Silencing of the long non-coding RNA LINC00265 triggers autophagy and apoptosis in lung cancer by reducing protein stability of SIN3A oncogene

Background:Long non-coding RNAs are important regulators in cancer biology and function either as tumor suppressors or as oncogenes.Their dysregulation has been closely associated with tumorigenesis.LINC00265 is upregulated in lung adenocarcinoma and is a prognostic biomarker of this cancer.However,the mechanism underlying its function in cancer progression remains poorly understood.Methods:Here,the regulatory role of LINC00265 in lung adenocarcinoma was examined using lung cancer cell lines,clinical samples,and xenografts.Results:We found that high levels of LINC00265 expression were associated with shorter overall survival rate of patients,whereas knockdown of LINC00265 inhibited proliferation of cancer cell lines and tumor growth in xenografts.Western blot andflow cytometry analyses indicated that silencing of LINC00265 induced autophagy and apoptosis.Moreover,we showed that LINC00265 interacted with and stabilized the transcriptional co-repressor Switch-independent 3a(SIN3A),which is a scaffold protein functioning either as a tumor repressor or as an oncogene in a context-dependent manner.Silencing of SIN3A also reduced proliferation of lung cancer cells,which was correlated with the induction of autophagy.These observations raise the possibility that LINC00265 functions to promote the oncogenic activity of SIN3A in lung adenocarcinoma.Conclusions:Ourfindings thus identify SIN3A as a LINC00265-associated protein and should help to understand the mechanism underlying LINC00265-mediated oncogenesis.

Muse cells decrease the neuroinflammatory response by modulating the proportion of M1 and M2 microglia in vitro

Neuroinflammation hinders repair of the central nervous system(CNS).Stem cell transplantation is a very promising approach for treatment of CNS injuries.However,it is difficult to select seed cells that can both facilitate nerve regeneration and improve the microenvironment in the CNS.In this study,we isolated multilineage-differentiating stress-enduring(Muse)cells from bone marrow mesenchymal stem cells.We explored the anti-inflammatory effect and mechanism of Muse cells in vitro by coculture of Muse cells with lipopolysaccharide-stimulated microglia.Our results showed that Muse cells effectively reduced the transcription and secretion of tumor necrosis factorαand interleukin-1βand increased the expression of transforming growth factor-βand interleukin-10 in microglia.In addition,Muse cells decreased the number of M1 microglia and increased the proportion of M2 microglia in an inflammatory environment more effectively than bone marrow mesenchymal stem cells.We also show that Muse cells inhibited the protein expression of toll-like receptor 4(TLR4)and myeloid differentiation primary response protein(MyD88)and inhibited the expression of the phosphorylated forms of transcription factor p65,nuclear factor(NF)-κB inhibitor alpha,and p38 mitogen-activated protein kinase(MAPK)in microglia.Therefore,we suggest Muse cells cause antineuroinflammatory effects by inhibition of the TLR4/MyD88/NF-κB and p38 MAPK signaling pathways in microglia.Our results shed light on the function of Muse cells in relation to CNS diseases and provide insight into the selection of seed cells.

Comprehensive overview of microRNA function in rheumatoid arthritis

MicroRNAs(miRNAs),a class of endogenous single-stranded short noncoding RNAs,have emerged as vital epigenetic regulators of both pathological and physiological processes in animals.They direct fundamental cellular pathways and processes by fine-tuning the expression of multiple genes at the posttranscriptional level.Growing evidence suggests that mi RNAs are implicated in the onset and development of rheumatoid arthritis(RA).RA is a chronic inflammatory disease that mainly affects synovial joints.This common autoimmune disorder is characterized by a complex and multifaceted pathogenesis,and its morbidity,disability and mortality rates remain consistently high.More in-depth insights into the underlying mechanisms of RA are required to address unmet clinical needs and optimize treatment.Herein,we comprehensively review the deregulated mi RNAs and impaired cellular functions in RA to shed light on several aspects of RA pathogenesis,with a focus on excessive inflammation,synovial hyperplasia and progressive joint damage.This review also provides promising targets for innovative therapies of RA.In addition,we discuss the regulatory roles and clinical potential of extracellular mi RNAs in RA,highlighting their prospective applications as diagnostic and predictive biomarkers.

