Abstract:Objective To investigate the effects of nuclear factor kappa B activator 1(Act1) on lung metastasis ofmelanoma in mice. Methods Mice were genetically engineered to enable the targeted suppression of Act1 in macrophages(anti-Act1). The lung metastasis model was generated by tail vein injection of B16-F10 melanoma cells. The extent of lungmetastasis was assessed pathology using HE staining of lung tissues. The infiltration of CD45+ leukocytes and CD68+macrophages and the proliferation index of tumor cells in lung tissues were evaluated by immunohistochemistry. Results The anti-Act1 mice developed fewer metastatic and micro-metastatic foci, with reduced CD45+ leukocyte and CD68+macrophage infiltration in the lung tissues, when compared with the C57 control mice. Cells of metastatic and micrometastaticfoci in the anti-Act1 mice demonstrated a reduced proliferation index, when compared with those of control animals. Conclusions Targeted suppression of Act1 in macrophages inhibits the lung metastasis of murine melanoma.

Abstract:Objective To explore the effect of Jianpi Yifei prescription (JPYF) on the expression of glutamatetransporter 2 (EAAT2) and the possible mechanism behind this. Methods Neonatal Sprague-Dawley rats within 24 h ofbirth were used and and the astrocytes of cerebral cortex were isolated under aseptic conditions, then purified, and culturedfor later experiments. The appropriate cell concentration was adjusted in plates for five groups: A, glutamic acid group (250μmoL/ L), B-D, JPYF prescription (final concentrations 0. 25, 0. 5, and 1 g/ kg) + glutamic acid group; and E, normalgroup, After the B-D groups had been treated with JPYF prescription (final concentrations of 0. 25, 0. 5, and 1 g/ kg) for24 h, glutamate at 250 μmol/ L was applied to the A-D groups for 4 h to induce an in vitro primary astrocyte injury model.Cell viability was determined by MTT assay. Determination of glutamic acid concentration in culture medium was performedby ultraviolet colorimetry. The expression of glutamate transporter protein in astrocytes was detected by immunofluorescenceand western blotting. The injury of spinal cord neurons was detected by Immunofluorescence. Results JPYF Fangsignificantly protected the astrocytes ( P < 0. 01), improved the expression of glutamate transporters ( P < 0. 05, P < 0. 01),reduced glutamate concentrations ( P < 0. 05, P < 0. 01), protectd neurons ( P < 0. 05, P < 0. 01), and showed a certaindose-related effect within the range of 0. 25-1 g.L^-1. Conclusions Within a certain dose range, JPYF Fang can reducethe damage of glutamate to neuronal cells, the mechanism of which may involve improving the expression of glutamate transporter and decreasing the concentration of glutamate in extracellular fluid, so as to protect neurons.

Abstract:Objective To establish a quail model of gout by simulating a clinical high-protein and high-calciumdiet, and to provide a basis for studying gout pathogenesis and drug screening for its prevention and treatment. Methods Tirty-six 30-day-old healthy male quails were randomly and equally divided into three groups according to body weight andblood uric acid level, namely, the control group, model I group, and model II group. The control group was fed the basaldiet, and the model groups were fed a high-protein high-calcium diet (dietary crude protein content of 29. 5% and calciumcontent of 7. 8%). The control group and the model I group were provided with drinking water ad libitum, while the modelII group was given drinking water restricted to 4 h daily. The experiment lasted for 50 days. The serum and fecal uric acidlevels were measured, renal function was determined, and histopathological examination was performed. Results Thehigh-protein and high-calcium diet significantly increased serum uric acid levels, significantly reduced fecal uric acidlevels, and did not change the serum creatinine and urea nitrogen levels. The high-protein and high-calcium diet combinedwith restricted drinking water aggravated the increase of blood uric acid level and renal urate deposition, causing goutchanges such as joint swelling and deformation. Conclusions A gout model can be established by feeding on a high-proteinand high-calcium diet and limiting the amount of drinking water. The pathogenesis of gout in this model is more consistentwith the etiology, pathogenesis, and clinical manifestations of gout in clinics, providing a reference for the research on gout pathogenesis and drug development.

