Spatial multi-omics at subcellular resolution via high-throughput in situ pairwise sequencing.

Technology for spatial multi-omics aids the discovery of new insights into cellular functions and disease mechanisms. Here we report the development and applicability of multi-omics in situ pairwise sequencing (MiP-seq), a method for the simultaneous detection of DNAs, RNAs, proteins and biomolecules at subcellular resolution. Compared with other in situ sequencing methods, MiP-seq enhances decoding capacity and reduces sequencing and imaging costs while maintaining the efficacy of detection of gene mutations, allele-specific expression and RNA modifications. MiP-seq can be integrated with in vivo calcium imaging and Raman imaging, which enabled us to generate a spatial multi-omics atlas of mouse brain tissues and to correlate gene expression with neuronal activity and cellular biochemical fingerprints. We also report a sequential dilution strategy for resolving optically crowded signals during in situ sequencing. High-throughput in situ pairwise sequencing may facilitate the multidimensional analysis of molecular and functional maps of tissues.

Detoxification and underlying mechanisms towards toxic alkaloids by Traditional Chinese Medicine processing: A comprehensive review.

BACKGROUND: Alkaloids have attracted enduring interest worldwide due to their remarkable therapeutic effects, including analgesic, anti-inflammatory, and anti-tumor properties, thus offering a rich source for lead compound design and new drug discovery. However, some of these alkaloids possess intrinsic toxicity. Processing (Paozhi) is a pre-treatment step before the application of herbal medicines in traditional Chinese medicine (TCM) clinics, which has been employed for centuries to mitigate the toxicity of alkaloid-rich TCMs. PURPOSE: To explore the toxicity phenotypes, chemical basis, mode of action, detoxification processing methods, and underlying mechanisms, we can gain crucial insights into the safe and rational use of these toxic alkaloid-rich herbs. Such insights have the great potential to offer new strategies for drug discovery and development, ultimately improving the quality of life for millions of people. METHODS: Literatures published or early accessed until December 31, 2023, were retrieved from databases including PubMed, Web of Science, and CNKI. The following keywords, such as "toxicity", "alkaloid", "detoxification", "processing", "traditional Chinese medicine", "medicinal plant", and "plant", were used in combination or separately for screening. RESULTS: Toxicity of alkaloids in TCM includes hepatotoxicity, nephrotoxicity, neurotoxicity, cardiotoxicity, and other forms of toxicity, primarily induced by pyrrolizidines, quinolizidines, isoquinolines, indoles, pyridines, terpenoids, and amines. Factors such as whether the toxic-alkaloid enriched part is limited or heat-sensitive, and whether toxic alkaloids are also therapeutic components, are critical for choosing appropriate detoxification processing methods. Mechanisms of alkaloid detoxification includes physical removal, chemical decomposition or transformation, as well as biological modifications. CONCLUSION: Through this exploration, we review toxic alkaloids and the mechanisms underlying their toxicity, discuss methods to reduce toxicity, and unravel the intricate mechanisms behind detoxification. These offers insights into the quality control of herbs containing toxic alkaloids, safe and rational use of alkaloid-rich TCMs in clinics, new strategies for drug discovery and development, and ultimately helping improve the quality of life for millions of people.

Targeting tumor suppressor p53 for organ fibrosis therapy.

Fibrosis is a reparative and progressive process characterized by abnormal extracellular matrix deposition, contributing to organ dysfunction in chronic diseases. The tumor suppressor p53 (p53), known for its regulatory roles in cell proliferation, apoptosis, aging, and metabolism across diverse tissues, appears to play a pivotal role in aggravating biological processes such as epithelial-mesenchymal transition (EMT), cell apoptosis, and cell senescence. These processes are closely intertwined with the pathogenesis of fibrotic disease. In this review, we briefly introduce the background and specific mechanism of p53, investigate the pathogenesis of fibrosis, and further discuss p53's relationship and role in fibrosis affecting the kidney, liver, lung, and heart. In summary, targeting p53 represents a promising and innovative therapeutic approach for the prevention and treatment of organ fibrosis.

[Retracted] Effect of microRNA-27b on cisplatin chemotherapy sensitivity of oral squamous cell carcinoma via FZD7 signaling pathway.

[This retracts the article DOI: 10.3892/ol.2019.10347.].

SIRT3: A potential therapeutic target for liver fibrosis.