Macrophage migration inhibitory factor facilitates astrocytic production of the CCL2 chemokine following spinal cord injury

Spinal cord injury causes accumulation of a large number of leukocytes at the lesion site where they contribute to excessive inflammation.Overproduced chemokines are responsible for the migratory process of the leukocytes,but the regulatory mechanism underlying the production of chemokines from resident cells of the spinal cord has not been fully elucidated.We examined the protein levels of macrophage migration inhibitory factor and chemokine C-C motif chemokine ligand 2 in a spinal cord contusion model at different time points following spinal cord injury.The elevation of macrophage migration inhibitory factor at the lesion site coincided with the increase of chemokine C-C motif chemokine ligand 2 abundance in astrocytes.Stimulation of primary cultured astrocytes with different concentrations of macrophage migration inhibitory factor recombinant protein induced chemokine C-C motif chemokine ligand 2 production from the cells,and the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine attenuated the stimulatory effect.Further investigation into the underlying mechanism on macrophage migration inhibitory factor-mediated astrocytic production of chemokine C-C motif chemokine ligand 2 revealed that macrophage migration inhibitory factor activated intracellular JNK signaling through binding with CD74 receptor.Administration of the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine following spinal cord injury resulted in the reduction of chemokine C-C motif chemokine ligand 2-recruited microglia/macrophages at the lesion site and remarkably improved the hindlimb locomotor function of rats.Our results have provided insights into the functions of astrocyte-activated chemokines in the recruitment of leukocytes and may be beneficial to develop interventions targeting chemokine C-C motif chemokine ligand 2 for neuroinflammation after spinal cord injury.

Multi-Classification of Polyps in Colonoscopy Images Based on an Improved Deep Convolutional Neural Network

Achieving accurate classification of colorectal polyps during colonoscopy can avoid unnecessary endoscopic biopsy or resection.This study aimed to develop a deep learning model that can automatically classify colorectal polyps histologically on white-light and narrow-band imaging(NBI)colonoscopy images based on World Health Organization(WHO)and Workgroup serrAted polypS and Polyposis(WASP)classification criteria for colorectal polyps.White-light and NBI colonoscopy images of colorectal polyps exhibiting pathological results were firstly collected and classified into four categories:conventional adenoma,hyperplastic polyp,sessile serrated adenoma/polyp(SSAP)and normal,among which conventional adenoma could be further divided into three sub-categories of tubular adenoma,villous adenoma and villioustublar adenoma,subsequently the images were re-classified into six categories.In this paper,we proposed a novel convolutional neural network termed Polyp-DedNet for the four-and six-category classification tasks of colorectal polyps.Based on the existing classification network ResNet50,Polyp-DedNet adopted dilated convolution to retain more high-dimensional spatial information and an Efficient Channel Attention(ECA)module to improve the classification performance further.To eliminate gridding artifacts caused by dilated convolutions,traditional convolutional layers were used instead of the max pooling layer,and two convolutional layers with progressively decreasing dilation were added at the end of the network.Due to the inevitable imbalance of medical image data,a regularization method DropBlock and a Class-Balanced(CB)Loss were performed to prevent network overfitting.Furthermore,the 5-fold cross-validation was adopted to estimate the performance of Polyp-DedNet for the multi-classification task of colorectal polyps.Mean accuracies of the proposed Polyp-DedNet for the four-and six-category classifications of colorectal polyps were 89.91%±0.92%and 85.13%±1.10%,respectively.The metrics of precision,recall and F1-score were also improved by 1%∼2%compared to the baseline ResNet50.The proposed Polyp-DedNet presented state-of-the-art performance for colorectal polyp classifying on white-light and NBI colonoscopy images,highlighting its considerable potential as an AI-assistant system for accurate colorectal polyp diagnosis in colonoscopy.

Matrix stiffening promotes chondrocyte senescence and the osteoarthritis development through downregulating HDAC3

Extracellular matrix(ECM)stiffening is a typical characteristic of cartilage aging,which is a quintessential feature of knee osteoarthritis(KOA).However,little is known about how ECM stiffening affects chondrocytes and other molecules downstream.This study mimicked the physiological and pathological stiffness of human cartilage using polydimethylsiloxane(PDMS)substrates.It demonstrated that epigenetic Parkin regulation by histone deacetylase 3(HDAC3)represents a new mechanosensitive mechanism by which the stiffness matrix affected chondrocyte physiology.We found that ECM stiffening accelerated cultured chondrocyte senescence in vitro,while the stiffness ECM downregulated HDAC3,prompting Parkin acetylation to activate excessive mitophagy and accelerating chondrocyte senescence and osteoarthritis(OA)in mice.Contrarily,intra-articular injection with an HDAC3-expressing adeno-associated virus restored the young phenotype of the aged chondrocytes stimulated by ECM stiffening and alleviated OA in mice.The findings indicated that changes in the mechanical ECM properties initiated pathogenic mechanotransduction signals,promoted the Parkin acetylation and hyperactivated mitophagy,and damaged chondrocyte health.These results may provide new insights into chondrocyte regulation by the mechanical properties of ECM,suggesting that the modification of the physical ECM properties may be a potential OA treatment strategy.

