Vertebral artery injury following combination Jefferson fracture of C1 and Type II odontoid fracture: A case report.

Traumatic posterior atlantoaxial dislocation combined with Jefferson fracture and odontoid process fracture with vertebral artery injury is rare. The management of such injury raises controversial issues and is still open to debate. A 74-year-old Chinese male presented with sustained neck pain and stiffness after falling from height. The patient was neurologically intact. Preoperative radiographs demonstrated a Jefferson burst fracture with a posterior dislocation of the atlantoaxial joints and odontoid process Anderson and D'alonzo type II fracture. A computed tomography angiography (CTA) showed an occluded left vertebral artery. Coil embolization in the proximal portion of the occluded vertebral artery was performed to prevent further cerebral infarction due to distal embolization of the thrombus. Then a second stage occipito-cervical fusion was performed to reconstruct cervical spine stability. A systematic screening of blunt trauma vertebral artery injuries through CTA is required when dealing with upper cervical fracture. For cases with vertebral artery occlusion secondary to cervical spine injury, endovascular treatment preceding cervical spine surgery is a feasible and a safe treatment.

Multi-phase features interaction transformer network for liver tumor segmentation and microvascular invasion assessment in contrast-enhanced CT.

Precise segmentation of liver tumors from computed tomography (CT) scans is a prerequisite step in various clinical applications. Multi-phase CT imaging enhances tumor characterization, thereby assisting radiologists in accurate identification. However, existing automatic liver tumor segmentation models did not fully exploit multi-phase information and lacked the capability to capture global information. In this study, we developed a pioneering multi-phase feature interaction Transformer network (MI-TransSeg) for accurate liver tumor segmentation and a subsequent microvascular invasion (MVI) assessment in contrast-enhanced CT images. In the proposed network, an efficient multi-phase features interaction module was introduced to enable bi-directional feature interaction among multiple phases, thus maximally exploiting the available multi-phase information. To enhance the model's capability to extract global information, a hierarchical transformer-based encoder and decoder architecture was designed. Importantly, we devised a multi-resolution scales feature aggregation strategy (MSFA) to optimize the parameters and performance of the proposed model. Subsequent to segmentation, the liver tumor masks generated by MI-TransSeg were applied to extract radiomic features for the clinical applications of the MVI assessment. With Institutional Review Board (IRB) approval, a clinical multi-phase contrast-enhanced CT abdominal dataset was collected that included 164 patients with liver tumors. The experimental results demonstrated that the proposed MI-TransSeg was superior to various state-of-the-art methods. Additionally, we found that the tumor mask predicted by our method showed promising potential in the assessment of microvascular invasion. In conclusion, MI-TransSeg presents an innovative paradigm for the segmentation of complex liver tumors, thus underscoring the significance of multi-phase CT data exploitation. The proposed MI-TransSeg network has the potential to assist radiologists in diagnosing liver tumors and assessing microvascular invasion.

GYY4137-induced p65 sulfhydration protects synovial macrophages against pyroptosis by improving mitochondrial function in osteoarthritis development.

INTRODUCTION: Osteoarthritis (OA) is the most common arthritis that is characterized by the progressive synovial inflammation and loss of articular cartilage. Although GYY4137 is a novel and slow-releasing hydrogen sulfide (H2S) donor with potent anti-inflammatory properties that may modulate the progression of OA, its underlying mechanism remains unclear. OBJECTIVES: In this study, we validated the protective role of GYY4137 against OA pathological courses and elucidated its underlying regulatory mechanisms. METHODS: Cell transfection, immunofluorescence staining, EdU assay, transmission electron microscopy, mitochondrial membrane potential measurement, electrophoretic mobility shift assay, sulfhydration assay, qPCR and western blot assays were performed in the primary mouse chondrocytes or the mouse macrophage cell line raw 264.7 for in vitro study. DMM-induced OA mice model and Macrophage-specific p65 knockout (p65f/f LysM-CreERT2) mice on the C57BL/6 background were used for in vivo study. RESULTS: We found that GYY4137 can alleviate OA progress by suppressing synovium pyroptosis in vivo. Moreover, our in vitro data revealed that GYY4137 attenuates inflammation-induced NLRP3 and caspase-1 activation and results in a decrease of IL-1ß production in macrophages. Mechanistically, GYY4137 increased persulfidation of NF-kB p65 in response to inflammatory stimuli that results in a decrease of cellular reactive oxygen species (ROS) accumulation and ameliorates mitochondrial dysfunctions. Using site-directed mutagenesis, we showed that H2S persulfidates cysteine38 in p65 protein and hampers p65 transcriptional activity, and p65 mutant impaired macrophage responses to GYY4137. CONCLUSION: These findings suggest a mechanism by which GYY4137 through redox modification of p65 participates in inhibiting NLRP3 activation by OA to regulate inflammatory responses. Thus, we propose that GYY4137 represents a promising novel therapeutic strategy for the treatment of OA.