Sirtuin3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase located in the mitochondria, which mainly regulates the acetylation of mitochondrial proteins. In addition, SIRT3 is involved in critical biological processes, including oxidative stress, inflammation, DNA damage, and apoptosis, all of which are closely related to the progression of liver disease. Liver fibrosis characterized by the deposition of extracellular matrix is a result of long termed or repeated liver damage, frequently accompanied by damaged hepatocytes, the recruitment of inflammatory cells, and the activation of hepatic stellate cells. Based on the functions and pharmacology of SIRT3, we will review its roles in liver fibrosis from three aspects: First, the main functions and pharmacological effects of SIRT3 were investigated based on its structure. Second, the roles of SIRT3 in major cells in the liver were summarized to reveal its mechanism in developing liver fibrosis. Last, drugs that regulate SIRT3 to prevent and treat liver fibrosis were discussed. In conclusion, exploring the pharmacological effects of SIRT3, especially in the liver, may be a potential strategy for treating liver fibrosis.

Regulatory role of PDK1 via integrated gene analysis of mitochondria-immune response in periodontitis.

AIMS: To investigate the association between mitochondrial events and immune response in periodontitis and related regulatory genes. MAIN METHODS: Gene expression profiles in gingival tissues were retrieved from the Gene Expression Omnibus. Mitochondria-immune response-related differentially expressed genes (MIR-DEGs) between the healthy and periodontitis samples were determined. WGCNA, GO, and KEGG were used to investigate the function and the enriched pathways of MIR-DEGs. The correlation between MIR-DEGs expression and clinical probing pocket depth was analyzed. The MIR-DEGs were further identified and verified in animal samples. A periodontitis model was established in C57BL/6 mice with silk ligation. Micro-computed tomography was used to assess alveolar bone loss. Western blot, quantitative real-time polymerase chain reaction, and immunohistochemical analyses further validated the differential expression of the MIR-DEGs. KEY FINDINGS: A total of ten MIR-DEGs (CYP24A1, PRDX4, GLDC, PDK1, BCL2A1, CBR3, ARMCX3, BNIP3, IFI27, and UNG) were identified, the expression of which could effectively distinguish patients with periodontitis from the healthy controls. Enhanced immune response was detected in the periodontitis group with that in the healthy controls, especially in B cells. PDK1 was a critical MIR-DEG correlated with B cell immune response and clinical periodontal probing pocket depth. Both animal and clinical periodontal samples presented higher gene and protein expression of PDK1 than the control samples. Additionally, PDK1 colocalized with B cells in both animal and clinical periodontal tissues. SIGNIFICANCE: Mitochondria participate in the regulation of the immune response in periodontitis. PDK1 may be the key mitochondria-related gene regulating B-cell immune response in periodontitis.

Traditional Chinese medicine in osteoporosis: from pathogenesis to potential activity.

Osteoporosis characterized by decreased bone density and mass, is a systemic bone disease with the destruction of microstructure and increase in fragility. Osteoporosis is attributed to multiple causes, including aging, inflammation, diabetes mellitus, and other factors induced by the adverse effects of medications. Without treatment, osteoporosis will further progress and bring great trouble to human life. Due to the various causes, the treatment of osteoporosis is mainly aimed at improving bone metabolism, inhibiting bone resorption, and promoting bone formation. Although the currently approved drugs can reduce the risk of fragility fractures in individuals, a single drug has limitations in terms of safety and effectiveness. By contrast, traditional Chinese medicine (TCM), a characteristic discipline in China, including syndrome differentiation, Chinese medicine prescription, and active ingredients, shows unique advantages in the treatment of osteoporosis and has received attention all over the world. Therefore, this review summarized the pathogenic factors, pathogenesis, therapy limitations, and advantages of TCM, aiming at providing new ideas for the prevention and treatment of OP.

Cornus officinalis with high pressure wine steaming enhanced anti-hepatic fibrosis: Possible through SIRT3-AMPK axis.

