[Clinical phenotype and genetic analysis of six Chinese patients affected with Acromicric dysplasia due to variants of FBN1 gene].

OBJECTIVE: To retrospectively analyze the clinical and genetic characteristics of six patients with Acromicric dysplasia due to variants of the FBN1 gene. METHODS: Six patients who had visited the Affiliated Hospital of Qingdao University between February 2018 and October 2020 were selected as the study subjects. Clinical data of the patients were collected. High-throughput sequencing was carried out. And candidate variants were verified by Sanger sequencing. RESULTS: All of the six patients had presented with severe short stature (< 3s), brachydactyly, short and broad hands and feet. Other manifestations included joint stiffness, facial dysmorphism, delayed bone age, liver enlargement, coracoid femoral head, and lumbar lordosis. Genetic testing revealed that all had harbored heterozygous variants of the FBN1 gene. Patient 1 had harbored a c.5183C>T (p.A1728V) missense variant in exon 42, which had derived from his father (patient 2). Patient 3 had harbored a c.5284G>A (p.G1762S) missense variant in exon 43, which had derived from her mother (patient 4). Patient 5 had harbored a c.5156G>T (p.C1719F) missense variant in exon 42, which was de novo in origin. Patient 6 had harbored a c.5272G>T (p.D1758Y) missense variant in exon 43, which was also de novo in origin. The variants carried by patients 1, 3 and 6 were known to be pathogenic. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), the FBN1: c.5156G>T was rated as a pathogenic variant (PS2+PM1+PM2_Supporting +PM5+PP3). CONCLUSION: All of the six patients had severe short stature and a variety of other clinical manifestations, which may be attributed to the variants of the FBN1 gene.

Alterations in the gut microbiota of toddlers with cow milk protein allergy treated with a partially hydrolyzed formula containing synbiotics: A nonrandomized controlled interventional study.

Formulas containing intact cow milk protein are appropriate alternatives when human milk (HM) is not feasible. However, for babies with a physician-diagnosed cow milk protein allergy (CMPA), hydrolyzed formulas are needed. We conducted a 3-month, open-label, nonrandomized concurrent controlled trial (ChiCTR2100046909) between June 2021 and October 2022 in Qingdao City, China. In this study, CMPA toddlers were fed with a partially hydrolyzed formula containing synbiotics (pHF, n = 43) and compared with healthy toddlers fed a regular intact protein formula (IF, n = 45) or HM (n = 21). The primary endpoint was weight gain; the secondary endpoints were changes in body length and head circumference of both CMPA and healthy toddlers after 3-month feeding; and the exploratory outcomes were changes in gut microbiota composition. After 3 months, there were no significant group differences for length-for-age, weight-for-age, or head circumference-for-age Z scores. In the gut microbiota, pHF feeding increased its richness and diversity, similar to those of IF-fed and HM-fed healthy toddlers. Compared with healthy toddlers, the toddlers with CMPA showed an increased abundance of phylum Bacteroidota, Firmicutes, class Clostridia, and Bacteroidia, and a decreased abundance of class Negativicutes, while pHF feeding partly eliminated these original differences. Moreover, pHF feeding increased the abundance of short-chain fatty acid producers. Our data suggested that this pHF partly simulated the beneficial effects of HM and shifted the gut microbiota of toddlers with CMPA toward that of healthy individuals. In conclusion, this synbiotic-containing pHF might be an appropriate alternative for toddlers with CMPA.

A Review of Three Chinese Cases of Acromicric/Geleophysic Dysplasia with FBN1 Mutations.