Deficiency of CBL and CBLB ubiquitin ligases leads to hyper T follicular helper cell responses and lupus by reducing BCL6 degradation.

Recent evidence reveals hyper T follicular helper (Tfh) cell responses in systemic lupus erythematosus (SLE); however, molecular mechanisms responsible for hyper Tfh cell responses and whether they cause SLE are unclear. We found that SLE patients downregulated both ubiquitin ligases, casitas B-lineage lymphoma (CBL) and CBLB (CBLs), in CD4+ T cells. T cell-specific CBLs-deficient mice developed hyper Tfh cell responses and SLE, whereas blockade of Tfh cell development in the mutant mice was sufficient to prevent SLE. ICOS was upregulated in SLE Tfh cells, whose signaling increased BCL6 by attenuating BCL6 degradation via chaperone-mediated autophagy (CMA). Conversely, CBLs restrained BCL6 expression by ubiquitinating ICOS. Blockade of BCL6 degradation was sufficient to enhance Tfh cell responses. Thus, the compromised expression of CBLs is a prevalent risk trait shared by SLE patients and causative to hyper Tfh cell responses and SLE. The ICOS-CBLs axis may be a target to treat SLE.

Complete miRNA-15/16 loss in mice promotes hematopoietic progenitor expansion and a myeloid-biased hyperproliferative state.

Dysregulated apoptosis and proliferation are fundamental properties of cancer, and microRNAs (miRNA) are critical regulators of these processes. Loss of miR-15a/16-1 at chromosome 13q14 is the most common genomic aberration in chronic lymphocytic leukemia (CLL). Correspondingly, the deletion of either murine miR-15a/16-1 or miR-15b/16-2 locus in mice is linked to B cell lymphoproliferative malignancies. However, unexpectedly, when both miR-15/16 clusters are eliminated, most double knockout (DKO) mice develop acute myeloid leukemia (AML). Moreover, in patients with CLL, significantly reduced expression of miR-15a, miR-15b, and miR-16 associates with progression of myelodysplastic syndrome to AML, as well as blast crisis in chronic myeloid leukemia. Thus, the miR-15/16 clusters have a biological relevance for myeloid neoplasms. Here, we demonstrate that the myeloproliferative phenotype in DKO mice correlates with an increase of hematopoietic stem and progenitor cells (HSPC) early in life. Using single-cell transcriptomic analyses, we presented the molecular underpinning of increased myeloid output in the HSPC of DKO mice with gene signatures suggestive of dysregulated hematopoiesis, metabolic activities, and cell cycle stages. Functionally, we found that multipotent progenitors (MPP) of DKO mice have increased self-renewing capacities and give rise to significantly more progeny in the granulocytic compartment. Moreover, a unique transcriptomic signature of DKO MPP correlates with poor outcome in patients with AML. Together, these data point to a unique regulatory role for miR-15/16 during the early stages of hematopoiesis and to a potentially useful biomarker for the pathogenesis of myeloid neoplasms.

Endothelial Cell-Derived Lactate Triggers Bone Mesenchymal Stem Cell Histone Lactylation to Attenuate Osteoporosis.

Blood vessels play a role in osteogenesis and osteoporosis; however, the role of vascular metabolism in these processes remains unclear. The present study finds that ovariectomized mice exhibit reduced blood vessel density in the bone and reduced expression of the endothelial glycolytic regulator pyruvate kinase M2 (PKM2). Endothelial cell (EC)-specific deletion of Pkm2 impairs osteogenesis and worsens osteoporosis in mice. This is attributed to the impaired ability of bone mesenchymal stem cells (BMSCs) to differentiate into osteoblasts. Mechanistically, EC-specific deletion of Pkm2 reduces serum lactate levels secreted by ECs, which affect histone lactylation in BMSCs. Using joint CUT&Tag and RNA sequencing analyses, collagen type I alpha 2 chain (COL1A2), cartilage oligomeric matrix protein (COMP), ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), and transcription factor 7 like 2 (TCF7L2) as osteogenic genes regulated by histone H3K18la lactylation are identified. PKM2 overexpression in ECs, lactate addition, and exercise restore the phenotype of endothelial PKM2-deficient mice. Furthermore, serum metabolomics indicate that patients with osteoporosis have relatively low lactate levels. Additionally, histone lactylation and related osteogenic genes of BMSCs are downregulated in patients with osteoporosis. In conclusion, glycolysis in ECs fuels BMSC differentiation into osteoblasts through histone lactylation, and exercise partially ameliorates osteoporosis by increasing serum lactate levels.