Abstract:Objective To study the protective effect of a Chinese medicine,Shenmai injection, on brain tissue in a mouse model of cerebral ischemia and explore its possible mechanism. Methods Thirty healthy adult male CD-1 micewere randomly divided into control, model, and experimental groups with 10 mice in each group. The mouse model of acutecerebral infarction was established by permanent middle cerebral artery occlusion. The experimental group was treated withShenmai injection. The control and model groups were administered the same dose of physiological saline. The red blood cellfunctional indexes were compared among groups. The neuonal apoptosis rate of brain tissue was determined by TUNELassay. Calpain-1 and Bcl-2 expression in the mouse cortex was detected by Western blot and qPCR. Results Comparedwith the control group, RBC-C3bR was significantly decreased and RBC-ICR was significantly increased in the experimentalgroup ( P < 0. 05). Compared with the model group, RBC-C3bR was significantly increased, and RBC-ICR was decreasedsignificantly in the experimental group( P < 0. 05). The number of TUNEL-positive cells in the brain tissue sections ofmodel and experimental groups was significantly higher than that of the control group ( P < 0. 05). The number of TUNELpositivecells in brain tissue sections of the experimental group was significantly lower than that of the model group ( P <0. 05). Compared with the control group, the expression levels of calpain-1 protein and mRNA in model and experimentalgroups were significantly increased, and the expression levels of Bcl-2 protein and mRNA were decreased significantly ( P <0. 05). Compared with the experimental group, the expression levels of calpain-1 protein and mRNA were significantlydecreased, and that of Bcl-2 protein and mRNA were increased significantly ( P < 0. 05). Conclusions Shenmai injectionimproves erythrocyte functions and inhibites neuronal apoptosis in this mouse model of cerebral infarction. The possiblemechanism of the protective effect of Shenmai injection on brain infarction may be the downregulating of expression of calpain-1 protein and upregulating of expression of anti-apoptotic protein Bcl-2 in the brain tissues.

Abstract:Objective To determine the serum cytokine levels in collagen-induced rheumatoid arthritis (RA)rats, cold-damp arthralgia rats, and damp-heat arthralgia rats by using antibody arrays. Methods A rheumatoid arthritismodel was established by intracutaneous injection of type II collagen and complete Freund’ s adjuvant (CFA). On thisbasis, cold-damp or damp-heat stimulation was applied to the RA rats in order to replicate cold-damp arthralgia or dampheatdamp-heat arthralgia. Serum cytokine levels in the rats were determined using antibody arrays. Results Comparedwith the normal group, the activin, CNTF, IFN-γ, and TNF-α levels were upregulated, while MIP-3α and MMP-8 weredownregulated in the RA group. The CINC-2α, GM-CSF, and IFN-γ levels were upregulated and MIP-3α wasdownregulated in the cold-damp arthralgia group. ICAM-1 was upregulated, while IFN-γ, MIP-3α, and RAGE weredownregulated in the damp-heat arthralgia group. Compared with those in the RA group, β-NGF, CINC-2α, MMP-8, andPDGF-AA were upregulated, while activin A and TNF-α were downregulated in the cold-damp arthralgia group. MMP-8 wasupregulated, and activin A, CNTF, IFN-γ, IL-1α, IL-6, MIP-3α, RAGE, and TNF-α were downregulated in the dampheatarthralgia group. Compared with the damp-heat arthralgia group, CINC-2α, IFN-γ, IL-1α, MIP-3α, PDGF-AA, andRAGE were upregulated in the cold-damp arthralgia group. Compared with that in the normal group, the ratio of IFN-γ/ IL-4was increased in the RA group and cold-damp arthralgia group, but was decreased significantly in the damp-heat arthralgiagroup. Compared with that in the RA group, the ratio increased in the cold-damp arthralgia group, and decreasedsignificantly in the damp-heat arthralgia group. Conclusions Diseases (RA) and syndromes (cold-damp or damp-heat)have a significant influence on serum cytokine expression profiles in rats, and there are clear differences among different models.