Inhibition of inflammatory mediator release from microglia can treat ischemic/hypoxic brain injury

Interleukin-1α and interleukin-1β aggravate neuronal injury by mediating the inf1αmmatory reaction following ischemic/hypoxic brain injury. It remains unclear whether interleukin-1α and interleukin-1β are released by microglia or astrocytes. This study prepared hippocampal slices that were subsequently subjected to oxygen and glucose deprivation. Hematoxylin-eosin staining verified that neurons exhibited hypoxic changes. Results of enzyme-linked immunosorbent assay found that interleukin-1α and interleukin-1β participated in this hypoxic process. Moreover, when hypoxic injury occurred in the hippocampus, the release of interleukin-1α and interleukin-1β was mediated by the P2X4 receptor and P2X7 receptor. Immunofluorescence staining revealed that during ischemia/hypoxia, the P2X4 receptor, P2X7 receptor, interleukin-1α and interleukin-1β expression was detectable in rat hippocampal microglia, but only P2X4 receptor and P2X7 receptor expression was detected in astrocytes. Results suggested that the P2X4 receptor and P2X7 receptor, respectively, mediated interleukin-1α and interleukin-1β released by microglia, resulting in hippocampal ischemic/hypoxic injury. Astrocytes were activated, but did not synthesize or release interleukin-1α and interleukin-1β.

Isoflurane-induced neuronal apoptosis in developing hippocampal neurons

We hypothesized that the P2X7 receptor may be the target of isoflurane, so we investigated the roles of the P2X7 receptor and inositol triphosphate receptor in calcium overload and neuronal apoptosis induced by isoflurane in cultured embryonic rat hippocampal neurons. Results showed that isoflurane induced widespread neuronal apoptosis and significantly increased cytoplasmic Ca^2＋ Blockade of P2X7 receptors or removal of extracellular Ca^2＋ combined with blockade of inositol triphosphate receptors completely inhibited apoptosis or increase in cytoplasmic Ca^2＋. Removal of extracellular Ca^2＋ or blockade of inositol triphosphate receptor alone could partly inhibit these effects of isoflurane. Isoflurane could directly activate P2X7-gated channels and induce inward currents, but did not affect the expression of P2X7 receptor protein in neurons. These findings indicate that the mechanism by which isoflurane induced neuronal apoptosis in rat developing brain was mediated by intracellular calcium overload, which was caused by P2X7 receptor mediated calcium influx and inositol triphosphate receptor mediated calcium release.

Potential risk of mitomycin C at high concentrations on peripheral nerve structure

Although the local application of mitomycin C may prevent epidural adhesion after laminectomy, mitomycin C can induce neurotoxicity in optic and acoustic nerves at high concentrations. To determine the safe concentration range for mitomycin C, cotton pads soaked with mitomycin C at different concentrations （0.1, 0.3, 0.5, and 0.7 mg/mL） were immediately applied for 5 minutes to the operation area of rats that had undergone laminectomy at L1. Rat sciatic nerves, instead of dorsal nerves, were used in this study. The results showed that mitomycin C at 0.1-0.5 mg/mL did not damage the structure and function of the sciatic nerve, while at 0.7 mg/mL, mitomycin C signiifcantly reduced the thickness of the sciatic nerve myelin sheath compared with lower concen-trations, though no functional change was found. These experimental ifndings indicate that the local application of mitomycin C at low concentrations is safe to prevent scar adhesion following laminectomy, but that mitomycin C at high concentrations （＆gt;0.7 mg/mL） has potential safety risks to peripheral nerve structures.