The calcium channel TRPV6 is a novel regulator of RANKL-induced osteoclastic differentiation and bone absorption activity through the IGF-PI3K-AKT pathway.

OBJECTIVES: Calcium ion signals are important for osteoclast differentiation. Transient receptor potential vanilloid 6 (TRPV6) is a regulator of bone homeostasis. However, it was unclear whether TRPV6 was involved in osteoclast formation. Therefore, the aim of this study was to evaluate the role of TPRV6 in bone metabolism and to clarify its regulatory role in osteoclasts at the cellular level. MATERIALS AND METHODS: Bone structure and histological changes in Trpv6 knockout mice were examined using micro-computed tomography and histological analyses. To investigate the effects of Trpv6 on osteoclast function, we silenced or overexpressed Trpv6 in osteoclasts via lentivirus transfection, respectively. Osteoclast differentiation and bone resorption viability were measured by tartrate-resistant acid phosphatase (TRAP) staining and pit formation assays. The expression of osteoclast marker genes, including cathepsin k, DC-STAMP, Atp6v0d2 and TRAP, was measured by qRT-PCR. Cell immunofluorescence and Western blotting were applied to explore the mechanisms by which the IGF-PI3K-AKT pathway was involved in the regulation of osteoclast formation and bone resorption by Trpv6. RESULTS: We found that knockout of Trpv6 induced osteoporosis and enhanced bone resorption in mice, but did not affect bone formation. Further studies showed that Trpv6, which was distributed on the cell membrane of osteoclasts, acted as a negative regulator for osteoclast differentiation and function. Mechanistically, Trpv6 suppressed osteoclastogenesis by decreasing the ratios of phosphoprotein/total protein in the IGF-PI3K-AKT signalling pathway. Blocking of the IGF-PI3K-AKT pathway significantly alleviated the inhibitory effect of Trpv6 on osteoclasts formation. CONCLUSIONS: Our study confirmed the important role of Trpv6 in bone metabolism and clarified its regulatory role in osteoclasts at the cellular level. Taken together, this study may inspire a new strategy for the treatment of osteoporosis.

Novel Bioactive Penicipyrroether A and Pyrrospirone J from the Marine-Derived Penicillium sp. ZZ380.

The marine-sourced fungus Penicillium sp. ZZ380 was previously reported to have the ability to produce a series of new pyrrospirone alkaloids. Further investigation on this strain resulted in the isolation and identification of novel penicipyrroether A and pyrrospirone J. Each of them represents the first example of its structural type, with a unique 6/5/6/5 polycyclic fusion that is different from the 6/5/6/6 fused ring system for the reported pyrrospirones. Their structures were elucidated by extensive nuclear magnetic resonance (NMR) and high resolution electrospray ionization mass spectroscopy (HRESIMS) spectroscopic analyses, electronic circular dichroism (ECD) and 13C NMR calculations and X-ray single crystal diffraction. Penicipyrroether A showed potent antiproliferative activity against human glioma U87MG and U251 cells with half maximal inhibitory concentration (IC50) values of 1.64-5.50 µM and antibacterial inhibitory activity with minimum inhibitory concentration (MIC) values of 1.7 µg/mL against methicillin-resistant Staphylococcus aureus and 3.0 µg/mL against Escherichia coli.

Bioactive Penicipyrrodiether A, an Adduct of GKK1032 Analogue and Phenol A Derivative, from a Marine-Sourced Fungus Penicillium sp. ZZ380.

Penicipyrrodiether A, an adduct of GKK1032 analogue and phenol A derivative, was isolated from a culture of marine-associated fungus Penicillium sp. ZZ380 and represents the first example of this type of fungal metabolite. Its structure was elucidated by extensive spectroscopic analyses, including 1D- and 2D-NMR, HRESIMS, MS/MS, and electronic circular dichroism calculation as well as single-crystal X-ray diffraction. Penicipyrrodiether A showed antibacterial activity in inhibiting the growth of methicillin-resistant Staphylococcus aureus with a MIC value of 5.0 µg/mL. Its plausible pathway for biosynthesis has been proposed.

