Simultaneous Determination of Four Aldehydes in Gas Phase of Mainstream Smoke by Headspace Gas Chromatography-Mass Spectrometry.

A method for simultaneous determination of acetaldehyde, propionaldehyde, acrolein, and crotonaldehyde in gas phase of cigarette mainstream smoke by headspace gas chromatography-mass spectrometry was developed and validated. Gas phase components of mainstream cigarette smoke were extracted with methanol, and then the samples were separated on a DB 624 (60 m, 0.32 mm x 1.8 mm) column, analyzed with headspace gas chromatography-mass spectrometry, and quantified by isotope internal standard. The linearities of acetaldehyde, propionaldehyde, acrolein, and crotonaldehyde were good (R 2>0.992). The recoveries of acetaldehyde, propionaldehyde, acrolein, and crotonaldehyde were between 78.5% and 115%. The relative standard deviations were less than 10%. The limits of detection and limits of quantitation were 0.014 µg/cigarette ~0.12 µg/cigarette and 0.045 µg/cigarette ~0.38 µg/cigarette, respectively. The method had advantage of high sensitivity, it did not require derivatization of 2,4-dinitrophenylhydrazine and avoided a large number of adverse reactions during the process of derivation to improve the accuracy of result, and it was suitable for quantitative analysis of four aldehydes in gas phase of cigarette mainstream smoke.

BDNF gene polymorphisms are associated with Alzheimer's disease-related depression and antidepressant response.

Brain-derived neurotrophic factor (BDNF) is needed to support neuronal survival and differentiation. It also promotes synaptic remodeling and modulates the function of many other neurotransmitters. The current study examined potential association between single nucleotide polymorphisms (SNPs) of the BDNF gene (G11757 C, C270T, G196A, G-712A) and Alzheimer's disease-related depression (AD-D). Participants included 336 patients with AD; 128 of these patients had AD-D. Response to 8-week paroxetine treatment was also assessed. The frequency of the 11757 C allele was significantly higher in AD-D than in the Alzheimer's disease without depression (AD-nD) patients (p = 0.003 after Bonferroni correction). The 196A allele occurred with significantly higher frequency in AD-D patients (p = 0.001 after Bonferroni correction versus AD-nD). Carriers of the A allele of G196A responded better to paroxetine treatment. These findings support an important role of BDNF polymorphism in AD-D.

[Clinical analysis of families with generalized epilepsy with febrile seizures plus].

OBJECTIVE: To investigate the clinical phenotypes and hereditary patterns of the generalized epilepsy with febrile seizures plus (GEFS+). METHODS: Detailed family trees were constructed by inquire and physical examinations for the probands of the 15 pedigrees of GEFS+. Some patients received electroencephalography, cranial CT or MRI examination. The seizures and epilepsy syndromes were classified according to the 2001 Seizure International Classification. The clinical data of GEFS+ were reviewed. RESULTS: The 15 families consisted of 196 individuals. Seventy-five individuals were confirmed with epilepsy. The phenotypes of 64 out of the 75 patients with epilepsy conformed to GEFS+. The 64 patients included 38 males and 26 females (1 deceased) and there was no gender difference in the morbility of GEFS+. The age at onset was all in childhood. GEFS+ had a diversity of phenotypes. Febrile seizures (FS) were confirmed in 44 patients, FS and myoclonic seizure in 1, febrile seizures plus (FS+) in 13, FS+ and absence seizure in 2, FS+ and myoclonic seizure in 1, and FS+ and focal seizure in 3. CONCLUSIONS: The heterogeneity of phenotypes and genetics may be the hallmarks of GEFS+. FS and FS+ are common phenotypes while FS+ and absence seizure, FS+ and myoclonic seizure, and FS+ and focal seizure are rare. If one of the parents is affected in a GEFS+ family, the susceptibility of their children to GEFS+ is the same no matter what gender of their children is. It is speculated that the hereditary pattern of GEFS+ conforms to autosomal dominant inheritance.