[Intellectual characteristics of children with attention deficit hyperactivity disorder and developmental dyslexia].

OBJECTIVE: To study the intellectual characteristics of children with attention deficit hyperactivity disorder (ADHD) and developmental dyslexia (DD). METHODS: A total of 55 children with ADHD and DD (ADHD+DD group), 150 children with ADHD alone (ADHD group), and 22 children with DD alone (DD group) were enrolled as subjects. Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV) was used to evaluate and compare intellectual characteristics among the three groups. RESULTS: There were significant differences in the scores of full-scale intelligence quotient (FSIQ), verbal comprehension index, perceptual reasoning index, and working memory index among the three groups (P < 0.05):the ADHD+DD group had significantly lower scores of FSIQ, verbal comprehension index, perceptual reasoning index, and working memory index than the ADHD group, as well as a significantly lower FSIQ score than the DD group. A comparison of the 10 core subtests in WISC-IV showed that compared with the ADHD group, the ADHD+DD group had significantly lower scores of similarities, vocabulary, comprehension, recitation, picture concepts, matrix reasoning, and letter-number sequencing (P < 0.05). Compared with the DD group, the ADHD+DD group had significantly lower scores of vocabulary, similarities, picture concepts, matrix reasoning, and recitation (P < 0.05). CONCLUSIONS: Compared with the children with ADHD alone, the children with ADHD and DD have more severe impairment of FSIQ, verbal comprehension, perceptual reasoning, and working memory, and therefore, it is suggested to enhance the training on similarities, vocabulary, matrix reasoning, picture concepts, and recitation for children with ADHD and DD in clinical practice.

Long non-coding RNA PVT1 encapsulated in bone marrow mesenchymal stem cell-derived exosomes promotes osteosarcoma growth and metastasis by stabilizing ERG and sponging miR-183-5p.

Exosomes secreted by bone marrow mesenchymal stem cells (BMSCs) promote osteosarcoma cell proliferation and migration, while the underlying mechanism remains unknown. Since the long non-coding RNA PVT1 has been reported to be upregulated in osteosarcoma cells and contributes to its growth and metastasis, we aim to investigate whether BMSC-derived exosomes promote osteosarcoma growth and metastasis via transporting PVT1 into osteosarcoma cells. The PVT1 expression in BMSC-derived exosomes was markedly higher than that in osteosarcoma cell-derived exosomes. The co-culturing of BMSC-derived exosomes and osteosarcoma cells (Saos-2, MG-63, and MNNG/HOS cell lines) significantly raised PVT1 expression of osteosarcoma cells. The direct binding between PVT1 and the oncogenic protein ERG was confirmed using RNA immunoprecipitation and RNA pull-down assays, and the transported PVT1 promotes osteosarcoma cell proliferation and migration via inhibiting degradation and ubiquitination of ERG. PVT1 also increased ERG expression through sponging miR-183-5p. In summary, our findings indicated that BMSC-derived exosomes encapsulate PVTl and transport it into osteosarcoma cells, and the transported PVT1 promotes tumor growth and metastasis by inhibiting ubiquitination and promoting expression of ERG in osteosarcoma cells. These data provide a novel insight into the mechanism of BMSC-derived exosomes in affecting osteosarcoma progression.

[Correlation between end-tidal carbon dioxide and partial pressure of arterial carbon dioxide in ventilated newborns].

OBJECTIVE: To study the correlation between end-tidal carbon dioxide (PetCO2) and partial pressure of arterial carbon dioxide (PaCO2) in ventilated newborns. METHODS: Thirty-one ventilated newborn underwent mainstream PetCO2 monitoring; meanwhile, arterial blood gas analysis was performed. The correlation and consistency between PetCO2 and PaCO2 were assessed. RESULTS: A total of 85 end-tidal and arterial CO2 pairs were obtained from 31 ventilated newborns. The mean PetCO2 (41±10 mm Hg) was significantly lower than the corresponding mean PaCO2 (46±11 mm Hg) (P<0.01). There was a significant positive correlation between PetCO2 and PaCO2 (r=0.92, P<0.01). The overall PetCO2 bias was 5.1±4.3 mm Hg (95% limits of consistency, -3.3 to 13.6 mmHg), and 5% (4/85) of the points were beyond the 95%CI. When the oxygenation index (OI) was less than 300 mm Hg (n=48), there was a significant positive correlation between PetCO2 and PaCO2 (r=0.85, P<0.01); the PetCO2 bias was 5.9±4.3 mm Hg (95% limits of consistency, -2.6 to 14.5 mm Hg), and 4.2% (2/48) of the points were beyond the 95%CI. When the OI was more than 300 mm Hg (n=37), there was also a significant positive correlation between PetCO2 and PaCO2 (r=0.91, P<0.01); the PetCO2 bias was 4.1±4.1 mm Hg (95% limits of consistency, -3.9 to 12.1 mm Hg), and 5% (2/37) of the points were beyond the 95%CI. CONCLUSIONS: There is a good correlation and consistency between PetCO2 and PaCO2 in ventilated newborns.