OBJECTIVE: This study aims to explore the clinical features and molecular diagnosis of FBN1-related acromelic dysplasia in Chinese patients. METHODS: The clinical and genetic features of three FBN1-related acromicric dysplasia (AD)/geleophysic dysplasia (GD) Chinese patients from two families were reviewed, and comprehensive medical evaluations were performed. Targeted next-generation sequencing was used to detect genetic mutations associated with short statures, including FBN1. Sanger sequencing was used to determine the de novo mutation origin. RESULTS: Patient 1 presented with short stature, short and stubby hands and feet, mild facial dysmorphism, hepatomegaly, delayed bone age and beak-like femoral heads. Patient 2 and this patient's father merely presented with short stature, wide and short hands, and beak-like femoral heads. One novel mutation, c.5272G>T(p.D1758Y), and one known mutation, c.5183C>T(p.A1728V), were identified in these patients. CONCLUSION: The clinical features varied among these patients. The variant c.5272G>T(p.D1758Y) is a novel mutation.

Six1 Promotes Epithelial-Mesenchymal Transition in Bronchial Epithelial Cells via the TGFß1/Smad Signalling Pathway.

INTRODUCTION: The homeodomain transcription factor sine oculis homeobox homolog 1 (Six1) plays a crucial role in embryogenesis and is not expressed in normal adult tissue but is expressed in many pathological processes, including airway remodelling in asthma. The current study aimed to reveal the effects of Six1 in regulating the airway remodelling and its possible mechanism. METHODS: A mouse model of ovalbumin-induced asthma-associated airway wall remodelling and a bronchial epithelial cell (16HBE) model of transforming growth factor ß1 (TGFß1)-induced epithelial-mesenchymal transition (EMT) were used to investigate the role of Six1. Then, 16HBE cells were transformed with Six1 expression vectors and treated with a TGFß1 pathway inhibitor to determine the role of Six1 in EMT. The effect of Six1 and its possible mechanism were assessed by immunohistochemistry, RT-PCR, and Western blot. RESULTS: Six1 expression was elevated in the lungs in an OVA mouse model of allergic asthma and in 16HBE cells treated with TGFß1. Six1 overexpression promoted an EMT-like phenotype with a decreased protein expression of E-cadherin and increased protein expression of α-smooth muscle actin (α-SMA) as well as fibronectin in 16HBE cells; these effects appeared to promote TGFß1 and phospho-Smad2 (pSmad2) production, which are the main products of the TGFß1/Smad signalling pathway, which could be reduced by a TGFß1 inhibitor. CONCLUSION: These data reveal that Six1 and TGFß1 are potentially a part of an autocrine feedback loop that induces EMT, and these factors can be reduced by blocking the TGFß1/Smad signalling pathway. As such, these factors may represent a promising novel therapeutic target for airway remodelling in asthma.

The efficacy and safety of Chinese herbal compound or combined with western medicine for pediatric adenoidal hypertrophy: A protocol for systematic review and meta-analysis.

BACKGROUND: Traditional Chinese medicine (TCM) or combined with western medicine in the treatment of pediatric adenoidal hypertrophy has been widely used in clinical practice, but the overall efficacy and safety is still unclear. This paper aims to evaluate the efficacy and safety analysis of TCM or combined with western medicine for pediatric adenoidal hypertrophy. METHODS: PubMed, EMbase, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), WanFang, the Chongqing VIP Chinese Science and Technology Periodical Database, and China biomedical literature database (CBM) were searched for randomized controlled trials of TCM or combined with western medicine for pediatric adenoidal hypertrophy from the date of establishment to July 2020, and Baidu Scholar, Google Scholar, International Clinical Trials Registry Platform (ICTRP), and Chinese Clinical Trials Registry (ChiCTR) were searched for unpublished grey literature. Two researchers independently applied RevMan 5.3 software for data extraction and risk assessment of bias. RESULTS: The effectiveness and safety of TCM or combined with western medicine for pediatric adenoidal hypertrophy is evaluated by means of the Adenoid (A) /(Nasopharyngeal (N) ratio, clinical efficacy, integral score of TCM syndromes, clinical single symptom score, disease specific quality of life for children with obstructive sleep apnea 18 items survey (OSA-18), Interleukin 4 (IL-4) and adverse reaction incidence. CONCLUSION: This study will provide theoretical support for the clinical application of TCM or combined with western medicine for pediatric adenoidal hypertrophy. OSF REGISTRATION NUMBER: DOI 10.17605/OSF.IO/J76AG.

