BACKGROUND:With the development of the aging trend of society,the incidence of femoral neck fractures is increasing.Currently,the preferred surgical treatment is cannulated screw internal fixation.However,post-surgical femoral neck shortening occurs in some cases,resulting in impaired hip functionality.OBJECTIVE:To investigate the incidence of femoral neck shortening following the use of half-threaded cannulated screws for internal fixation in patients with femoral neck fractures,to analyze the effect on hip function,and to identify factors contributing to neck shortening.METHODS:A retrospective analysis was conducted on the medical records of 102 patients treated with half-threaded cannulated screws in an inverted triangle setup for femoral neck fractures at Affiliated Hai'an Hospital of Nantong University from January 2016 to January 2021.This group included 36 males and 66 females at the mean age of(57.2±7.7)years,with 34 cases of Garden type Ⅰ and Ⅱ fractures and 68 of Garden type Ⅲ and Ⅳ fractures.The mean bone mineral density value T was-2.8 SD.The Harris score was used to evaluate the hip function.During the follow-up period,the occurrence of femoral neck shortening was determined using X-ray imagery,and the factors influencing this shortening were examined using both univariate and multivariate regression analyses.RESULTS AND CONCLUSION:(1)Among the 102 patients with femoral neck fractures,30 patients developed femoral neck shortening,accounting for 29.4％.72 patients had no femoral neck shortening(70.6％).(2)The Harris score for patients experiencing neck shortening was significantly lower than that for patients without shortening(P＜0.05).(3)The study identified several factors associated with femoral neck shortening following the internal fixation of femoral neck fractures included age,gender,bone mineral density value T,preoperative Garden classification,and quality of reduction.These factors not only affect the shortening of the femoral neck after surgery,but are also directly related to the functional performance of the patient's hip joint.(4)Femoral neck shortening after surgery for femoral neck fracture is associated with various clinical parameters,especially the patient's age,gender,bone mineral density,preoperative classification,and accuracy of reduction during surgery.

BACKGROUND:With the development of the aging trend of society,the incidence of femoral neck fractures is increasing.Currently,the preferred surgical treatment is cannulated screw internal fixation.However,post-surgical femoral neck shortening occurs in some cases,resulting in impaired hip functionality.OBJECTIVE:To investigate the incidence of femoral neck shortening following the use of half-threaded cannulated screws for internal fixation in patients with femoral neck fractures,to analyze the effect on hip function,and to identify factors contributing to neck shortening.METHODS:A retrospective analysis was conducted on the medical records of 102 patients treated with half-threaded cannulated screws in an inverted triangle setup for femoral neck fractures at Affiliated Hai'an Hospital of Nantong University from January 2016 to January 2021.This group included 36 males and 66 females at the mean age of(57.2±7.7)years,with 34 cases of Garden type Ⅰ and Ⅱ fractures and 68 of Garden type Ⅲ and Ⅳ fractures.The mean bone mineral density value T was-2.8 SD.The Harris score was used to evaluate the hip function.During the follow-up period,the occurrence of femoral neck shortening was determined using X-ray imagery,and the factors influencing this shortening were examined using both univariate and multivariate regression analyses.RESULTS AND CONCLUSION:(1)Among the 102 patients with femoral neck fractures,30 patients developed femoral neck shortening,accounting for 29.4％.72 patients had no femoral neck shortening(70.6％).(2)The Harris score for patients experiencing neck shortening was significantly lower than that for patients without shortening(P＜0.05).(3)The study identified several factors associated with femoral neck shortening following the internal fixation of femoral neck fractures included age,gender,bone mineral density value T,preoperative Garden classification,and quality of reduction.These factors not only affect the shortening of the femoral neck after surgery,but are also directly related to the functional performance of the patient's hip joint.(4)Femoral neck shortening after surgery for femoral neck fracture is associated with various clinical parameters,especially the patient's age,gender,bone mineral density,preoperative classification,and accuracy of reduction during surgery.

