Objective To study the effect of Jade -Screen Powder (JSP)on regulating expression of 5 microRNAs associated with helper T cells in asthmatic mouse model.Methods Forty Balb /c mice were randomly di-vided into 4 groups,1 0 mice for each group,namely normal control,asthma model,JSP treatment and Dexamethasone treatment.The mouse models of allergic inflammation on both upper and lower airways were established by ovalbumin sensitization and challenge.Interleukin(IL)-1 3 and IL -1 7 expressions were detected from lung homogenates by ELISA.Hematoxylin and eosin staining was also performed to observe the pathological changes in the lung tissue.The expressions of miR -1 46a,miR -1 46b,miR -21 0,miR -1 26 and miR -21 a were detected by quantitative real time PCR from splenocytes.Results The lower levels of IL -1 3 [(6.382 ±1 .690)μg/L]and IL -1 7 [(24.21 2 ± 1 .250)μg/L]were found in JSP treatment group compared with those in the asthma model group [(20.1 54 ±7.960)μg/L;(50.31 2 ±5.770)μg/L,rseparately],there was significant difference in IL -1 3 between JSP group and the asthma model group,as well as IL -1 7 (t =3.785,P =0.005;t =9.891 ,P =0.000).Same findings were found in Dexamethasone treated group as well [IL -1 3:(9.366 ±3.460)μg/L,IL -1 7:(29.1 32 ±4.960)μg/L;t =2.779, P =0.024;t =6.225,P =0.000].However,upregulation of miR -21 0 was observed in JSP treatment group (2.052 ± 0.871 )compared with that in the asthma model group (4.034 ±1 .379)(3.95 folds,t =2.71 8,P =0.026).Mean-time,the expression of miR -1 26 in JSP group (4.920 ±0.924)and Dexamethasone group (3.862 ±1 .51 0)in-creased compared with asthma model group (6.024 ±0.447)(2.1 5 folds,t =2.405,P =0.043,and 4.48 folds,t =-3.069,P =0.01 5).Conclusions Th2 and Th1 7 T cells participate in the pathogenesis of asthma and the asthmatic process can be inhibited by JSP.JSP may affect the helper T cells by regulating miR -21 0 and miR -1 26.

OBJECTIVE: To explore the distribution of inflammatory cells and positive expression of P-se- lectin glycoprotein ligand-1 (PSGL-1) in infant brainstem tissue from hand-foot-mouth disease related fatal brainstem encephalitis. METHODS: Twenty brainstem samples from infants suffered from brainstem en- cephalitis were collected as the experimental group. Ten brainstem samples from infants died of non- brain diseases and injuries were collected as the control group. The distribution of inflammatory cells and the expression of PSGL-1 in the two groups were examined by immunohistochemical method. The characteristics of the positive cells were observed. RESULTS: In brainstem tissue of the experimental group, there were sleeve infiltrations of inflammatory cells around the vessels and in the glial nodule. Microglia was the most and following was neutrophils around the vessels and in the glial nodule. There was a significant statistical difference among microglias, neutrophils and lymphocytes (P < 0.05). There was no sleeve infiltration in the control group. PSGL-1 protein was expressed widely in inflammatory cells in the experimental group, especially in the inflammatory cells around the vessels and in the glial nodule. But PSGL-1 positive staining could be observed significantly less in the control group comparing with the experimental group (P < 0.05). CONCLUSION Microglia is the main type of inflammatory cells involved in the progress of the fatal disease. Moreover, PSGL-1 could participate in the pathogenesis of hand-foot-mouth disease related fatal brainstem encephalitis.
Brain Stem/pathology* ; Encephalitis/pathology* ; Hand, Foot and Mouth Disease/pathology* ; Humans ; Infant ; Membrane Glycoproteins/metabolism* ; Microglia/pathology* ; Neutrophils/pathology*

