Objective:This study aims to explore the relationship between non-suicidal self-injurious (NSSI) behaviors and childhood trauma and peer rejection in adolescents with depressive disorders and, to examine whether childhood trauma and peer rejection can predict NSSI behaviors in these adolescents.Methods:A total of 412 depressed adolescents (263 with NSSI and 149 without NSSI) were included in the test data set, while another 161 depressed adolescents (99 with NSSI and 62 without NSSI) were in the validation set. This study firstly analyzed the differences in the scores of the Children's Depression Inventory (CDI), Childhood Trauma Questionnaire (CTQ), and Social Peer Rejection Scale (SPR) between the two groups using the test set. Then, a hierarchical logistic regression model was used to analyze the independent effects of these environmental factors on NSSI behaviors and to determine the diagnostic model. Finally, the diagnostic model was applied using the validation data set to calculate the actual predictive efficacy of the model.Results:Compared to those without NSSI, adolescent patients with NSSI showed significantly higher scores in CDI ( t=10.04, P<0.001), CTQ ( t=9.11, P<0.001), SPR ( t=5.30, P<0.001), and their subscale scores. Then, the scores of the low self-esteem factor of CDI ( OR=1.12, P=0.002), the emotional neglect factor of CTQ ( OR=1.08, P=0.037), and the insult factor ( OR=1.10, P=0.050) and somatic aggression factor ( OR=0.89, P=0.049) of SPR were significantly associated with NSSI behaviors. The diagnostic model was well established (area under the ROC curve=0.84, P<0.001). In addition, in the validation data set, the diagnostic model had a significant predictive effect (area under the ROC curve=0.85, P<0.001). Conclusion:Childhood emotional neglect and peer insult might be crucially influential factors triggering NSSI behaviors among adolescents with depressive disorders. Childhood trauma and peer rejection were of considerable importance when diagnosing and predicting the development of NSSI behaviors in depressive adolescents.

Objective:This study aims to explore the relationship between non-suicidal self-injurious (NSSI) behaviors and childhood trauma and peer rejection in adolescents with depressive disorders and, to examine whether childhood trauma and peer rejection can predict NSSI behaviors in these adolescents.Methods:A total of 412 depressed adolescents (263 with NSSI and 149 without NSSI) were included in the test data set, while another 161 depressed adolescents (99 with NSSI and 62 without NSSI) were in the validation set. This study firstly analyzed the differences in the scores of the Children's Depression Inventory (CDI), Childhood Trauma Questionnaire (CTQ), and Social Peer Rejection Scale (SPR) between the two groups using the test set. Then, a hierarchical logistic regression model was used to analyze the independent effects of these environmental factors on NSSI behaviors and to determine the diagnostic model. Finally, the diagnostic model was applied using the validation data set to calculate the actual predictive efficacy of the model.Results:Compared to those without NSSI, adolescent patients with NSSI showed significantly higher scores in CDI ( t=10.04, P<0.001), CTQ ( t=9.11, P<0.001), SPR ( t=5.30, P<0.001), and their subscale scores. Then, the scores of the low self-esteem factor of CDI ( OR=1.12, P=0.002), the emotional neglect factor of CTQ ( OR=1.08, P=0.037), and the insult factor ( OR=1.10, P=0.050) and somatic aggression factor ( OR=0.89, P=0.049) of SPR were significantly associated with NSSI behaviors. The diagnostic model was well established (area under the ROC curve=0.84, P<0.001). In addition, in the validation data set, the diagnostic model had a significant predictive effect (area under the ROC curve=0.85, P<0.001). Conclusion:Childhood emotional neglect and peer insult might be crucially influential factors triggering NSSI behaviors among adolescents with depressive disorders. Childhood trauma and peer rejection were of considerable importance when diagnosing and predicting the development of NSSI behaviors in depressive adolescents.