Objective:To discuss the effect of berberine hydrochloride(BBR)on autophagy in the HeLa cells infected with herpes simplex virus type 1(HSV-1),and to clarify its related mechanism.Methods:The HeLa cells at logarithmic growth phase were added with 0,10,20,40,80,120,and 160 μmol·L-1 BBR,respectively,and cultured for 24 h.In addition,the HeLa cells were divided into HSV-1 group(the cells were infected with HSV-1),L-BBR group(were infected with HSV-1 and then treated with 20 μmol·L-1 BBR for 24 h),M-BBR group(were infected with HSV-1 and then treated with 40 μmol·L-1 BBR for 24 h),H-BBR group(were infected with HSV-1 and then treated with 80 μmol·L-1 BBR for 24 h),and 740 Y-P group(were infected with HSV-1 and then treated with 80 μmol·L-1 BBR and 10 μmol·L-1 740 Y-P for 24 h)for viral infection and corresponding drug treatment.MTT method was used to detect the activities of microtubule-associated protein 1 light chain 3(LC3)the HeLa cells after treated with different concentrations of BBR;plaque reduction assay was used to detect the proliferation ability of HSV-1 in the HeLa cells in various groups;real-time fluorescence quantitative PCR(RT-qPCR)method was used to detect the mRNA expression levels of virus replication-related genes in the HeLa cells in various groups;immunofluorescence method was used to detect the formation of autophagosomes in the HeLa cells in various groups;flow cytometry was used to detect the apoptotic rate of the HeLa cells in various groups;Western blotting method was used to detect the expression levels of autophagy and the phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)pathway pathway-related proteins in the HeLa cells in various groups.Results:The MTT method results showed that compared with 0 μmol·L-1 BBR group,the activities of the HeLa cells in 120 and 160 μmol·L-1 BBR groups were significantly decreased(P<0.05),which had certain toxicity to the cells;20,40,and 80 μmol·L-1 BBR were selected for subsequent experiments.The plaque reduction assay results showed that compared with HSV-1 group,the plaque forming units(PFUs)in the HeLa cells in L-BBR group,M-BBR group,and H-BBR group were significantly decreased(P<0.05)in a dose-dependent manner;compared with H-BBR group,the PFUs in the HeLa cells in 740 Y-P group were significantly increased(P<0.05).The RT-qPCR results showed that compared with HSV-1 group,the mRNA expression levels of infected cell protein 0(ICP0),infected cell protein 22(ICP22),infected cell protein 8(ICP8),thymidine kinase(TK),glycoprotein B(gB),and glycoprotein D(gD)in the HeLa cells in L-BBR group,M-BBR group,and H-BBR group were significantly decreased(P<0.05)in a dose-dependent manner;compared with H-BBR group,the expression levels of ICP0,ICP22,ICP8,TK,gB,and gD mRNA in the HeLa cells in 740 Y-P group were significantly increased(P<0.05).The immunofluorescence method results showed that compared with HSV-1 group,the number of LC3 autophagosomes formed in the HeLa cells in L-BBR group,M-BBR group,and H-BBR group was increased;compared with H-BBR group,the number of LC3 autophagosomes formed in the HeLa cells in 740 Y-P group was decreased.The flow cytometry results showed that compared with HSV-1 group,the apoptotic rates of the HeLa cells in L-BBR group,M-BBR group,and H-BBR group were significantly increased(P<0.05)in a dose-dependent manner;compared with H-BBR group,the apoptotic rate of the HeLa cells in 740 Y-P group was significantly decreased(P<0.05).The Western blotting method results showed that compared with HSV-1 group,the expression levels of Beclin-1 and B-cell lymphoma 2(Bcl-2)/adenovirus E1B 19kDa protein interacting protein protein(BNIP)2 proteins and the ratios of LC3-Ⅱ/LC3-Ⅰ in the HeLa cells in L-BBR group,M-BBR group,and H-BBR group were significantly increased(P<0.05)in a dose-dependent manner;compared with H-BBR group,the expression levels of Beclin-1 and BNIP proteins and the LC3-Ⅱ/LC3-Ⅰ ratio in the HeLa cells in 740 Y-P group were significantly decreased(P<0.05);compared with HSV-1 group,the expression levels of cysteine-containing aspartate protein hydrolase 1(Caspase-1),cysteine-containing aspartate protein hydrolase 3(Caspase-3),and Bcl-2 associated X protein(Bax)proteins in the HeLa cells in L-BBR group,M-BBR group,and H-BBR group were significantly increased(P<0.05),and the expression level of Bcl-2 protein was significantly decreased(P<0.05)in a dose-dependent manner;compared with H-BBR group,the expression levels of Caspase-1,Caspase-3,and Bax proteins in the HeLa cells in 740 Y-P group were significantly decreased(P<0.05),and the expression level of Bcl-2 protein was significantly increased(P<0.05);compared with HSV-1 group,the ratios of phosphorylated PI3K(p-PI3K)/PI3K,phosphorylated AKT(p-AKT)/AKT,and phosphorylated mTOR(p-mTOR)/mTOR in the HeLa cells in L-BBR group,M-BBR group,and H-BBR group were significantly decreased(P<0.05)in a dose-dependent manner;compared with H-BBR group,the ratios of p-PI3K/PI3K,p-Akt/Akt,and p-mTOR/mTOR in the HeLa cells in 740 Y-P group were significantly increased(P<0.05).Conclusion:BBR can promote the autophagy process in the HeLa cells infected with HSV-1 by regulating the PI3K/AKT/mTOR pathway,induce autophagy-dependent apoptosis,and significantly inhibit the virus replication.