[Analysis of clinical features and genetic variants in an infant with Bloom syndrome].

OBJECTIVE: To analyze the clinical features and genetic variants in a 13-month-old child with Bloom syndrome. METHODS: Clinical data of the child was collected. Genetic variants were detected by high-throughput sequencing and Sanger sequencing. RESULTS: The child was born at full term but was small for gestational age. His clinical features included loss of appetite, severe growth retardation, microcephaly, and small mandible. Genetic testing found that he had carried compound heterozygous c.1068+3A>C and c.1069-1G>C variants of the BLM gene, both of which were unreported previously. CONCLUSION: Bloom syndrome is mainly characterized by severe growth retardation in infancy. The novel variants have expanded the variant spectrum of the BLM gene.

Correlation between oxidative stress and NF-κB signaling pathway in the obesity-asthma mice.

In this study, a mice model of obesity-asthma was established. We investigated the correlation between oxidative stress and NF-κB signaling pathway in the lung tissues, together with the effects of acetylcysteine. The animals were fed on a high-fat diet, and then ovalbumin (OVA) sensitization was utilized to establish the obesity-asthma model. N-acetylcysteine was used to treat asthma, animals treated with budesonide served as control. The malondialdehyde (MDA) in the lung tissues was determined, together with the activity of glutathione (GSH). EMAS assay was utilized to measure the nuclear factor-κB-P65 (NF-κB-P65) in lung tissues. Western blot analysis was performed to determine the expression of inhibitor kappa B-α (IκB-α) and inhibitor kappa B kinase-ß (IKK-ß). The MDA in the asthma groups showed significantly elevation (P < 0.01), and the GSH showed significant decrease (P < 0.01), especially in the obesity-asthma group. The efficiency of N-acetylcysteine was superior to that of the budesonide in the decline of MDA and elevation of GSH (P < 0.01). In both asthma groups, the expression of IKK-ß and transcription of NF-κB-P65 in the lung tissues showed significant elevation (P < 0.01), and IκB-α showed significant decline (P < 0.01), especially in the obesity-asthma group. There was decline of IKK-ß and NF-κB-P65 and elevation of IκB-α in the N-acetylcysteine group, which was even significantly in the Budesonide group (P < 0.01). There was a positive correlation between MDA and NF-κB activation in the lung tissues in all the asthma groups and treatment groups (P < 0.05). Obesity-asthma mice showed higher oxidative stress and activation of NF-κB compared with that of the asthma mice. There was a positive correlation between MDA and NF-κB activation in the lung tissues in the asthma groups. N-acetylcysteine was more effective in reducing the oxidative stress compared to the budesonide.

MiR-204-5p Inhibits Transforming Growth Factor-ß1-Induced Proliferation and Extracellular Matrix Production of Airway Smooth Muscle Cells by Regulating Six1 in Asthma.

BACKGROUND: Transforming growth factor-ß1 (TGF-ß1)-in-duced proliferation of airway smooth muscle cells plays critical roles in the development of airway remodeling. Six1 (sine oculis homeobox homolog 1) has been demonstrated to be involved in airway inflammation and remodeling in asthmatic mice. OBJECTIVES: The aim of this work was to investigate the potential role of miR-204-5p in the proliferation and extracellular matrix (ECM) production of airway smooth muscle cells in asthma. METHODS: Real-time PCR was used to measure the expression of miR-204-5p in asthmatic airway smooth muscle cells. Cell viability and apoptosis were detected to evaluate the effect of miR-204-5p on airway smooth muscle cells. Dual-luciferase reporter experiments were applied to identify the target genes of miR-204-5p. RESULTS: MiR-204-5p was downregulated notably in asthmatic airway smooth muscle cells as well as cells stimulated with TGF-ß1. Overexpression of miR-204-5p markedly suppressed the TGF-ß1-induced proliferation of airway smooth muscle cells and the deposition of ECM, whereas the inhibition of miR-204-5p significantly enhanced the proliferation of airway smooth muscle cells and upregulated the level of fibronectin and collagen III. Furthermore, subsequent analyses demonstrated that Six1 was a direct target of miR-204-5p, and Western blot further indicated that miR-204-5p negatively regulated the expression of Six1. Most importantly, the restoration of Six1 expression reversed the inhibitory effect of miR-204-5p on TGF-ß1-induced proliferation and ECM production. CONCLUSIONS: MiR-204-5p inhibits TGF-ß1-in-duced proliferation and ECM production of airway smooth muscle cells by regulating Six1, identifying a potential therapeutic target for preventing airway remodeling in asthma.