Objective:This study aims to explore the structural characteristics of the abnormal brain cortex in patients with autism by analyzing the neuroanatomical differences between patients with autism and the healthy controls.Methods:This study analyzed the brain imaging data of patients with autism ( n=525) and healthy controls ( n=569) extracted from the database of the Autism Brain Imaging Data Exchange (ABIDE) which collected data from 20 sites around the world. The cerebral cortex thickness was estimated using the FreeSurfer software based on the data of brain structure and was compared between patients with autism and the healthy controls using the t test. At the same time, according to their age, all participants were divided into three groups, which were younger than 12 years old group(150 patients and 151 controls), 12 to 18 years old group (210 patients and 233 controls), and older than 18 years old group (159 patients and 183 controls), and the cortical thickness was compared between patients with autism and healthy controls in different age groups using the t test respectively. Results:Based on the comparison of the thickness of the cerebral cortex between the autism group and the control group, it was found that compared with the control group, patients with autism showed a significant increase in cortical thickness in the occipital face area of both left and right sides of the brain (left side: size=1 043.95 mm 2, Z=4.31, MNI coordinates: x=-13.1, y=-102.4, z=2.4; right side: size=1 364.13 mm 2, Z=5.14, MNI coordinates: x=14.4, y=-101.3, z=3.1) and significant atrophy of cortical thickness at the posterior part of the superior frontal gyrus on the right side of the brain (size=485.86 mm 2, Z=4.71, MNI coordinates: x=6.8, y=-13.1, z=61.6). Comparisons of cerebral cortical thickness in different age groups found that patients younger than 12 years old showed a significant reduction in cortical thickness in the middle and posterior right superior frontal gyrus (right side: size=914.44 mm 2, Z=4.86, MNI coordinates: x=19.7, y=32.4, z=41.1) and inferior temporal gyrus (left side: size=638.16 mm 2, Z=-4.36, MNI coordinates: x=-34.7, y=-32.5, z=-22.8) compared to the healthy controls of the same age. Patients within 12 to 18 years old showed a reduction in the cortical thickness of the posterior upper frontal gyrus and an increase in the occipital facial area compared to the corresponding healthy controls. No significant difference in the thickness of the cortex was found between patients older than 18 years and the healthy controls of the same age. Conclusion:Abnormal cortical thickness in the occipital face area and posterior part of the superior frontal gyrus could be the characteristics of neurodevelopment in patients with autism, especially in younger children with autism.

Objective:The study aims to explore the abnormal characteristics in cerebral cortex among children with different subtypes of attention deficit hyperactivity disorder (ADHD).Methods:Four hundred and twelve samples were obtained from the Healthy Brain Network project of American Child Mind Institute. There were 288 children with ADHD (all subjects: age,M=10.03,SD=3.11; 151 of ADHD-C, 20 of ADHD-H, and 117 of ADHD-I) and 124 healthy controls (age,M=9.98,SD=2.98). Using FreeSurfer software, we processed the brain structure images and obtained the cortical volume, cortical thickness and surface area for each subject. Analysis of Variance (ANOVA) and post hoc comparison analyses were conducted.Results:ANOVA analysis showed significant differences of the cortical volume located in the left superior parietal gyrus ( Z=5.94) and superior temporal gyrus ( Z=5.49) among the 3 subtypes of ADHD children and the healthy controls (Monte Carlo, P<0.05). Compared with the healthy controls, ADHD-H group exhibited an increased cortical volume in the left superior parietal gyrus ( Z=6.79), while the ADHD-I group had a decreased volume in the left superior temporal gyrus ( Z=-5.12) and lateral occipital cortex ( Z=-6.40). ADHD-C group also had a decreased volume in the left lateral occipital cortex ( Z=-3.37). Among 3 subtypes of ADHD patients, both ADHD-I and ADHD-C groups had a smaller volume in the left superior parietal gyrus than that of the ADHD-H group (ADHD-I: Z=-7.33,MNI coordinate:x=-26.8,y=-60.6,z=45.4; ADHD-C: Z=-7.14,MNI coordinate:x=-26.6,y=-60.2,z=45.4). Additionally, there was no statistical difference in cortical volume between the ADHD-I and ADHD-C group (Monte Carlo, P>0.05). Subsequent supplementary analyses showed that the sample size and age had no significant effect on the above results. Moreover, analysis of cortical thickness and the surface area showed that the abnormality of the cortical volume in different ADHD subtypes was mainly determined by the surface area of the cerebral cortex. Conclusion:Cortical measures in the superior parietal gyrus might be the crucial features that distinguishes the different subtypes of ADHD. These results enable us to further explore the neurodevelopmental mechanism of ADHD and guide the precise and specific clinical treatment.

