Objective:To explore the aeromedical assessment standard and follow-up situation for the civil pilots treated by intracranial aneurysm interventional embolism surgery.Methods:The information about diagnosis and treatment, aeromedical identification and follow-up of 8 pilots treated by intracranial aneurysm interventional embolism surgery from June 2012 to November 2020 were collected and analyzed retrospectively, and relevant literatures were reviewed.Results:Eight unruptured aneurysms were detected accidentally in 7 patients during medical examination, and 1 ruptured aneurysm was detected due to subarachnoid hemorrhage. Seven pilots with unruptured aneurysms were waivered for flight after at least 1-year grounding for observation, with the restrictions of limited flying time and barred duty from being a captain (double restrictions). Then the restrictions were gradually cancelled after 1-year waiver and the follow-up was extended for 4-7 years. The pilot with ruptured aneurysms was waivered after 2-year grounded observation with double restrictions. He gave up the aeromedical assessment because of memory loss after returning flight for 1 year and the follow-up was terminated then.Conclusions:The aeromedical assessment for the pilot with intracranial aneurysm interventional embolism surgery should consider the objective and clinical characteristics, imaging findings, EEG, cognitive performance, flight ability, as well as the individual assessment upon pilot′s wishes. The pilots who resume flying should be followed up for an extended period.

Objective:To explore the aeromedical assessment standard and follow-up situation for the civil pilots treated by intracranial aneurysm interventional embolism surgery.Methods:The information about diagnosis and treatment, aeromedical identification and follow-up of 8 pilots treated by intracranial aneurysm interventional embolism surgery from June 2012 to November 2020 were collected and analyzed retrospectively, and relevant literatures were reviewed.Results:Eight unruptured aneurysms were detected accidentally in 7 patients during medical examination, and 1 ruptured aneurysm was detected due to subarachnoid hemorrhage. Seven pilots with unruptured aneurysms were waivered for flight after at least 1-year grounding for observation, with the restrictions of limited flying time and barred duty from being a captain (double restrictions). Then the restrictions were gradually cancelled after 1-year waiver and the follow-up was extended for 4-7 years. The pilot with ruptured aneurysms was waivered after 2-year grounded observation with double restrictions. He gave up the aeromedical assessment because of memory loss after returning flight for 1 year and the follow-up was terminated then.Conclusions:The aeromedical assessment for the pilot with intracranial aneurysm interventional embolism surgery should consider the objective and clinical characteristics, imaging findings, EEG, cognitive performance, flight ability, as well as the individual assessment upon pilot′s wishes. The pilots who resume flying should be followed up for an extended period.

OBJECTIVETo study the anti-cancer effect of matrine (Mat) on U937 cell line and its possible molecular mechanism.

METHODThe cells were cultured in medium containing either 0.1, 0.2, 0.3, 0.4, or 0.5 g x L(-1) of Mat. The morphological alteration was observed by inverted microscopy and electron microscopy. Cell proliferation was analyzed by Try pan blue staining and MTT. The method of Western Blot was used to detect phosphorylation activity of MAPK.

RESULTMatrine had a significant inhibitory effect on proliferation of U937 cell line at the concentration of 0.2 g x L(-1). Treated with matrine of 0.2 g x L(-1) for 48 h, U937 cells became smaller and appeared more round than previously. The number of U937 cells showing apoptosis increased with elevation of the concentration of the matrine. Matrine had an ability of inhibiting the activity of ERK and increasing the activities of p38 and JNK to some degree in U937 cells.

CONCLUSIONMatrine can inhibit the proliferation of U937 cell line in vitro and induce its apoptosis possibly through inhibiting the activity of ERK and increasing the activities of p38 and JNK in U937 cells.

Alkaloids ; pharmacology ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Humans ; MAP Kinase Signaling System ; drug effects ; Quinolizines ; pharmacology ; U937 Cells

OBJECTIVEThe objective of this paper was to study the change of P38MAPK and Fas in the apoptosis of THP-1 cells induced by allicin.

METHODThe proliferation inhibition rates of THP-1 cells after various treatments were examined by MTT assay. Apoptosis rate was determined with Annexin V- FITC/PI double staining by flow cytometry. The expression and distribution change of the phosphorylation p38MAPK (P-p38MAPK) were detected by immunohistochemical staining. The changes of P-p38 MAPK and Fas proteins were detected by Western blot.

RESULTThe proliferations of leukemia cell line THP-1 are inhibited by allicin. MTT assay showed that allicin can inhibit the proliferation of the THP-1 cell, and the inhibition was dependent on both dose and time. The IC50 of 72 hours was 12.8 mg x L(-1). Apoptosis rate detected by Annexin V-FITC/PI was proportional to the concentration of the allicin. After the immunohistochemical staining test, the P-p38MAPK was located in the cell nucleus and plasma, showing deep brown, when adding allicin to THP-1 cell. Western blot test showed that the P-p38MAPK proteins expression was proportional to the concentration of Allicin and was also dose dependent. The levels of P-p38MAPK in negative control group, 1/2 IC50 of 72 hours group and IC50 of 72 hours group were 0.259 8 +/- 0.013 2, 0.61 2 +/- 0.008 3 and 0.505 6 +/- 0.005 5 respectively, and the levels of Fas proteins were 0.287 4 +/- 0.008 9, 0.426 8 +/- 0.007 9 and 0.597 1 +/- 0.010 9 respectively. The difference was statistically significant when compared with the negative control group (P < 0.01).

CONCLUSIONAllicin can significantly induce THP-1 cells apoptosis, and its mechanism may be related to the activation of P38MAPK/Fas.

Apoptosis ; drug effects ; Cell Line, Tumor ; Humans ; Neoplasms ; drug therapy ; metabolism ; physiopathology ; Phosphorylation ; Signal Transduction ; drug effects ; Sulfinic Acids ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; genetics ; metabolism