Abstract:Objective To explore the influence of edaravone on cerebral edema in neonatal rats with hypoxicischemicencephalopathy (HIE) and on the CD163/ HO-1 signaling pathway. Methods A total of 120 SD neonatal rats (7days old) were included here, 90 of which underwent double ligation of the proximal and distal ends the left commoncarotid artery to establish a hypoxic-ischemic brain damage (HIBD) model. After ligation and hypoxia the rats were thendivided into a model group and an edaravone group. The remaining 30 rats had only separated the common carotid arterywithout ligation as a sham operation group. The rats in the edaravone group were immediately intraperitoneally injected with2 mg/ kg edaravone after model establishment, once a day for 5 consecutive days. The model group and the sham operationgroup were given the same amount of saline intraperitoneally at the same time. After operation, the biological behaviors ofthe neonatal rats were observed. After modeling for 24 h,the morphology of brain tissue in neonatal rats was observed byTTC staining. Changes of the water content in brain tissue of neonatal SD rats were detected at 6, 12, and 24 h, and 2, 3,and 5 days after model establishment. CD163 and HO-1 mRNA expression levels were determined by quantitativefluorescence PCR (qRT-PCR). CD163 and HO-1 protein expression levels were tested using western blotting. Results After operation, 90 neonatal rats showed lethargy, malaise, and convulsions. Those symptoms were clearly alleviated aftertreatment with edaravone compared with those in the model group, and improved within 3 days. At 24 h after modelestablishment, TTC staining showed that the left hemisphere was edematous and had a pale color in the model group, andalso had a slightly larger volume than the right hemisphere. The degree of injury of brain tissue significantly decreased afteredaravone treatment. The infarct size in the left hemisphere of the rats in the model group and the edaravone group wassignificantly greater than that in the sham operation group ( P < 0. 05), and the infarct size in the edaravone-treated groupwas significantly smaller than that in the model group ( P < 0. 05). At 6 h after modeling, water contents of brain tissue inthe model group and edaravone group were significantly higher than that in the sham operation group ( P < 0. 05), and brainwater content was the highest at 2 days. The water content in brain tissue of neonatal rats treated with edaravone wassignificantly lower than that in the model group ( P < 0. 05). qRT-PCR and western blotting showed that CD163 and HO-1mRNA/ protein expression levels in brain tissue of neonatal rats in the model group and edaravone group were significantlyincreased compared with those in the sham operation group ( P < 0. 05). CD163 and HO-1 mRNA/ protein expression levelsin neonatal rats were significantly higher than those in the model group after edaravone treatment ( P < 0. 05). Conclusions Edaravone can clearly reduce the degrees of cerebral edema and cerebral infarction in neonatal rats with HIBD. The mechanism behind this may be related to activation of the CD163/ HO-1 signaling pathway.

Abstract:Objective To compare the effects of two hemostatic methods including 3M vetbond tissue adhesiveand electrocoagulation in a rat model of uremia. Methods Male SD rats were divided into groups A and B. To induce theuremia model, all rats underwent right and 2/3 left kidney resection. 3M vetbond tissue adhesive was used in the group Afor hemostasis, while electric coagulation was used in group B. The amount of bleeding and the duration of left renal bloodflow blockage during operation were assessed. The postoperative survival rates of the two groups were compared. Thecreatinine values of all rats after operation were measured, and rats for which the creatinine value was two to three timeshigher than normal were further regarded as a uremic model. Kidney tissues were examined by pathology. Results Theserum creatinine after the application of both hemostatic method after 5/6 renal resection was 2-3 times higher than thenormal level. Left renal blood flow blockage of group A was (59. 97 ±7. 56) s and that of group B was (174. 1±15. 28) s( P <0. 05). The blood loss of the group A during left renal resection was (0. 11±0. 037) mL, and that of group B was(0. 24 ±0. 056) mL ( P <0. 05). Pathology of renal tissues in both groups indicated glomerular ischemic shrinkage andtubular interstitial fibrosis. The postoperative survival rate of group A was significantly higher than that of the group B ( P <0. 05). Conclusions 3M vetbond tissue adhesive is more effective than electrocoagulation to shorten the bleeding time,decrease the bleeding amount, or increase the postoperative survival rate.