Cornus officinalis, a medicinal and edible plant known for its liver-nourishing properties, has shown promise in inhibiting the activation of hepatic stellate cells (HSCs), crucial indicators of hepatic fibrosis, especially when processed by high pressure wine steaming (HPWS). Herein, this study aims to investigate the regulatory effects of cornus officinalis, both in its raw and HPWS forms, on inflammation and apoptosis in liver fibrosis and their underlying mechanisms. In vivo liver fibrosis models were established by subcutaneous injection of CCl4, while in vitro HSCs were exposed to transforming growth factor-ß (TGF-ß). These findings demonstrated that cornus officinalis with HPWS conspicuously ameliorated histopathological injury, reduced the release of proinflammatory factors, and decreased collagen deposition in CCl4-induced rats compared to its raw form. Utilizing ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometer (UHPLC-QTOF-MS) combined with network analysis, we identified that the pharmacological effects of the changed components of cornus officinalis before and after HPWS, primarily centered on the adenosine phosphate (AMP)-activated protein kinase (AMPK) pathway. Of note, cornus officinalis activated AMPK and Sirtuin 3 (SIRT3), promoting the apoptosis of activated HSCs through the caspase cascade by regulating caspase3, caspase6 and caspase9. siRNA experiments showed that cornus officinalis could regulate AMPK activity and its mediated-apoptosis through SIRT3. In conclusion, cornus officinalis exhibited the ability to reduce inflammation and apoptosis, with the SIRT3-AMPK signaling pathway identified as a potential mechanism underlying the synergistic effect of cornus officinalis with HPWS on anti-liver fibrosis.

Adenine-induced animal model of chronic kidney disease: current applications and future perspectives.

Chronic kidney disease (CKD) with high morbidity and mortality all over the world is characterized by decreased kidney function, a condition which can result from numerous risk factors, including diabetes, hypertension and obesity. Despite significant advances in our understanding of the pathogenesis of CKD, there are still no treatments that can effectively combat CKD, which underscores the urgent need for further study into the pathological mechanisms underlying this condition. In this regard, animal models of CKD are indispensable. This article reviews a widely used animal model of CKD, which is induced by adenine. While a physiologic dose of adenine is beneficial in terms of biological activity, a high dose of adenine is known to induce renal disease in the organism. Following a brief description of the procedure for disease induction by adenine, major mechanisms of adenine-induced CKD are then reviewed, including inflammation, oxidative stress, programmed cell death, metabolic disorders, and fibrillation. Finally, the application and future perspective of this adenine-induced CKD model as a platform for testing the efficacy of a variety of therapeutic approaches is also discussed. Given the simplicity and reproducibility of this animal model, it remains a valuable tool for studying the pathological mechanisms of CKD and identifying therapeutic targets to fight CKD.

Current-sensitive Hall effect in a chiral-orbital-current state.

Chiral orbital currents (COC) underpin a novel colossal magnetoresistance in ferrimagnetic Mn3Si2Te6. Here we report the Hall effect in the COC state which exhibits the following unprecedented features: (1) A sharp, current-sensitive peak in the magnetic field dependence of the Hall resistivity, and (2) A current-sensitive scaling relation between the Hall conductivity σxy and the longitudinal conductivity σxx, namely, σxy ∝ σxxα with α reaching up to 5, which is exceptionally large compared to α ≤ 2 typical of all solids. The novel Hall responses along with a current-sensitive carrier density and a large Hall angle of 15% point to a giant, current-sensitive Hall effect that is unique to the COC state. Here, we show that a magnetic field induced by the fully developed COC combines with the applied magnetic field to exert the greatly enhanced transverse force on charge carriers, which dictates the COC Hall responses.

Three-dimensional chromatin analysis reveals Sp1 as a mediator to program and reprogram HPV-host epigenetic architecture in cervical cancer.

Human papillomavirus (HPV) is predominantly associated with HPV-related cancers, however, the precise mechanisms underlying the HPV-host epigenetic architectures in HPV carcinogenesis remain elusive. Here, we employed high-throughput chromosome conformation capture (Hi-C) to comprehensively map HPV16/18-host chromatin interactions. Our study identified the transcription factor Sp1 as a pivotal mediator in programming HPV-host interactions. By targeting Sp1, the active histone modifications (H3K27ac, H3K4me1, and H3K4me3) and the HPV-host chromatin interactions are reprogrammed, which leads to the downregulation of oncogenes located near the integration sites in both HPV (E6/E7) and the host genome (KLF5/MYC). Additionally, Sp1 inhibition led to the upregulation of immune checkpoint genes by reprogramming histone modifications in host cells. Notably, humanized patient-derived xenograft (PDX-HuHSC-NSG) models demonstrated that Sp1 inhibition promoted anti-PD-1 immunotherapy via remodeling the tumor immune microenvironment in cervical cancer. Moreover, single-cell transcriptomic analysis validated the enrichment of transcription factor Sp1 in epithelial cells of cervical cancer. In summary, our findings elucidate Sp1 as a key mediator involved in the programming and reprogramming of HPV-host epigenetic architecture. Inhibiting Sp1 with plicamycin may represent a promising therapeutic option for HPV-related carcinoma.