Aim To investigate the curative effects of resveratrol on OVA induced allergic rhinitis in mice and the underlying immune mechanisms. Methods Balb/c mice (female, 6 weeks) were divided randomly into normal control ( NC) group, allergic rhinitis (AR) group, high dose resveratrol treatment group (RH), low dose resveratrol treatment group (RL), and dexamethasone treatment group ( Dex). RL, RH and Dex group were oral administered with resveratrol 30 mg • kg"1, resveratrol 100 mg • kg"1 and dexamethasone 10 mg • kg"1, respectively. After the treat-ment , the sneezing and nasal rubbing behaviors of mice in all the group were recorded and HE was performed to assess the inflammatory cell infiltration in nasal tissues. The sera levels of allergic cytokines were determined with ELISA assay. The percentage of CD4+ GA- TA3 + T cells in spleen of each group was further recorded by flow cytometry. Results Compared with AR group, treatment with resveratrol (100 mg - kg"1) reduced the sneezing and nasal rubbing behaviors signifi-cantly and improved inflammatory cell infiltration in nasal tissues. The up-regulated sera levels of IL-4, IL- 13 and OVA-sIgE in AR group were reversed by RH, and ratios CD4+ GATA3 + Th2 cells in spleen of RH were also down-regulated parallelly. Conclusions RH treatment could improve the allergic related symptoms of OVA-induced allergic rhinitis, which is associated with down-regulated sera levels of IL-4, IL-13 and OVA-sIgE and ratios of CD4+ GATA3 + Th2 cells in spleen of mouse model.

OBJECTIVETo explore the coincidence of lipid peroxidation and neurobehavioral function changes in coke oven workers.

METHODSOne hundred and thirty-four coke oven workers were divided into three groups: 35 in the oven-bottom group, 49 in the oven-side group and 50 in oven-top group. WHO recommended NCTB was performed on coke oven workers and 36 controls from material conservation department; The contents of total superoxide dismutases (T-SOD), glutathione (GSH) and malondialdehyde (MDA) in blood were determined by test kits.

RESULTSCompared with the controls, the coke oven workers showed lower levels of T-SOD and GSH (P < 0.01), significantly higher MDA levels in blood (P < 0.01), higher score on negative mood state, lower scores on positive mood state, and poorer performance in NCTB test (P < 0.05). Further analysis revealed that there was a weak positive correlation between neurobehavioral function changes and the level of lipid peroxidation with a coefficient lower than 0.25.

CONCLUSIONThe level of lipid peroxidation in coke oven workers' blood increased and coincided with neurobehavioral function impairment.

Adult ; Affect ; Anxiety ; Case-Control Studies ; Coke ; Fatigue ; Glutathione ; blood ; Humans ; Lipid Peroxidation ; Male ; Malondialdehyde ; blood ; Middle Aged ; Occupational Exposure ; adverse effects ; Superoxide Dismutase ; blood ; Young Adult

OBJECTIVETo investigate the effects of carbon disulfide (CS(2)) inhalation on the lipid levels of ApoE knockout gene mice and C57BL/6J mice.

METHODSFifty-one male ApoE gene knockout mice were randomly divided into four groups: CS(2)-exposed normal diet group, CS(2)-unexposed normal diet group, CS(2)-exposed high-fat diet group, and CS(2)-unexposed high-fat diet group. Fifty male C57BL/6J mice were divided into four groups in the same way. The exposed groups received 1000 mg/m3 CS(2) by static inhalation (5h/d, 5d/w) for four weeks. The weight of each mouse was determined and recorded once a week. On the 14th day of exposure, six mice in each group were randomly selected to measure serum total cholesterol (TC) levels. On the 28th day of exposure, the serum levels of TC and low-density lipoprotein (LDL) in the remaining mice were measured.

RESULTSThe mean weight gain of exposed groups was less than that of the unexposed groups. On the 14th and 28th days of experiment, the TC levels of the CS2-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P < 0.01 for both). On the 14th day of experiment, the TC levels of the CS(2)-unexposed high-fat diet group were significantly higher than those of the CS(2)-unexposed normal-diet group among C57BL/6J mice group (P < 0.05). On the 28th day of experiment, the LDL levels of the CS(2)-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P = 0.003).

CONCLUSIONCS(2) exposure, high-fat diet, and ApoE gene knockout can elevate blood lipids in mice, thus increasing the risk of atherosclerosis.

