Botanical characterization, phytochemistry, biosynthesis, pharmacology clinical application, and breeding techniques of the Chinese herbal medicine Fritillaria unibracteata.

Fritillaria unibracteata (FRU) belongs to the genus Fritillaria of the Liliaceae family. It is one of the original plants of the Chinese medicinal material "Chuanbeimu" and also a biological resource featured in the Tibetan Plateau of China. The dried bulbs of FRU are used in traditional Chinese medicine. The chemical constituents of FRU that have been isolated and identified include alkaloids, sterols, organic acids and their esters, nucleosides and volatile oils. FRU has antitussive, expectorant, anti-asthmatic, anti-inflammatory, antibacterial, acute lung injury-reducing, antifibrosis, antitumor, and other pharmacological effects. This valuable plant has an extremely high market demand, and over the years, due to over-exploitation, FRU has now been listed as a key species that is endangered and scarcely cultivated in China as a traditional Chinese medicinal herb. However, research on FRU is rare, and its effective components, resource control, and mechanisms of action need further study. This review systematically discusses the herbal characteristics, resource distribution, chemical composition, biosynthesis, pharmacological effects, clinical application, and breeding techniques of FRU, hoping to provide a reference for further research and the use of FRU.

Orchestrating NK and T cells via tri-specific nano-antibodies for synergistic antitumor immunity.

The functions of natural killer (NK) and T cells in innate and adaptive immunity, as well as their functions in tumor eradication, are complementary and intertwined. Here we show that utilization of multi-specific antibodies or nano-antibodies capable of simultaneously targeting both NK and T cells could be a valuable approach in cancer immunotherapy. Here, we introduce a tri-specific Nano-Antibody (Tri-NAb), generated by immobilizing three types of monoclonal antibodies (mAbs), using an optimized albumin/polyester composite nanoparticle conjugated with anti-Fc antibody. This Tri-NAb, targeting PDL1, 4-1BB, and NKG2A (or TIGIT) simultaneously, effectively binds to NK and CD8+ T cells, triggering their activation and proliferation, while facilitating their interaction with tumor cells, thereby inducing efficient tumor killing. Importantly, the antitumor efficacy of Tri-NAb is validated in multiple models, including patient-derived tumor organoids and humanized mice, highlighting the translational potential of NK and T cell co-targeting.

Progress in nanoparticle-based regulation of immune cells.

Immune cells are indispensable defenders of the human body, clearing exogenous pathogens and toxicities or endogenous malignant and aging cells. Immune cell dysfunction can cause an inability to recognize, react, and remove these hazards, resulting in cancers, inflammatory diseases, autoimmune diseases, and infections. Immune cells regulation has shown great promise in treating disease, and immune agonists are usually used to treat cancers and infections caused by immune suppression. In contrast, immunosuppressants are used to treat inflammatory and autoimmune diseases. However, the key to maintaining health is to restore balance to the immune system, as excessive activation or inhibition of immune cells is a common complication of immunotherapy. Nanoparticles are efficient drug delivery systems widely used to deliver small molecule inhibitors, nucleic acid, and proteins. Using nanoparticles for the targeted delivery of drugs to immune cells provides opportunities to regulate immune cell function. In this review, we summarize the current progress of nanoparticle-based strategies for regulating immune function and discuss the prospects of future nanoparticle design to improve immunotherapy.

Apatinib plus chemotherapy versus chemotherapy alone as neoadjuvant therapy in locally advanced gastric carcinoma patients: a prospective, cohort study.