[Genetic factors in the occurrence of neonatal unconjugated hyperbilirubinemia].

OBJECTIVE: To study association of uridine-diphosphate-glucuronosyltransferase1A1 (UGT1A1) Gly71Arg, UGT1A1 promoter TATA-box and glucose-6-phosphate dehydrogenase (G6PD) gene mutations with the occurrence of neonatal unconjugated hyperbilirubinemia. METHODS: The TATA-box, exon 1 and exon 5 of the UGT1A1 gene and the exon 12 of G6PD gene were amplified by PCR. The products of PCR were analyzed by direct DNA sequencing. Clones for the mutations of the UGT1A1 gene and the G6PD gene were constructed in order to identify the results of the products of PCR. Seventy-two neonates with unconjugated hyperbilirubinemia (case group) and 65 healthy neonates (control group) were enrolled. The genotypes and allele frequencies of the polymorphisms of UGT1A1 Gly71Arg and UGT1A1 TATA-box were compared between the two groups. The effects of UGT1A1 Gly71Arg, UGT1A1 promoter TATA-box and G6PD gene mutations on the development of neonatal unconjugated hyperbilirubinemia were estimated using logistic regression models. RESULTS: There were significant differences in the genotype distribution of Gly71Arg polymorphism of UGT1A1 gene between the case and control groups (P<0.01). The Arg allele frequency of the polymorphisms of UGT1A1 gene in the case group was significantly higher than in the control group (P<0.01). There were no significant differences in the genotype distribution of the UGT1A1 promoter TATA-box between the two groups (P>0.05). The OR and 95%CI values of UGT1A1 Gly71Arg, UGT1A1 TATA-box and G6PD gene mutations associated with the development of neonatal unconjugated hyperbilirubinemia were 5.468 (2.274, 12.818), 0.688 (0.266, 1.778) and 5.081 (1.070, 24.133) respectively. CONCLUSIONS: UGT1A1 Gly71Arg and G6PD gene mutations may be involved in the development of neonatal unconjugated hyperbilirubinemia.

Hospitalized children with 2009 influenza a (H1N1) infection in Shenzhen, China, November-December 2009.

OBJECTIVES: During the winter outbreak of 2009 influenza A (H1N1) infection in China, the number of confirmed cases and the fatal cases has grown rapidly. We describe the clinical characteristics of hospitalized children with 2009 influenza A (H1N1) infection in Shenzhen, China, November-December 2009. METHODS: Using a standardized form, we collected data on 148 hospitalized children. 2009 influenza A (H1N1) infection was confirmed in nasopharyngeal swab specimens with the use of a real-time reverse transcriptase-polymerase chain reaction assay. RESULTS: Of the 148 hospitalized children with 2009 influenza A (H1N1) infection, 81 (55%) were 5 years of age or older and 85% of the patients were previously healthy. The common presenting symptoms were fever (94%), cough (89%), runny nose (36.5%), vomiting (24%), sore throat (19.6%), wheezing (18%), abdominal pain (16%), mental status changes (9%), seizures (6%), diarrhea (6%), myalgia (6%), and chest pain (4%). Twenty-nine (20%) patients were admitted to an ICU, 10 (7%) patients required mechanical ventilation. The overall complication rate was 65.5%, they were pneumonia in 94 (64%), neurologic complications in 18 (12%), parapneumonic effusion in 12 (8%) and myocarditis in 7 (5%). One hundred seven (72%) patients received oseltamivir treatment, 34 (23%) received within 48 hr after the onset of symptoms. All patients received antibiotics before admission or on admission. One hundred forty-four (97%) patients were discharged; four (3%) previously healthy patients died, three died from severe encephalopathy, one died from secondary fungal meningitis. CONCLUSION: Hospitalized children with 2009 influenza A (H1N1) infection can have a wide range of presentation and clinical complications including neurologic complications. The severe cases and deaths concentrate in previously healthy older children.

[Characteristics of severely and critically ill children with 2009 influenza A (H1N1) virus infection].