Abstract:Objective To investigate the effect of astragaloside IV on the apoptosis of HT22 cells after oxygen andglucose deprivation/ reoxygenation. Methods HT22 cells in the logarithmic growth phase were randomly divided into fourgroups: Control, Model, AS-IV, and DMSO. In addition to the Control group, cells in other groups were reoxygenated after6 h of oxygen and glucose deprivation. Cell morphology was observed using an inverted microscope, the CCK-8 method wasused to test the cell survival rate, the LDH assay was performed to detect cell damage, and Bax/ Bcl-2 immunofluorescenceand flow cytometry was used to detect apoptosis. Results HT22 cells in the control group were bipolar or multipolar, withobvious synapses, multiple synapses being woven into a network, and strong cell refractivity. Meanwhile, in the modelgroup, the axons of the cell bodies decreased, the cells shrank and became rounded, the cytoplasm agglutinated, and thenumber of intercellular connections decreased. However, the cell injury in the AS-IV group was significantly alleviatedcompared with that in the model group. Compared with the findings in the control, cell viability was significantly reduced,LDH leakage was significantly increased, and the Bax/ Bcl-2 ratio and apoptosis rate were significantly increased in themodel group ( P < 0. 05). Compared with the model group, cell viability was significantly increased and LDH leakage, Bax/Bcl-2 ratio, and the apoptosis rate were significantly decreased in the AS-IV group ( P < 0. 05). There were no significantdifferences between the DMSO group and the model group. Conclusions Astragaloside IV may exert protective effect on OGD/ R HT22 cells by inhibiting apoptosis.

Abstract:Objective To investigate the effects of different doses of ovalbumin (OVA) on the serum levels ofIgE, IL-4, and IFN-γ, on the number of eosinophils (EOS) in bronchoalveolar lavage fluid (BALF), and on lunghistopathology in the BALB/ c mice with bronchial asthma, to determine the optimal OVA dose. Methods BALB/ c micewere randomly divided into a normal group, model 1 group (OVA 20 μg), model 2 group (OVA 50 μg), model 3 group(OVA 100 μg), and dexamethasone acetate group (OVA 100 μg). In addition to the normal group, the other groups ofmice were sensitized by intraperitoneal injection of the corresponding doses of OVA, and stimulated by 1% OVA atomizationto establish bronchial asthma models. The serum levels of IgE, IL-4, and IFN-γ were determined by ELISA. The number ofEOS in BALF was calculated by Wright staining, and the pathological changes of lung tissue were observed by HE staining.Results Compared with the normal group, the serum levels of IgE, IL-4, and IFN-γ and EOS in BALF were significantlyincreased in all groups ( P <0. 05). Inflammatory cell infiltration, bronchial epithelial cell degeneration, bronchial smoothmuscle cell hyperplasia, and other pathological changes were observed in the lung tissues. Especially, in the OVA 50 μggroup, the changes in the IgE, IL-4, and IFN-γ levels and lung histopathological changes were more pronounced. Conclusions All the three doses of OVA can induce asthma in BALB/ c mice successfully, and the asthma model inducedby 50 μg of OVA had more pronounced alterations. It is recommended that 50 μg of OVA be used as the appropriate dosage for establishing an asthma model in BALB/ c mice.

Abstract:Objective To investigate the effects of metformin, aerobic exercise alone or in combination on thevascular oxidative stress in type 2 diabetic rats. Methods Rat models of type 2 diabetes were established by feeding ahigh-fat diet combined with low dose streptozotocin (STZ). Rats were assigned into five groups: normal control (NC),diabetes control (DC), diabetes swimming (DS), diabetes metformin (DM), and diabetes metformin plus swimming(DMS). After undergoing the respective interventions for 8 weeks, indicators of vascular morphology, protein expression inthe vascular tissue, and serum indicators were tested by histopathology using HE staining, western blotting, and ELISA.Results All the DS, DM, and DMS groups showed decrease to different degrees in fasting blood glucose and insulinlevels. Compared with the DC group, the DS, DM, and DMS groups exhibited significant increases in the protein expressionof Nrf2 and HO-1, and exhibited a clear decrease in the expression of NOX4. The activities of SOD in the DS and DMSgroups were higher than in the DC group. MDA levels in the DM and DMS groups were lower than in the DC group. Theconcentrations of TNF-α and VCAM-1 were decreased to varying degrees in the DS, DM, and DMS groups. Conclusions Metformin and aerobic exercise may relieve vascular oxidative stress in type 2 diabetic rats, by regulating the balance between Nrf2 and NOX4.