BACKGROUND: Apatinib, a small molecule targeting VEGFR2, is commonly used for advanced gastric cancer treatment. This prospective cohort study further investigated the efficacy and safety of neoadjuvant apatinib plus chemotherapy in locally advanced gastric carcinoma patients. METHODS: Ninety-six locally advanced gastric carcinoma patients were divided into the apatinib plus chemotherapy group (N = 45) and chemotherapy group (N = 51) according to their chosen treatment. Apatinib was administered (375 mg/day), and S-1 plus oxaliplatin (SOX) or oxaliplatin plus capecitabine (CapOx) was given as chemotherapy, for 3 cycles with 3 weeks a cycle before surgery. RESULTS: The objective response rate (62.2% vs. 37.3%, P = 0.015) and pathological response grade (P = 0.011) were better; meanwhile, the tumor-resection rate (95.6% vs. 84.3%, P = 0.143) and pathological complete response rate (23.3% vs. 9.3%, P = 0.080) exhibited increasing trends (without statistical significance) in the apatinib plus chemotherapy group compared with the chemotherapy group. Additionally, the apatinib plus chemotherapy group achieved prolonged disease-free survival (DFS) (P = 0.019) and overall survival (OS) (P = 0.047) compared with the chemotherapy group. After adjusted by multivariate Cox's regression analysis, neoadjuvant apatinib plus chemotherapy was still superior to chemotherapy regarding DFS (hazard ratio (HR): 0.277, P = 0.014) and OS (HR: 0.316, P = 0.038). Notably, the incidences of adverse events between the two groups were not different (P > 0.050). Moreover, the most common adverse events of neoadjuvant apatinib plus chemotherapy were leukopenia (42.2%), fatigue (37.8%), hypertension (37.8%), and anemia (31.1%). CONCLUSION: Neoadjuvant apatinib plus chemotherapy realizes better clinical response, pathological response, survival profile, and non-inferior safety profile compared to chemotherapy in locally advanced gastric carcinoma.

MIL-101-Cr/Fe/Fe-NH2 for Efficient Separation of CH4 and C3H8 from Simulated Natural Gas.

Adsorptive separation based on porous solid adsorbents has emerged as an excellent effective alternative to energy-intensive conventional separation methods in a low energy cost and high working capacity manner. However, there are few stable mesoporous metal-organic frameworks (MOFs) for efficient purification of methane from other light hydrocarbons in natural gas. Herein, we report a series of stable mesoporous MOFs, MIL-101-Cr/Fe/Fe-NH2, for efficient separation of CH4 and C3H8 from a ternary mixture CH4/C2H6/C3H8. Experimental results show that all three MOFs possess excellent thermal, acid/basic, and hydrothermal stability. Single-component adsorption suggested that they have high C3H8 adsorption capacity and commendable selectivity for C3H8 and C2H6 over CH4. Transient breakthrough experiments further certified the ability of direct separation of CH4 from simulated natural gas and indirect recovery of C3H8 from the packing column. Theoretical calculations illustrated that the van der Waals force proportional to the molecular weight is the key factor and that the structural integrity and defect can impact separation performances.

Cell graph neural networks enable the precise prediction of patient survival in gastric cancer.

Gastric cancer is one of the deadliest cancers worldwide. An accurate prognosis is essential for effective clinical assessment and treatment. Spatial patterns in the tumor microenvironment (TME) are conceptually indicative of the staging and progression of gastric cancer patients. Using spatial patterns of the TME by integrating and transforming the multiplexed immunohistochemistry (mIHC) images as Cell-Graphs, we propose a graph neural network-based approach, termed Cell-Graph Signature or CGSignature, powered by artificial intelligence, for the digital staging of TME and precise prediction of patient survival in gastric cancer. In this study, patient survival prediction is formulated as either a binary (short-term and long-term) or ternary (short-term, medium-term, and long-term) classification task. Extensive benchmarking experiments demonstrate that the CGSignature achieves outstanding model performance, with Area Under the Receiver Operating Characteristic curve of 0.960 ± 0.01, and 0.771 ± 0.024 to 0.904 ± 0.012 for the binary- and ternary-classification, respectively. Moreover, Kaplan-Meier survival analysis indicates that the "digital grade" cancer staging produced by CGSignature provides a remarkable capability in discriminating both binary and ternary classes with statistical significance (P value < 0.0001), significantly outperforming the AJCC 8th edition Tumor Node Metastasis staging system. Using Cell-Graphs extracted from mIHC images, CGSignature improves the assessment of the link between the TME spatial patterns and patient prognosis. Our study suggests the feasibility and benefits of such an artificial intelligence-powered digital staging system in diagnostic pathology and precision oncology.

Pressure Loading Induces DNA Damage in Human Hepatocyte Line L02 Cells via the ERK1/2-Dicer Signaling Pathway.