Objective:This study aims to explore the structural characteristics of the abnormal brain cortex in patients with autism by analyzing the neuroanatomical differences between patients with autism and the healthy controls.Methods:This study analyzed the brain imaging data of patients with autism ( n=525) and healthy controls ( n=569) extracted from the database of the Autism Brain Imaging Data Exchange (ABIDE) which collected data from 20 sites around the world. The cerebral cortex thickness was estimated using the FreeSurfer software based on the data of brain structure and was compared between patients with autism and the healthy controls using the t test. At the same time, according to their age, all participants were divided into three groups, which were younger than 12 years old group(150 patients and 151 controls), 12 to 18 years old group (210 patients and 233 controls), and older than 18 years old group (159 patients and 183 controls), and the cortical thickness was compared between patients with autism and healthy controls in different age groups using the t test respectively. Results:Based on the comparison of the thickness of the cerebral cortex between the autism group and the control group, it was found that compared with the control group, patients with autism showed a significant increase in cortical thickness in the occipital face area of both left and right sides of the brain (left side: size=1 043.95 mm 2, Z=4.31, MNI coordinates: x=-13.1, y=-102.4, z=2.4; right side: size=1 364.13 mm 2, Z=5.14, MNI coordinates: x=14.4, y=-101.3, z=3.1) and significant atrophy of cortical thickness at the posterior part of the superior frontal gyrus on the right side of the brain (size=485.86 mm 2, Z=4.71, MNI coordinates: x=6.8, y=-13.1, z=61.6). Comparisons of cerebral cortical thickness in different age groups found that patients younger than 12 years old showed a significant reduction in cortical thickness in the middle and posterior right superior frontal gyrus (right side: size=914.44 mm 2, Z=4.86, MNI coordinates: x=19.7, y=32.4, z=41.1) and inferior temporal gyrus (left side: size=638.16 mm 2, Z=-4.36, MNI coordinates: x=-34.7, y=-32.5, z=-22.8) compared to the healthy controls of the same age. Patients within 12 to 18 years old showed a reduction in the cortical thickness of the posterior upper frontal gyrus and an increase in the occipital facial area compared to the corresponding healthy controls. No significant difference in the thickness of the cortex was found between patients older than 18 years and the healthy controls of the same age. Conclusion:Abnormal cortical thickness in the occipital face area and posterior part of the superior frontal gyrus could be the characteristics of neurodevelopment in patients with autism, especially in younger children with autism.

Objective:The study aims to explore the abnormal characteristics in cerebral cortex among children with different subtypes of attention deficit hyperactivity disorder (ADHD).Methods:Four hundred and twelve samples were obtained from the Healthy Brain Network project of American Child Mind Institute. There were 288 children with ADHD (all subjects: age,M=10.03,SD=3.11; 151 of ADHD-C, 20 of ADHD-H, and 117 of ADHD-I) and 124 healthy controls (age,M=9.98,SD=2.98). Using FreeSurfer software, we processed the brain structure images and obtained the cortical volume, cortical thickness and surface area for each subject. Analysis of Variance (ANOVA) and post hoc comparison analyses were conducted.Results:ANOVA analysis showed significant differences of the cortical volume located in the left superior parietal gyrus ( Z=5.94) and superior temporal gyrus ( Z=5.49) among the 3 subtypes of ADHD children and the healthy controls (Monte Carlo, P<0.05). Compared with the healthy controls, ADHD-H group exhibited an increased cortical volume in the left superior parietal gyrus ( Z=6.79), while the ADHD-I group had a decreased volume in the left superior temporal gyrus ( Z=-5.12) and lateral occipital cortex ( Z=-6.40). ADHD-C group also had a decreased volume in the left lateral occipital cortex ( Z=-3.37). Among 3 subtypes of ADHD patients, both ADHD-I and ADHD-C groups had a smaller volume in the left superior parietal gyrus than that of the ADHD-H group (ADHD-I: Z=-7.33,MNI coordinate:x=-26.8,y=-60.6,z=45.4; ADHD-C: Z=-7.14,MNI coordinate:x=-26.6,y=-60.2,z=45.4). Additionally, there was no statistical difference in cortical volume between the ADHD-I and ADHD-C group (Monte Carlo, P>0.05). Subsequent supplementary analyses showed that the sample size and age had no significant effect on the above results. Moreover, analysis of cortical thickness and the surface area showed that the abnormality of the cortical volume in different ADHD subtypes was mainly determined by the surface area of the cerebral cortex. Conclusion:Cortical measures in the superior parietal gyrus might be the crucial features that distinguishes the different subtypes of ADHD. These results enable us to further explore the neurodevelopmental mechanism of ADHD and guide the precise and specific clinical treatment.