Abstract:Objective To investigate the neuroprotective effects of artesunate on experimental autoimmuneencephalomyelitis (EAE) and on autophagy in mice. Methods Forty-eight female C57BL/6 mice were randomly dividedinto four groups: control group, model group, and artesunate low- and high-dose groups, with 12 mice in each group. TheEAE model was induced by MOG35-55 peptide. The mice in the low- and high-dose groups were intraperitoneally injectedwith artesunate (10 or 50 mg/ (kg·d)) for 10 consecutive days. The symptoms of the mice in each group were observed.Demyelination lesions in the brain tissues were observed by luxol fast blue (LFB) staining. The expression levels ofautophagy protein markers LC3-I and LC3-II were detected through western blot analysis. Results ①The mice in thecontrol group did not develop neurological symptoms. The mice in the model group and artesunate groups developed tovarying degrees of gait instability, hindlimb weakness, and paralysis. Compared with the model group, the latent period andpeak period were delayed and neurofunctional deficiency scores were decreased in the artesunate groups. The effects in thehigh-dose group were more pronounced than those in the low-dose group ( P < 0. 05). There was no significant difference inpeak period between the low- and high-dose artesunate groups ( P > 0. 05). ② LFB staining showed that the myelin sheathof brain tissue in the model group was loose, disordered, and had low staining intensity, while these findings were improvedin the artesunate groups. ③ Western blot analysis showed that the optical density values of LC3-I, LC3-II, and LC3-II/LC3-I in the model group were higher than those in the control group ( P < 0. 01). These values were lower in the artesunategroups than in the model group ( P < 0. 01), and the findings in the high-dose artesunate group were more pronounced thanthose in the low-dose artesunate group ( P < 0. 05). Conclusions Artesunate has neuroprotective effects on EAE mice andcan reduce demyelination in brain tissue. The mechanism involved may be related to the alleviation of autophagy by downregulation of LC3-I, LC3-II, and LC3-II/ LC3-I expressions.

Abstract:Objective To investigate the prevalence of bovine coronavirus (BCV) in bovine herds and bovinederivedbioproducts. Methods A fluorescent quantitative PCR (FQ-PCR) method for BCV was developed based on a pairof primers and a TaqMan probe, in accordance with the published sequence of BCV. Results The assay could specificallydetect BCV and had good sensitivity, with a limit of detection of 40 copies. The FQ-PCR method achieved a good linearrelationship within the template concentration range from 10³to 10⁷copies/ μL, with a correlation of 0. 999. Theamplification efficiency of the assay was 96. 195%. A total of 64 bovine rectal swabs and 33 bovine-derived bioproducts weresubjected to the FQ-PCR assay, and the positivity rates were 1. 5% and 6%, respectively. The positive sample wasamplified with another pair of primers for the N gene. Conclusions The results of this study demonstrated that the PCRproduct had 99% similarity to BCV, suggesting the existence of a BCV epidemic in bovine herds and the potential risk of BCV contamination in bovine-derived bioproducts.

Abstract:Objective To investigate the mechanism of expression of the chemokine CCL22 in human normal liverLO2 cells after infected with hepatitis B virus(HBV). Methods LO2 cells were first infected with HBV virus and theexpression of IL-32 was detected by ELISA. Then, exogenous human recombinant IL-32 protein was used to stimulatehuman acute leukemia cell line THP-1 or HEB and THP-1 cells co-cultured with HBV, and TNF-α expression was detectedby ELISA. Second, exogenous human recombinant TNF-α protein was applied for stimulation or co-cultured LO2 and THP-1 cells were infected with HBV. LO2 cells were used to detect the phosphorylation of CREB protein by western blotting withspecific antibody and to detect the expression of the chemokine CCL22 by ELISA. Results HBV induced IL-32 expressionin LO2 cells ( P < 0. 05),and virus-induced IL-32 in turn induced the secretion of TNF-α by THP-1 cells ( P < 0. 05).TNF-α induced activation of the CREB pathway in LO2 cells. This activation then promoted the expression of the chemokineCCL22 in LO2 cells ( P < 0. 05). Conclusions LO2 cells co-cultured under conditions of HBV infection and in thepresence of THP-1 can express CCL22. The mechanism behind this may involve HBV inducing IL-2 expression in LO2cells, and then IL-32 induces the secretion of TNF-α by THP-1 cells, after which TNF-α promotes the HBV-infection. LO2 cells to express chemokine CCL22.

