Traditional open thyroid surgery often leaves a scar on the neck,which can affect cosmetic outcomes.Therefore,various endoscopic thyroidectomy approaches via extra-cervical approaches have been developed.However,due to the unique anatomical characteristics of the neck and limitations of endoscopic instruments,conventional endoscopic techniques have certain drawbacks.Robot-assisted endoscopic thyroid surgery can help overcome these limitations.At present,robotic surgical systems remain expensive and the associated surgical costs are high,limiting their widespread adoption.Most surgeons are still relatively unfamiliar with the technique.Nevertheless,with ongoing technological advancements and cost reductions,robot-assisted surgery holds great promise for broader application.Based on years of large-scale experience in endoscopic thyroid surgery at our center,and drawing upon both domestic and international experiences with robotic thyroidectomy,this paper summarizes and proposes a seven-step protocol for robot-assisted endoscopic thyroidectomy via the bilateral axillo-breast approach,aiming to provide a practical reference for the clinical adoption of this technique.

Locally advanced thyroid cancer (LATC) can seriously invade the important organs of the neck, such as the trachea, esophagus and carotid artery, and has a poor prognosis. It is one of the leading causes of death in thyroid cancer. Diagnosis and treatment for LATC often involve multidisciplinary fields, the difficulty and risk of surgical are very high, and high-quality multidisciplinary comprehensive diagnosis and treatment can obtain a better prognosis. In order to realize the proceduralization, standardization and normalization of the LATC diagnosis and treatment model, the seven-step method for diagnosis and treatment of LATC is summarized by our center.

Locally advanced thyroid cancer (LATC) can seriously invade the important organs of the neck, such as the trachea, esophagus and carotid artery, and has a poor prognosis. It is one of the leading causes of death in thyroid cancer. Diagnosis and treatment for LATC often involve multidisciplinary fields, the difficulty and risk of surgical are very high, and high-quality multidisciplinary comprehensive diagnosis and treatment can obtain a better prognosis. In order to realize the proceduralization, standardization and normalization of the LATC diagnosis and treatment model, the seven-step method for diagnosis and treatment of LATC is summarized by our center.

Traditional open thyroid surgery often leaves a scar on the neck,which can affect cosmetic outcomes.Therefore,various endoscopic thyroidectomy approaches via extra-cervical approaches have been developed.However,due to the unique anatomical characteristics of the neck and limitations of endoscopic instruments,conventional endoscopic techniques have certain drawbacks.Robot-assisted endoscopic thyroid surgery can help overcome these limitations.At present,robotic surgical systems remain expensive and the associated surgical costs are high,limiting their widespread adoption.Most surgeons are still relatively unfamiliar with the technique.Nevertheless,with ongoing technological advancements and cost reductions,robot-assisted surgery holds great promise for broader application.Based on years of large-scale experience in endoscopic thyroid surgery at our center,and drawing upon both domestic and international experiences with robotic thyroidectomy,this paper summarizes and proposes a seven-step protocol for robot-assisted endoscopic thyroidectomy via the bilateral axillo-breast approach,aiming to provide a practical reference for the clinical adoption of this technique.

Liver fibrosis and cirrhosis are the common outcomes of various chronic liver diseases after progression,and studies have shown that liver fibrosis and early liver cirrhosis can be reversed.Compound traditional Chinese medicine prescriptions have a marked therapeutic effect in reversing liver fibrosis and early liver cirrhosis,and their mechanism of action remains unclear.By reviewing related articles in China and globally,this article summarizes the six main phenotypic mechanisms involved in the efficacy of compound traditional Chinese medicine prescriptions,i.e.,inhibiting liver inflammation and regulating liver immune response,regulating hepatic stellate cell activation and extracellular matrix(ECM)generation,promoting ECM degradation,reversing hepatic sinusoidal capillarization,regulating hepatocyte regeneration,and regulating gut microbiota,and in addition,this article also analyzes the advances and shortcomings in current studies on each phenotype.Future studies on compound traditional Chinese medicine prescriptions should focus on experimental exploration and rescue experiments to verify the above phenotypes and further explore the upstream and downstream signaling pathways with a marked effect.This article aims to help clarify the direction and ideas of studies on the therapeutic mechanism of compound traditional Chinese medicine prescriptions,in order to provide a basis for clarifying the scientific essence of compound traditional Chinese medicine prescriptions.