Regulation of TRPV5 transcription and expression by E2/ERα signalling contributes to inhibition of osteoclastogenesis.

The increasing of osteoclasts formation and activity because of oestrogen (E2) deficiency is very important in the aetiology of postmenopausal osteoporosis. Our previous studies showed that E2 inhibited osteoclastic bone resorption by increasing the expression of Transient Receptor Potential Vanilloid 5 (TRPV5) channel. However, the exact mechanism by which E2 increases TRPV5 expression is not fully elucidated. In this study, Western blot, quantitative real-time PCR, tartrate-resistant acid phosphatase staining, F-actin ring staining, chromatin immunoprecipitation and luciferase assay were applied to explore the mechanisms that E2-induced TRPV5 expression contributes to the inhibition of osteoclastogenesis. The results showed that silencing or overexpressing of TRPV5 significantly affected osteoclasts differentiation and activity. Silencing of TRPV5 obviously alleviated E2-inhibited osteoclastogenesis, resulting in increasing of bone resorption. E2 stimulated mature osteoclasts apoptosis by increasing TRPV5 expression. Further studies showed that E2 increased TRPV5 expression through the interaction of the oestrogen receptor α (ERα) with NF-κB, which could directly bind to the fragment of -286 nt ~ -277 nt in the promoter region of trpv5. Taken together, we conclude that TRPV5 plays a dominant effect in E2-mediated osteoclasts formation, bone resorption activity and osteoclasts apoptosis. Furthermore, NF-κB plays an important role in the transcriptional activation of E2-ERα stimulated TRPV5 expression.

Anti-glioma Natural Products Downregulating Tumor Glycolytic Enzymes from Marine Actinomycete Streptomyces sp. ZZ406.

Marine natural products are important resources for discovering novel anticancer drugs. In this study, an extract prepared from the culture of a sea anemone-derived actinomycete Streptomyces sp. ZZ406 in soluble starch and casein-related liquid medium was found to have activity in inhibiting the proliferation of glioma cells and reducing the production of lactate in glioma cells. Chemical investigation of this active crude extract resulted in the isolation of four new compounds and seven known ones. Structures of the new compounds were determined by a combination of extensive NMR analyses, HRESIMS and MS-MS data, electronic circular dichroism calculation, chemical degradation, and Marfey's method. New compound 1 showed potent activity against the proliferation of different glioma cells with IC50 values of 4.7 to 8.1 µM, high selectivity index (>12.3 to 21.3), and good stability in human liver microsomes. Western blot analysis revealed that compound 1 remarkably downregulated the expressions of several important glioma glycolytic enzymes. The data from this study suggested that compound 1 might have potential as a novel anti-glioma agent to be further investigated.

Anti-colorectal cancer effects of tripolinolate A from Tripolium vulgare.

Tripolinolate A (TLA) is recently identified as a new compound from a halophyte plant Tripolium vulgare and has been shown to have significant in vitro activity against the proliferation of colorectal cancer and glioma cells. This study was designed to further investigate the effects of TLA on the proliferation of human normal cells, and the apoptosis and cell cycle in colorectal cancer cells, and the growth of tumors in the colorectal cancer-bearing animals. The data obtained from this study demonstrated that: 1) TLA had much less cytotoxicity in the human normal cells than the colorectal cancer cells; 2) TLA remarkably induced apoptosis in the human colorectal cancer cells and blocked cell cycle at G2/M phase, and 3) TLA had significant anti-colorectal cancer activity in the tumor-bearing animals.

Rare Polyene-polyol Macrolides from Mangrove-derived Streptomyces sp. ZQ4BG.

Bioactive natural products from mangrove-derived actinomycetes are important sources for discovery of drug lead compounds. In this study, an extract prepared from culture of an actinomycete Streptomyces sp. ZQ4BG isolated from mangrove soils was found to have activity in inhibiting proliferation of glioma cells. Large culture of this mangrove actinomycete in Gause's liquid medium resulted in isolation of seven novel polyene-polyol macrolides, named as flavofungins III-IX (3-9), together with known flavofungins I (1) and II (2) and spectinabilin (10). Structures of these isolated compounds were elucidated by extensive NMR analyses and HRESIMS data. The stereochemical assignments were achieved by a combination of NOE information, universal NMR database, and chemical reactions including preparation of acetonide derivatives and Mosher esters. Flavofungins IV-VIII (4-8) are rare 32-membered polyene-polyol macrolides with a tetrahydrofuran ring, while flavofungin IX (9) represents the first example of this type of macrolide with a unique oxepane ring. Flavofungins I (1) and II (2) and spectinabilin (10) showed anti-glioma and antifungal activities.