Administration, Inhalation ; Animals ; Apolipoproteins E ; genetics ; Atherosclerosis ; Body Weight ; Carbon Disulfide ; toxicity ; Diet, High-Fat ; adverse effects ; Gene Knockout Techniques ; Lipid Metabolism ; drug effects ; Lipids ; blood ; Lipoproteins, LDL ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout

Objective To observe the influence of rotenone on the distribution of alpha-synuclein (ASN) in rat model of Parkinson's disease (PD). Methods Wistar rats were randomly divided into two groups and received 2 mg/kg rotenone (s.c.) or sunflower oil (as control group) for about 4 weeks. The hippocampus, substantia nigra and striatum of brain were observed. Hematoxylin and eosin stain were used to observe the Lewy body like inclusion. The expression of tyrosine hydroxylase (TH) or ASN protein was determined by anti-TH or anti-alpha-synuclein immunohistochemistry, respectively. Results In control rats, ASN protein distributed widely in brain, especially in hippocampus, cortex and striatum. Rotenone obviously increased TH positive neurons and fibers loss in substantia nigra and striatum (P < 0.05). In rotenone treated rats, ASN positive cells increased in global brain but not distributed in an even manner. In substantia nigra, ASN positive stuff was found aggregate in both cytoplasm and nucleus, and some formed spherical inclusion; in striatum, ASN positive neurites end aggregated and agglomerated around neurons; and in hippocampus, few dot-like ASN were aggregated in cell body, and no notable change was found in nucleus. Conclusion In rotenone administrated PD rats, ASN protein aggregated in several brain regions but most obviously in striatum and substantia nigra, and the distribution region of ASN was changed from peri-synapse to the cytoplasm and nucleus of dopaminergic neuron.

OBJECTIVETo construct a cell model of 4.1R gene knockout in murine macrophage cell line RAW264.7 using CRISPR/Cas9 technique.

METHODSThree high?grade small?guide RNAs (sgRNAs) that could specifically identify 4.1R gene were synthesized and inserted into lentiCRISPRv2 plasmid. RAW264.7 cells were infected with sgRNA?Cas9 lentivirus from 293T cells transfected with the recombinant sgRNA?lentiCRISPRv2 plasmid, and the positive cells were screened using puromycin and the monoclonal cells were obtained. The expression of 4.1R protein in the monoclonal cells was measured by Western blotting, and the mutation site was confirmed by sequence analysis. Result A 4.1R gene knockout RAW264.7 cell line was obtained, which showed a 19?bp deletion mutation in the 4.1R gene sequence and obviously enhanced proliferation.

CONCLUSIONWe successfully constructed a 4.1R gene knockout macrophage cell line using CRISPR/Cas9 technique, which may facilitate further investigation of the function of 4.1R in macrophages.

OBJECTIVETo observe the effects of maternal exposure to nano-alumina during pregnancy on the neurodevelopment in offspring mice.

METHODSFemale ICR mice began to be exposed to nano-alumina 10 d before mating, and the nano-alumina exposure lasted till offspring mice were born. All the female mice were randomly divided into 5 groups: solvent control group (saline), nano-carbon group (11.76 mg/ml), micro-alumina group (50 mg/ml), 50 nm alumina group (50 mg/ml), and 13 nm alumina group (50 mg/ml). All the mice were treated by nasal drip (10 µl/time) 3 times daily till offspring mice were born. Physiological indices, reflex and sensory function test, endurance test, Morris water maze test, positioning and navigation test, and open field test were used to evaluate the neurodevelopment of newborn mice.

RESULTSOn day 28, the body weight of 13 nm alumina group (16.73±4.04 g) was significantly lower than that of solvent control group (20.45±2.50 g) (P<0.01); the 13 nm alumina group had significantly delayed time to ear opening compared with the solvent control group (4.91±0.78 d vs 4.45±0.50 d, P<0.01); compared with the solvent control group, the nano-carbon group, micro-alumina group, 50 nm alumina group, and 13 nm alumina group had significantly delayed time to eruption of teeth (10.05±0.23 d vs 10.32±0.48 d, 10.75±0.45 d, 10.32±0.47 d, and 10.79±0.49 d, P<0.05 or P<0.01). On days 4 and 7 after birth, compared with the solvent control group, other groups had significantly decreased proportions of mice which passed the cliff avoidance test (P < 0.05 or P < 0.01). On days 12 and 14 after birth, compared with the solvent control group, the nano-carbon group, 50 nm alumina group, and 13 nm alumina group had significantly reduced pre-suspension time in the endurance test (P < 0.05 or P < 0.01). The Morris water maze and positioning and navigation tests showed that the 13 nm alumina group had a significantly increased 5 d incubation period compared with the solvent control group (P < 0.05); compared with the solvent control group, other groups had significantly reduced numbers of platform crossings (P < 0.05 or P < 0.01). The open field test showed that the nano-carbon group and 13 nm alumina group had reduced numbers of rearings compared with the solvent control group (P < 0.05); compared with the solvent control group, other groups had significantly reduced numbers of modifications (P < 0.01).