OBJECTIVE: To analyze the clinical characteristics of severely and critically ill children with 2009 influenza A (H1N1) infection. METHOD: Clinical data of 150 cases with 2009 influenza A (H1N1) virus infection confirmed with the use of a real-time polymerase-chain-reaction assay on nasopharyngeal swab specimens were analyzed. RESULT: Among 150 severely and critically ill children with 2009 influenza A (H1N1) virus infection, 103 were male, 47 were female; the median age was 5 years, 81(55%) were 5 years of age or older; 21 (14%) had underlying chronic diseases. The most common presenting symptoms were fever (95%), cough (89%), vomiting (23%), wheezing (19%), abdominal pain (16%), lethargy (7%), seizures (6%), myalgia (6%), and diarrhea (6%). The common laboratory abnormalities were increased or decreased white blood cells counts (40%), elevated of CRP (33%), LDH (29%), CK (25%) and AST (19%). Clinical complications included pneumonia (65%), encephalopathy (12%), myocarditis (5%), encephalitis (1%) and myositis (1%). All patients had received antibiotics before admission or on admission; 73% of patients had received oseltamivir treatment, 23% of patients had received corticosteroids; 32 (21%) were admitted to an ICU, 13 patients were intubated and mechanically ventilated. Fourteen patients with dyspnea who were irresponsive to the treatment experienced bronchoalveolar lavage with flexible bronchoscopy, and the branching bronchial casts were removed in 5 patients. Totally 145 (97%) patients were discharged, five (3%) died, three previously healthy patients died from severe encephalopathy, one patient died from ARDS, one previously healthy patient died from secondary fungal meningitis. CONCLUSION: Severely and critically ill children with 2009 influenza A (H1N1) virus infection may occur mainly in older children without underlying chronic disease. The clinical spectrum and laboratory abnormality of the patients can have a wide range. Neurologic complications may be common and severe encephalopathy can lead to death in previously healthy children. Early use of bronchoalveolar lavage with flexible bronchoscopy may reduce death associated with pulmonary complications.

[Protective effects and mechanisms of recombinant human superoxide dismutase in acute lung injury of rats following meconium aspiration].

OBJECTIVE: To evaluate the protective effects of recombinant human superoxide dismutase (rhSOD) in acute lung injury (ALI) following meconium aspiration. METHODS: Thirty-two healthy male Sprage-Dawley rats were divided into two groups, 8 were used as control (saline group) by infusing 1 ml/kg saline through endotracheal tube; the other 24 rats were used to establish model of ALI by infusing 1 ml/kg of 20% human newborn meconium suspension through endotracheal tube, and then were randomized to 3 groups (8 each): meconium group with no administration of saline or rhSOD; meconium + saline group by infusing 1 ml/kg saline through endotracheal tube; meconium + rhSOD group by infusing 20 mg/kg rhSOD dissolved in 1 ml/kg saline through endotracheal tube. The rats were killed 24 h after treatment. The measurements included bronchoalveolar lavage fluid (BALF) cell counts, protein, BALF protein/plasma protein (pulmonary permibility index, PPI), lactic dehydrogenase (LDH), pulmonary myeloperoxidase (MPO) and superoxide dismutase (SOD) activity, malonyldialdehyde (MDA) and nitric oxide (NO) level. Lung injury score was also evaluated. RESULTS: Compared with the saline group, the rats in the meconium group had significantly increased BALF cell counts (4.04 +/- 1.01 vs. 0.53 +/- 0.19), protein (2.54 +/- 0.74 vs. 0.67 +/- 0.26), PPI (0.50 +/- 0.18 vs. 0.12 +/- 0.05), LDH (263.50 +/- 97.84 vs. 17.38 +/- 3.58), pulmonary MPO (1.49 +/- 0.22 vs. 0.62 +/- 0.16), MDA (3.30 +/- 0.85 vs. 1.40 +/- 0.35), NO (12.77 +/- 5.00 vs. 4.89 +/- 1.32) and lung injury score (9.88 +/- 2.10 vs. 2.25 +/- 1.04), P < 0.01 for all, whereas pulmonary SOD activity had no statistically significant differences (103.28 +/- 24.53 vs. 94.49 +/- 12.93, P > 0.05). There were no statistically significant differences between meconium + saline group and meconium group (all P > 0.05). Compared with the meconium + saline group, meconium + rhSOD group had decreased BALF cell counts (3.13 +/- 0.77 vs. 4.68 +/- 1.40, P < 0.01), LDH (162.63 +/- 76.90 vs. 273.75 +/- 111.83, P < 0.05), pulmonary MPO activity (1.23 +/- 0.28 vs. 1.54 +/- 0.24, P < 0.05), MDA (2.46 +/- 0.42 vs. 3.50 +/- 0.82, P < 0.01), NO level (9.17 +/- 2.34 vs. 13.04 +/- 4.38, P < 0.05), lung injury score (8.63 +/- 1.30 vs. 10.00 +/- 1.07, P < 0.05) and increased pulmonary SOD activity (134.45 +/- 23.30 vs. 106.79 +/- 17.77, P < 0.05), but there were no statistically significant differences in BALF protein and PPI between these two groups. CONCLUSION: Inflammation and lipid peroxidation might play important roles in the pathogenesis of ALI with meconium aspiration, a single early administration of 20 mg/kg rhSOD intratracheally can reduce lung damage in rats following meconium aspiration.