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Objective To investigate the role and underlying mechanism of cathepsin B in myocar-dial injury in mice with diabetic cardiomyopathy(DCM).Methods Twenty 8-week-old male SPF C57BL/6 mice were randomly divided into wild-type(WT)group and WT DCM group,with 10 mice in each group.Another 20 8-week-old male SPF-grade mice with cathepsin B knockout(KO)were randomly and equally assigned to KO group and KO DCM group.HE staining was used to observe morphological changes,Prussian blue staining was employed to detect iron deposition,while immunohistochemical staining with 4-hydroxynonenal(4-HNE)was used to assess lipid peroxidation level in the myocardial tissues.Western blotting was performed to detect the expression of heme oxygenase-1(HO-1),superoxide dismutase 2(SOD2),and nuclear factor E2-related factor 2(Nrf2),while RT-PCR was applied to evaluate the expressions of Nrf-2,HO-1,and phospholipid hydroperoxide glutathione peroxidase 4(GPX4).Results Compared to the WT DCM group,the KO DCM group presented improved cell arrangement in cardiac tissues and sig-nificant reduction in inflammatory cell infiltration.Furthermore,the KO DCM group displayed a significant decrease in iron deposition compared to the WT DCM group.Additionally,the KO DCM group exhibited a significant reduction in 4-HNE expression compared to the WT DCM group.The protein levels of Nrf2,SOD2,and HO-1 were significant increased in the KO DCM group than the WT DCM group(0.68±0.21 vs 0.39±0.13,0.59±0.10 vs 0.28±0.09,1.03±0.10 vs 0.48±0.04,P＜0.05).Moreover,elevated mRNA levels of GPX4,Nrf2 and HO-1 were also observed in the KO DCM group than the WT DCM group(0.65±0.09 vs 0.40±0.10,0.61±0.11 vs 0.34±0.11,0.62±0.12 vs 0.39±0.09,P＜0.05).Conclusion Cathepsin B exacerbates myocardial injury in DCM mice through ferroptosis.
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Objective To investigate the clinical efficacy of double locking mini-plates for fixation of the comminuted fracture of the first metacarpal base.Methods Twenty-four patients with the comminuted fracture of the first metacarpal base were treated by double locking mini-plates in our hospital from January 2013 to January 2016.They were 17 males and 7 females,from 27 to 65 years of age (average,33.5 years).By the Green classification,6 cases were type Ⅰ,13 cases type Ⅱ and 5 cases type Ⅲ.All the fractures were closed.The average time from injury to surgery was 2.3 days (from 8 hours to 7 days).After open reduction via the palmar-radial incision,the fracture was fixated with 2 mini-plates,one locking T-plate on the radial side and one straight locking plate on the dorsal side.Fracture healing time,pain and finger function were followed up postoperatively.Visual analogue scale (VAS) was used to evaluate the pain at 12 months and scoring for digital total range of motion to assess the function of the affected finger at the final follow-up.Results The 24 patients obtained follow-up for 8 to 28 months (average,18 months).All the Fractures healed after 9 to 12 weeks (average,10.5 weeks).The VAS scores at 12 months ranged from 0 to 3 (average,1.5).The function of the affected finger at the final follow-up was excellent in 20 cases and good in 4,giving an excellent to good rate of 100％.Two patients complained of pain after frequent motion of the finger.No complications like skin problems,dislocation of the first metacarpal base,implant failure,necrosis or irritation of the soft tissue were observed during follow-up.No angulation or rotational deformity occurred after fracture union.Conclusion Fixation with double locking mini-plates can effectively treat comminuted fractures of the first metacarpal base,because it can provide rigid stabilization which promotes early functional exercise of the finger,and prevents joint stiffness as well.
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Objective To observe the dynamic changes of Notch1 protein expression in the subventricular zone (SVZ) after traumatic cerebral injury (TBI) in rats,and to explore the correlation between Notch signaling pathway and neural stem cells (NSCs) proliferation after TBI.Methods Ninety-six SD rats were randomly divided into sham-operated group (only opening the scalp and shall window,n=16),control group (without any treatment,n=16) and experimental group (establishing medium-sized TBI models with Feeney's free fall method,n=64);rats in the experimental group were divided into 4 sub groups according to the execution times (one,three,7 and 14 d after TBI,n=16).Immunofluorescence staining was performed to detect the Notchl/nestin labeled cell expressions in SVZ of rats,and Notch1 protein expression was detected by Western blotting.Results Immunofluorescence results showed that the Notch1/nestin double staining positive cells in the right SVZ brain tissues of the experimental group on the first day of TBI had peak level,which was 2-3 times of the control group;and then,it gradually declined and basically returned to normal on 144 day of TBI;the differences between the 4 subgroups were statistically different (P＜0.05).The positive cell counts in the subgroups of first,third,and 74 d after TBI were statistically different as compared with those in the control group and sham operated group (P＜0.05).Western blotting results indicated that there was no significant difference in the Notch1 protein expression between control group and sham operated group;Notch1 protein expression in SVZ of the experimental group had peak level on the first day of TBI,gradual decline was noted after that,and normal level was noted on the 14th d of TBI.Conclusion TBI can activate the Notch1 protein expression,which induces the opening of Notch signaling pathway so as to affect the regulation of NSCs proliferation.