Use of FK506 and bone marrow mesenchymal stem cells for rat hind limb allografts

Dark Agouti rat donor hind limbs were orthotopically transplanted into Lewis rat recipients to verify the effects of bone marrow mesenchymal stem cells on neural regeneration and functional recovery of allotransplanted limbs in the microenvironment of immunotolerance, bone marrow mesenchymal stem cells were intramuscularly （gluteus maximus） injected with FK506 （tacrolimus） daily, and were transplanted to the injured nerves. Results indicated that the allograft group not receiving therapy showed severe rejection, with transplanted limbs detaching at 10 days after transplantation with complete necrosis. The number of myelinated axons and Schwann cells in the FK506 and FK506 ＋ bone marrow mesenchymal stem cells groups were significantly increased. We observed a lesser degree of gastrocnemius muscle degeneration, and increased polymorphic fibers along with other pathological changes in the FK506 ＋ bone marrow mesenchymal stem cells group. The FK506 ＋ bone marrow mesenchymal stem cells group showed significantly better recovery than the autograft and FK506 groups. The results demonstrated that FK506 improved the immune microenvironment. FK506 combined with bone marrow mesenchymal stem cells significantly promoted sciatic nerve regeneration, and improved sensory recovery and motor function in hind limb allotransplant.

Effects of Xianzhong Injection on the Function of Knee Joint and the Content of Insulin-Like Growth Factor-1 in Rabbits of Early Osteoarthritis

Objective: To evaluate the effect of Xianzhong Injection (仙仲注射液) into the articular cavity on the function of the joints and the content of insulin-like growth factor-1(IGF-1) in rabbits with early knee osteoarthritis (OA). Methods: 120 rabbits were randomly divided into five groups: blank group, model group (injecting 0.5ml of normal saline, once a week), positive control group (injecting 0.5ml of sodium hyaluronate, once a week), Xianzhong group I (injecting 0.5ml of Xianzhong Injection, once a week), Xianzhong group II (injecting 0.5ml of Xianzhong Injection, twice a week). Changes of the articular function and IGF-1 levels in the serum and joint fluid were investigated 8 weeks later. Results: The function of knee joint in the Xianzhong group I and II was improved significantly as compared with that in the model group (P<0.01), and there was no significant difference between the Xianzhong group I and the positive control group (P>0.05), but a significant difference was seen between the Xianzhong group I and the Xianzhong group II (P<0.05); in the positive control group, the Xianzhong group I and the Xianzhong group II , the levels of IGF-1 in the joint fluid and serum were significantly increased as compared with that in the model group (P﹤0.01). Conclusion: Xianzhong Injection can improve the function of knee joint in rabbits with early knee OA, and can substitute sodium hyaluronate Injection for treating this disease.

Evolution and current status of the subclassification of intermediate hepatocellular carcinoma

The staging and treatment of intermediate hepatocellular carcinoma(HCC)remains controversial.According to the recommendations of Barcelona Clinic Liver Cancer staging system,patients with intermediate HCC are candidates for transcatheter arterial chemoembolization.However,not all patients with intermediate HCC benefit from transcatheter arterial chemoembolization.Therefore,it is meaningful to propose a novel staging system of intermediate HCC in order to allocate different treatments for different subgroups.Bolondi et al proposed the first subclassification system of intermediate HCC.Subsequently,investigators performed studies to validate the feasibility of Bolondi’s criteria and proposed several novel staging systems.The present study reviewed the literatures and provided a general overview of the evolution and current status of the subclassification of intermediate HCC.We propose to expand the indication of liver resection and add radical treatments as the first option of the treatment for patients with intermediate HCC.

Variant TP53BP1 rs560191 G>C is associated with risk of gastric cardia adenocarcinoma in a Chinese Han population

Objective： To investigate the association between gastric cardia adenocarcinoma （GCA） and ten functional single nueleotide polymorphisms （SNPs）, including TPY3BPI rs560191 G〉C, CASP8 rs1035142 G〉T, CASP7 rs3127075 G〉C, CASP7 rs7907519 C〉A, and six C1 orf 10/CRNN variants. We performed a hospital- based case-control study to evaluate the genetic effects of these SNPs. Methods： Two hundred and forty-three GCA cases and 476 controls were enrolled in this study. A custom- by-design 48-Plex SNPscanTM Kit was used to determine their genotypes. Results： When the TP^3BP1 rs560191 GG homozygote genotype was used as the reference group, the GC genotype was associated with a significantly increased risk of GCA. The CC genotype was not associated with the risk of GCA compared with the GG genotype. None of the CASP8 rs1035142 G〉T, CASP7 rs3127075 G〉C, CASP7 rs7907519 C〉A or the six ClorflO/CRNN polymorphisms showed a significant difference in genotype distributions between the cases and the controls. Conciusions： The results demonstrated that the functional polymorphism TP53BPI rs560191 G〉C might contribute to GCA susceptibility. However, the statistical power of our study was limited. Large, well- designed studies and further functional investigations are needed to confirm our findings.