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 explore the surgical intervention strategy for metastatic cervical lymph nodes surrounding the carotid artery in head and neck squamous cell carcinoma.Methods:A total of 62 patients with advanced head and neck tumors and carotid wrap by disease treated in Department of Otorhinolaryngology and Head and Neck Surgery, the Affiliated BenQ Hospital of Nanjing Medical University between June 2019 and December 2023 were reviewed, of whom 9 patients presented with metastatic squamous cell carcinoma in cervical lymph nodes of unknown primary or with no recurrence of primary lesion and all the 9 patients were males, aged from 48 to 79 years old, with≤level 2 of Eastern Cooperative Oncology Group-Performance Status (ECOG-PS). Radiographically common carotid artery (CCA) and/or internal carotid artery (ICA) were surrounded by≥270° with tumor. All the 9 patients received implantation of covered stent in carotid artery and radical resection of metastatic cervical lymph nodes. The success rate, complications, surgery-related complications, local recurrence rate, quality of life (QOL) and overall survival (OS) were analyzed. The QOL of patients was compared by paired rank sum test, and P<0.05 indicated statistically significant difference. The OS was analyzed by Kaplan-Meier. Results:The success rate of stent implantation was 100%, with no implantation-related complications. R0 resection was performed in 8 cases and R1 resection in 1 case. The QOL of patients after surgery was improved, and the improvements in "pain", "mood" and "anxiety" were statistically significant( Z values were -2.236, -2.460 and -2.200, respectively, and all P values were<0.05). Follow-up was 1-18 months, with a median of 7 months, and 1 case was lost to follow-up. Local recurrence occurred in 3 patients with an incidence of 37.5% (3/8). OS was 59.9% at 12 months after surgery. Conclusion:Implantation of covered stent in carotid artery combined with radical resection is an effective method for the treatment of cervical lymph node metastasis.

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.

The liver reserve function refers to the compensatory ability to maintain liver function after damage, providing implication for the resection of hepatic malignant tumor. Hepatobiliary scintigraphy imaging can provide quantitative evaluation of liver blood perfusion, and has advantages on the evaluation of liver reserve function and the prediction of postoperative complications. 99Tc m-galactosyl serum albumin (GSA) and 99Tc m-mebrofenin are commonly used imaging agents for hepatobiliary scintigraphy imaging assessment of liver reserve function. This article reviews the application and progress of hepatobiliary scintigraphy in liver reserve function assessment.

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.

Objective:To summarize the clinical, imaging, muscle pathological and gene mutational features of patients with late-onset mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS).Methods:Three patients with late-onset MELAS, admitted to Department of Neurology, Jiaozuo People's Hospital Affiliated of Xinxiang Medical University from January 1997 to December 2021 were chosen; all patients were screened for mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) mutations by second-generation gene sequencing. The clinical, imaging, muscle pathological and gene mutational features of patients with late-onset MELAS were analyzed retrospectively.Results:The main clinical manifestations of these late-onset MELAS patients included stroke-like attacks, headache, hearing and vision loss, cognitive decline and mental disorder. The muscle tension and muscle strength of both upper extremities in these 3 patients were normal. Increased muscle tension and active tendon reflexes, and positive pathological signs in both lower extremities were noted in 2 patients. Head MRI showed abnormal long T1 and long T2 signals in temporal occipital parietal cortex and subcortex in 3 patients, and CT showed calcification in bilateral globus pallidus in 1 patient. Ragged red fibers (RRF) and ragged blue fibers (RBF) were found in the muscle biopsies of 3 patients, and cytochrome oxidase (COX)-negative muscle fibers were found in 2 patients. MT-TL1 gene m.3243A>G mutation was detected in all 3 patients by genetic testing, among which mutation in the blood of 2 patients was 15% and 17%, respectively, and mutation in the muscle tissues of 1 patient was 73%. Conclusion:Muscle pathology indicates high RRF percentage in patients with late-onset MELAS; and m.3243A>G spot mutation is the most common mutation type in late-onset MELAS, and m.3243A>G mutation ratio in muscle tissues is obviously higher than that in blood.