Alteration of liver tissue mechanical microenvironment is proven to be a key factor for causing hepatocyte injury and even triggering the occurrence of hepatocellular carcinoma; however, the underlying mechanisms involved are not fully understood. In this study, using a customized, pressure-loading device, we assess the effect of pressure loading on DNA damage in human hepatocytes. We show that pressure loading leads to DNA damage and S-phase arresting in the cell cycle, and activates the DNA damage response in hepatocytes. Meanwhile, pressure loading upregulates Dicer expression, and its silencing exacerbates pressure-induced DNA damage. Moreover, pressure loading also activates ERK1/2 signaling molecules. Blockage of ERK1/2 signaling inhibits pressure-upregulated Dicer expression and exacerbates DNA damage by suppressing DNA damage response in hepatocytes. Our findings demonstrate that compressive stress loading induces hepatocyte DNA damage through the ERK1/2-Dicer signaling pathway, which provides evidence for a better understanding of the link between the altered mechanical environment and liver diseases.

Clinical Aspects of Gut Microbiota in Hepatocellular Carcinoma Management.

Liver cancer, predominantly hepatocellular carcinoma (HCC), is the third leading cause of cancer-related deaths worldwide. Emerging data highlight the importance of gut homeostasis in the pathogenesis of HCC. Clinical and translational studies revealed the patterns of dysbiosis in HCC patients and their potential role for HCC diagnosis. Research on underlying mechanisms of dysbiosis in HCC development pointed out the direction for improving the treatment and prevention. Despite missing clinical studies, animal models showed that modulation of the gut microbiota by probiotics may become a new way to treat or prevent HCC development.

Immunomodulating nano-adaptors potentiate antibody-based cancer immunotherapy.

Modulating effector immune cells via monoclonal antibodies (mAbs) and facilitating the co-engagement of T cells and tumor cells via chimeric antigen receptor- T cells or bispecific T cell-engaging antibodies are two typical cancer immunotherapy approaches. We speculated that immobilizing two types of mAbs against effector cells and tumor cells on a single nanoparticle could integrate the functions of these two approaches, as the engineered formulation (immunomodulating nano-adaptor, imNA) could potentially associate with both cells and bridge them together like an 'adaptor' while maintaining the immunomodulatory properties of the parental mAbs. However, existing mAbs-immobilization strategies mainly rely on a chemical reaction, a process that is rough and difficult to control. Here, we build up a versatile antibody immobilization platform by conjugating anti-IgG (Fc specific) antibody (αFc) onto the nanoparticle surface (αFc-NP), and confirm that αFc-NP could conveniently and efficiently immobilize two types of mAbs through Fc-specific noncovalent interactions to form imNAs. Finally, we validate the superiority of imNAs over the mixture of parental mAbs in T cell-, natural killer cell- and macrophage-mediated antitumor immune responses in multiple murine tumor models.

Comparison of clinical outcomes with hip replacement versus PFNA in the treatment of intertrochanteric fractures in the elderly: A systematic review and meta-analysis (PRISMA).

BACKGROUND: The purpose of this meta-analysis was to evaluate the clinical efficacy and safety of HR and PFNA in the treatment of intertrochanteric fractures in the elderly. METHODS: We carried out this review according to the principle of preferred reporting items for systematic reviews and meta-analyses (PRISMA) guideline. The clinical randomized controlled trials (RCTs), prospective cohort studies, retrospective cohort studies (RCSs), and case-control studies involving HR and PFNA in the treatment of intertrochanteric fractures in the elderly from 2000 to 2020 were compared by searching Web of Science, Pubmed, the Cochrane Library, and Embase. The quality of the included cohort study (CS) lines was evaluated using the Newcastle-Ottawa Scale (NOS). The quality of the included RCT lines was evaluated using Jadad. Forest plots were drawn by RevMan5.4 software based on the results and the data were analyzed. RESULTS: After screening, a total of 9 articles were included, of which one was a clinical RCT and eight were RCSs with 1374 patients. The operative time of the PFNA group was shorter [WMD = 15.20; 95% CI (13.17, 17.23), P < .05] and the intraoperative blood loss was less [WMD = 178.81; 95% CI (97.24, 260.38), P < .05] than the HR group, while the first weight-bearing time of the HR group was shorter [WMD = -7.70; 95% CI (-10.54, -4.86), P  < .05] than the PFNA group. There was no significant difference in the length of hospital stay, HHS, postoperative orthopedic complications, and postoperative medical complications between the 2 groups. CONCLUSION: With the development of HR technology and minimally invasive technology, the trauma caused by surgery is decreasing. Under the premise of improving perioperative management, such as optimizing the preoperative preparation and postoperative management, shortening the operative time, reducing intraoperative blood loss, and actively managing co-existing diseases, HR has more advantages than PFNA in the treatment of senile intertrochanteric fractures.

microRNA-935-modified bone marrow mesenchymal stem cells-derived exosomes enhance osteoblast proliferation and differentiation in osteoporotic rats.

