OBJECTIVE: To evaluate the effectiveness of double joystick technique assisted closed reduction and Kirschner wire internal fixation in the treatment of Gartland type Ⅲ supracondylar fractures of the humerus (SCFH) in children. METHODS: A retrospective study was conducted on 28 cases of Gartland type Ⅲ SCFH with complete data available, who underwent closed reduction and Kirschner wire internal fixation with the double joystick technique between August 2022 and July 2024. There were 23 boys and 5 girls, with an average age of 6.4 years (range, 1-12 years). All fractures resulted from falls and were classified as extension-type. X-ray film showed the radial displacement of the distal fragment in 15 cases and unlar displacement in 13 cases. The interval from injury to operation was 3-36 hours (mean, 19.5 hours). X-ray film re-examination was conducted to evaluate the fracture healing, and the Baumann angle of affected elbow joint and carrying angle of bilateral elbow joints were measured. Elbow joint function was evaluated using the range of motion (flexion and extension) and the Flynn criteria. The above indicators were compared between affected and healthy sides. RESULTS: All operation were successfully completed. The operation time ranged from 15 to 40 minutes (mean, 25.2 minutes). The length of hospital stay was 2-5 days (mean, 3.5 days). All patients were followed up 3-24 months (mean, 11.8 months). X-ray film confirmed fracture healing in all patients, with a mean healing time of 5.4 weeks (range, 4-6 weeks). At last follow-up, the Baumann angle of the affected elbow joint was (73.50±3.46)°, and the carrying angle and the range of motion in flexion and extension of the affected elbow joint were significantly less than the contralateral side (P<0.05). According to the Flynn criteria, the elbow joint function of the affected elbow was evaluated as excellent in 25 cases and good in 3 cases, with an excellent and good rate of 100%. CONCLUSION The double joystick technique is a safe and effective method which can facilitate the closed reduction and Kirschner wire internal fixation of Gartland type Ⅲ SCFH in children without increasing risk of complications.
Humans ; Male ; Female ; Humeral Fractures/diagnostic imaging* ; Fracture Fixation, Internal/instrumentation* ; Child ; Retrospective Studies ; Bone Wires ; Child, Preschool ; Fracture Healing ; Treatment Outcome ; Infant ; Elbow Joint/physiopathology* ; Range of Motion, Articular ; Closed Fracture Reduction/methods*

Iron overload is strongly associated with heart disease. Ferroptosis is a new form of regulated cell death indicated in cardiac ischemia-reperfusion (I/R) injury. However, the specific molecular mechanism of myocardial injury caused by iron overload in the heart is still unclear, and the involvement of ferroptosis in iron overload-induced myocardial injury is not fully understood. In this study, we observed that ferroptosis participated in developing of iron overload and I/R-induced cardiomyopathy. Mechanistically, we discovered that Parkin inhibited iron overload-induced ferroptosis in cardiomyocytes by promoting the ubiquitination of long-chain acyl-CoA synthetase 4 (ACSL4), a crucial protein involved in ferroptosis-related lipid metabolism pathways. Additionally, we identified p53 as a transcription factor that transcriptionally suppressed Parkin expression in iron-overloaded cardiomyocytes, thereby regulating iron overload-induced ferroptosis. In animal studies, cardiac-specific Parkin knockout mice (Myh6-CreER ^T2 /Parkin ^fl/fl ) fed a high-iron diet presented more severe myocardial damage, and the high iron levels exacerbated myocardial I/R injury. However, the ferroptosis inhibitor Fer-1 significantly suppressed iron overload-induced ferroptosis and myocardial I/R injury. Moreover, Parkin effectively protected against impaired mitochondrial function and prevented iron overload-induced mitochondrial lipid peroxidation. These findings unveil a novel regulatory pathway involving p53-Parkin-ACSL4 in heart disease by inhibiting of ferroptosis.