MiR-448-5p inhibits TGF-ß1-induced epithelial-mesenchymal transition and pulmonary fibrosis by targeting Six1 in asthma.

MicroRNAs (miRNAs) are small yet versatile gene tuners that regulate a variety of cellular processes, including cell growth and proliferation. The aim of this study was to explore how miR-448-5p affects airway remodeling and transforming growth factor-ß1 (TGF-ß1)-stimulated epithelial-mesenchymal transition (EMT) by targeting Sine oculis homeobox homolog 1 (Six1) in asthma. Asthmatic mice models with airway remodeling were induced with ovalbumin solution. MiRNA expression was evaluated using quantitative real-time polymerase chain reaction. Transfection studies of bronchial epithelial cells were performed to determine the target genes. A luciferase reporter assay system was applied to identify whether Six1 is a target gene of miR-448-5p. In the current study, we found that miR-448-5p was dramatically decreased in lung tissues of asthmatic mice and TGF-ß1-stimulated bronchial epithelial cells. In addition, the decreased level of miR-448-5p was closely associated with the increased expression of Six1. Overexpression of miR-448-5p decreased Six1 expression and, in turn, suppressed TGF-ß1-mediated EMT and fibrosis. Next, we predicted that Six1 was a potential target gene of miR-448-5p and demonstrated that miR-448-5p could directly target Six1. An SiRNA targeting Six1 was sufficient to suppress TGF-ß1-induced EMT and fibrosis in 16HBE cells. Furthermore, the overexpression of Six1 partially reversed the protective effect of miR-448-5p on TGF-ß1-mediated EMT and fibrosis in bronchial epithelial cells. Taken together, the miR-448-5p/TGF-ß1/Six1 link may play roles in the progression of EMT and pulmonary fibrosis in asthma.

Association of childhood depressive symptoms behaviors with family factors / 中国学校卫生

Objective@#To explore the relationship between childhood depressive symptoms with behaviors and family factors, and to provide a new perspective for comprehensive treatment of depressive children.@*Methods@#A total of 58 children diagnosed with depressive disorder were recruited as case group in Department of Child Health, Affiliated Hospital of Qingdao University. At the same time, 88 healthy children were selected as age and gender-matched control group. Depressive symptoms, behaviors and family factors in the two groups were investigated. SPSS 22.0 statistical software was used to describe and analyze the data.@*Results@#The total score of CBCL scale in the case group was significantly higher than that in the control group(43.29±30.93, 20.24±12.93, P<0.01), and the number of positive factors was significantly higher than that in the control group(2.57±3.14, 0.97±1.80, P<0.01). The scores of introversion, extroversion, depression, compulsion, hyperactivity, aggression and social withdrawal in the case group were significantly higher than those in the control group(30.29±26.10, 17.10±16.53; 26.29±26.88, 17.45±16.99; 10.14±10.23, 3.48±3.14; 7.29±7.31, 4.83±5.26; 7.00±7.01, 4.86±4.38; 12.86±11.60, 8.38±8.90; 4.29±5.14, 2.72±3.01, P<0.01). There was no significant difference between the two groups in the scores of physical complaints and disciplinary violations (P>0.05). The scores of somatization, hostility and terror of SCL-90 in parents of children in case group were significantly higher than those in control group(17.58±4.05, 15.81±4.00; 9.66±2.67, 8.69±2.45; 8.03±1.49, 7.50±0.88, P<0.05). The score of SDS scale was positively correlated with the total score of CBCL scale, the number of positive factors, introversion, extroversion, depression, compulsion, hyperactivity, aggression and social withdrawal, and negatively correlated with parents’ marital status (P<0.01).@*Conclusion@#Depression is a common emotional disorder in childhood, which has a negative impact on learning and social performance. In the comprehensive treatment of children with depression, the importance of child behavior therapy and parental psychological counseling should be fully considered for mental health improvement.