AIMS: The involvement of several microRNAs (miRNAs) in osteogenic differentiation has been indicated recently. Also, exosomes, derived from different cells, could shuttle specific miRNAs to other cell systems. Nevertheless, the effect and mechanism of microRNA-935 (miR-935)-containing exosomes in osteoblasts remain basically unclear. The current work was set to inspect the relevance of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (BMSC-exo) carrying miR-935 to osteoporotic rats. METHODS: The extracted BMSCs and purchased osteoblasts were cultured, followed by exosome isolation and identification. After cell grouping, osteoblasts were co-cultured with BMSCs. CCK-8, alizarin red staining as well as ALP staining were performed to detect osteoblast proliferation and activity. The binding connection between miR-935 and signal transducer and activator of transcription 1 (STAT1) was measured by dual-luciferase reporter gene assays. The expression profiles of miR-935, STAT1 and osteoblast-related proteins were assessed by RT-qPCR and Western blot. A rat model with osteoporosis was induced, and the BMD, BV/TV, Tb.N, Tb.Th and Tb.Sp values in rat bone tissues were observed by Micro-CT. RESULTS: BMSC-exo inhibited STAT1 levels by the delivery of miR-935 into osteoblasts, while STAT1 silencing promoted ALP activity in osteoblasts and mineralized nodules. STAT1 was identified as a target gene of miR-935. Moreover, in vivo experiments showed that in ovariectomized rats, silencing of miR-935 significantly reduced BMD, BV/TV, Tb.N, Tb.Th and increased Tb.Sp. CONCLUSION: BMSC-exo carry miR-935 to promote osteoblast proliferation and differentiation through targeting STAT1.

Body Composition Analysis of 10 Years versus 5 Years of Adjuvant Endocrine Therapy in Patients with Nonmetastatic Breast Cancer.

OBJECTIVE: Our study aims to investigate the association of extended adjuvant endocrine therapy with disease-free survival (DFS), muscle mass, muscle strength, and visceral adipose tissue in patients with nonmetastatic breast cancer and the effect of extended endocrine therapy on body composition. Patients and Methods. Patients (N = 90) with nonmetastatic breast cancer aged between 60 and 65 years old were prospectively recruited in this study, compromising a cohort of subjects rece iving 5 years or 10 years of adjuvant endocrine therapy. Patients' DFS was compared between these two groups. Patients' body composition including muscle and fat using CT scans, muscle strength, and gait speed was evaluated in these two groups. RESULTS: Dietary behavior was recorded with the food frequency questionnaire (FFQ). Patients' age, body weight, and body mass index (BMI) did not differ between the two groups. An extended adjuvant endocrine therapy into 10 years could translate into DFS benefit (123.8 vs. 102.2 months, P=0.038). Patients receiving 10 years of adjuvant endocrine therapy had less skeletal muscle and more visceral fat compared with patients receiving 5 years of adjuvant endocrine therapy. The skeletal muscle index was 50.3 ± 1.6 cm2/m2 versus 46.5 ± 1.3 cm2/m2 in the 10 years or 5 years of adjuvant endocrine therapy group (P=0.042). The visceral fat was 28.9 ± 2.9 cm2/m2 versus 55.0 ± 3.2 cm2/m2 in the 10 years or 5 years of adjuvant endocrine therapy group (P=0.011). The muscle strength, gait speed, and FFQ results in the two groups not reaching statistical difference. CONCLUSION: In conclusion, breast cancer patients with 10 years of adjuvant endocrine therapy had DFS benefit, but with more muscle loss and adipose tissue deposits compared to patients receiving 5 years of adjuvant endocrine therapy.

An All-in-One Nanomedicine Consisting of CRISPR-Cas9 and an Autoantigen Peptide for Restoring Specific Immune Tolerance.