Design of Implant Prosthesis for Bone Injury Repair Considering Stress Shielding Effect

The failure of bone injury repair surgery is mostly due to the stress shielding effect caused by the difference of elastic modulus between the implant prosthesis and human bone,result-ing in a great damage to patients.To solve this problem,in this study,the influencing factors of the elastic modulus of implant prosthesis were investigated,the relationship between the elastic modulus of the implanted prosthesis and the influencing factors was analyzed,and then a design method of the implant prosthesis to reduce the stress shielding effect by adjusting the unit module to control the elastic modulus was established.This method was used for the biomechanical simula-tion to simulate the displacement and stress distribution between the implant prosthesis and the surrounding bone tissue,and then the reliability of the method was verified.The implant prosthe-sis with an elastic modulus consistent with that of the experimental dog bone was made by this method,and used for the animal experiments.The effects of implant prosthesis with different mod-ulus on the growth of surrounding bone tissue were observed,and at the same time,the reliability of the implant design method and the results of biomechanical simulation were verified.It is con-firmed that this method can effectively reduce the stress concentration of implant prosthesis by more than 15.4%and increase the growth of bone tissue by more than 21%.

Salubrinal alleviates traumatic spinal cord injury through suppression of the eIF2α/ATF4 pathway in mouse model

Spinal cord injury(SCI)remains an intractable clinical challenge of neurosurgery,it can be divided into two stages:uncontrollable primary injury induced by mechanical damage and controllable secondary injury regulated by continuous cell death.The apoptosis was the one of most important events in secondary injury,previous studies revealed that excessive endoplasmic reticulum(ER)stress breaks down the homeostasis and triggers apoptosis in the spinal cord.To deter or alleviate the secondary jury,we screen one of fat-soluble compounds,salubrinal,which was an inhibitor of eIF2αdephosphorylation can repair SCI by inhibiting ER stress in mice after SCI.Administration of salubrinal effectively represses apoptosis,protects neuronal cell,and promotes the restoration of locomotor function in mice SCI models.Furthermore,the level of phosphorylated eIF2αwas raised in the presence of salubrinal,but the protein expression of ATF4 and CHOP was downregulated.Unexpectedly,transcriptional expression of CHOPregulated pro-apoptotic genes was decreased.These data suggest salubrinal suppress ER stress by targeting eIF2α/ATF4 pathways and reduces cell death after SCI.It is suggested that the mitigation of secondary lesion by inhibiting ER stress induced apoptosis in the early phase of SCI is promising treatment strategy.

Relationship between Muscle Strength, Muscle Mass and BMD in Postmenopausal Female of Zhuang in Guangxi Province of China

Objective: To explore the correlation between muscle strength, muscle mass and bone mineral density (BMD) in Zhuang female population, body composition analysis and grip strength, and to analyze the possible influencing factors of BMD. Methods: 182 postmenopausal women were selected from Guangxi Province of China. Broadband ultrasound attenuation (BUA) was used to evaluate BMD. Grip dynamometer to assess muscle strength. Height, weight and muscle mass of each part were measured by body composition measuring instrument. Body mass index (BMI), skeletal muscle mass index (SMI) and limb skeletal muscle mass (SM) were calculated according to the measurement results. Results: BUA, grip strength and SMI in postmenopausal women of Zhuang nationality showed a decreasing trend with age (p p p r = 0.305, p Conclusion: With the increase of age, the decline rate of muscle strength of postmenopausal Zhuang women in Guangxi is slower than that of BMD and muscle mass. SM can better reflect the BMD level of the body than SMI, and the LSM is the main influencing factor of BMD.

Relationship Between Symptom Distress,Functional Status and Quality of Life in Patients with Low Back Myofascial Pain Syndrome