Targeted inhibition of Six1 attenuates allergic airway inflammation and remodeling in asthmatic mice.

Asthma is an inflammatory disease of the airways, characterized by lung eosinophilia, mucus hypersecretion by goblet cells and airway hyperresponsiveness to inhaled allergens. The purpose of this study was to evaluate the effects of Six1 on airway inflammation and remodeling and the underlying mechanisms in a murine model of chronic asthma. Female BALB/c mice were randomly divided into four groups: phosphate-buffered saline control, ovalbumin (OVA)-induced asthma group, OVA+siNC and OVA+siSix1. In this mice model, Six1 expression level was significantly elevated in OVA-induced asthma of mice. Additionally, downregulation of Six1 dramatically decreased OVA-challenged inflammation, infiltration, and mucus production. Moreover, silencing of Six1 resulted in decreased levels of immunoglobulin E and inflammatory mediators and reduced inflammatory cell accumulation, as well as inhibiting the expression of important mediators including matrix metalloproteinase MMP-2 and MMP-9, which is related to airway remodeling. Further analysis indicated that silencing of Six1 can significantly inhibit NF-kB pathway activation in the lungs. .In conclusion, these findings indicated that the downregulation of Six1 effectively inhibited airway inflammation and reversed airway remodeling, which suggest that Six1 represents a promising therapeutic strategy for human allergic asthma.

KLF6SV1 siRNA inhibits proliferation of human lens epithelial cells.

PURPOSE: To investigate whether transfection with Krüppel-like factor 6 splice variant 1 (KLF6SV1) siRNA can inhibit proliferation of human lens epithelial cell (HLEC). METHODS: Plasmid containing KLF6SV1 siRNA was used to decrease the level of KLF6SV1 protein in HLEC. The expression of protein27 kinase inhibition protein 1 (p27(kip1)) and proliferation cell nuclear antigen (PCNA) was tested with western blot. Cell proliferation was assayed by 3-(4,5-dimethylthiazolyl-2-)-2,5-diphenyltetrazoliumbromide (MTT) assay and bromodeoxyuridine (BrdU) incorporation. RESULTS: KLF6SV1 siRNA can decrease KLF6SV1 expression which leads to increased levels of p27(kip1) and decreased expression of PCNA in HLEC. Cells transfected with pKLF6SV1 siRNA showed less viability compared with the control group in vitro. CONCLUSIONS: KLF6SV1 siRNA can effectively inhibit HLEC proliferation. It can be regarded as a novel target to treat posterior capsular opacity (PCO).

[The significance of the expression of Col IV and LN in nasal and paranasal sinus malignant tumor].

OBJECTIVE: To study the pathological relationship between the expression of Col IV and LN in nasal and paranasal sinus malignant tumor (NPMT). METHOD: The immunohistochemical technique was used to detected the expression of Col IV and LN in NPMT, para-cancer tissues and non-cancer tissues. RESULT: There was a significance on the expression of the Col IV and LN in NPMT, para-cancer tissues and non-cancer tissues (P<0.01), and no significance in endepidermis and soft connective tissue of the NPMT (P>0.05). CONCLUSION: The Col IV and LN perhaps participate in tumorigenesis of NPMT, and may play the homoioplastic role in different pathological types of the NPMT.

[Study about eye complication of nasopharyngeal carcinoma].