Nanotechnology has shown great promise in treating diverse diseases. However, developing nanomedicines that can cure autoimmune diseases without causing systemic immunosuppression is still quite challenging. Herein, we propose an all-in-one nanomedicine comprising an autoantigen peptide and CRISPR-Cas9 to restore specific immune tolerance by engineering dendritic cells (DCs) into a tolerogenic phenotype, which can expand autoantigen-specific regulatory T (Treg) cells. In brief, we utilized cationic lipid-assisted poly(ethylene glycol)-b-poly(lactide-co-glycolide) (PEG-PLGA) nanoparticles to simultaneously encapsulate an autoimmune diabetes-relevant peptide (2.5mi), a CRISPR-Cas9 plasmid (pCas9), and three guide RNAs (gRNAs) targeting costimulatory molecules (CD80, CD86, and CD40). We demonstrated that the all-in-one nanomedicine was able to effectively codeliver these components into DCs, followed by simultaneous disruption of the three costimulatory molecules and presentation of the 2.5mi peptide on the genome-edited DCs. The resulting tolerogenic DCs triggered the generation and expansion of autoantigen-specific Treg cells by presenting the 2.5mi peptide to CD4+ T cells in the absence of costimulatory signals. Using autoimmune type 1 diabetes (T1D) as a typical disease model, we demonstrated that our nanomedicine prevented autoimmunity to islet components and inhibited T1D development. Our all-in-one nanomedicine achieved codelivery of CRISPR-Cas9 and the peptide to DCs and could be easily applied to other autoimmune diseases by substitution of different autoantigen peptides.

Programmable Delivery of Immune Adjuvant to Tumor-Infiltrating Dendritic Cells for Cancer Immunotherapy.

Tumor-infiltrating dendritic cells (TIDCs) are mostly immature and immunosuppressive, usually mediating immune inhibition. The utilization of cytosine-guanine oligodeoxynucleotides (CpG ODNs) to stimulate the activation of TIDCs has been demonstrated to be effective for improving antitumor immunity. However, a series of biological barriers has limited the efficacy of previous nanocarriers for delivering CpG to TIDCs. Herein, we developed a dual-sensitive dendrimer cluster-based nanoadjuvant for delivering CpG ODNs into TIDCs. We show that the tumor acidity triggers the rapid release of CpG conjugated polyamidoamine (PAMAM) dendrimers from the nanoadjuvant, thus facilitating its perfusion deep into tumors and phagocytosis by TIDCs. Thereafter, the reductive condition of the endolysosomes led to the subsequent release of CpG, which promotes the DCs activation and enhances antitumor immunotherapies. Programmable delivery of immune adjuvant efficiently overcomes the barriers for targeted delivery to TIDCs and provides a promising strategy for improving cancer immunotherapy.

PSMC6 promotes osteoblast apoptosis through inhibiting PI3K/AKT signaling pathway activation in ovariectomy-induced osteoporosis mouse model.

There is now increasing evidence which suggests a key role for osteoblast apoptosis in the pathogenesis of postmenopausal osteoporosis. Here, we evaluated the role and mechanism of proteasome 26S subunit, ATPase (PSMC) 6, a protein that is highly expressed in bone. Gene expression pattern had been extracted based on database of Gene Expression Omnibus (GEO). GEO2R was employed for analyses, while the DAVID database was adopted to further analyze the gene ontology (GO) as well as Kyoto Encyclopedia of Genomes pathway (KEGG) enrichment. Then, the Search Tool Retrieval of Interacting Genes (STRING) was utilized to carry out interaction regulatory network for the top 200 differentially expressed genes (DEGs). A key gene, called PSMC6, was identified by Cytoscape 3.6.0. The OVX osteoporosis model was established in female C57BL/6 mice by full bilateral ovariectomy. According to our findings, PSMC6 gene knockout would elevate bone mineral density (BMD) and the phosphorylation level of PI3K protein and increased the protein level of cleaved caspase-3/-9 in OVX osteoporosis mice. Further, MTT, bromodeoxyuridine, and flow cytometry assays revealed that PSMC6 inhibition promoted the progression of cell cycle and cell proliferation, whereas, PSMC6 overexpression promoted the apoptosis and inhibited cell cycle progression and cell proliferation in vitro. Besides, we found that PI3K activation significantly decreased PSMC6-induced osteoblast apoptosis and promoted cell proliferation through regulating the protein levels of p53, cyclinD1, and cleaved caspase-3/9. In conclusion, PSMC6 aggravated the degree of OVX-induced osteoporosis by inhibiting the PI3K/AKT signal transduction pathway, thereby promoting the apoptosis of osteoblasts.

LncRNA NKILA integrates RXFP1/AKT and NF-κB signalling to regulate osteogenesis of mesenchymal stem cells.

