Humans ; Indium ; toxicity

Asbestos ; adverse effects ; Humans ; Lung Neoplasms ; chemically induced ; Mesothelioma ; chemically induced ; Peritoneal Neoplasms ; chemically induced

Brain Neoplasms ; pathology ; Humans ; Neurocytoma ; pathology

Humans ; Nitrogen Oxides ; poisoning ; Pulmonary Edema ; chemically induced

Cranial Fossa, Anterior ; Humans ; Liposarcoma, Myxoid ; diagnostic imaging ; metabolism ; pathology ; Magnetic Resonance Imaging ; Male ; Middle Aged ; S100 Proteins ; metabolism ; Skull Base Neoplasms ; diagnostic imaging ; metabolism ; pathology ; Tomography, X-Ray Computed

Actins ; metabolism ; Adult ; Desmin ; metabolism ; Electromyography ; Humans ; Male ; Microscopy, Electron, Transmission ; Muscle, Skeletal ; pathology ; ultrastructure ; Myopathies, Nemaline ; metabolism ; pathology

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

OBJECTIVETo investigate the expression of protein kinase C (PKC) in the spinal dorsal horn of rats with formalin-induced pain and the effect of intrathecal ketamine on PKC expression.

METHODSThirty-two SD rats were randomly divided into 4 equal groups, namely the control group, intrathecal saline group (NS), 50 µg ketamine group (K1) and 100 µg ketamine group (K2). The rats were anesthetized with 10% chloral hydrate, and a microspinal catheter was inserted intrathecally into the lumbar region. Five days later, the rats in groups, K1 and K2 were subjected to intrathecal administration of 50 and 100 µg ketamine (10 µl), respectively, followed by 10 µl saline, and those in NS group received 20 µl saline only. Thirty minutes later, 5% formalin (50 µl) was subcutaneously injected into the left hindpaw. The pain intensity score (PIS) was utilized to assess antinociceptive behavior within 1 h after formalin injection. Twenty-four hours later, the left hindpaw thickness was measured and the expression of PKC in the spinal dorsal horn in the L5 segment was assayed using immunohistochemistry.

RESULTSCompared to group NS, groups K1 and K2 showed significantly decreased PIS (P<0.01) in the second phase of formalin-induced pain; 24 h later, the left hindpaw thickness of group NS increased obviously in comparison with that in the control group (P<0.01), whereas the thickness was significantly reduced in group K1 and K2 as compared to that in group NS (P<0.05). The number of immunoreactive cells and the immunohistochemical score of PKC in the spinal dorsal horn were significantly higher in group NS than in group C (P<0.01), but significantly lower in groups K1 and K2 than in group NS (P<0.05).

CONCLUSIONIntrathecal ketamine produces obvious antinociception against formalin-induced pain in rats and inhibits the enhanced PKC expression in the spinal dorsal horn in response to formalin-induced pain, suggesting the important role of PKC in nociceptive signal transmission and modulation in the spinal cord.

Animals ; Formaldehyde ; adverse effects ; Injections, Spinal ; Ketamine ; administration & dosage ; pharmacology ; Male ; Pain ; chemically induced ; metabolism ; Pain Measurement ; Posterior Horn Cells ; metabolism ; Protein Kinase C ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; drug effects ; metabolism

This study was aimed to investigate the effect of baicalin on proliferation and apoptosis of HL-60 cells and its mechanism. Cell proliferation was assayed by using Cell Counting Kit-8. The morphological changes of HL-60 cells were examined by light microscopy and nucleolus morphological changes were observed by fluorescent microscopy after Hoechst 33342 staining. The early cell apoptosis was detected by using flow cytometry with Annexin V-FITC/PI double staining. The expression of caspase-3, caspase-9, Bcl-2 and Bax mRNA was detected by RT-PCR and Western blot assay was carried out to examine Bax, Bcl-2, caspase-8 and cleaved caspase-3 expression. The results showed that Baicalin inhibited the proliferation of HL-60 cells in a time- and concentration-dependent manner. HL-60 cells exhibited typical morphological features (for example, cell shrinkage, membrane blebbing and formation of apoptotic bodies). Cell apoptosis in early stage could be detected, the expression of caspase-3, caspase-9 and Bax mRNA was obviously up-regulated, while the Bcl-2 expression down-regulated, and accordingly Bcl-2/Bax ratio decreased. Such results were consistent with the expression of these proteins. In addition, the expression of cleaved caspase-8 protein was induced significantly after treated with baicalin. It is concluded that baicalin can significantly inhibit the proliferation of HL-60 cells and induce the apoptosis of HL-60 cells, which may occur through decreasing Bcl-2/Bax ratio by intrinsic pathway and through extrinsic pathway. It suggests that baicalin may be a promising drug for the therapy of acute myeloid leukemia.
Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Cell Proliferation ; drug effects ; Flavonoids ; pharmacology ; HL-60 Cells ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; bcl-2-Associated X Protein ; metabolism