Objective:To investigate the clinical phenotypes, muscle magnetic resonance imaging (MRI) and pathological changes, and genetic characteristics of myfibrillar myopathies (MFMs) cuased by MYOT gene mutation. Methods:(1) The clinical data of a MFMs family caused by a de novo frameshift mutation in MYOT gene admitted to Department of Neurology, Jiaozuo People's Hospital Affiliated to Xinxiang Medical University in February 2021 were collected. Electromyography, muscle MRI, and pathological examination were used to confirm the changes of the muscle lesions. MYOT gene mutation in the proband and other patients was detected by next generation sequencing (NGS) and Sanger sequencing, respectively. The 3D structure models of myotilin protein before and after gene mutation were predicted by AlphaFold3 and pymol3. (2) Literature on MFMs caused by MYOT gene mutation was searched from Pubmed and China National Knowledge Infrastructure from the establishment of these databases to July 2024; clinical and genetic characteristics of MFMs caused by MYOT gene mutation were summarized. Results:(1) In the 9 patients from this family, 8 had onset in adolescence (16-20 years old). Unilateral or bilateral hand muscle weakness as the first symptoms appeared in most patients, and then, hand muscle atrophy gradually appeared and slowly progressed to the proximal limbs. Electromyography showed myogenic damage. Muscle MRI showed patchy long T1 and long T2 signal intensity in the bilateral anterior tibial muscles. Muscle pathological staining showed typical rimbed vacuoles, cytoplasm, smear-like muscle fibers and desmin abnormal deposition in some muscle fibers; electron microscopy revealed disorganized myofibril structures, focal myofibril lysis, Z-band streaming, and subsarcolemmal or myofibril mitochondrial accumulation. Heterozygous mutation in MYOT gene c.680_683del (p.Val227GlufsTer10) locus was noted in 8 patients and daughter of the proband. Bioinformatics analysis suggested that MYOT gene c.680_683del mutation could cause premature termination of myotilin translation, leading to the production of a truncated protein, thereby disrupting its normal structure and function. (2) Eighty-nine patients with MFMs caused by MYOT gene mutation in previous literature mainly manifested as chronic progressive weakness of the distal or proximal limbs, with some involving the myocardium, respiratory muscles, or peripheral nerves. A total of 12 MYOT gene mutations were identified, with p. Ser60phe being the most common mutation. Except for p.Tyr4_his9del, being an in-frame mutation, the others were missense mutations. Conclusion:MFMs caused by MYOT gene mutation exhibit obvious clinical heterogeneity, characterized by very slow progression of muscle weakness; MYOT gene locus c.680_683del (p.Val227GlufsTer10) is a de novo heterozygous mutation.

Objective To observe the value of cranial ultrasound for perioperative patients with acute severe traumatic brain injury(sTBI).Methods Data of 55 sTBI patients who underwent craniotomy were retrospectively analyzed.The patients were divided into observation group(n=15)and control group(n=40)according to received perioperative cranial ultrasound or not.The general data and surgical data were compared between groups,and ultrasonic data of observation group were analyzed.Results The proportions of good prognosis 1 and 6 months after operation in observation group were both higher than those in control group,while the incidence of cerebral infarction in observation group was lower than that in control group(all P＜0.05).No significant difference of general data nor other surgical data was found between groups(all P＞0.05).Acute encephalocele occurred in 1 case in observation group during operation,and cranial ultrasound accurately showed the contralateral secondary epidural hematoma.Increased intracranial pressure in different degrees were found in all 15 cases(15/15,100％)in observation group after operation with transcranial color coded Doppler(TCCD)or transcranial Doppler(TCD),while cerebral vascular spasm was observed in 5 cases(5/15,33.33％),among them 4 cases(4/5,80.00％)were diagnosed cerebral infarction based on CT examination.Conclusion Cranial ultrasound could be used to evaluate changes of sTBI in perioperative period and guide adjusting treatment strategy in time,being valuable for reducing risk of postoperative cerebral infarction and improving prognosis.

Objective:To analyze the clinical characteristics, muscle imaging and pathological features of patients with anti-signal recognition particle positive immune-mediated necrotizing myopathy (SRP-IMNM).Methods:Nine patients with SRP-IMNM were collected in the Neuromuscular Disease Center of Jiaozuo People′s Hospital from May 2018 to May 2023, who were confirmed by skeletal muscle pathology and myositis-specific autoantibodies detection, and their clinical manifestations, muscle imaging and muscle pathology characteristics were systematically summarized.Results:Among the 9 patients with SRP-IMNM, there were 7 females and 2 males. The age of onset ranged from 18 to 59 years. All the patients presented proximal muscle weakness. Seven patients experienced neck weakness, and dysphagia was present in 5 patients. Laboratory examinations showed elevated serum creatine kinase levels in all 9 patients (1 866-6 725 U/L). Eight patients were combined with other antibodies positivity, except for anti-SRP antibody. Among them, 7 patients were combined with anti-Ro-52 antibody positivity, 4 patients combined with anti-Ro-52 antibody positivity alone, and 3 patients combined with 3 or more positive antibodies simultaneously. Those patients who presented with interstitial lung disease and cardiac involvement were all combined with other antibodies positivity. Seven patients completed thigh muscle magnetic resonance imaging (MRI), which showed diffuse skeletal muscle oedema, partial muscle atrophy and fatty replacement, primarily affecting the posterior thigh muscle group. Two patients underwent shank muscle MRI. The soleus involvement was evident, while the tibialis anterior muscle and gastrocnemius muscles were involved in 1 patient. All 9 patients showed varying degrees of scattered muscle fiber necrosis and regeneration on muscle biopsies. In 1 patient, a small amount of inflammatory cell infiltration was observed. Pipestem capillaries were observed in 4 patients. Immunohistochemical staining revealed a small number of CD68-positive lymphocytes in 8 patients. Additionally, 5 patients showed upregulation of major histocompatibility complex Ⅰ expression on the muscle fiber membrane, while 6 patients showed deposition of membrane attack complex (C5b-9) on non-necrotic muscle fibers and capillaries. P62 staining showed homogeneous fine-granular in sarcoplasm in 6 patients.Conclusions:In addition to proximal muscle weakness, patients with SRP-IMNM often experience neck weakness and dysphagia. Those with multiple antibodies are more likely to develop interstitial lung disease and cardiac involvement. SRP-IMNM patients have diffuse oedema in the affected muscles, and the posterior thigh muscles are more prone to atrophy and fatty tissue formation. C5b-9 deposition and pipestem capillaries are significant pathological features of SRP-IMNM, which provide additional evidence for clinical diagnosis.