Sini Decoction (SNT) is a traditional formula recognized for its efficacy in warming the spleen and stomach and dispersing cold. However, elucidating the mechanism of action of SNT remains challenging due to its complex multiple components. This study utilized a synergistic approach combining two-dimensional fluorescence difference in gel electrophoresis (2D-DIGE)-based drug affinity responsive target stability (DARTS) with label-free quantitative proteomics techniques to identify the direct and indirect protein targets of SNT in myocardial infarction. The analysis identified 590 proteins, with 30 proteins showing significant upregulation and 51 proteins showing downregulation when comparing the SNT group with the model group. Through the integration of 2D-DIGE DARTS with proteomics data and pharmacological assessments, the findings indicate that protein disulfide-isomerase A3 (PDIA3) may serve as a potential protein target through which SNT provides protective effects on myocardial cells during myocardial infarction.
Myocardial Infarction/genetics* ; Proteomics/methods* ; Drugs, Chinese Herbal/chemistry* ; Animals ; Protein Disulfide-Isomerases/genetics* ; Male ; Two-Dimensional Difference Gel Electrophoresis/methods* ; Humans ; Rats ; Rats, Sprague-Dawley ; Electrophoresis, Gel, Two-Dimensional

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective To observe the effects of Baishile Capsules on neonatal neuronal activity and synaptic plasticity in hippocampus of depression model rats;To explore its mechanism of antidepressant.Methods Totally 32 SD rats were randomly divided into blank group,model group,fluoxetine group(5.4 mg/kg)and Baishile Capsules group(2.88 g/kg),with 8 rats in each group.The depression rat model was established by chronic unpredictable mild stress and single cage feeding,and drugs were administered at the same time as modeling for 21 consecutive days.Forced swimming test and open field test were used to evaluate the depressive-like behavior of rats,Golgi staining was used to observe the synaptic morphology of hippocampal neurons,and immunofluorescence was used to detect the positive expressions of BrdU/GABA-B,BrdU/c-fos,BrdU/GAP-43,BrdU/MAP-2 and CXCR4 in hippocampal tissue.Results Compared with the blank group,the immobility time of forced swimming experiment in the model group increased,and the horizontal and vertical time of open field experiment decreased significantly(P<0.01);the hippocampal neurons dendrites and dendritic spines atrophied,the density decreased,the branches became shorter,synaptic structure becomes blurred,and the longest and total lengths of synaptic branches significantly decreased(P<0.01);the positive expressions of GABA-B,c-fos,GAP-43 and MAP-2 proteins in hippocampal neonatal neurons decreased(P<0.05,P<0.01),and the expression of CXCR4 in hippocampal tissue decreased significantly(P<0.01).Compared with the model group,the immobility time of the forced swimming experiment in fluoxetine group and Baishile Capsules group significantly reduced,and the horizontal and vertical activity time of the open field experiment significantly increased(P<0.01);the number of dendritic spines in hippocampal neurons increased,synaptic damage improved,and the length of the longest and total branches of synapses significantly increased(P<0.01);the positive expressions of GABA-B,c-fos,GAP-43 and MAP-2 in hippocampal neonatal neurons significantly increased(P<0.05,P<0.01),and the positive expression of CXCR4 in hippocampal tissue significantly increased(P<0.01).Conclusion Baishile Capsules can regulate hippocampal synaptic plasticity and nerve regeneration by improving the activity and function of hippocampal neonatal neurons in depression model rats,exerting antidepressant effects.

The anatomical structure of the gingival papilla around the implant is special, and it is difficult to recover after injury. The reduction of its height will have a negative impact on function and esthetics, and it is one of the many problems in implant treatment at present. This paper analyzes the influencing factors of implant gingival papilla height from three aspects: anatomical factors, implant surgical design and implant restorative design, including the classical influencing factors such as the shape of natural teeth, interproximal distance between the implant and the adjacent tooth, soft tissue grafting, and contour of implant restorations, as well as the hot and controversial influencing factors in recent years such as the thickness of soft tissues around the implant, the implant surgical timing, the flap design, and the surgical incision, in order to provide reference for clinicians in the process of implant treatment for gingival papilla preservation and reconstruction.