Objective To explore the clinical features and risk factors of poor prognosis in neonatal necrotizing enterocolitis(NEC).Methods A retrospective study was carried out in the infants with NEC admitted to 6 cooperative hospitals in Guangdong Province between January 2005 and December 2014.The clinical features and risk factors of poor prognosis in preterm and full-term infants diagnosed NEC,early onset and late onset NEC were analyzed.Results A total of 449 cases who met the criteria were admitted during the study time.The mortality was 23.6％ (106/449 cases),of which the preterm group was 24.6％ (58/238 cases) while the full-term group was 22.7％ (48/211 cases),the early onset group was 22.1％ (45/204 cases) while the late onset group was 24.3％ (57/235 cases).The median number of NEC onset in preterm group was 11 d after birth while the number of the full-term group was 6 d.Full-term infants who diagnosed NEC were more likely to manifest themselves as abdominal distension (52.1％ vs.42.0％,x2 =4.597,P =0.032),vomiting(36.5％ vs.17.2％,x2 =21.428,P =0.000) and bloody stool(30.3％ vs.21.4％,x2 =4.653,P =0.031);but in the onset of NEC,preterm infants more likely to have feeding intolerance (21.0％ vs.12.8％,x2=5.309,P =0.021).The early onset group of full-term NEC was much common in twins or multiplets(9.4％ vs.1.1％,x2 =6.226,P =0.013),which rate of surgical therapy was much higher (41.0％ vs.27.0％,P =0.036) and the breast-feeding rate before NEC was lower than the late onset group(14.5％ vs.32.6％,x2 =9.500,P =0.002),the differences were statistically significant.The gestational age and birth weight were bigger in the early onset group of preterm NEC[(33.8 ±2.5) weeks vs.(32.2 ±2.8) weeks,t =4.261,P =0.000;(2.1 ±0.5) kg vs.(1.7 ± 0.5) kg,t =4.735,P =0.000)],but length of stay was shorter than the late onset group (18.0 d vs.26.5 d,P =0.000).Logistic regression analysis showed that the risk factors of poor prognosis of full-term NEC were shock,peritonitis and sepsis;while risk factors of poor prognosis of preterm NEC were small for gestational age infant,pulmonary hemorrhage,shock,intestinal perforation and sepsis;the risk factors of poor prognosis of the early onset group of full-term NEC was shock;while those of the late onset group were shock and peritonitis;the risk factors of poor prognosis in the early onset group of preterm NEC were shock and sepsis,while those in the late onset group were pulmonary hemorrhage,shock,intestinal perforation and sepsis.Conclusions Compared to the preterm NEC,the onset time of full-term NEC was earlier and the clinical manifestations were more typical.Early identification and management of shock,peritonitis,intestinal perforation,sepsis and pulmonary hemorrhage can reduce the risk of poor prognosis of neonate NEC.

OBJECTIVETo observe the effects of manganese sulfate on blood pressure, myocardial ultrastructure and heart organ index of rats.

METHODSForty male SPF SD rats were randomly divided into 4 groups: control group (0 mg/kg), 5 mg/kg dose group, 15 mg/kg dose group and 25 mg/kg dose group, 10 rats each group. Intraperitoneal injection was performed for six months, by five times each week, the rat blood pressure was measured by tail cuff method, and the heart organ index of the rats was computed. Three rats were selected from each group randomly, and the myocardial ultrastructure of the rats was observed by using transmission electron microscopy (TEM). The BMD and BMDL between manganese sulfate injected dose and the rats heart organ index were evaluated by BMD (Benchmark Dose).

RESULTSThere was no significant of blood pressure between the experimental group and the control group (P > 0.05).The heart organ indexes of the four groups were 0.24% ± 0.10%, 0.25% ± 0.02%, 0.26% ± 0.02%, and 0.24% ± 0.02%. Statistical significance of heart organ indexes was found between the 15 mg/kg dose group and the control group (P < 0.05). Observed by TEM, we found that-different degrees of mitochondrial crest fracture or disappear, mitochondria swelling, hydropic change and myocardial fibers degeneration happened in the rats of the three exposed groups, but not the control group. The BMD and BMDL were calculated as 9.33 mg/kg and 4.28 mg/kg in the study of manganese sulfate injected dose and the rats heart organ index.

CONCLUSIONChronic manganese poisoning can lead to myocardial mitochondria superfine lesions, myocardial fiber damage and heart organ index change in rats.

Animals ; Male ; Manganese Compounds ; Mitochondria ; drug effects ; ultrastructure ; Myocardium ; ultrastructure ; Myocytes, Cardiac ; drug effects ; ultrastructure ; Rats ; Rats, Sprague-Dawley ; Sulfates ; toxicity ; Toxicity Tests