As a real-time,rapid and non-invasive method for monitoring the occurrence and development of various diseases and evaluating the health status of the body,breath detection has attracted wide attention in the application of early lung cancer screening.However,there is significant variability in the reported specific biomarkers of lung cancer,making it difficult to reach a unified consensus.Meanwhile,the pathways for the generation of volatile organic compounds(VOCs)in exhaled breath of lung cancer patients remain unclear,and further research on the detailed metabolic mechanisms is required.Therefore,this review comprehensively summarizes the VOCs detected in the exhaled breath of lung cancer patients from relevant literature in the past five years,deeply analyzes the production mechanism of these VOCs and the internal correlation with the disease,and evaluates the performance of the lung cancer prediction models constructed based on these VOCs,in order to provide reference for clinical and subsequent researches.

As a real-time,rapid and non-invasive method for monitoring the occurrence and development of various diseases and evaluating the health status of the body,breath detection has attracted wide attention in the application of early lung cancer screening.However,there is significant variability in the reported specific biomarkers of lung cancer,making it difficult to reach a unified consensus.Meanwhile,the pathways for the generation of volatile organic compounds(VOCs)in exhaled breath of lung cancer patients remain unclear,and further research on the detailed metabolic mechanisms is required.Therefore,this review comprehensively summarizes the VOCs detected in the exhaled breath of lung cancer patients from relevant literature in the past five years,deeply analyzes the production mechanism of these VOCs and the internal correlation with the disease,and evaluates the performance of the lung cancer prediction models constructed based on these VOCs,in order to provide reference for clinical and subsequent researches.

ObjectiveTo explore the antidepressant effect of Sophora flavescens seed extract and its molecular mechanism. MethodA mouse depression model was established by intraperitoneal injection of lipopolysaccharide（LPS）， and normal group， model group， fluoxetine group（2.5 mg·kg^-1）， and S. flavescens seed low， medium and high dose groups（200， 400， 800 mg·kg^-1） were set up for 7 d of consecutive gavage. Then the antidepressant effect of S. flavescens seed extract was evaluated by using open field test， elevated plus maze test and forced swimming test. Pathological morphological changes in the hippocampal tissue was observed by hematoxylin-eosin（HE） staining. Protein expression levels of G₁/S-specific cyclin D₁（Cyclin D₁）， Wnt1， β-catenin and phosphorylated glycogen synthase kinase-3β（p-GSK-3β） in mouse brain tissues were detected by Western blot. Hippocampal cell apoptosis was detected by terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate（dUTP） nick end labeling（TUNEL）. ResultThe results of mouse behavioral experiments showed that compared with the normal group， the speed of movement in the open field and the distance of movement in the central area of the open field， and the time spent on the open arms of the elevated plus maze were significantly reduced in the model group（P<0.01）， while immobility time in the forced swimming test was significantly increased（P<0.05）. Compared with the model group， the S. flavescens seed medium and high dose groups had increased speed of movement in the open field test and time spent on the open arms of the elevated plus maze test（P<0.05， P<0.01）， and decreased immobility time in the forced swimming test（P<0.05）， the distance of movement in the central area of the open field test increased in the high dose group（P<0.05）. HE staining results showed that compared with the normal group， the hippocampal neuron structure of mice in the model group was damaged. Compared with the model group， after treatment of S. flavescens seed extract， the pathological state of the mouse hippocampal neuron structure was alleviated， and the neurons increased， were neatly arranged， and the cytoplasm was clear. Western blot results showed that the protein expression levels of Wnt1 and β-catenin in mouse brain tissue were significantly decreased（P<0.01）， while the protein expression levels of Cyclin D₁ and p-GSK-3β were significantly increased（P<0.01） after LPS injection. Compared with the model group， protein expression levels of Wnt1 and β-catenin in brain tissue of S. flavescens seed medium and high dose groups were significantly increased（P<0.01）， while the protein expression levels of Cyclin D₁ and p-GSK-3β were significantly decreased（P<0.01）. TUNEL staining results showed that the hippocampal cell apoptosis rate in the model group was significantly increased compared with that of the normal group（P<0.01）， while the hippocampal cell apoptosis rate in the S. flavescens seed medium and high dose groups was significantly decreased compared with that of the model group（P<0.01）. ConclusionS. flavescens seed extract can effectively improve the severity of depression in LPS-induced depressed mice， and its molecular mechanism is related to the regulation of neuroinflammation and hippocampal neuronal apoptosis mediated by Wnt/β-catenin signaling pathway.

Objective: To clarify the characteristics of the A20 regulatory changes by analyzing mutations in the non-coding region of the A20 gene in patients with T-cell lymphoma leukemia (T-LCL) . Methods: PCR and nucleotide sequence analysis were used to detect mutations in the non-coding region of the A20 gene, and DNA samples from PBMCs of 52 cases of T-LCL and 99 healthy controls. Results: A missense mutation (c.-672T>G) was detected in the A20 gene promoter from one T-LCL patient, which has been registered as a SNP (rs139054966) in gene bank. Meanwhile, a new mutation was detected in the 3′ UTR mRNA (3916 (C>G) ) . These two mutations were absent in other T-LCL samples and controls. Conclusion The rs139054966 (c.-672T>G) and 3916 (C>G) mutations in the A20 gene were detected in T-LCL patients for the first time. There was also rs139054966 located on the binding region of the transcription factor P53, and its significance remained to be further clarified.

OBJECTIVE: Although the therapeutic method of stroke is progressed very quickly in recent years, the incidence of its post-depression is up to 40%. Poststroke depression many affect neural function recovery, for which, to understand it is advantageous of improving living quality of stroke patients.DATA SOURCE: The literatures relevant to poststroke depression were looked up from China medical nuclear journals and studies at home and abroad in recent 5 years on www.google.com, Medline. The Retrieval words: stroke, depression, incidence, relevant factors.STUDY SELECTION: Totally 42 relevant papers were selected on experimental and clinical studies on poststroke depression. The original literatures of non-randomized study were excluded and those of nonblind study were not excluded.DATA EXTRACTION: Of 42 papers, 10 papers were deleted because of repetition of various degrees and 32 papers were sorted out in category and 10 of those were selected as reference.DATA SYNTHESIS: The incidence of poststroke depression is about 40%, resulting from the co-factors of society, psychology and biology.It is viewed generally that the high risk phase of depression is in a couple of year after stroke and the duration of poststroke depression is various. The severity of neural functional deficits in recovery phase is affected by poststroke depression. Moderate and severe depression may delay the recovery of neural function and poststroke depression can also result in poor recovery of daily living capacity of patients, affect patients' cognition and increase the incidence of dementia. Concerning to clinical observation, a remarkable progression has been achieved on treatment of poststroke depression.CONCLUSION: The incidence of poststroke depression is very high,associated with multiple factors. Poststroke depression influences harmfully on neural function, cognition and daily living capacity. Active intervention and treatment provide a certain action on reducing the incidence of poststroke depression.

AIM: To study the relationship between nitric oxide (NO) and gastric mucosal injury induced by reserpine in rats. METHODS: Sixteen healthy male Wistar rats were randomly divided into control group and experimental group (n=8). NO contents and malondialdehyde(MDA) contents in plasma, gastric mucosa of the rats were respectively determined with Cadmium-reduct plus Greiss and TBA; nitric oxide synthase in gastric walls of the rats were observed using NADPH-diaphorase histochemistry and quantitatively measured with image analyzer.RESULTS: The NO contents in both plasma and gastric mucosa of experimental group were significantly lower than that in control group (P