Comparison of Radiofrequency Ablation and Craniotomy Microvascular Decompression for Treatment of Hemifacial Spasm.

BACKGROUND: Hemifacial spasm (HFS) is distinguished by sudden and involuntary spasms of the facial muscles, predominantly on one side of the face. Microvascular decompression (MVD) is an efficacious surgical technique for treating HFS; however, MVD may occasionally lead to noteworthy postoperative complications. Previously, we reported the successful utilization of an innovative awake computed tomography-guided percutaneous puncture of the stylomastoid foramen for administering radiofrequency ablation (RFA) therapy in the treatment of HFS. STUDY DESIGN: Prospective clinical research study. SETTING: Department of Anesthesiology and Pain Medical Center, Ningbo, China. OBJECTIVES: The aim of this study was to compare and contrast the clinical outcomes and adverse reactions associated with attempts to use RFA and MVD to manage primary HFS. METHODS: Three hundred patients received either RFA or MVD treatment (Group R and Group M). We tracked and recorded each patient's cure rate, remission rate, intraoperative and postoperative complications, short-term and long-term therapeutic outcomes, hospitalization duration, hospitalization expenses, and operation time. RESULTS: One hundred and fifty-eight patients were placed in the R group, and 142 patients were sorted into the M group. In the R group, 87.34% of patients showed improvement, 9.49% experienced relief, and 3.16% experienced treatment failure. Similarly, in the M group, 85.92% of patients showed improvement, 10.56% experienced relief, and 3.52% experienced treatment failure. The difference in therapeutic efficacy between the 2 groups was not significant. However, the M group had significantly lower recurrence rates at 3 months, 6 months, and one year post-operation than the R group did. Notably, the M group also experienced a higher rate of postoperative complications. Among the complications reported in the M group were 25 cases of dizziness or headache (17.6%) following the operation, 22 cases of hearing damage, including one case of complete hearing loss on the side involved, and 28 cases of peripheral nerve injury with abnormal skin sensation. Postoperative facial paralysis occurred in 15 patients, including 10 cases of moderate to severe facial paralysis that were relieved to grade II after one year. In comparison, the R group had 40 cases of grade II and 53 cases of grade III, and no cases of more severe facial paralysis were found. There were also 13 cases of peripheral nerve injury, such as local skin numbness and tenderness. Importantly, there were no cases of facial hematoma, intracranial hemorrhage, infection, or any other complications in either group, and no fatalities occurred during the study period. LIMITATIONS: The limitations of this study are the exclusion of transient postoperative complications, the lack of in-person follow-up with patients, and the potential underestimation of certain complications. CONCLUSION: The short-term outcome was found to be comparable between the 2 treatment modalities. Notably, RFA demonstrates both safety and efficacy as a method for managing primary HFS; however, the procedure may lead to mild facial paralysis. In situations during which surgery is contraindicated, especially among elderly or high-risk surgical patients, percutaneous facial nerve RFA at the stylomastoid foramen may be considered as an alternative therapeutic approach.

An algorithm for power transmission line fault detection based on improved YOLOv4 model.

In response to the escalating demand for real-time and accurate fault detection in power transmission lines, this paper undertook an optimization of the existing YOLOv4 network. This involved the substitution of the main feature extraction network within the original YOLOv4 model with a lighter EfficientNet network. Additionally, the inclusion of Grouped Convolution modules in the feature pyramid structure replaced conventional convolution operations. The resulting model not only reduced model parameters but also effectively ensured detection accuracy. Moreover, in enhancing the model's reliability, data augmentation techniques were employed to bolster the robustness of the power transmission line fault detection algorithm. This optimization further utilized the DIoU loss function to stabilize target box regression. Comparative experiments demonstrated the improved YOLOv4 model's superior performance in terms of loss function optimization while significantly enhancing detection speed under equivalent configurations. The parameter capacity was reduced by 81%, totaling merely 43.65 million, while the frame rate surged by 85% to achieve 24 frames per second. These experimental findings validate the effectiveness of the algorithm.

Investigation of New Accelerometer Based on Capacitive Micromachined Ultrasonic Transducer (CMUT) with Ring-Perforation Membrane.

