased,and LVEDP was increased in I/R and SSP groups.Compared with I/R group,LVSP,+ dp/dtmax,-dp/dtmax,NOS activity and NO content were significantly increased,LVEDP was decreased,Bcl-2 expression was down-regulated,and the expression of Beclin 1 and caspase-3 was up-regulated in SSP group,and no significant changes were found in each index in SSP+ L and L groups.Compared with SSP group,LVSP,+ dp/dtmax,-dp/dtmax,NOS activity and NO content were significantly decreased,LVEDP was increased,Bcl-2 expression was down-regulated,and the expression of Beclin 1 and caspase-3 was up-regulated in SSP + L group.Conclusion The mechanism by which sevoflurane postconditioning reduces I/R injury may be related to promoted NO product and inhibited autophagy and cell apoptosis in isolated rat hearts.

Objective To evaluate the role of the mitochondrial ATP-sensitive potassium (mito-KATP)channel in sevoflurane preconditioning-induced delayed cardioprotection against ischemia-reperfusion (I/R) injury in isolated rat hearts.Methods Seventy-two adult male Sprague-Dawley rats were randomly divided into 6 groups (n =12 each):control group (group CON),I/R group,sevoflurane control group (group SEVO),sevoflurane preconditioning group (group SWO P),5-hydroxydeconoate (5-HD) + sevoflurane preconditioning group (group 5-HD+ SWOP) and 5-HD control group (group 5-HD).The rats were exposed to 33％ pure oxygen for 1 h in groups CON and I/R.The rats were exposed to 2.5％ sevoflurane for 1 h in groups SEVO and SWOP.5-HD (a mito-KATP channel inhibitor) 10 mg/kg was injected intraperitoneally 30 min before sevoflurane preconditioning in group 5-HD + SWOP.5-HD 10 mg/kg was injected intraperitoneally in group 5-HD.The hearts were immediately removed and perfused in a Langendorff apparatus.The hearts were made globally ischemic for 30 min followed by 120 min reperfusion in groups I/R,SWOP,5-HD + SWOP and 5-HD.The expression of phosphorylated protein kinase C-epsilon (p-PKC-ε) and caspase-8 was measured by Western blot immediately before ischemia (T0) and at 120 min of reperfusion (T1).The myocardial infarct volume was measured by TTC staining.Results Compared with group CON,the myocardial infarct volume was significantly increased at T1 in groups I/R,SWOP,5-HD +SWOP and 5-HD,p-PKC-ε expression was up-regulated at T0 in groups SEVO and SWOP and at T1 in groups I/R,SWOP,5-HD + SWOP and 5-HD,and caspase-8 expression was down-regulated at T1 in group SEVO (P ＜0.05).Compared with group I/R,the myocardial infarct volume was significantly decreased at T1 in groups SWOP and 5-HD + SWOP,p-PKC-ε expression was up-regulated at T0 in groups SEVO and SWOP,and caspase-8 expression was down-regulated at T1 in group SWOP (P ＜ 0.05).Compared with group SWOP,the myocardial infarct volume was significantly increased,p-PKC-ε expression was down-regulated at T0,and caspase-8 expression was up-regulated at T1 in group 5-HD + SWOP (P ＜ 0.05).Conclusion The mito-KATP channel is involved in sevoflurane preconditioning-induced delayed cardioprotection against I/R injury in isolated rat hearts through upregulation of p-PKC-ε expression before ischemia and inhibition of cell apoptosis during reperfusion.

Objective:To explore the risk factors of seroma after laparoscopic totally extraperitoneal hernia repair.Methods:The clinical data of 236 patients underwent laparoscopic totally extraperitoneal hernia repair from July 2018 to June 2021 in Jiaozhou Central Hospital of Qingdao City were retrospectively analyzed. The related risk factors of seroma after laparoscopic totally extraperitoneal hernia repair were analyzed.Results:Among 236 patients, the seroma occurred in 36 cases (seroma group), the incidence of seroma was 15.25%; no seroma occurred in 200 cases (non-seroma group). There were statistical differences in the duration of disease ≥5 years, scrotal hernia, internal inguinal ring defect ≥3 cm, rupture of hernia sac, experience of operators <5 years between 2 groups ( P<0.01 or <0.05); there were no statistical difference in age, body mass, type of patch, preoperative complications (including diabetes, chronic obstructive pulmonary disease and cardiac cerebrovascular disease) and operative time between 2 groups ( P>0.05). Multivariate Logistic regression analysis result showed that the duration of disease ≥5 years, scrotal hernia, rupture of hernia sac and experience of operators<5 years were independent influencing factors of seroma after laparoscopic totally extraperitoneal hernia repair ( OR = 5.147, 5.006, 0.044 and 3.315; 95% CI 1.513 to 17.516, 1.845 to 13.583, 0.008 to 0.240 and 1.029 to 10.679; P<0.01 or<0.05). Conclusions:The duration of disease ≥5 years, scrotal hernia, rupture of hernia sac and experience of operators<5 years are independent influencing factors of seroma after laparoscopic totally extraperitoneal hernia repair, and preoperative assessment of risk factors is helpful to reduce the incidence of seroma.

Objective To investigate the effect ofbiglycan (BGN) on neural apoptosis in mice with early brain injury (EBI) after subarachnoid hemorrhage (SAH).Methods SAH models were induced by endovascular perforation in young male C57BL/6J mice.(1) Totally,48 mice were randomly divided into sham-operated group,SAH 6 h group,SAH 12 h group,SAH 24 h group,SAH 48 h group,and SAH 72 h group (n=8);the BGN protein and mRNA expressions were detected by Western blotting and real-time quantitative PCR (qRT-PCR).(2) Totally,16 mice were randomly divided into sham-operated group and SAH 48 h group (n=8);immunofluorescent double staining was conducted to explore the BGN expression in the neurons of brain tissues.(3) Totally,24 mice were randomly divided into sham-operated group,sham+control lentivirus group,and sham+BGN lentivirus group (n=8);BGN lentiviral vector and control lentivirus were administered intracerebroventricularly 7 d before sham-operation;qRT-PCR was performed to explore the BGN mRNA expression.(4) Totally,48 mice were randomly divided into sham-operated group,SAH+control lentivirus group,and SAH+BGN lentivirus group (n=16);BGN lentiviral vector and control lentivirus were administered intracerebroventricularly 7 d before SAH;neurological scores were detected by modified Garcia scale and beam balance tests;TUNEL was used to detect the neuronal apoptosis,and Western blotting was performed to explore the expressions of nuclear transcription factor kappa B (NF-κB) and phosphorylated-(p-) NF-κB.Results (1) Mice in the SAH 48 h group had the highest BGN protein and mRNA expressions,which showed statistical differences as compared with the sham-operated group (P＜0.05).(2) A majority of BGN expressions were detected in the neurons 48 h after SAH.(3) The sham+BGN lentivirus group had statistically lower BGN mRNA expression than the sham+control lentivirus group (P＜0.05).(4) As compared with those in the SAH+control lentivirus group,both scores of modified Garcia scale and beam balance tests were significantly higher in SAH+BGN lentivirus group (6.125±1.246 vs.13.000±1.309;1.125±1.126 vs.2.875±0.835),and neural apoptosis ratio and ratio of p-NF-κB/NF-κB were significantly lower in the SAH+BGN lentivirus group (51.950％±11.166％ vs.31.938％±7.705％;1.161±0.156 vs.0.886±0.142,P＜0.05).Conclusion Inhibition of BGN can effectively reduce neuronal apoptosis in mice with EBI after SAH,and attenuate neurological deficits.