OBJECTIVE: To explore the eye complication of nasopharyngeal carcinoma (NPC), to analysis the clinical manifestation, CT characteristics and pathological diagnosis of eye complications of NPC and to provide the base for early diagnosis of NPC. METHOD: To retrospectively study of 82 cases eye complications in 562 cases NPC, to study their clinical manifestation, CT characteristics and pathological diagnosis. RESULT: The clinical studies showed that eye complication cases were occurred in 82 cases of 562 NPC cases (14.6%). Thirty-six cases in left and 37 cases in right eye, 9 cases in bilateral eyes. Sixty-five cases came from Guangdong, while the others 17 cases come from 5 provinces. There were 9 kinds of eye manifestation. CT appearances: 40 cases suffered from skull base distracted, 6 cases with orbit involved, 2 cases ( in left eyes) with orbit metastasis, 12 cases with nose-sinus involved, 68 case with parapharyngeal space involved, 49 cases with soft issue in wall of styloid process involved (there were many kind of shows in the same case, so the data were repeated in these cases). CONCLUSION: There were multiplicity and complexity in eye complication of NPC. Ophthalmologists should think highly of these cases.

[Cluster analysis in micrangium detection in malignant nasal and paranasal sinus tumor].

OBJECTIVE: To study the application of cluster analysis in micrangium detection in malignant nasal and paranasal sinus tumor. METHODS: Microvessel density (MVD) counting and cluster analysis were used to detect the micrangium in patients with malignant nasal and paranasal sinus tumor to assess the association between the malignancy and MVD. RESULTS: According to cluster analysis, the MVD counting could be clustered into two groups, and the MVD showed significant differences between the tumor tissues, adjacent normal tissue and the control group (P<0.01), a result consistent with that by analysis of variance of the MVD. CONCLUSION: Cluster analysis can be used in clustering of MVD counting in malignant nasal and paranasal sinus tumor to simplify MVD counting, and offers an important analytic method for micrangium analysis in tumors.

[Inhibition of growth and proliferation of Hep-2 cells by targeting c-myc gene using small interference RNA technology].

OBJECTIVE: To investigate the effect of small interfering RNA (siRNA) targeting c-myc gene in Hep-2 cells. METHOD: siRNA targeting c-myc mRNA was designed and synthesized. In vitro cultured Hep-2 cells were transfected with lipofectamine 2000 and the inhibitory effect was detected by MTT, morphology, real time PCR assay. RESULT: 1) The MTT result showed the c-myc siRNA to be able effectively to suppress the Hep-2 cell multiplication; 2) The real time PCR result showed c-myc at mRNA level inhibition ratio at 94% in group S3; 3) The morphology result showed the c-myc siRNA to be able effectively to suppress the Hep-2 cell multiplication, the cell heteromorphism was diminished. CONCLUSION: siRNA targeting c-myc can remarkably suppress the Hep-2 cell growth and multiplication.

[Clinical significance of the expression of p53, p63 and p73 in nasal and paranasal sinus carcinoma].

OBJECTIVE: To study the clinical significance of the expression of p53, p63 and p73 protein and the correlation of p53 and p63 in nasal and paranasal sinus carcinoma (NPSC). METHOD: The immunohistochemical technique was used to detect the expression of p53, p63 and p73 in 67 cases of NPSC, para-cancer tissues and non-cancer tissues. RESULT: The positive rate of p53 and p63 protein in NPSC was significantly higher than that in park cancer tissues and non-cancer tissues (P<0.01), and there were a positive correlation between the expression of p53 and p63 protein in NPSC (P<0.01). But the expression of p73 had no significant difference among NPSC, para-cancer tissues and non-cancer tissues (P>0.05). CONCLUSION: There are positive correlation between p53 and p63 protein in NPSC, and they may play an important role in the tumorgenesis of NPSC. The p73 may not be associated with tumorgenesis of NPSC.

[Recombinant adeno-associated virus conducted NgR(DN) enhances axonal regeneration of optic nerve after trauma: experiment with rats].