Capacitive micromachined ultrasonic transducer (CMUT) has been widely studied due to its excellent resonance characteristics and array integration. This paper presents the first study of the CMUT electrostatic stiffness resonant accelerometer. To improve the sensitivity of the CMUT accelerometer, this paper innovatively proposes the CMUT ring-perforation membrane structure, which effectively improves the acceleration sensitivity by reducing the mechanical stiffness of the elastic membrane. The acceleration sensitivity is 10.9 (Hz/g) in the acceleration range of 0-20 g, which is 100% higher than that of the conventional CMUT structure. This research contributes to the acceleration measurement field of CMUT and can effectively contribute to the breakthrough of vibration acceleration monitoring technology in aerospace, medical equipment, and automotive electronics.

The Role of Rv1476 in Regulating Stress Response and Intracellular Survival of Mycobacterium tuberculosis.

The virulence of Mycobacterium tuberculosis (M. tuberculosis) is related to many factors, including intracellular survival, cell wall permeability, and cell envelope proteins. However, the biological function of the M. tuberculosis membrane protein Rv1476 remains unclear. To investigate the potential role played by Rv1476, we constructed an Rv1476 overexpression strain and found that overexpression of Rv1476 enhanced the intracellular survival of M. tuberculosis, while having no impact on the growth rate in vitro. Stress experiments demonstrated that the Rv1476 overexpression strain displayed increased susceptibility to different stresses compared to the wild-type strain. Transcriptome analysis showed that Rv1476 overexpression causes changes in the transcriptome of THP-1 cells, and differential genes are mainly enriched in cell proliferation, fatty acid degradation, cytokine-cytokine receptor interaction, and immune response pathways. Rv1476 overexpression inhibited the expression of some anti-tuberculosis-related genes, such as CCL1, IL15, IL16, ISG15, GBP5, IL23, ATG2A, IFNß, and CSF3. Altogether, we conclude that Rv1476 may play a critical role for M. tuberculosis in macrophage survival.

Self-heating mitochondrion-induced free radical blast for immunogenic cell death stimulation and HCC immunotherapy.

Hepatocellular carcinoma (HCC) is an immunosuppressive tumor associated with high mortality. Photothermal and photodynamic therapies have been applied to induce immunogenic cell death (ICD) in HCC, successfully eliciting immune responses but facing limitations in penetration depth in clinical trials. Here, intrinsic mitochondrial hyperthermia was used to trigger thermosensitive drug release. The mitochondria were further self-heated through 2,4-dinitrophenol uncoupling, dramatically promoting free radical initiation and inducing tumor ICD. The synthesized mitochondrial-targeting TPP-HA-TDV nanoparticles specifically generated free radicals in the mitochondria without external stimulation, and obviously enhanced the release of ICD markers, subsequently evoking immune responses. The results showed that mitochondrial hyperthermia could be an endogenous target for thermosensitive drug release. Furthermore, self-heating mitochondria-induced free radical blast could be an efficient therapeutic for deep-seated tumor therapy.

Transcriptomic analysis of the hypoxia-inducible factor 1α impact on the gene expression profile of chicken fibroblasts under hypoxia.

Hypoxia-inducible factor 1 (HIF-1) is a transcriptional regulator that mediates cellular adaptive responses to hypoxia. Hypoxia-inducible factor 1α (HIF-1α) is involved in the development of ascites syndrome (AS) in broiler chickens. Therefore, studying the effect of HIF-1α on the cellular transcriptome under hypoxic conditions will help to better understand the mechanism of HIF-1α in the development of AS in broilers. In this study, we analyzed the gene expression profile of the chicken fibroblast cell line (DF-1) under hypoxic conditions by RNA-seq. Additionally, we constructed the HIF-1α knockdown DF-1 cell line by using the RNAi method and analyzed the gene expression profile under hypoxic conditions. The results showed that exposure to hypoxia for 48 h had a significant impact on the expression of genes in the DF-1 cell line, which related to cell proliferation, stress response, and apoptosis. In addition, after HIF-1α knockdown more differential expression genes appeared than in wild-type cells, and the expression of most hypoxia-related genes was either down-regulated or remained unchanged. Pathway analysis results showed that differentially expressed genes were mainly enriched in pathways related to cell proliferation, apoptosis, and oxidative phosphorylation. Our study obtained transcriptomic data from chicken fibroblasts at different hypoxic times and identified the potential regulatory network associated with HIF-1α. This data provides valuable support for understanding the transcriptional regulatory mechanism of HIF-1α in the development of AS in broilers.

