Craniosynostosis is a prevalent congenital craniofacial anomaly characterized by premature fusion of cranial sutures. It is of great social significance for the study and prevention of the genetic mechanism of craniosynostosis. Mutant genes such as FGFR1, FGFR2, FGFR3, TWIST1, MSX2, RAB, ERF related to craniosynostosis has been identified in humans, leading to the generation of a large number of recombinant animal models with similar functional acquisition or loss mutations to simulate various manifestations of craniosynostosis. The similarity of craniofacial development and molecular pathways between mice and humans makes them a good animal model for studying craniosynostosis. This article reviews the research progress of mouse models related to syndromic, non-syndromic craniosynostosis and craniosynostosis with non-human gene mutations, in order to provide a more comprehensive and systematic understanding of the genetic pathogenesis and treatment of this disease.

Parotid hypertrophy is a non-neoplastic, non-inflammatory and chronic salivary gland enlargement, which leads to facial "swelling", especially in the lower and lateral parts of the face, weakens the aesthetic feeling, and adversely affects the mental health of patients to a certain extent. However, there is no standard clinical treatment. In recent years, studies have explored and confirmed that botulinum toxin type A injection showed a good clinical effect in the treatment of parotid hypertrophy. With the aim of providing reference for the clinical treatment, the authors summarize the potential mechanism, Methods and complications of botulinum toxin type A treating parotid hypertrophy.

Acromegaly is a chronic disease predominantly caused by the hypersecretion of growth hormone (GH), typically due to a pituitary adenoma. The characteristic craniofacial deformities include pronounced zygomatic arches, frontal bossing, prognathism, dental malocclusion and macroglossia. It’s recommended that facial reconstructive interventions be deferred until the patient’s serum GH levels have been consistently normalized for at least 12 months. This review summarized the current knowledge on diagnosis, screening and facial management strategies for this disease.

Craniosynostosis is a prevalent congenital craniofacial anomaly characterized by premature fusion of cranial sutures. It is of great social significance for the study and prevention of the genetic mechanism of craniosynostosis. Mutant genes such as FGFR1, FGFR2, FGFR3, TWIST1, MSX2, RAB, ERF related to craniosynostosis has been identified in humans, leading to the generation of a large number of recombinant animal models with similar functional acquisition or loss mutations to simulate various manifestations of craniosynostosis. The similarity of craniofacial development and molecular pathways between mice and humans makes them a good animal model for studying craniosynostosis. This article reviews the research progress of mouse models related to syndromic, non-syndromic craniosynostosis and craniosynostosis with non-human gene mutations, in order to provide a more comprehensive and systematic understanding of the genetic pathogenesis and treatment of this disease.

Parotid hypertrophy is a non-neoplastic, non-inflammatory and chronic salivary gland enlargement, which leads to facial "swelling", especially in the lower and lateral parts of the face, weakens the aesthetic feeling, and adversely affects the mental health of patients to a certain extent. However, there is no standard clinical treatment. In recent years, studies have explored and confirmed that botulinum toxin type A injection showed a good clinical effect in the treatment of parotid hypertrophy. With the aim of providing reference for the clinical treatment, the authors summarize the potential mechanism, Methods and complications of botulinum toxin type A treating parotid hypertrophy.

Acromegaly is a chronic disease predominantly caused by the hypersecretion of growth hormone (GH), typically due to a pituitary adenoma. The characteristic craniofacial deformities include pronounced zygomatic arches, frontal bossing, prognathism, dental malocclusion and macroglossia. It’s recommended that facial reconstructive interventions be deferred until the patient’s serum GH levels have been consistently normalized for at least 12 months. This review summarized the current knowledge on diagnosis, screening and facial management strategies for this disease.

Objective:This study aims to obtain the prevalence and features associated with Violence Against Children (VAC) in China and, thus, formulate a prevention strategy.Methods:The mortality-related data of VAC was sourced from the National Disease Surveillance Points System (DSP) during 2013-2021. We analyzed the DSP data regarding children aged 0-17 years old who died from violence. The hospital cases of VAC was sourced from the National Injury Surveillance System (NISS), 2013-2021. We analyzed the data from NISS with the parameter of "intentional injury" caused by VAC in children aged between 0-17 years. Using robust linear regression, we analyze the time trend in the proportion of violence incidence. To understand the variations in the incidence of different types of violence across genders, we apply the chi-square test and adjusted Pearson residuals.Results:The overall trend of death caused by VAC has declined; it was reduced to 0.14/100 000 in 2021 from 0.33/100 000 in 2013. In 2021, male VAC mortality (0.15/100 000) was higher than females (0.13/100 000). The proportion of VAC cases to all injury cases has declined from 3.34% in 2013 to 2.29% in 2021. Among 9 344 VAC cases supervised by hospitals in 2021, the number of males (7 503 cases) was around 4 times that of females (1 841 cases), and the top three modes of violence were blunt tools (64.77%), falls (7.46%) and sharp instruments (6.18%), and 45 cases of sexual violence included 38 girls and 7 boys.Conclusions:The declining death rate due to VAC may be related to the benign development of Chinese society. Prevention strategies targeting training in parenting skills and problem-solving should be prioritized.

