Osteoarthritis (OA) is a common disease among elders and athletes. Mitogen-activated protein kinases (MAPKs) are molecules of stress sensitivity which play a significant role in the occurrence and development of OA. MAPKs are closely related with chondrocyte apoptosis and cartilage degradation. This paper reviewed the related studies between OA and MAPKs.

OBJECTIVETo investigate the temporal changes of serum interleukin-37 (IL-37) concentration following acute ST-segment elevation myocardial infarction (ASTEMI) and the relationship between IL-37 and C-reactive protein (CRP) in patients with ASTEMI.

METHODSThis analysis was conducted in a cohort of 20 patients with an established diagnosis of ASTEMI and 26 patients admitted for chest pain but with normal findings in coronary angiography (control) between June 2012 and December 2013. Venous blood was collected at days 1, 3, 5, and 7 after myocardial infarction for measurement of serum IL-37 and CRP levels using enzyme-linked immunosorbent assay (ELISA).

RESULTSCompared with the control group, the patients in ASTEMI group showed a significant acute elevation of IL-37 level on day 1 following myocardial infarction; IL-37 level reached the peak on day 3 and began to decrease on day 5, followed by a significant decrease on day 7. The time course of post-infarction CRP changes was consistent with that of IL-37 variations and showed a positive correlation the latter (r=0.63, P<0.05).

CONCLUSIONIL-37 may participate in the inflammatory responses in ASTEMI.

C-Reactive Protein ; metabolism ; Coronary Angiography ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-1 ; blood ; Myocardial Infarction ; blood

Objective To investigate the temporal changes of serum interleukin-37 (IL-37) concentration following acute ST-segment elevation myocardial infarction (ASTEMI) and the relationship between IL-37 and C-reactive protein (CRP) in patients with ASTEMI. Methods This analysis was conducted in a cohort of 20 patients with an established diagnosis of ASTEMI and 26 patients admitted for chest pain but with normal findings in coronary angiography (control) between June 2012 and December 2013. Venous blood was collected at days 1, 3, 5, and 7 after myocardial infarction for measurement of serum IL-37 and CRP levels using enzyme-linked immunosorbent assay (ELISA). Results Compared with the control group, the patients in ASTEMI group showed a significant acute elevation of IL-37 level on day 1 following myocardial infarction; IL-37 level reached the peak on day 3 and began to decrease on day 5, followed by a significant decrease on day 7. The time course of post-infarction CRP changes was consistent with that of IL-37 variations and showed a positive correlation the latter (r=0.63, P<0.05). Conclusion IL-37 may participate in the inflammatory responses in ASTEMI.

Objective To investigate the temporal changes of serum interleukin-37 (IL-37) concentration following acute ST-segment elevation myocardial infarction (ASTEMI) and the relationship between IL-37 and C-reactive protein (CRP) in patients with ASTEMI. Methods This analysis was conducted in a cohort of 20 patients with an established diagnosis of ASTEMI and 26 patients admitted for chest pain but with normal findings in coronary angiography (control) between June 2012 and December 2013. Venous blood was collected at days 1, 3, 5, and 7 after myocardial infarction for measurement of serum IL-37 and CRP levels using enzyme-linked immunosorbent assay (ELISA). Results Compared with the control group, the patients in ASTEMI group showed a significant acute elevation of IL-37 level on day 1 following myocardial infarction; IL-37 level reached the peak on day 3 and began to decrease on day 5, followed by a significant decrease on day 7. The time course of post-infarction CRP changes was consistent with that of IL-37 variations and showed a positive correlation the latter (r=0.63, P<0.05). Conclusion IL-37 may participate in the inflammatory responses in ASTEMI.

