Objective To study the protective effect of chlorogenic acid(CGA)on the apoptosis of PC12 cells induced byβ-amyloid protein23-35(Aβ25-35)and its mechanism. Methods The cells model of death was estab-lished by Aβ25-35 (20 μmol/L)-induced PC12 cells. The cells were interfered with 5 different concentrations of CGA. CCK-8 assay was used to detect cells viability to determine the 3 concentrations of CGA in future experi-ments. The cells were divided randomly into control group ,model group and interference groups with 3 different concentrations of CGA. Cells apoptosis rates were detected by flow cytometry;colorimetry method was used to detect MDA,SOD and GSH-Px. The mitochondrial membrane potential(MMP)was detected by fluorescent staining and the expression of caspase-3 by western blot. Results Compared with model group,the cells viability of CGA groups were increased but the apoptosis rates were reduced;the activity of SOD and GSH-Px were increased but the level of MDA,MMP and caspase-3 were decreased(P<0.05). Conclusions CGA has a protective effect on Aβ25-35-induced PC12 cells apoptosis and it may be related to the improvement of cellular antioxidation capacity and mitochondrial damage.

OBJECTIVETo investigate the effect of siRNA silencing the role of C-Jun N-terminal Kinase (JNK) gene in excessive endoplasmic reticulum stress on lung ischemia/reperfusion injury.

METHODSMouse model of pulmonary ischemia reperfusion injury (PIRI) in situ was established with unilateral lung in vivo. Seventy experimental mice were randomly allocated into seven groups (n = 10): Sham group (Sham group), ischemia reperfusion group (I/R), PBS+ Lipofectamine2000TM transfection reagent group (I/R + PBS+ Lipo group), negative control group (I/R+ SCR group), JNK-siRNA group (I/R + siRNA(JNK1), siRNA(JNK2), siRNA(JNK3)). Mice were euthanized after experimental time out, and left lung tissue was extracted. Wet/dry lung weight ratio (W/D) and total lung water content (TLW) were tested. Light microscope, alveolar damage quantitative evaluation index (IQA) and electron microscope were observed. The expression levels of JNK and glucose regulatex protein(GRP78) were detected by RT-PCR and Western blot. Apoptosis of lung tissue was determined by TUNEL.

RESULTSCompared with Sham group, all indicators above of I/R + PBS + Lipo group and I/R + SCR group were significantly increased (P < 0.01), and compared with I/R group, those indicators of the three groups all had no notable difference; those indicators were not statistically different between I/R + PBS + Lipo group and I/R + SCR group, and compared to the three groups, the above indicators in JNK-siRNA group were lower (P < 0.05, P < 0.01) except that the expression levels of GRP78 was not statistically different.

CONCLUSIONI/R induces excessive ERS in lung tissue, in which JNK pathway participates in apoptosis, leading to lung tissue injury.

Animals ; Apoptosis ; Endoplasmic Reticulum Stress ; Heat-Shock Proteins ; metabolism ; JNK Mitogen-Activated Protein Kinases ; genetics ; Lung ; physiopathology ; Lung Injury ; genetics ; MAP Kinase Signaling System ; Mice ; RNA, Small Interfering ; Reperfusion Injury ; genetics

OBJECTIVETo investigate the effects of cyclosporine A (CsA), a powerful inhibitor of mitochondrial permeability transition pore (MPTP), on pneumocyte apoptosis, the release of cytochrome C and the activity of caspase-3 after lung ischemia/reperfusion, and explore the mechanisms.

METHODSSingle lung in situ ischemia/reperfusion animal model was used. 30 SD rats were randomly divided into three groups (n = 10): sham (S) group, ischemia/reperfusion (I/R) group and cyclosporine A (CsA) group. Apoptosis of pneumocyte was assessed by TUNEL method, cytochrome C (CytC) in cytoplasm was detected by immunohistochemistry techniques, and the activity of caspase-3 was measured with spectrophotometer.

RESULTSThe content of CytC in cytoplasm, the activity of caspase-3, and the value of apoptosis index (AI) in ischemia/reperfusion group were evidently higher than that in S group (P < 0.01). CsA suppressed apoptosis as well as CytC release and caspase-3 activity (P < 0.01).

CONCLUSIONCsA can prevent the release of cytochrome C, block the apoptosis of pneumocyte accordingly maybe by closing the MPTP.

Alveolar Epithelial Cells ; cytology ; drug effects ; Animals ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cyclosporine ; pharmacology ; Cytochromes c ; metabolism ; Lung ; blood supply ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology

OBJECTIVETo study the occupational exposure limit of dimethoxymethane (DMM) in workplace air.

