Objective:To explore the role of Semaphorins 3A(Sema 3A) and its receptor Neuropilin-1 (Nrp1) in the development of chronic periodontitis of rats and clinical samples.Methods:20 SD rats were divided into 2 groups.Rats in the experimental group were induced into chronic periodontitis models.Rats in control group were not treated.After 8 weeks,maxilla of all the rats were collected for micro-CT scanning and IHC staining.The distance from cementoenamel junction to alveolar bone crest(CEJ-ABC) and the IOD of Sema3A/Nrp1 positive staining in rats were analyzed.20 clinical samples of chronic periodontitis(n =10) and normal periodontal tissues (n =10) were collected for immunofluorescence and qRT-PCR analysis.Results:The CEJ-ABC distance of chronic periodontitis group was higher than that of the control group(P ＜ 0.05).The IOD of Sema3A/Nrp1 in experimental group was lower than that of the control group (P ＜ 0.05) and with a negative correlation with bone loss (P ＜ 0.05).Immunofluorescence and qRT-PCR analysis showed that the expression level of Sema3a/Nrpl in clinical samples with chronic periodontitis was also lower than that of the healthy subjects(P ＜ 0.05).Conclusion:The reduced Sema3A/Nrp1 plays an important role in the development of bone destruction in chronic periodontitis.

Objective To explore the efficacy of ketogenic diet( KD) in the treatment of status epi-lepticus( SE) and whether KD could protect the brain,and propose a new thought on SE patients′reasonably individualized treatment, brain protection and prognosis improvement. Methods From Sep 2013 to Jan 2015,all the patients diagnosed as SE were advised to apply KD treatment; the patients who refused KD treatment were included in the control group,while the patients who accepted KD treatment were included in the treatment group. Based on the SE treatment principles,the control group applied traditional anti-convulsive therapy,while the treatment group applied traditional therapy combined with KD treatment. Before the treat-ment and after the epilepsy control,the patients′ serum was collected to test neuron specific enolase( NSE) and S100βlevels,and the duration of epilepsy control was recorded. Results The treatment group included a total of 10 patients; 3 patients had a good efficacy and obtained seizure-free after the treatment; clinical seizures declined significantly in 6 patients. The treatment group′s overall response rate was 9/10,which was higher than that of the control group(5/8)(P<0. 01). The treatment group′s duration to gain efficacy was shorter than that of the control group[(5. 2 ± 2. 9) d vs. (9. 8 ± 1. 5) d,P<0. 01]. After the treatment,the patients′NSE and S100β in both groups were significantly decreased than those before the treatment ( P<0. 001 or P<0. 05). After the treatment,the serum NSE and S100β of the patients in the treatment group were lower than those in the control group,with statistically significant difference(P<0. 05). Conclusion Frequent epileptic seizures and SE would impair the patient′s brain. Controlling the epileptic seizures actively could lower the severity of brain injury. KD could effectively control the epileptic seizure and had neuropro-tective effects.

Objective To analyze a rare genotype with β-thalassemia intermadia.Methods Phenotypic analysis was performed using routine hematological tests to measure red blood cell parameters and high performance liquid chromatography (HPLC)was used to measure hemoglobin fractions.The β-globin gene mutations were conducted using reverse-dot-blot and DNA sequencing of the breakpoint region were characterized with gap-PCR.Results The proband had a trait of thalassemia intermedia with reduced hemoglobin (86 g/L).The proband's father had a trait of microcytic hypochromic with reduced mean corpuscular volume(MCV),mean corpuscular hemoglobin (MCH) (63.7 fl and 20.4 pg,respectively) and an elevated level of HbA2.He had the phenotype of heterozygosity for β-thalassemia.The preband's mother,grandmother and sister had a trait of heterezygote for hereditary persistence of fetal hemoglobin (HPFH) with elevated level of HbF,which were 28.3%,21.1% and 33.7%,respectively.After molecular characterization of the family members,the proband was identified as a patient with β-thalassemia intermedia caused by co-existence of β-thalassemia(β41-42) and HPFH-6.The father was heterozygoas for β-thaiassemia (β41-42/βN) and the mother,grandmother and sister were all heterozygons for HPFH-6.Condusions A rare β-thalassemia intermedia case resulting from compound heterezygote of β41-42 with HPFH-6 is found.This study may provide clinical experiences for antenatal diagnosis.

Clinical and imageological characteristics of Paget's disease of bone in 7 patients who were treated in our hospital from 1991 to 2007 were analyzed. The data showed (1) 6 patients had the symptoms of bone pain and bone deformity, with more long bones involved; (2) Serum alkaline phosphatase was over normal range; (3) Imageology showed that osteoclasia was usually combined with bone sclerosis; (4) All the patients were treated with bisphosphonates; (5) 2 patients with serious bone deformity were treated with orthomorphia. Paget's disease of bone is a kind of metabolic bone disease with the characteristics of osteoclasia combined with bone sclerosis. The main features are bone pain and bone abnormality. Bisphosphonates are the first choice of drugs. Patients with serious bone deformity should be treated with orthomorphia.