OBJECTIVE: To investigate the effect of recombinant adeno-associated virus conducted NgRDN on the axonal regeneration of optic nerve after trauma. METHODS: Two kinds of adeno-associated virus (AAV), AAV-NgRDN-EGFP containing dominant negative form of Nogo receptor and enhanced green fluorescent protein (EGFP) and rAAV-NgR-EGFP containing Nogo-66 receptor (NgR) and EGFP, were constructed. 45 adult Wistar male rats were randomly divided into three equal groups, all with both eyes as experimental eyes: Groups A, B, and C to undergo injection of rAAV-EGFP, rAAV-NgR-EGFP, and rAAV-NgRDN-EGFP respectively into the vitreous; and each group was subdivided into 3 equal subgroups: subgroups 1 underwent injection of rAAV only, subgroups 2 underwent injection of rAAV and lens trauma, and subgroups 3 underwent injection of rAAV and zymosan. The rats in the Subgroups A2, B2, and C2 underwent. Crush of the optic nerve 2 mm behind the eyeball with optic nerve forceps 3 weeks after the injection. Four days after the crush the right eyes were taken out and the retinal explants were cultured in 2 kinds of culture fluid: with or without myelin. The growth of axons at the edge of retinal explants was observed by immunofluorescent staining with betaIII tubulin. Two weeks after the crush the other eyes were taken out to isolate the optic nerves. Immunofluorescence assay was used to detect the expression of growth associated protein-43 (GAP-43) of optic nerve. The axonal regeneration of optic nerve was observed. RESULTS: betaIII tubulin staining showed that on the condition of culture fluid without myelin both rAAV-NgR-EGFP and rAAV-NgRDN-EGFP showed no effects on the axonal regeneration of retinal ganglion cells (RGCs). However, on the condition of culture fluid with myelin the count of axonal regeneration and the length of regenerated axons of Group B were (13+/-4) and (36 microm+/-4 microm), both significantly lower than those of Group A [(21+/-4) and (83 microm+/-11 microm) respectively, both P<0.01]. There were not significant differences in count of axonal regeneration and length of regenerated axons between Subgroups C1 and A1. The count of axonal regeneration and length of regenerated axons of Subgroups C2 were (317+/-45) and (508 microm+/-44 microm), both significantly higher than those of Subgroup C3 [(238+/-30) and (365 microm+/-48 microm) respectively, both P<0.01], and the values of both Subgroups C2 and C3 were significantly higher than those of Subgroups A2 and A3. The GAP43-positive area in the optic nerve of Group C was significantly larger than that of Group A (P<0.01), and that of Group B was significantly smaller than that of Group A (P<0.01). The GAP43-positive area in the optic nerve of Subgroup A2 was (18.71+/-1.72)x100 microm2, significantly larger than that of Subgroup A3 [(12.75+/-1.02)x100 microm2, P<0.01], and that of Subgroup A3 was significantly larger than that of Subgroup A1 (P<0.01). There were not significant differences in the GAP43-positive area among the subgroups in Group B. CONCLUSION: Transfection of rAAV-NgRDN-EGFP into RGC in an activated status enhances axonal regeneration of optic nerve. NgRDN AAV can inhibit effectively the role of NgR.

[The clinical significance of the expression of p63 gene in laryngeal squamous cell carcinoma].

OBJECTIVE: To study the expression and clinical significance of p63 gene in laryngeal squamous cell carcinoma(LSCC). METHOD: The immunohistochemical technique was used to detected the expression of p63 in 63 cases of LSCC, 45 cases of para-cancer tissues, 24 cases of lymph node metastasis, 40 cases of non lymph node metastasis and 25 normal tissues. RESULT: The positive overexpression rate of the p63 gene in LSCC (95.24%) and in matched metastatic lymph node (83.3%) was significantly higher than para cancer tissues, non metastasis lymph node and normal tissues (P<0.01). p63 gene expression was not correlation with the clinical stages,clinical typing and pathological classification of the LSCC(P >0.05). CONCLUSION: p63 gene had important clinic significance to the diagnosis and differential diagnosis of the LSCC. It perhaps participate in regulation of tumorigenesis in LSCC, and it may play negative feedback action in the development of LSCC.