Objective:To investigate the clinical phenotypes, muscle magnetic resonance imaging (MRI) and pathological changes, and genetic characteristics of myfibrillar myopathies (MFMs) cuased by MYOT gene mutation. Methods:(1) The clinical data of a MFMs family caused by a de novo frameshift mutation in MYOT gene admitted to Department of Neurology, Jiaozuo People's Hospital Affiliated to Xinxiang Medical University in February 2021 were collected. Electromyography, muscle MRI, and pathological examination were used to confirm the changes of the muscle lesions. MYOT gene mutation in the proband and other patients was detected by next generation sequencing (NGS) and Sanger sequencing, respectively. The 3D structure models of myotilin protein before and after gene mutation were predicted by AlphaFold3 and pymol3. (2) Literature on MFMs caused by MYOT gene mutation was searched from Pubmed and China National Knowledge Infrastructure from the establishment of these databases to July 2024; clinical and genetic characteristics of MFMs caused by MYOT gene mutation were summarized. Results:(1) In the 9 patients from this family, 8 had onset in adolescence (16-20 years old). Unilateral or bilateral hand muscle weakness as the first symptoms appeared in most patients, and then, hand muscle atrophy gradually appeared and slowly progressed to the proximal limbs. Electromyography showed myogenic damage. Muscle MRI showed patchy long T1 and long T2 signal intensity in the bilateral anterior tibial muscles. Muscle pathological staining showed typical rimbed vacuoles, cytoplasm, smear-like muscle fibers and desmin abnormal deposition in some muscle fibers; electron microscopy revealed disorganized myofibril structures, focal myofibril lysis, Z-band streaming, and subsarcolemmal or myofibril mitochondrial accumulation. Heterozygous mutation in MYOT gene c.680_683del (p.Val227GlufsTer10) locus was noted in 8 patients and daughter of the proband. Bioinformatics analysis suggested that MYOT gene c.680_683del mutation could cause premature termination of myotilin translation, leading to the production of a truncated protein, thereby disrupting its normal structure and function. (2) Eighty-nine patients with MFMs caused by MYOT gene mutation in previous literature mainly manifested as chronic progressive weakness of the distal or proximal limbs, with some involving the myocardium, respiratory muscles, or peripheral nerves. A total of 12 MYOT gene mutations were identified, with p. Ser60phe being the most common mutation. Except for p.Tyr4_his9del, being an in-frame mutation, the others were missense mutations. Conclusion:MFMs caused by MYOT gene mutation exhibit obvious clinical heterogeneity, characterized by very slow progression of muscle weakness; MYOT gene locus c.680_683del (p.Val227GlufsTer10) is a de novo heterozygous mutation.

Objective:To summarize the characteristics of clinical, muscle pathology and gene mutation of late-onset reducing body myopathy caused by FHL1 gene mutation, in order to improve clinicians′ understanding of this disorder. Methods:The clinical, muscle pathology and muscle magnetic resonance imaging data of the proband from a family diagnosed as reducing body myopathy in Jiaozuo People′s Hospital in December 2021 were collected. Genetic tests and pedigree verification were conducted on the proband and her son.Results:The proband was a 59-year-old female with progressive, asymmetrical limb weakness and muscular atrophy. Her mother, sister and brother had similar symptoms. Electromyography showed myogenic and neurogenic damage. Muscle magnetic resonance imaging indicated that the lesion mainly involved the posterior muscles of the thigh and calf, as well as the gluteus maximus. The muscle pathology showed eosinophilic granular inclusion bodies and rimmed vacuoles in the muscle fibers of the lesion. The structure of myofibrils was disordered and abnormal protein deposition was observed. The gene sequencing showed the FHL1 gene p.C150S heterozygous variation. Conclusions:Late-onset reducing body myopathy is characterized by progressive asymmetric proximal limb muscle weakness, partially involving distal limb muscles and gluteus maximus. Muscle pathology shows the characteristic pathological changes of many kinds of myofibrillar myopathies. FHL1 gene mutation is an important basis for diagnosis.