The aim of this study was to identify antigens for a vaccine or drug target to control rabbit coccidiosis. A combination of 2-dimensional electrophoresis, immunoblotting, and mass spectrometric analysis were used to identify novel antigens from the sporozoites of Eimeria stiedae. Protein spots were recognized by the sera of New Zealand rabbits infected artificially with E. stiedae. The proteins were characterized by matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF/TOF-MS) analysis in combination with bioinformatics. Approximately 868 protein spots were detected by silver-staining, and a total of 41 immunoreactive protein spots were recognized by anti-E. stiedae sera. Finally, 23 protein spots were successfully identified. The proteins such as heat shock protein 70 and aspartyl protease may have potential as immunodiagnostic or vaccine antigens. The immunoreactive proteins were found to possess a wide range of biological functions. This study is the first to report the proteins recognized by sera of infected rabbits with E. stiedae, which might be helpful in identifying potential targets for vaccine development to control rabbit coccidiosis.
Coccidiosis* ; Computational Biology ; Eimeria ; Electrophoresis ; HSP70 Heat-Shock Proteins ; Immunoblotting ; Mass Spectrometry ; Rabbits ; Sporozoites

Exercise is benefic for osteoporosis, without clear molecular biology mechanism. The osteoprotegerin/receptor activator of nuclear factor-κB ligand/receptor activator of nuclear factor-κB (OPG/RANKL/RANK) signal pathway contributes to osteoporosis, which can be mediated by mechanical force. Research progress on osteoporosis and the stress sensitive signal pathway OPG/RANKL/RANK were reviewed in this paper.

BACKGROUND:Croton cream can activate ERK pathways and have anti-apoptotic effects on neuronal cells.It is not clear whether it synergistically exerts anti-apoptotic effects by inhibiting the activation of JNK and p38 pathways. OBJECTIVE:To explore the effects and mechanisms of croton cream on neuronal damage and apoptosis in the ischemic cortex of rats with cerebral ischemia-reperfusion injury. METHODS:(1)Ninety Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream low-dose group,croton cream medium-dose group,croton cream high-dose group and nimodipine group,with 15 rats in each group.Except for the sham operation group,animal models of middle cerebral artery occlusion were prepared in rats by the thread method.Rats in the three croton cream groups were given 20,40,and 60 mg/kg croton cream,respectively.Rats in the sham operation and model groups were given the same amount of normal saline,once a day,for 7 consecutive days.The optimal concentration of croton cream,namely the high dose of croton cream,was selected based on neurological deficit score,TTC staining,brain tissue water content,hematoxylin-eosin staining and Nissl staining.(2)Another 120 Sprague-Dawley rats were randomly divided into sham operation group,model group,croton cream group,JNK inhibitor group,croton cream+JNK inhibitor group,p38 MAPK inhibitor group,croton cream+p38 MAPK inhibitor group,and nimodipine group,with 15 rats in each group.Animal models of middle cerebral artery occlusion were prepared using the thread method in all the groups except in the sham operation group.Thirty minutes before modeling,10 μL of SP600125(JNK inhibitor)and 10 μL of SB203580(p38 MAPK inhibitor)were injected into the lateral ventricle of the rats,respectively.Rats in croton cream groups were intragastrically given 60 mg/kg croton cream.Seven days later,the JNK/p38 MAPK signaling pathway,apoptosis-related proteins and cell apoptosis were detected by western blot,TUNEL staining and flow cytometry,respectively. RESULTS AND CONCLUSION:(1)Compared with the sham operation group,neurological deficit score,cerebral water content,cerebral infarction volume and apoptosis rate were significantly increased in the model group(P<0.05),where nerve cells showed scattered distribution.Compared with the model group,neurological deficit score,water content of brain tissue and cerebral infarction volume were significantly decreased in the croton cream medium-dose group,high-dose group and nimodipine group(P<0.05),and the pathological morphology of nerve cells was significantly improved.(2)Compared with the JNK inhibitor group,p-JNK/JNK,p-p38/p38 and Bax expressions in rat brain tissue and the apoptotic rate were significantly decreased in the croton cream+inhibitor groups(P<0.05),while the expression of and Bcl-2 was significantly increased(P<0.05).To conclude,croton cream may inhibit the activation of JNK/p38 MAPK signaling pathway and reduce neuronal apoptosis to achieve neuroprotective effects in rats with cerebral ischemia-reperfusion injury.