Objective: To investigate the diagnosis and treatment of one patient with pneumocephalus caused by congenital mastoid dysplasia, and to clarify the clinical features, diagnostic methods and treatment strategies of intracranial accumulation of pneumocephalus. Methods: The patient with ineffective right upper limb activity accompanied stupid speech for 12 h was admitted to hospital. After admission, the head CT and MRI examination were performed again, and the patient was diagnosed as pneumocephalus. The paitent scheduled for stoma repair, neurotrophic treatment, infection prevention and other symptomatic treatments were performed after operation; the patient was instructed avoid cough forcefully, blowing nose, defecating and sneezing to increase the intracranial pressure. Results: Due to congenital dysplasia of mastoid wall, local thinning bones and intense swimming choking cough of the patient destroyed the intracranial pressure balance to form pneumocephalus, the patient scheduled for stoma and damaged dura repair; when discharged from hospital, the patient's right upper limb muscle strength and language function returned to normal; the head CT results showed that pneumocephalus disappeared completely. Conclusion: Pneumocephalus is common in clinic, and its reason is diversiform; it should be combined with the patient's history and imaging findings to explore the causes, the most reasonable treatment measures should be performed in order to relieve the patient's symptoms of increased intracranial pressure, and promote the recovery of neural function.

OBJECTIVETo investigate the association and interaction between smoking and the nicotine acetylcholine receptor subunits alpha 5(CHRNA5) gene polymorphisms on lung cancer in Chinese men.

METHODSA case-control study was employed with a total of 204 male lung cancer patients and 821 healthy control subjects enrolled in the study. All the subjects were interviewed under a structured questionnaire with the contents on socio-demographic status and smoking behavior. Venous blood samples were collected to measure single nucleotide polymorphism of rs17486278 in CHRNA5. A series of multivariate logistic regression models were performed to assess the association and interaction between smoking and the CHRNA5 gene polymorphisms on lung cancer.

RESULTSAfter controlling for potential confounding factors, data from the multivariate logistic regression analysis showed that individuals with smoking >15 cigarettes per day would significantly increase the risk of lung cancer when compared to the non-smokers (OR = 3.49, 95%CI:2.29-5.32). However, no associations between CHRNA5 rs17486278 polymorphisms and lung cancer were found. Furthermore, those who smoked 1-15 cigarettes per day had a positive interactive effect between rs17486278 CC genotype and lung cancer (OR = 16.13, 95% CI:1.27-205.33). Results from further stratified analysis on smoking behaviors and rs17486278 genotypes indicated that when compared with non-smokers on rs17486278 AA genotype, those individuals who smoked 1-15 cigarettes per day with rs17486278 CC genotype, individuals smoking >15 cigarettes per day with AA genotype and individuals smoking >15 cigarettes per day with AC genotype, all had a higher risk of developing lung cancer, with their OR value as 8.14(95% CI:1.17-56.56), 3.84 (95% CI:1.30-11.40) and 5.32 (95% CI:1.78-15.93), respectively.

CONCLUSIONThere was an interaction between smoking and CHRNA5 gene polymorphism on lung cancer.

Asian Continental Ancestry Group ; Case-Control Studies ; Genotype ; Humans ; Logistic Models ; Lung Neoplasms ; genetics ; Male ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Receptors, Nicotinic ; genetics ; Risk ; Smoking