Abstract:Objective To study the protective effect and mechanism of action of sevoflurane on the acute lunginjury in rabbits with one-lung ventilation. Methods Thirty-six rabbits were randomly divided into three groups: shamoperationgroup, one-lung ventilation group, and one-lung ventilation + sevoflurane group. The sevoflurane concentration inthe one-lung ventilation + sevoflurane group was varied to create several subgroups. The level of arachidonic acid in lungtissue of rabbits was determined by ELISA, and the W/ D value of lung was measured. The morphological changes of lungtissue were examined pathology. The expression levels of Clara cell secretory protein ( CCSP ) and cytoplasmicphospholipase A₂ (C-PLA₂) mRNA in the lung tissue were determined by RT-qPCR. The expression levels of CCSP andC-PLA₂ protein in lung tissue were detected by western blotting. Results The level of arachidonic acid, the degree of lunginjury, and the expression of C-PLA₂ protein and mRNA in the lung tissue of the one-lung ventilation group weresignificantly higher than those of the sham operation group ( P < 0. 05), while the expression levels of CCSP protein andmRNA were significantly lower ( P < 0. 05). Arachidonic acid, lung injury, C-PLA₂ protein, and mRNA expression in thelung tissue of rabbits in the one-lung ventilation + sevoflurane group were lower than those in the one-lung ventilation group( P < 0. 05), while CCSP protein and mRNA expression levels were increased. The level of arachidonic acid, the degree oflung injury, and the expression of C-PLA₂ protein and mRNA in lung tissue of the one-lung ventilation + sevoflurane groupwere decreased with increasing sevoflurane concentration ( P < 0. 05), but there were no significant differences in theexpression of CCSP protein and mRNA. Conclusions The protective mechanism of sevoflurane against lung injury inducedby one-lung ventilation may be related to downregulation of the C-PLA₂ pathway and reduction of arachidonic acid production in the lung tissue.

Abstract:Objective To study the effects of methylene blue and sevoflurane on oxidative stress indexes andinflammatory factors in serum and lung tissue in rats with lung ischemia-reperfusion injury. Methods Sixty male Sprague-Dawley rats were divided into four groups according to random number table, sham operation group (blank control group),lung ischemia-reperfusion group ( IR control group), methylene blue pretreatment group ( MB group), sevofluranepretreatment group (S group), 15 in each group. After establishing a model of lung ischemia-reperfusion injury, the ratswere treated respectively, and interleukin-1β (IL-1β) and interleukin-6 (IL-6) were detected in serum and lung tissues.Inflammatory markers such as tumor necrosis factor-α ( TNF-α) and oxidative stress indicators such as superoxidedismutase (SOD), malondialdehyde (MDA), reactive oxygen species (ROS), and adenosine triphosphate (ATP),hemorheology and the effects of lung wet weight and dry weight were assessed. Results The lung wet/ dry mass ratios inthe MB and S groups were significantly higher than that in the sham operation group and significantly lower than that in theIR group ( P < 0. 05). There was no significant difference in wet/ dry weight ratios between the MB group and the S group( P > 0. 05). The levels of SOD and ATP in the MB and S groups were significantly lower than those in the sham operationgroup and significantly higher than those in the IR group, while MDA and ROS were significantly higher than those in thesham operation group and significantly lower than those in the IR group, all showed statistical significance ( P < 0. 05).There was no significant difference in the indexes of oxidative stress in the MB and S groups ( P > 0. 05). The inflammatoryindex levels of lung tissue and serum in the MB and S groups were significantly higher than those in the sham operationgroup and significantly lower than those in the IR group ( P < 0. 05). There was no significant difference in inflammatoryindex levels between the MB and S groups ( P > 0. 05). The erythrocyte deformation index, erythrocyte aggregation index,and plasma viscosity in the MB group and S group at the T1 and T2 phases were lower than those in the T0 phase, andthose in the MB group at the T1 and T2 phases were lower than those in the S group ( P < 0. 05). Conclusions Methyleneblue and sevoflurane can improve the index of oxidative stress in the lung tissue, reduce the level of inflammatory factors inthe serum and lung tissue, and improve the edematous state in IR injury rats. However, methylene blue can decrease the blood viscosity more significantly, which can effectively reduce the risk of thrombosis.