Cytotoxic Bagremycins from Mangrove-Derived Streptomyces sp. Q22.

New bagremycins C-E (3-5) and bagrelactone A (6), together with known bagremycins A (1) and B (2), 4-hydroxystyrene (7), and 4-hydroxystyrene 4-O-α-d-galactopyranoside (8), were isolated from a mangrove-derived actinomycete, Streptomyces sp. Q22. Structures of these new compounds were elucidated based on their NMR and HRESIMS spectroscopic data as well as chemical degradation. Bagremycin C (3) is a unique analogue with an N-acetyl-(S)-cysteine moiety, while bagrelactone A (6) represents the first example of this type of bagremycin-derived macrolide. Bagremycin C (3) was active against four glioma cell lines, with IC50 values in the range from 2.2 to 6.4 µM, induced apoptosis in human glioma U87MG cells in a dose- and time-dependent manner, and arrested the U87MG cell cycle at the G0/G1 phase.

Antiproliferative cyclodepsipeptides from the marine actinomycete Streptomyces sp. P11-23B downregulating the tumor metabolic enzymes of glycolysis, glutaminolysis, and lipogenesis.

Two cyclodepsipeptides and a known cyclodepsipeptide valinomycin were isolated from a culture of the marine actinomycete Streptomyces sp. P11-23B. Their structures were established based on NMR, HRESIMS, and MS-MS spectroscopic interpretation as well as by chemical degradation. Both streptodepsipeptides P11A and P11B inhibited proliferation of different glioma cell lines, with IC50 values ranging from 0.1 µM to 1.4 µM. Streptodepsipeptide P11A was found to block the cell cycle at the G0/G1 phase and induce apoptosis in glioma cells. Further investigation demonstrated that streptodepsipeptide P11A downregulated expression of HK2, PFKFB3, PKM2, GLS, and FASN, important tumor metabolic enzymes. Data from this study suggested that targeting multiple tumor metabolic regulators might be one anti-glioma mechanism of streptodepsipeptide P11A. A possible mechanism for this class of streptodepsipeptides is reported herein.

A new curvularin glycoside and its cytotoxic and antibacterial analogues from marine actinomycete Pseudonocardia sp. HS7.

Five curvularin macrolides (1-5) were isolated from the cultured broth of marine actinomycete Pseudonocardia sp. HS7 that was obtained from the cloacal aperture of sea cucumber Holothuria moebii. The structures of these isolates were characterized as (11S,15R)-11-hydroxycurvularin (1), (11R,15R)-11-hydroxycurvularin (2), curvularin-7-O-α-D-glucopyranoside (3), trans-dehydrocurvularin (4) and curvularin (5) based on their NMR and HRESIMS data as well as chemical degradation. Compound 3 is a new macrolide with a rare α-D-glucopyranose substituent. Compounds 1-4, 5a and 5c (the acyl products of 5), suppressed the proliferation of all six tested cancer cell lines and 4 is the most active compound with IC50 values ranging from 0.59 to 3.39 µM. The 11-hydroxycurvularins 1 and 2 also showed antibacterial activity inhibiting the growth of Escherichia coli.

Comparison of the outcome of early and delayed surgical treatment of complete acromioclavicular joint dislocation.

PURPOSE: The aim of this study is to compare the clinical and radiographic results and the complication rate between early and delayed surgical treatment of acromioclavicular joint (ACJ) dislocation. METHODS: Publications in the management of ACJ dislocation are identified from the PubMed database between January 1993 and December 2013 using "acromioclavicular joint" and "dislocation" as keywords. The eligibility criteria included are as follows: (1) ACJ dislocation; (2) intervention, early compared with delayed surgical treatment or the surgical treatment for acute compared with chronic ACJ dislocation; (3) human; and (4) English articles. Exclusion criteria consist of the following: (1) type I and type II ACJ dislocation, (2) no definition of the time of early and delayed surgery in studies, (3) no comparison between the clinical result of early and delayed surgery in studies, (4) laboratory studies, radiographic studies, biomechanical studies, (5) the cases including fractures or revisions in studies, and (6) systematic analyses. RESULTS: Eight studies comparing early and delayed surgical treatment of ACJ dislocation are included in this systematic review. According to Constant scores and shoulder subjective value, early surgery has better functional outcomes than delayed surgery in the treatment of ACJ dislocation (P < 0.05). Partial-dislocation/re-dislocation is found at 26.0 % in early and 38.1 % in delayed surgical treatment (P < 0.05). The rate of CC ossification in early surgical treatment is found as the same as the delayed. The complication rates are found at 12.5 % in early surgical treatment and 17.7 % in the delayed, which is not significantly different. CONCLUSION: Early surgical treatment may have superiority to the delayed procedure in the management of ACJ dislocation with better functional outcomes and more satisfied reduction. However, high-quality evidence studies are required to provide stronger support for this opinion in the future. LEVEL OF EVIDENCE: IV.