Mesenchymal stem cells (MSCs) are previously found to have potential capacity to differentiate into osteocytes when exposed to specific stimuli. However, the detailed molecular mechanism during this progress remains largely unknown. In the current study, we characterized the lncRNA NKILA as a crucial positive regulator for osteogenesis of MSCs. NKILA attenuation significantly inhibits the calcium deposition and alkaline phosphatase activity of MSCs. More interestingly, we defined that NKILA is functionally involved in the regulation of RXFP1/PI3K-AKT and NF-κB signalling. Knockdown of NKILA dramatically down-regulates the expression of RXFP1 and then reduces the activity of AKT, a downstream regulator of RXFP1 signalling which is widely accepted as an activator of osteogenesis. Moreover, we identify NF-κB as another critical regulator implicated in NKILA-mediated osteogenic differentiation. Inhibition of NF-κB can induce the expression of RUNX2, a master transcription factor of osteogenesis, in a HDAC2-mediated deacetylation manner. Thus, this study illustrates the regulatory function of NKILA in osteogenesis through distinct signalling pathways, therefore providing a new insight into searching for new molecular targets for bone tissue repair and regeneration.

PLEXIN-B2 promotes the osteogenic differentiation of human bone marrow mesenchymal stem cells via activation of the RhoA signaling pathway.

Plexin-B2 (PLXNB2), a transmembrane protein is found in various tissues. Recent studies have indicated the presence of PLXNB2 in large quantity in the growth plates of Sprague-Dawley rats and are believed to be potentially involved in their skeletal development. This study endeavored to analyze the effect of PLXNB2 on the osteogenic differentiation of BMSCs by using gene overexpression and knockdown assays. The results of our study revealed that PLXNB2 was upregulated during BMSCs differentiation into an osteoblastic lineage. By determining the expression levels of specific markers and mineral deposition, the study established that PLXNB2 promotes the osteogenic differentiation of human BMSCs through the activation of the RhoA signaling pathway. In conclusion, the study identified PLXNB2 as a novel regulator that enhanced the osteogenic differentiation of human BMSCs. The enhancing effect of PLXNB2 on osteogenesis of human BMSCs was mediated through activation of RhoA signaling. The results of our study imply that pharmacological targeting of PLXNB2 may initiate a possible improvement in bone formation.

Comparison of sartorius muscle-pedicle and circumflex iliac deep bone flap grafts in the treatment of early non-traumatic osteonecrosis of femoral head in young adults.

OBJECTIVE: The aim of this study was to retrospectively compare and evaluate the midterm curative effect of two different bone flap grafts in the treatment of early non-traumatic osteonecrosis of the femoral head (ONFH). METHODS: A total of 180 patients (199 hips) with early non-traumatic ONFH received surgical treatment by sartorius muscle-pedicle bone flap graft (SMBF) (104 patients, 64 males and 40 females; mean age 34.67 ± 3.24 years) or circumflex iliac deep bone flap graft (CIDBF) (76 patients, 44 males and 32 females; mean age: 35.54 ± 3.37 years) from July 2004 to July 2009. The comparison between the groups was made with Harris score before and after surgery, length of incision, operative time, amount of bleeding, postoperative X-ray. Association Research Circulation Osseous (ARCO) staging was performed. RESULTS: The preoperative Harris hip score of two groups were 68.26 ± 1.26 and 69.35 ± 1.31, respectively. Patients' ARCO staging indicated 36 hips of stage IIa, 115 hips of stage IIb and 48 hips of stage IIc. The etiology of ONFH mainly including hormones (93 patients), alcohol (64 patients) and other (23 patients). The mean follow-up time of SMBF and CIDBF groups were (51.78 ± 2.35) and (52.73 ± 3.71) months, respectively. The time of removing sutures, operation time, amount of bleeding and length of incision in SMBF group were superior to those in the CIDBF group, and those differences between the SMBF and CIDBF groups were not significant (all p values > 0.28). The Harris score between the two groups was similar after operation and postoperative 12 month, and the difference was not statistically significant (p > 0.05), whereas the difference of the postoperative 24 and 48 months was statistically significant (p Ë‚ 0.05). X-ray analysis showed improvement of osteonecrosis in both two groups after surgery, and as time went on, the total hip amount decreased, the replacement amount increased. CONCLUSION: Both bone flap grafts appear to be effective methods for treatment of early osteonecrosis of femoral head (ARCOⅡ), and the SMBF is a relatively simple technique and easy for mastering, and it is a reliable method for clinical application. LEVEL OF EVIDENCE: Level III, Therapeutic Study.