METHODSLiterature research was conducted on DMM; information on its physicochemical properties, toxicology, and occupational epidemiology was collected. Upon analyzing these data, an occupational exposure limit of DMM in workplace air was proposed according to the guidelines and principles of developing occupational exposure limits for harmful factors in workplaces.

RESULTSA total of 165 air samples were collected from DMM manufacturers, 14 of which had a DMM concentration over 3000 mg/m(3), accounting for 8.48% of all samples. Compared with the control group, the exposed employees had a significantly increased incidence of discomfort symptoms when exposed to more than 6000 mg/m(3) DMN (P < 0.01).No significant differences in the constituent ratios of abnormal results in physical examinations were found between the exposure groups and control group (P > 0.05).

CONCLUSIONWe recommend to set the permissible concentration-time weighed average to 3100 mg/m(3) as the occupational exposure limit of DMM in workplace air in China. This occupational exposure limit standard meets the relevant requirements of toxicology and occupational epidemiology, as well as fits well with our country's current economical and technological levels. This standard has high applicability in China's domestic settings.

Air Pollutants, Occupational ; analysis ; China ; Humans ; Inhalation Exposure ; Methyl Ethers ; analysis ; Occupational Exposure ; analysis ; Threshold Limit Values ; Workplace

OBJECTIVETo explore the effect of curcumin (CUR) on cycteinyl aspirate specific protease-12 (Caspase-12) and pneumocyte apoptosis in pulmonary ischemia/reperfusion (I/R) injury mice.

METHODSThe in vivo unilateral in situ pulmonary I/R injury mouse model was established in C57BL/6J mice. Sixty experimental mice were randomly divided into six groups by random digit table, i. e., the sham-operation group (Sham), the I/R group, the I/R + dimethyl sulfoxide group (I/R + DMSO), the I/R + low dose CUR pre-treated group (I/R + CUR-100), the I/R + middle dose CUR pre-treated group (I/R + CUR-150), the I/R + high dose CUR pre-treated group (I/R + CUR-200), 10 in each group. Mice were euthanized and their left lungs were excised. Wet lung weight to dry lung weight (W/D) and the total lung water content (TLW) were tested. The morphological changes of the lung tissue were observed and index of quantitative evaluation for alveolar damage (IQA) detected under light microscope. The ultra-microstructure of the lung tissue was observed under electron microscope. The mRNA and protein expression levels of Caspase-12 and glucose regulated protein (GRP78) were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Apoptosis index (AI) of the lung tissue was determined by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) method.

RESULTSCompared with the Sham group, expression levels of Caspase-12, GRP78 mRNA and protein all significantly increased in the I/R group (P < 0.05); W/D, TLW, IQA, and AI were all notably higher (P < 0.05, P < 0.01); the morphological and ultrastructural injury of the lung tissue were notably observed in I/R group. Compared with the I/R + DMSO group, expression levels of GRP78 mRNA and protein were increasingly higher in the I/R + CUR-100 group, the I/R + CUR-150 group, and the I/R +CUR-200 group (P < 0.05), expression levels of Caspase-12 mRNA and protein were lower (P < 0.05); W/D, TLW, IQA, and AI also decreased (P < 0.05, P < 0.01); the morphological and ultrastructural injury of the lung tissue were gradually alleviated in the I/R + CUR groups.

CONCLUSIONCUR had better effect on the lung protection against I/R injury, which might be related to inhibition for pneumocyte apoptosis associated with Caspase-12 in excessive unfolded protein response (UPR).

Animals ; Apoptosis ; drug effects ; Caspase 12 ; metabolism ; Curcumin ; pharmacology ; Heat-Shock Proteins ; metabolism ; Lung ; blood supply ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury ; metabolism ; pathology ; prevention & control

AIMTo observe protective effects of safflower injection (SI) on lung ischemia/reperfusion injury (LIRI) and investigate its potential mechanism.

METHODSRabbit lung model of ischemia/reperfusion injury was constituted in vivo. The rabbits were randomly divided into three groups: sham-operation group (S group), ischemia/reperfusion group (I/R group) and ischemia/reperfusion plus safflower injection group (SI group). Malondialdehyde (MDA) content, superoxide dismutase (SOD) and xanthine oxidase (XO) activities in serum were measured. The lung tissue sampled at the end of the experiment was assayed for wet/dry weight ratio (W/D), injured alveoli rate (IAR) and ultrastructural changes were observed under electron microscope. The expression of COX-1 and COX-2 were measured by immunohistochemistry (IHC). The expressions of COX-1mRNA and COX-2mRNA were observed by in situ hybridization (ISH).