Objective:To explore the relationship between symptomatic functional status and quality of life of patients with low back myofascial pain syndrome(MPS).Methods:From July 2021 to June 2022,106 patients with low back myofascial pain syndrome in the Affiliated Hospital of Hebei University were selected as the research subjects.A total of 106 MPS patients were investigated with general information questionnaire,Memory Symptom Assessment Scale(MSAS),Oswestry Disability Index(ODI)and Short Form Questionnaire(SF-36).The relationship between quality of life and symptom distress and dysfunction was observed and analyzed based on symptom distress and dysfunction scores,SF-36 scores,and so on.Results:The total score of MSAS was 1.79±0.91.The overall symptom distress of the patients was moderate.The ODI score was 18.46±5.95.The functional disability of the patients was classified as moderately impaired.The MSAS-PHYS,MSAS-PSYCH,MSAS-GDI three scale scores were 2.14±0.75,1.69±0.88,1.55±0.46,respectively,and the variability of the three scales is relatively large;the dimension scores were significantly lower than those of the conventional scoring models,and P<0.05,indicating a statistical difference;the scores of each dimension of the patient’s quality of life were compared with the scores of symptom distress and functional status.The higher the symptom distress score,the lower the quality of life,with P<0.05,indicating a statistical difference;the higher the score of each dimension of functional status,the better the quality of life,showing a positive correlation,and P<0.05,indicating a statistical difference.Conclusion:MPS patients face a number of physical and psychological symptoms,and their functional status is limited.Nursing staff should implement health education and intervention measures according to the actual situation of the patients,so as to improve the quality of their lives.

Study on the Application Effect of Enhanced Recovery After Surgery (ERAS) in Patients Undergoing Spinal Fracture Surgery

Objective:To study the application effect of the Enhanced Recovery After Surgery(ERAS)model in patients undergoing spinal fracture surgery.Methods:A randomized controlled trial was designed,and 86 patients undergoing spinal fracture surgery were randomly divided into the ERAS group and the conventional care group.Postoperative recovery outcomes of the two groups were compared.Results:The ERAS group showed better outcomes in terms of postoperative pain scores,activities of daily living,length of hospital stay,and adherence to rehabilitation training compared to the conventional care group,with shorter hospital stays and lower medical expenses(P<0.05).Conclusion:The ERAS model significantly improves the postoperative recovery quality of patients undergoing spinal fracture surgery,reduces hospital stay and medical costs,and increases patient satisfaction.

仙灵骨葆对骨质疏松性骨折骨痂血管形成的影响

背景:骨质疏松对骨折愈合早期的影响尚存争议,仙灵骨葆对骨质疏松性骨折愈合的影响及其机制尚有待深入研究。目的:观察骨质疏松对大鼠股骨干骨折愈合的影响,以及仙灵骨葆对骨质疏松性骨折愈合的作用。方法:将50只雌性12周龄Sprague-Dawley大鼠随机分成5组:假手术组、骨折组、去卵巢组、去卵巢+骨折组及治疗组,后3组切除大鼠双侧卵巢制备去卵巢模型,骨折模型于去卵巢后4周制备,为股骨干中段横行骨折。治疗组在去卵巢及骨折基础上灌胃给予仙灵骨葆250mg/(kg·d)。给药3周,取去卵巢+骨折组、骨折组和治疗组大鼠骨折侧标本行X射线摄像仪摄片后,测量其骨密度,苏木精-伊红染色观察骨痂组织的病理学改变并计数血管,免疫组织化学染色检测骨痂组织骨形态发生蛋白2的表达。结果与结论:去卵巢处理后大鼠的骨密度、计算机X射线摄像仪摄片评分显著降低(P<0.05),仙灵骨葆可在一定程度上提高去卵巢后骨折大鼠的骨密度及X射线摄像仪摄片评分,但差异无显著性意义(P>0.05);仙灵骨葆可提高去卵巢后骨折大鼠骨痂组织的血管数量(P<0.05),但对骨形态发生蛋白2的表达无影响。提示,去卵巢后大鼠骨折早期愈合过程延迟,仙灵骨葆可促进骨质疏松大鼠骨折愈合早期血管的形成。

髋部骨折后下肢深静脉血栓形成家兔模型的建立

背景:目前各种方法诱导下肢深静脉血栓的动物模型缺乏统一的标准。目的:建立髋部骨折后下肢深静脉血栓形成兔模型。方法:采用专用击打装置,用位于28cm高度的击打物击打家兔后下肢左侧大腿根部;建立兔髋部骨折模型,另一侧兔后下肢不击打设为对照侧。4周后选取下肢髂静脉行彩色多普勒超声以及凝血功能的检查血栓形成情况。结果与结论:家兔经打击后经彩色多普勒超声检查存在下肢深静脉血栓,血栓长度(124±37)mm。对照侧无下肢深静脉血栓形成。血栓形成率81.8%,死亡率为9.1%。结果证实,实验成功建立的兔髋部骨折后下肢深静脉血栓形成模型,简单可行。