[Progress in clinical diagnosis and treatment of multiple primary lung cancer].

With the application of high-resolution chest imaging system and lung cancer screening program, patients with multiple primary lung cancer (MPLC) are becoming a growing population in clinical practice. However, the diagnostic criteria of MPLC and its differentiation from intrapulmonary metastasis of lung cancer (IM) are still controversial, especially in cases with similar histology. On the basis of reviewing the existing literature, this paper discusses the changes of the diagnostic criteria of MPLC and the differential diagnosis methods of imaging, histology and molecular genetics of MPLC and IM, and briefly introduces the application of multidisciplinary diagnosis, algorithm, predictive model and artificial intelligence in the differential diagnosis of MPLC. In addition, we also discuss the latest progress in the treatment of MPLC. Radical surgery is the main method for the treatment of MPLC. Stereotactic body radiation therapy (SBRT) is safe and feasible for inoperable MPLC patients, and targeted therapy and immunotherapy can also be used in MPLC after appropriate patient selection.

[Current status of job burnout in in-service sailors from 13 provinces and cities in China].

Objective: To investigate the current status of job burnout in in-service sailors, and to provide a basis for the development of intervention measures for job burnout in sailors. Methods: From September 2015 to May 2016, stratified cluster random sampling was used to select 6 172 in-service sailors from 13 provinces and cities as research subjects. General demographic data including age, education background, and household registration and occupational characteristics such as job position, navigating zone, and nature of employment were collected. The Maslach Burnout Inventory-General Survey (MBI-GS) was used to measure the levels of emotional exhaustion, depersonalization, low occupational efficiency, and job burnout, and the influencing factors for job burnout were also analyzed. Results: Of all 6 172 in-service sailors, 112 (1.8%) had a positive result in emotional exhaustion, 870 (14.1%) had a positive result in depersonalization, and 3 517 (57.0%) had a positive result in low occupational efficiency. Of all sailors, 63.3% had job burnout, among whom 54.1% had mild burnout, 8.7% had moderate burnout, and 0.5% had severe burnout. There was a significant difference in the score of job burnout between the sailors with different ages, education backgrounds, types of household registration, job positions, navigating zones, ornature of employment (P<0.05). Age, education background, household registration, job position, navigating zone, and nature of employment were major influencing factors for job burnout in in-service sailors (P<0.05) , and there was a higher level of job burnout in the sailors with an age of 30-39 years, education background of junior college or above, urban registration, a job position of second mate/third engineer, a navigating zone of coastal lines, orthe nature of employment of freelance sailor. Conclusion: There is a high incidence rate of job burnout among in-service sailors, and the sailors with a young age, urban registration, a navigating zone of coastal lines, or thenature of employment of freelance sailor tend to have low occupational efficiency. Related measures should be adopted for active intervention.

Involvement of platelet-activating factor in cell death induced under ischemia/postischemia-like conditions in an immortalized hippocampal cell line.

The involvement of platelet-activating factor (PAF) in cell damage induced by ischemia/postischemia-like conditions was studied in a hippocampus-derived cell line, HN33.11. Cells exposed to N2-saturated glucose-free HEPES-buffered saline (ischemia) for 5 h followed by 18 h of incubation in serum-free control medium (postischemia reincubation) remained 67.4 +/- 2.4% viable in comparison with sham-treated cells. Analysis of DNA fragmentation in combination with Hoechst 33258 staining indicates that apoptosis is the dominant mode of cell death in the present model. PAF level during 10 h of ischemia was unchanged. However, an increase in PAF accumulation was found early during the reincubation period that followed 5 h of ischemia. Peak PAF concentrations were noted at 2 h after initiation of reincubation and rapidly declined to control level after 7 h of reincubation. Consistent with a role of PAF in mediating cell death under ischemia/postischemia reincubation in this model, the PAF antagonist BN 50739 exerted a dose-dependent protective effect. Maximal protection (85.7 +/- 5.4%) of the cells from ischemia/reincubation-induced cell damage was achieved at 0.1 microM BN 50739. The PAF antagonist lacked any protective effect against ischemia-induced cell death. On the other hand, the addition of the stable PAF analogue 1-O-hexadecyl-2-N-methylcarbamyl-sn-glycero-3-phosphocholine (MC-PAF) at the onset of ischemia potentiated ischemia/reincubation-induced apoptosis--an effect that was blocked by BN 50739. Pretreatment of HN33.11 cells with the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid acetoxymethyl ester (BAPTA-AM) also provided a protective effect against ischemia/reincubation-induced cell damage. BAPTA-AM increased cell viability by 50%. Pretreatment with BAPTA-AM also decreased ischemia/reincubation-induced PAF accumulation in HN33.11 cells. The results suggest that PAF, acting via a PAF receptor, is at least in part mediating apoptosis under ischemia/postischemia-like conditions in HN33.11 cells.

Guanine nucleotide regulatory proteins, Gq and Gi1/2, mediate platelet-activating factor-stimulated phosphoinositide metabolism in immortalized hippocampal cells.

Platelet-activating factor (PAF) may be a neuromodulator involved in neural cell differentiation, cerebral inflammation, and ischemia. The PAF receptor is a member of the G protein-coupled receptor superfamily. In the present study, we sought to define the specific G protein(s) that mediate PAF-stimulated phosphoinositide (PI) metabolism in an immortalized hippocampal cell line, HN33.11. PAF increased the production of 3H-labeled inositol phosphates (IPs) with EC50 values of 1.2-1.5 nM. The effect of PAF on 3H-IPs formation was completely blocked by the PAF antagonist BN 50739 at a concentration of 300 nM. Pertussis toxin pretreatment attenuated PAF-stimulated 3H-IPs production by 20-30% (p < 0.05). Consistent with a role for Gi1/2 in this response, antiserum against G alpha i1/2 blocked the response to a similar degree. Pretreatment of permeabilized cells with G alpha q/11 antiserum attenuated the response by 70% (p < 0.05), suggesting a role for Gq/11 in mediating the PAF response in this cell line. Stimulation with PAF increased [alpha-32P]-GTP binding to both G alpha q and G alpha i1/2 proteins. Moreover, specific [3H]PAF binding sites coprecipitated with G alpha q and G alpha i1/2 proteins. The results suggest that PAF-stimulated PI metabolism in HN33.11 cells is mediated by both Gq and Gi1/2 proteins.