RESULTSIn I/R group, XO and MDA increased and SOD decreased in serum, while the same changes happened in SI group but less severely(P<0.01). The value of W/D and IAR was much higher in I/R group than S group, but decreased in SI group. Electron microscope showed obvious ultrastructural injury brought by LIRI in I/R group, which was greatly attenuated in SI group. The IHC and ISH demonstrated that COX-2 and COX-2mRNA in pulmonary tissue of I/R group were significantly higher than those of SI group (P < 0.01). The difference of COX-1 and COX-1mRNA in pulmonary tissue among the three groups was not significant.

CONCLUSIONThe ischemia/reperfusion lung injury insults induced the regulation of COX-2 in lung. Safflower injection may attenuate lung ischemia/reperfusion injury through inhibiting cyclooxygenase-2 expression.

Animals ; Carthamus tinctorius ; Cyclooxygenase 1 ; metabolism ; Cyclooxygenase 2 ; metabolism ; Lung ; drug effects ; enzymology ; physiopathology ; Malondialdehyde ; blood ; Rabbits ; Reactive Oxygen Species ; metabolism ; Reperfusion Injury ; metabolism ; Superoxide Dismutase ; blood ; Xanthine Oxidase ; blood

Objective To investigate the relationship between learning and memory deficit and demyelination of the corpus callosum in twelve-month old APP/PS1 transgenic mice. Methods Twelve twelve-month old APP/PS1 transgenic mice were as AD group, and age-matched wild type (WT) littermates were as WT group. Learning and memory ability was tested with Morris water maze, and the mor-phology of nerve fiber of corpus callosum was detected with Luxol Fast Blue staining. Immunohistochemistry was used to detect myelin ba-sic protein (MBP) in the corpus callosum. Thioflavine S staining was used to detect amyloid plaque in the corpus callosum. Results Com-pared with WT group, the latency increased (Z>2.873, P<0.01) and the times crossing the location of the platform decreased (t=-7.339, P<0.001) in AD group. The nerve fibers were sparse and disorganized, with a lot of vacuoles in the corpus callosum of AD group. The positive expression of MBP in the corpus callosum was significantly decreased (t=-4.481, P<0.001) in AD group compared with WT group. There were amyloid plaques in the corpus callosum of AD group. Conclusion Twelve-month old APP/PS1 transgenic mice exhibit learning and memory deficit, which may be attributed to the deposition of the amyloid plaque mediated demyelinated injury of the corpus callosum.

Objective: To compare the effects of various interventions on the incidence of central line-associated bloodstream infection (CLABSI) . Methods: The clinical data of 218 patients with central venous catheterization were retrospectively analyzed. Infected patients were treated as CLABSI group and non-infected patients as control group. Results: Of the 218 patients, 24 patients were developed CLABSI. There was no significant difference in sex, age, primary infection status and puncture site between CLABSI group and control group. Univariate analysis showed that axillary vein puncture could significantly reduce the incidence of CLABSI (P=0.028), and the infection rate of axillary vein puncture per 1000 days under B-ultrasound was significantly reduced by 0.93‰. The average indwelling days of deep venous catheter in patients with pulse puncture were significantly longer than those in other groups (47.32 days vs 19.90 days). The average indwelling days in patients with axillary vein puncture positioned by B ultrasound were longer than those in patients with other parts of vein puncture positioned by B ultrasound (P < 0.05). Logistic multiple regression analysis showed that the main risk factors for CLABSI were anatomically located puncture (P = 0.031) and non-axillary venous catheterization (P = 0.068). Conclusions Choosing axillary vein as the position of deep venous catheterization and using ultrasound-guided central venous puncture can reduce the incidence of CLABSI and prolong the average catheterization time.

OBJECTIVETo study the diagnosis and treatment of a second primary malignant tumor induced by previous radiotherapy.

METHODSFrom March 1970 to March 1997, 108 nasopharyngeal cancer (NPC) patients who developed a second primary malignant tumor induced by radiotherapy were treated. There were squamous carcinoma 43 (39.8%), sarcoma 26 (24.1%), malignant fibrous histiocytoma 14 (13.0%), adenoid cystic carcinoma 12 (11.1%), thyroid papillary adenocarcinoma 8 (7.4%) and malignant melanoma 5 (4.6%). Fifty patients underwent operation, 32 received radiotherapy, 18 received chemotherapy and 8 received operation combined with chemotherapy.

RESULTSThe 3- and 5-year tumor-free survival rates were 64.0% and 36.0% in the operation group. They were 34.4% and 18.8% in the radiotherapy group.

CONCLUSIONSurgery, if not contra-indicated, is the first choice for the second primary malignant tumor induced by radiotherapy. Aggressive treatment for these patients is, hence, indicated clinically.

Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Neoplasms, Radiation-Induced ; diagnosis ; mortality ; therapy ; Neoplasms, Second Primary ; diagnosis ; mortality ; therapy ; Radiotherapy ; adverse effects ; Survival Rate