Abstract:Objective To study the safety of the Chang Wei Ning Capsule and to provide a reference for clinicalapplication. Methods Forty mice (males and females) were randomly divided into a Chang Wei Ning Capsule group and anormal control group, each containing twenty mice. Mice of the test group received 32 g/ kg body weight Chang Wei NingCapsule, while those of the control group received the same volume of pure water. A detailed observation of the mice,including examination of viscera morphology by naked eye, was conducted until day 14 post-drug administration. Onehundred and twenty rats (males and females) were randomly divided into a normal control group and three different ChangWei Ning Capsule dosage groups (9, 3, 1 g/ kg bodyweight). The rats received consecutive intragastric administrations ofChang Wei Ning Capsule over a 13-week period. In addition to observing the general condition of the animals, body weight,blood, hepatic function and renal function measurements, and a histopathology analysis, were performed after the 13 weektreatment duration and at four weeks-post drug withdrawal. Results No toxic reaction was observed in mice that receivedintragastric administrations of Chang Wei Ning Capsule (32 g/ kg). No abnormal reaction was also observed in the rats of alldosage groups that received intragastric Chang Wei Ning Capsule over a 13-week period. Conclusions The maximumadministered dose of Chang Wei Ning capsule in mice was 32 g/ kg body weight in a single-dose toxicity test. No observed adverse effects were observed in rats receiving up to 9 g/ kg drug per day in repeated-dose toxicity tests.

Abstract:Objective To establish an enzyme-linked immunosorbent assay (ELISA) method for detectingantibody to feline panleukopenia virus (FPV) and apply this method for FPV antibody detection in cats. Methods TheFPV antigen was raised in CRFK cells and purified by ultracentrifugation. The purified FPV antigens were coated inmicrotiter plates and goat anti-cat IgG-HRP was used as the detection antibody. After a series of experiments on theoptimization of reaction conditions, the ELISA method was established. Experiments were carried out to evaluate thesensitivity, specificity, repeatability and stability. Results The optimal working densities of the purified FPV antigens andthe enzyme-labeled antibody were 5 μg/ mL and 1∶6000, respectively. The inter-assay and intra-assay average coefficientsof variation were 8. 68% and 7. 14%, respectively. The detection sensitivity was more than 1 ∶5000. There was no crossreactionwith feline herpesvirus type 1 (FHV-1) and feline calicivirus (FCV). Compared with the results of the ELISA kitfrom the European Veterinary Laboratory (EVL), the concordance between the two methods was 90. 7%. Conclusions The established ELISA method exhibites satisfactory duplication, stability, specificity, and sensitivity. This method can be used for the antibody detection of FPV in cats.

Abstract:Objective In this study, the ¹¹¹In-labeled bleomycin complex (¹¹¹ In-BLMC) was used as a Single-Photon Emission Computed Tomography (SPECT)-tracking agent to differentiate the high-grade and low-grade gliomas innude mice. Methods Thirty-four nude mice with gliomas,induding 22 high-grade and 12 low-grade gliomas,were used inthis study.SPECT was performed 10 min after the injection of ¹¹¹In-BLMC to the mice. Semi-quantitative analysis by imagingwas performed at the early and delayed phases. The ¹¹¹In-BLMC early- and delayed-phase uptake indexes and retentionindexes were obtained. Results All SPECTs were positive for ¹¹¹In-BLMC markers. In the high-grade glioma group, theearly- and delayed-phase ¹¹¹In-BLMC uptake indexes and retention indexes were (3. 47± 1. 66) and (5. 193± 1. 49),respectively. In the low-grade glioma group, the mid-, early-, and delayed-phase ¹¹¹In-BLMC uptake indexes and retentionindexes were (1. 59±1. 68) and (2. 99±1. 36), respectively, both differences were statistically significant ( P < 0. 01).When the intake index was < 1. 898, the sensitivity of diagnosis of low-grade glioma was 66. 67% and the specificity was85. 71% ( P < 0. 01); when the retention index was < 3. 155, the sensitivity of diagnosis of low-grade glioma was58. 33%,and the specificity was 63. 66% ( P < 0. 01). Conclusions ¹¹¹In-BLMC-labeled glioma SPECT can provide somehelp for preoperative tumor grading. The uptake index and the retention index enable a relatively accurate judgment of the degree of malignancy of gliomas.