Signaling lymphocyte-activation molecule SLAMF1 augments mycobacteria BCG-induced inflammatory response and facilitates bacterial clearance.

Tuberculosis, which is caused by intracellular mycobacterium Mycobacterium tuberculosis (Mtb), remains one of the most serious global public health concerns. The mechanisms by which innate immunity regulates the inflammatory responses and affects mycobacterial infection remain unclear. In this study, signaling lymphocyte-activation molecule family 1 (SLAMF1) was significantly upregulated in Mycobacterium bovis Bacille Calmette-Guérin (BCG)-infected RAW264.7 cells. Overexpression of SLAMF1 significantly increased the production of inflammatory factors TNF-α and IL-1ß, as well as chemokine MCP-1, both in vitro and in vivo upon mycobacteria BCG infection. By contrast, knockdown of SLAMF1 significantly decreased the production of TNF-α, IL-1ß, and MCP-1. Western blot analysis indicated that the NF-κB signaling pathway may contribute to the elevated inflammatory response promoted by SLAMF1, as evidenced by higher levels of phosphorylated p65 and IκBα detected with SLAMF1 overexpression. Furthermore, SLAMF1 upregulation facilitated bacterial clearance in infected RAW264.7 cells and in the lungs of infected mice. In conclusion, we demonstrated that BCG infection significantly upregulated SLAMF1, which enhanced inflammatory response by activating the NF-κB signaling pathway and facilitated bacterial clearance in BCG-infected RAW264.7 cells and mice.

Synthesis and bioactivity of tripolinolate A from Tripolium vulgare and its analogs.

A new coniferol derivative, named as tripolinolate A (1), and 11 known compounds (2-12) were isolated from whole plants of Tripolium vulgare Nees. The structure of this new compound was determined as 4-(2S-methylbutyryl)-9-acetyl-coniferol based on its NMR and HRESIMS spectral analyses. A simple and efficient method was designed to prepare tripolinolate A and its 19 analogs including nine new chemical entities for bioactive assay. Tripolinolate A and its analog 4,9-diacetyl-coniferol were found to be the two most active compounds that significantly inhibited the proliferation of different cancer cell lines with IC50 values ranging from 0.36 to 12.9µM and induced apoptosis in tumor cells. Structure-activity relationship analysis suggested that the molecular size of acyl moieties at C-4 and C-9 position might have an effect on the activity of this type of coniferol derivatives.

Lumbar pedicle cortical bone trajectory screw.

OBJECTIVE: The purpose of this study was to demonstrate the lumbar pedicle cortical bone trajectory (CBT) screw fixation technique, a new fixation technique for lumbar surgery. DATA SOURCES: The data analyzed in this review are mainly from articles reported in PubMed published from 1994 to 2014. STUDY SELECTION: Original articles and critical reviews relevant to CBT technique and lumbar pedicle fixation were selected. RESULTS: CBT technique was firstly introduced as a new fixation method for lumbar pedicle surgery in 2009. The concepts, morphometric study, biomechanical characteristics and clinical applications of CBT technique were reviewed. The insertional point of CBT screw is located at the lateral point of the pars interarticularis, and its trajectory follows a caudocephalad path sagittally and a laterally directed path in the transverse plane. CBT technique can be used for posterior fixation during lumbar fusion procedures. This technique is a minimally invasive surgery, which affords better biomechanical stability, fixation strength and surgical safety. Therefore, CBT technique has the greatest benefit in lumbar pedicle surgery for patients with osteoporosis and obesity. CONCLUSION: CBT technique is a better alternative option of lumbar pedicle fixation, especially for patients with osteoporosis and obesity.