Double network(DN)hydrogels have the ability to precisely adjust physical and chemical properties,change the interac-tion between biomaterials and cells or biomolecules,which can better fulfill clinical needs.DN have been widely used in tissue engi-neering and regenerative medicine.This article summarizes the advantages of DN hydrogels used in bone tissue regeneration,and intro-duces the effect of DN hydrogel systems on the behavior of loading cells,drug delivering in bone reparation,and the application of DN hydrogel system in microenvironment construction,bioactive composite materials,and antibacterial activity to meet the needs of bone regeneration.

Double network(DN)hydrogels have the ability to precisely adjust physical and chemical properties,change the interac-tion between biomaterials and cells or biomolecules,which can better fulfill clinical needs.DN have been widely used in tissue engi-neering and regenerative medicine.This article summarizes the advantages of DN hydrogels used in bone tissue regeneration,and intro-duces the effect of DN hydrogel systems on the behavior of loading cells,drug delivering in bone reparation,and the application of DN hydrogel system in microenvironment construction,bioactive composite materials,and antibacterial activity to meet the needs of bone regeneration.

Objective:To explore the effects of life events, family environment and coping style on self-injury behavior in adolescents with first-episode depression.Methods:From July 2019 to December 2022, a total of 110 adolescent patients with first-episode depression were selected in the Psychiatry Department of the First Affiliated Hospital of Zhengzhou University. According to whether the patients had self-injury behavior, the patients were divided into group without self-injury( n=54)and group with self-injury( n=56).Patients in the two groups were evaluated by a general clinical data questionnaire, adolescent self-rating life events checklist (ASLEC), family environment scale-Chinese version(FES-CV), simplified coping style questionnaire (SCSQ), 24 items Hamilton depression scale (HAMD-24), Hamilton anxiety scale (HAMA) and 90 symptom checklist-90 (SCL-90). Statistical analysis including t-test, χ2 test and binary Logistic regression analysis were performed on the enrolled data by SPSS 25.0 statistical software. Results:Among 110 patients, there were 56 patients(50.9%) exhibited self-injury behavior.The scores of ASLEC(51.04±5.99, 48.02±6.86), intimacy(3.70±1.85, 4.59±1.60), emotional expression(3.84±1.80, 4.69±1.96), positive coping styles(15.84±5.85, 18.22±4.84), negative coping styles(12.50±3.23, 11.06±3.64), and HAMA(20.63±2.86, 19.48±2.55) showed statistically significant differences between the group with and without self-injury ( t=-2.46, 2.72, 2.36, 2.32, -2.20, -2.21, all P<0.05). Binary Logistic regression analysis showed that life events ( B=0.079, OR=1.083, 95% CI=1.008-1.163, P=0.030), negative coping style ( B=0.173, OR=1.188, 95% CI=1.033-1.367, P=0.016), HAMA ( B=0.225, OR=1.252, 95% CI=1.057-1.482, P=0.009) were risk factors for self-injury, while intimacy ( B=-0.264, OR=0.768, 95% CI=0.593-0.995, P=0.046) and positive coping styles ( B=-0.092, OR=0.912, 95% CI=0.834-0.997, P=0.044) were protective factors for self-injury. Conclusion:The self-injury behavior of adolescents with first-episode depression may be related to negative life events, early adverse family environment and coping style.

Objective:To explore the effects of depressive symptoms on sleep quality in adolescents with depressive disorder, and the mediating roles of cognitive fusion and sleep belief.Methods:A sample of 210 adolescents with first episode depressive disorder aged 12-18 years were recruited to complete 17-item Hamilton depression scale (HAMD-17), Pittsburgh sleep quality index (PSQI), cognitive fusion questionnaire (CFQ), and dysfunctional beliefs and attitudes about sleep scale (DBAS-16) from November 2021 to July 2022. SPSS 26.0 software was used to perform descriptive analysis and correlation analysis. The mediating effect was tested by Bootstrap analysis using PROCESS V 3.4 Macro program.Results:The incidence of low sleep quality in adolescents with depressive disorder was 69.0%(145/210). HAMD-17 score was (22.4±7.9), PSQI score was (9.7±3.7), CFQ score was (51.6±7.8), DBAS-16 score was (43.5±8.4).PSQI was positively correlated with the scores of HAMD-17 and CFQ( r=0.613, 0.463, both P<0.001).HAMD-17 was positively correlated with CFQ score ( r=0.488, P<0.001).DBAS-16 was negatively correlated with scores of PSQI, HAMD-17 and CFQ( r=-0.326, -0.284, -0.354, all P<0.001). The direct effect of depression on sleep quality was 0.230(95% CI=0.169-0.293). The indirect effect of depression on sleep quality through two pathways, the separate mediating effect value of cognitive fusion was 0.041 (95% CI=0.011-0.074), and the chain mediating effect value of cognitive fusion and sleep beliefs was 0.008(95% CI=0.001-0.020). Conclusion:Depressive symptoms can directly affect sleep quality of depressive disorder adolescents and indirectly through cognitive fusion and sleep beliefs.