Objective To investigate the application effect of a bedside ultrasound-guided intestinal cleaning program in patients with severe acute pancreatitis.Methods A total of 51 patients with severe acute pancreatitis admitted to the ICU of a tertiary A hospital in Shandong from March to September 2023 were selected by convenience sampling method,and they were divided into an experimental group and a control group according to random number table method.The experimental group was given the bedside ultrasound-guided intestinal cleaning program,and the control group was given the routine intestinal cleaning program.Acute gastrointestinal injury ultrasonography score,the incidence of grade Ⅲ acute gastrointestinal injury and intra-abdominal pressure were compared between the 2 groups before intervention,on the 3rd and 5th day.Results There was an interaction effect between time and group in the comparison of acute gastrointestinal injury ultrasonography scores in the 2 groups(F=7.478,P<0.001);simple effect analysis showed that acute gastrointestinal injury ultrasonography scores in the experimental group were lower than those in control group on the 3rd and 5th day,with statistically significant differences(P<0.05).The incidence of grade Ⅲ acute gastrointestinal injury in the experimental group(23%)was lower than that in the control group(60%),with statistically significant differences(P<0.05).The intra-abdominal pressure had an interaction effect between the 2 groups(F=47.128,P<0.001);simple effect analysis showed that the intra-abdominal pressure in the experimental group was lower than that in the control group on the 3rd and 5th day,with statistically significant differences(P<0.05).Conclusion The bedside ultrasound-guided intestinal cleaning program can improve acute gastrointestinal injury and reduce intra-abdominal hypertension in patients with severe acute pancreatitis.

Objective:To evaluate the value of monitoring regional cerebral oxygen saturation (rSO 2) in the prognosis of comatose children in pediatric intensive care unit (PICU). Methods:A total of 127 coma children who admitted to PICU at Henan Children′s Hospital from January 2019 to September 2021 were collected and divided into mild[Glasgow coma score(GCS): 13-15], moderate(GCS: 9-12) and severe coma(GCS: 3-8) groups according to GCS.A cerebral oxygen monitor was used to monitor the rSO 2 of all children before treatment, and on the 3rd, 7th and 14th day after treatment.The outcomes were assessed according to the pediatric cerebral performance category (PCPC), and the children were divided into recovery group(PCPC score: 1), disability group(PCPC score: 2-4) and poor prognosis group(PCPC score: 5-6). Multiple linear regression and receiver operating characteristic(ROC) curve were used to analyze the correlation between rSO 2 and PCPC score. Results:rSO 2 in mild, moderate and severe coma groups before treatment were (78.06±3.21)%, (66.07±6.05)%, and (52.87±6.49)%, respectively ( F=209.263, P<0.05). rSO 2 before treatment was positively correlated with GCS( r=0.806, P<0.05). There were significant differences in rSO 2 among recovery group, disability group and poor prognosis group before treatment and that on the 3rd, 7th and 14th day after treatment ( P<0.05). Notably, rSO 2 in recovery group was higher than that in disability group, and rSO 2 in disability group was higher than that in poor prognosis group.The rSO 2 of three groups showed an increasing trend over time ( P<0.05). Multiple linear regression analysis showed that rSO 2 on the 7th and 14th day of treatment were independent prognostic factors ( OR -0.042, 95% CI -0.082~0.003, P<0.05; OR -0.047, 95% CI -0.094~0.000, P<0.05). ROC analysis showed that rSO 2 on the 7th day of treatment had a relatively higher prognostic value for children in coma, and the area under the ROC curve for predicting the prognosis of abnormal brain function and no wakefulness were 0.741 and 0.746, respectively. Conclusion:Monitoring rSO 2 has predictive value for the prognosis of brain function of coma children in PICU, in which the prognostic value of rSO 2 on the 7th day after treatment is relatively higher and can be used as a reference index for prognosis assessment of coma children in PICU.

OBJECTIVE: Acetaminophen (APAP) overdose is a common cause of liver injury. This study aimed to investigate the protective effect of honokiol (Hon) against APAP-induced hepatotoxicity and its potential mechanism. METHODS: C57BL/6 mice were administrated with Hon (10 and 30 mg/kg) after APAP (300 mg/kg) treatment. On 1.5 h and 5 h after Hon treatment, mice were sacrificed. Serum and liver were collected. And then, liver injury-related indexes, APAP metabolism-related indexes, mitochondrial respiratory chain function-related indexes, and mitochondrial membrane function-related protein expression were evaluated. RESULTS: It was found that Hon significantly decreased serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) activity and glutathione (GSH) depletion, increased hepatic catalase (CAT) and GSH peroxidase (GSH-Px) activities, reduced hepatic MDA and 3-nitrotyrosine contents, inhibited hepatic CYP1A2 activity and APAP protein adducts (APAP-CYS) formation. Meanwhile, oxidative phosphorylation capacity of complex I and electron transfer capacity of complex IV in mitochondrial respiratory chain was increased, whereas the release of H₂O₂ in the mitochondria was decreased following Hon treatment. Furthermore, Hon markedly down-regulated p-JNK in both cytosol and mitochondria, and obviously inhibited the release of apoptosis inducing factor (AIF) and endonuclease G (EndoG) from mitochondria to cytosol. CONCLUSION Hon alleviated APAP-induced liver injury through the following pathways: Reducing the production of APAP-CYS by inhibiting CYP1A2 activity; Ameliorating hepatic oxidative stress by increasing the levels of hepatic CAT, GSH-Px and GSH; Improving mitochondrial respiratory chain function by promoting oxidative phosphorylation capacity of complex I and electron transfer capacity of complex IV; Improving the function of mitochondrial membrane by inhibiting p-JNK and its translocation to mitochondria, thereby reducing the release of AIF and EndoG.