Objective:To analyze the gene mutations of 18 patients with plasminogen (PLG) deficiency and to explore the clinical manifestations caused by PLG gene mutations.Methods:This study belongs to observational study-descriptive study: case series.Clinical data from 18 patients with PLG deficiency admitted to the First Affiliated Hospital of Wenzhou Medical University from January 1st, 2021 to May 31st, 2025 were collected. The age ranged from 16 to 70 years old, with an average of 48 years old. Among them, there were 10 males and 8 females. Anticoagulant blood samples were taken before treatment to measure and analyze plasminogen activity (PLG:A), plasminogen antigen (PLG:Ag), protein C activity, protein S activity, fibrinogen, antithrombin activity, D-dimer, and fibrin (fibrinogen) degradation products. PCR direct sequencing was used to analyze the 19 exons and flanking sequences of the PLG gene in these patients, and reverse sequencing was employed to verify the suspected mutations.Results:For the 18 patients, cranial MRI showed fresh cerebral infarction lesions, and PLG:A levels ranged from 19% to 67%, while no other lab indicators showed significant abnormalities, all presenting with dysplasminogenemia. Genetic analysis revealed five types of PLG gene mutations: c.1858G>A (p.Ala620Thr) heterozygous mutation, c.1858G>A (p.Ala620Thr) homozygous mutation, c.398A>G (p.His133Arg) heterozygous mutation, c.2108G>A (p.Gly703Asp) heterozygous mutation, and c.1702G>A (p.Gly568Arg) heterozygous mutation. Among the above, the c.1858G>A heterozygous mutation was the most common, and c.398A>G and c.1702G>A were identified for the first time.Conclusion:Patients with plasminogen deficiency caused by PLG gene defects are prone to occur cerebral infarction events, which may be related to impaired fibrinolytic function due to PLG gene mutations.

Objective:To explore the clinical efficacy of layered thinning superficial circumflex iliac artery perforator (SCIP) flap based on color Doppler ultrasound (CDU) positioning.Methods:The study was a retrospective observational study. From February 2023 to February 2024, 14 patients who met the inclusion criteria were admitted to the Department of Hand Surgery of Beijing Jishuitan Hospital Affiliated to Capital Medical University, including 11 males and 3 females, aged 15 to 60 years. The wound area was from 7 cm×4 cm to 14 cm×11 cm. Before the flap transplantation surgery, CDU was used to accurately locate the deep fascial exit point of the superficial branch of the superficial circumflex iliac artery. During the surgery, the SCIP flap was thinned in layers to repair the hand and forearm wounds of 11 patients and foot wounds of 3 patients. The flap incision area ranged from 8 cm×5 cm to 15 cm×12 cm. The donor area wounds of flaps were sutured directly. During the surgery, the deep fascial exit point of the superficial branch of the superficial circumflex iliac artery in the flap donor area was observed and compared with the result of CDU positioning before the surgery, and the flap thickness was measured. The flap survival and occurrence of adverse reactions were observed after the surgery. During follow-up, the appearance and texture of flaps, and the wound healing in the donor area was observed. At the last follow-up, the function of the wrist and hand in the affected limbs was evaluated according to the trial standards for evaluation of partial function of upper extremity by the Hand Surgery Society of Chinese Medical Association, and the function of the foot and ankle in the affected limbs was evaluated according to the scoring standard of American Orthopaedic Foot and Ankle Society.Results:During the surgery, the deep fascial exit point of the superficial branch of the superficial circumflex iliac artery in the flap donor area was consistent with the result of CDU positioning before the surgery, and the distance between them was less than 10 mm. The flap thickness was 5 to 8 mm with an average of 6.2 mm. All the flaps survived after surgery. During the follow-up of 5 to 12 months, the flaps had good appearance and texture, all the wounds in the donor areas healed with only linear scar left. At the last follow-up, the function of the wrist and hand in the affected limbs was evaluated as excellent in 9 cases, good in one case, and fair in one case; the function of the foot and ankle in the affected limbs was evaluated as excellent in one case and good in two cases.Conclusions:CDU examination can provide precise preoperative perforator positioning for layered thinning of SCIP flap and contribute to the optimization of flap design, so as to avoid the problem of flap necrosis caused by improper preoperative design to some extent and improve the safety of surgery. In addition, the layered thinning SCIP flap results in less damage to the donor area and is beneficial for the recovery of the affected limb function, which is worthy of clinical promotion.