Adsorption of Pb(II) by UV-aged microplastics and cotransport in homogeneous and heterogeneous porous media.

To investigate the adsorption effects of aged microplastics (MPs) on Pb(II) and their co-transport properties in homogeneous (quartz sand) and heterogeneous (quartz sand with apple branches biochar) porous media, we explored the co-transport of UV-irradiated aged MPs and coexisting Pb(II) along with their interaction mechanisms. The UV aging process increased the binding sites and electronegativity of the aged MPs' surface, enhancing its adsorption capacity for Pb(II). Aged MPs significantly improved Pb(II) transport through homogeneous media, while Pb(II) hindered the transport of aged MPs by reducing electrostatic repulsion between these particles and the quartz sand. When biochar, with its loose and porous structure, was used as a porous medium, it effectively inhibited the transport capacity of both contaminants. In addition, since the aged MPs cannot penetrate the column, a portion of Pb(II) adsorbed by the aged MPs will be co-deposited with the aged MPs, hindering Pb(II) transport to a greater extent. The transport experiments were simulated and interpreted using two-point kinetic modeling and the DLVO theory. The study results elucidate disparities in the capacity of MPs and aged MPs to transport Pb(II), underscoring the potential of biochar application as an effective strategy to impede the dispersion of composite environmental pollutants.

LPS-TLR4 pathway exaggerates alcoholic hepatitis via provoking NETs formation.

BACKGROUND: Intrahepatic infiltration of neutrophils is a character of alcoholic hepatitis (AH) and neutrophil extracellular traps (NETs) are an important strategy for neutrophils to fix and kill invading microorganisms. The gut-liver axis has been thought to play a critical role in many liver diseases also including AH. However, whether NETs appear in AH and play role in AH is still unsure. METHODS: Serum samples from AH patients were collected and LPS and MPO-DNA were detected. WT, NE KO, and TLR4 KO mice were used to build the AH model, and the intestinal bacteria were eliminated at the same time and LPS was given. Then the formation of NETs and AH-related markers were detected. RESULTS: The serum MPO-DNA and LPS concentration was increased in AH patients and a correlation was revealed between these two indexes. More intrahepatic NETs formed in AH mice. NETs formation decreased with antibiotic intervention and restored with antibiotic intervention plus LPS supplement. While NETs formation failed to change with gut microbiome or combine LPS supplement in TLR4 KO mice. As we tested AH-related characters, liver injury, intrahepatic fat deposition, inflammation, and fibrosis alleviated with depletion of NE. These related marks were also attenuated with gut sterilization by antibiotics and recovered with a combined treatment with antibiotics plus LPS. But the AH-related markers did show a difference in TLR4 KO mice when they received the same treatment. CONCLUSION: Intestinal-derived LPS promotes NETs formation in AH through the TLR4 pathway and further accelerates the AH process by NETs.

Preliminary report on a novel technique for endoscopic transaxillary thyroidectomy: a case-control study.

BACKGROUND: Endoscopic transaxillary approaches to thyroidectomy have been well described and gasless transaxillary endoscopic thyroidectomy (GTET) is the most popular method. However, this require a single long axillary incision which is longer than most remote access thyroidectomy procedures. The authors improved the GTET and provided a novel way to access the thyroid. The purpose of this study was to test the feasibility of our novel transaxillary thyroidectomy procedure and to attempt to reduce the size of the scar and reduce the flap creation area. METHODS: One hundred sixteen patients who underwent our novel transaxillary thyroidectomy procedure were compared with the patients who underwent open and GTET procedures. The patients' demographics, outcomes, and complications were analyzed. RESULTS: Although the operation time (121.48±23.91 mins) was longer in the novel endoscopic group compare to the open group, it was shorter than GTET group. Intraoperative blood loss was similar between the groups. However, the novel procedure group had more drainage volume within 48 postoperative hours compare to other two groups. Despite the VAS pain score did not reveal a difference between the open and novel endoscopic procedure, it was lower in the novel procedure than GTET. The hospital stay days did not show a difference between the two groups. The number of resected central lymph nodes was similar between the groups. Differences did not reveal between the groups regarding to the complications rate. CONCLUSION: Our results showed that our novel transaxillary thyroidectomy procedure is feasible and safe. This procedure can be an alternative endoscopic transaxillary method for thyroidectomy.