Abstract:Objective To determine the main components of SPF golden hamster milk and compare them withcow milk, human milk, and infant formula milk. Methods Sixty female lactating homsters (1~10 days) were selectedand separated from their offspring for more than 4 h. The milk of the female homsters was collected by an artificial lactationmethod and preserved by freezing. The milk was collected every other day; 2 ml of milk was obtained on average from eachfemale. Testing of the milk composition was performed in accordance with the Chinese National Standards. Results Goldenhamster milk water content was 86. 9 g/100 g, crude protein 6. 95 g/100 g, crude fat 2. 4 g/100 g, lactose 2. 61 g/100 g,and ash 0. 83 g/100 g, with pH 6. 61. Its water content was close to that of cow’s milk and human milk, while its proteincontent was higher. The protein of golden hamster milk is higher than milk?Human milk and infant formula..The fat ofgolden hamster milk is lower than cow’s milk,human milk and infant formula..The lactose of golden hamster milk is lowerthan cow’s milk,human milk and infant formula. Conclusions The main features of golden hamster milk are high protein,low fat, and low sugar, which can provide the basis for the artificial lactation and formulation of sterile golden hamster milk.

Abstract:Genetic quality control of laboratory animals is important for laboratory animal production, scientificresearch, and the biomedical industry. However, problems with the genetic quality of laboratory animals have continued fora long time, because it has hysteresis and concealment. The major professional groups working with laboratory animals areanimal experimenters, supervisors, and administrators. Based on the possible problems with genetic quality in theproduction of and experiments on laboratory animals, combined with practical experience of animal management and animalexperiments for scientific research, this paper analyzes the possible causes of these problems, and provides advice andsolutions for these to be applied, during the training of professionals and the teaching of medical students. Througheducation, theoretical explanations, and examples in the training and teaching processes, as well as strengthening theunderstanding of the importance of genetic quality control among professionals, the aim is to guarantee the genetic quality oflaboratory animals and improve the authenticity and accuracy of animal experiments. This paper also provides a reference for non-technical personnel to discover, analyze and solve the genetic quality of experimental animals.

Abstract:Bronchiolitis obliterans (BO) is a clinical syndrome characterized by chronic obstruction of thebronchioles. Pathologically, BO is characterized by partial or complete occlusion of the bronchioles. Pathological typesinclude constrictive bronchiolitis and proliferative bronchiolitis. Ideal animal models have contributed to characterizing thepathogenesis of BO and exploring new therapeutic schedules. Animal models of BO have been established by differentmethods. These models each have their own advantages and limitations. This article reviews the recent progress in research on animals models of nontransplant BO.

Abstract:Single-nucleotide polymorphism (SNP) markers are genetic markers in which a single nucleotidevariation occurs at a specific position in the genome. Characterized by their high abundance, density, and easy genotyping,SNP markers have been widely used in animal and plant breeding, as disease resistance markers, and for the screening ofheterosis and identification of disease-related genes. In the present paper, we first present the application of SNP arrays foranalyzing animal population genetic structure, genetic mapping, and for characterizing marker-assisted selection, kinship,and heterosis. Second, we describe the relationship between SNP loci and animal models of human diseases, which canprovide a valuable reference for the improved application of SNP molecular marker technology in animal genetic breeding,and the establishment and genetic analysis of animal models of human diseases.

Abstract:Graves’ disease (GD), the most common clinical type of hyperthyroidism, is a common organ-specificautoimmune disease. Although its etiology involves genetic and environmental factors, the exact pathogenesis of GD remainsunclear. Extensive genome-wide association studies ( GWAS) have identified various genes that contribute to thedevelopment of GD. This article reviews progress in our identification of susceptibility genes for GD, and provides a preliminary discussion on the genetic mechanism that promote GD onset.