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 analyze the status of respiratory pathogen detection and the clinical features in children with Mycoplasma pneumoniae pneumonia (MPP). Methods:A prospective, multicenter study was conducted to collect clinical data, including medical history, laboratory examinations and multiplex PCR tests of children diagnosed with MPP from 4 hospitals in China between November 15 th and December 20 th, 2023. The multiplex PCR results and clinical characteristics of MPP children in different regions were analyzed. The children were divided into severe and mild groups according to the severity of the disease. Patients in the severe group were further divided into Mycoplasma pneumoniae (MP) alone and Multi-pathogen co-detection groups based on whether other pathogens were detected besides MP, to analyze the influence of respiratory pathogen co-detection rate on the severity of the disease. Mann-Whitney rank sum test and Chi-square test were used to compare data between independent groups. Results:A total of 298 children, 136 males and 162 females, were enrolled in this study, including 204 children in the severe group with an onset age of 7.0 (6.0, 8.0) years, and 94 children in the mild group with an onset age of 6.5 (4.0, 7.8) years. The level of C-reactive protein, D-dimer, lactic dehydrogenase (LDH) were significantly higher (10.0 (5.0, 18.0) vs. 5.0 (5.0, 7.5) mg/L, 0.6 (0.4, 1.1) vs. 0.5 (0.3, 0.6) mg/L, 337 (286, 431) vs. 314 (271, 393) U/L, Z=2.02, 2.50, 3.05, all P<0.05), and the length of hospitalization was significantly longer in the severe group compared with those in mild group (6.0 (6.0, 7.0) vs. 5.0 (4.0, 6.0) d, Z=4.37, P<0.05). The time from onset to admission in severe MPP children was significantly shorter than that in mild MPP children (6.0 (5.0, 9.5) vs. 9.0 (7.0, 13.0) d, Z=2.23, P=0.026). All patients completed the multiplex PCR test, with 142 cases (47.7%) MPP children detected with 21 pathogens including adenovirus 25 cases (8.4%), human coronavirus 23 cases (7.7%), rhinovirus 21 cases (7.0%), Streptococcus pneumoniae 21 cases (7.0%), influenza A virus 18 cases (6.0%). The pathogens with the highest detection rates in Tianjin, Shanghai, Wenzhou and Chengdu were Staphylococcus aureus at 10.7% (8/75), adenovirus at 13.0% (10/77), adenovirus at 15.3% (9/59), and both rhinovirus and Haemophilus influenzae at 11.5% (10/87) each. The multi-pathogen co-detection rate in severe MPP children was significantly higher than that in mild MPP group (52.9% (108/204) vs. 36.2% (34/94), χ2=10.62, P=0.005). Among severe MPP children, there are 89 cases in the multi-pathogen co-detection group and 73 cases in the simple MPP group. The levels of LDH, D-dimer and neutrophil counts in the multi-pathogen co-detection group were significantly higher than those in the simple MPP group (348 (284, 422) vs. 307 (270, 358) U/L, 0.8 (0.5, 1.5) vs. 0.6 (0.4, 1.0) mg/L, 4.99 (3.66, 6.89)×10 9vs. 4.06 (2.91, 5.65)×10 9/L, Z=5.17, 4.99, 6.11, all P<0.05). Conclusions:The co-detection rate of respiratory pathogens, LDH and D-dimer in children with severe MPP were higher than those with mild MPP. Among severe MPP children the stress response of children in co-detection group was more serious than that of children with simple MPP.

Fanconi anemia (FA) is an inheritable disorder that presents with bone marrow failure, developmental anomalies, and an increased susceptibility to cancer. The etiology of this condition stems from a genetic mutation that disrupts the proper repair of interstrand DNA cross-links (ICLs). The resultant dysregulation of the DNA damage response mechanism can induce genomic instability, thereby elevating the mutation rates and the likelihood of developing cancer. The FA pathway assumes a pivotal role in safeguarding genome stability through its involvement in the repair of DNA cross-links and the maintenance of overall genomic integrity. A mutation in the germ line of any of the genes responsible for encoding the FA protein results in the development of FA. The prevalence of aberrant FA gene expression in somatic cancer, coupled with the identification of a connection between FA pathway activation and resistance to chemotherapy, has solidified the correlation between the FA pathway and cancer. Consequently, targeted therapies that exploit FA pathway gene abnormalities are being progressively developed and implemented. This review critically examines the involvement of the FA protein in the repair of ICLs, the regulation of the FA signaling network, and its implications in cancer pathogenesis and prognosis. Additionally, it explores the potential utility of small-molecule inhibitors that target the FA pathway.

Objective:To evaluate the short-term and long-term efficacy of Heidelberg triangle dissection in surgical treatment for pancreatic head cancer.Methods:The clinicopathological data of 97 patients with pancreatic head cancer who underwent pancreaticoduodenectomy at Cangzhou Central Hospital from Jan 2017 to Jan 2020 were retrospectively analyzed. After propensity score matching, 33 patients were included into the Heidelberg group and 36 patients in the control group.Results:There were no significant difference between Heidelberg group and control group in preoperative general conditions and postoperative major complications, while there were more cases with safe surgical margin > 1 mm (81.8% vs. 58.3%, P=0.034) and a significantly higher total number of lymph node dissection (11.24±2.35 vs. 9.50±2.76, P=0.006). In the survival analysis, the cumulative recurrence rate at 12 months (0.182±0.067 vs. 0.444±0.083, P=0.023) and 18 months (0.424±0.086 vs. 0.667±0.079, P=0.024) were better off in the Heidelberg group, and the local recurrence rate in the Heidelberg group was significantly lower than that in the control group (15.3 % vs. 36.1 %, P=0.037). However, there was no statistical difference in the overall survival time between the two groups. Conclusion:Dissection of Heidelberg triangle in radical resection of pancreatic head cancer reduces tumor local recurrence ,while fails to provide survival benefit.

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 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.