CONCLUSIONMaternal exposure to nano-alumina (13 nm) during pregnancy has inhibitory effects on the physical development and early behavioral development in newborn mice and can also inhibit the learning and memory abilities and adaptability to new environment in offspring mice. The neurodevelopmental toxicity of nano-alumina to newborn mice increases as the particle sizes of nano-alumina decrease, which has been demonstrated by the endurance test and number of rearings.

Aluminum Oxide ; toxicity ; Animals ; Animals, Newborn ; Behavior, Animal ; Body Weight ; Female ; Maternal Exposure ; Maze Learning ; Mice ; Mice, Inbred ICR ; Motor Activity ; Nanostructures ; toxicity ; Pregnancy

OBJECTIVETo explore the value of (18)F-FDG PET/CT in the diagnosis and treatment evaluation in patients with pretreatment or recurrent extranodular natural killer/T-cell lymphoma nasal type (ENTCL).

METHODS(18)F-FDG PET/CT images and clinical records of 35 cases (67 scans) of pathologically confirmed ENTCL treated in our hospital within the last 9 years were analyzed. The imaging characteristics of the upper aerodigestive tract (UAT) and the non-aerodigestive tract (NUAT) lesions were analyzed. Lesion distribution, clinical stages, SUVmax and patient survival data were compared between pretreatment and recurrent cases.

RESULTSs All the ENTCL lesions were hypermetabolic. The UAT lesions involved mainly the nasal cavity and pharynx, while the NUAT lesions may involve the lymph nodes and all the organs. UAT lesions were more common in pretreatment cases while NUAT lesions tended to increase in recurrent cases. The SUVmax of pretreatment and recurrent lesions were 10.4∓4.4 and 9.6∓5.2, and showed no significant difference among patients with different lesion distribution patterns, clinical stages, or treatment history. The tumor remission rate evaluated by PET/CT were higher in cases with an initial diagnosis than in those with recurrence [(89.5% (17/19) vs 33.3% (5/15), P<0.005)]. Cox regression analysis revealed no significant differences in the survival rates among patients with different treatment history, clinical stages, lesion distribution patterns, or SUVmax levels (P>0.05).

CONCLUSION(18)F-FDG PET/CT can sensitively detect the pretreatment or recurrent lesions in ENTCL patients and helps in accurate tumor staging and curative effect evaluation.

Fluorodeoxyglucose F18 ; Humans ; Lymphoma, Extranodal NK-T-Cell ; diagnostic imaging ; Neoplasm Recurrence, Local ; Neoplasm Staging ; Positron Emission Tomography Computed Tomography

OBJECTIVETo investigate the role of Snitrosylation of protein disulphide isomerasec in methamphetamine (METH)-induced expression of alpha synuclein (αSN) in mouse hippocampus and striatum neurons.

METHODSForty C57BL/6 mice were randomized equally into saline control group, METH group, L-NNA (a NOS inhibitor) group and L-NNA plus METH group. All the agents were injected intraperitoneally at an interval of 12 h, and a total of 8 injections were administered; in L-NNA plus METH group, METH was injected 30 min after LNNA in each treatment. Western Blotting was used to detect the expression of nitric oxide synthase (NOS), αSN, PDI and Snitrosylation of protein disulphide isomerase (PDI-SNO) in the hippocampus and striatum of the mice, and nitric oxide (NO) levels were determined using a NO assay kit.

RESULTSIn METH group, the levels of NOS, PDISNO, αSN and NO all increased significantly compared with those in the control group (P<0.05). Combined treatment with L-NNA and METH, compared with METH alone, resulted in significantly lowered expression of NOS, NO, PDI-SNO and αSN in the hippocampus and striatum of the mice (all P<0.05). No significant differences were found in NOS, NO, PDI-SNO or αSN expressions among METH+L-NNA, L-NNA and control groups (P>0.05).

CONCLUSIONMETH induces the activation of NOS and increases NO level to cause the occurrence of PDI-SNO, leading subsequently to increased expression of αSN in mouse striatum and hippocampus. L-NNA, the inhibitor of NOS, can partly relieve nervous system toxicity induced by METH.