Abstract:Objective To observe the effect of astragaloside IV on inflammatory factors and ultrastructure in rats with cerebral ischemia reperfusion. Methods A cerebral ischemia reperfusion injury model was established in Sprague- Dawley (SD) rats by middle cerebral artery occlusion. Forty male SD rats were randomly divided into a sham operation group, model group (cerebral ischemia reperfusion injury group), astragaloside IV group and nimodipine group ( positive drug group). All groups except the sham operation group were reperfused for 24 hours after 2 hours of cerebral ischemia. In the treatment groups, astragaloside IV and nimodipine were respectively injected intraperitoneally one week before model establishment. The Zea Longa scoring method was used to detect neurological deficits of rats in each group. TTC staining was used to detect the volume of cerebral infarction. The ELISA method was used to detect the inflammatory factor levels in brain tissue, including tumor necrosis factoR-α ( TNF-α), interleukin - 6 ( IL-6) and interleukin - 1β ( IL-1β). Nissl staining was used to observe neuronal damage in the cerebral cortex. Transmission electron microscopy was used to observe the ultrastructural changes of neurons in the cerebral cortex. Results In the sham operation group, no neurological deficits or cerebral infarction was observed, and abundant nerve cells and Nissl bodies were present. The cells were arranged neatly, and the ultrastructure was clear and normal. Compared with the sham operation group, neurological impairment was more serious in the model group. The cerebral infarction volume was significantly increased (P<0. 05). The inflammatory factor content (TNF-α, IL-6 and IL-1β) was increased (P<0. 05). The cells had a disorderly arrangement, the nuclei were deformed and showed pyknosis, and the chromatin was unevenly distributed. Compared with the model group, the neurological function of rats in astragaloside IV and nimodipine groups was improved, the cerebral infarction volume was decreased (P<0. 05), the TNF-α, IL-6 and IL-1β content was significantly decreased (P<0. 05), the cell arrangement was more orderly, the cell nucleus was regular, and the chromatin distribution was more uniform. Conclusions Astragaloside IV can inhibit cerebral ischemia reperfusion injury and improve the ultrastructural changes of nerve cells in rats. Its mechanism may be related to alleviation of the inflammatory reaction.

Abstract:Objective To investigate the effect of Siwuyin on the migration and invasion of esophageal cancer cells and explore the molecular mechanisms of this effect. Methods Different concentrations (600 μg / mL, 300 μg / mL, 150 μg / mL, 70 μg / mL, and 30 μg / mL) of Siwuyin were applied to the human esophageal cancer cell line Eca109. The blank control group did not undergo any treatment. IncuCyte software was used to evaluate the scratch closure rate and to screen the effective concentration and intervention time of Siwuyin. The effect of Siwuyin on cell invasion was observed using a transwell system, while laser confocal microscopy was used to observe the effect of Siwuyin on the cytoskeleton of microfilaments. In addition, RNA-Seq sequencing and information analyses were used to determine the effect of Siwuyin on RNA in esophageal cancer cells. Results The scratch assay result demonstrated that when the concentration of Siwuyin was 150 μg / mL, cell migration ability was significantly inhibited ( P < 0. 05). Results from the transwell experiments revealed that Siwuyin significantly inhibited the invasion of esophageal cancer cells ( P< 0. 05). Furthermore, laser confocal microscopy demonstrated that Siwuyin significantly inhibited the epithelial-mesenchymal transition of esophageal cancer cells. Finally, RNA-Seq analysis revealed that Siwuyin altered the metabolic pathways of alanine, aspartic acid, and glutamate in esophageal cancer cells, and this effect mainly inhibited the production of fumaric acid. Conclusions Siwuyin can significantly inhibit the migration and invasion of esophageal cancer cells and inhibits the accumulation of fumarate.

Abstract:Objective To observe the survival and liver differentiation of Green Fluorescent Protein ( GFP) labeled human umbilical cord mesenchymal stem cells ( GFP-hUCMSCs ) in SD rats during the embryonic stage, to investigate the feasibility of establishing a human-rat chimeric liver in the embryonic stage of rats. Methods Lentiviral containing GFP gene was used to transfect and to label human umbilical cord mesenchymal stem cells, and then GFP- hUCMSCs were injected into the experimental group rat embryos. After embryonic rats birth, the Frozen liver sections were used, and the migration and distribution of the GFP-hUCMSCs were observed in the liver tissue. While the expression of human-related proteins in the rat liver were detected by immunohistochemical method . The control group was injected with an equal volume of normal saline. Results GFP signal were detected in liver tissue from the experimental group at 45 d,75 d, and 120 d after birth. Correspondingly, expression of the human hepatocyte-related proteins ALB, HNF3β, and HNF4α was detected in the liver tissue, but these proteins content at 120 d was extremely small, and partly not detected. The control group was negative. Conclusions In embryonic rats injected with hUCMSCs, the presence of GFP signal and the expression of the human hepatocyte-related proteins ALB, HNF3β, and HNF4α can be detected in the liver at 75 d after birth, and gradually decrease over time.

Abstract:Objective To investigate the function of interferon-induced transmembrane protein 3 ( IFITM3) and determine the mechanism by which IFITM3 restricts viruses in African green monkeys (AGMs), IFITM3 was cloned from organs of AGMs, and IFITM3 cDNA and protein expression levels was analyzed. Methods RT-PCR was employed to clone the full-length cDNA from the heart, lung, liver, kidney, brain, lymphoid system, and skin. IFITM3 gene expression was analyzed in different organs by RT-PCR, and data were calculated with DNAman software. Additionally, the location of IFITM3 protein was investigated using pathology and immunohistochemistry assays. Results The IFITM3 gene was found in several cells and organs, including lymphocytes, skin, heart, brain, liver, kidney, lung and spleen. The IFITM3 cDNA was almost 440 bp (442~ 448 bp) and shared 93% homogeneity with Macaca mulatta. Predictive analysis of the IFITM3 protein of AGMs indicated that the protein contained five transmembrane domains and several highly conserved specific sites. The highest expression of the IFITM3 gene was observed in the spleen, and the lowest expression level was found in the brain according to RT-PCR detection. However, a high level of IFITM3 protein was found in the spleen and lymphocytes in immunohistochemistry experiments. Conclusions Based on the comprehensive expression of IFITM3 in AGM organs, especially in the spleen and lymphocytes, IFITM3 may be involved in the immunological response of AGMs and may have an important anti-viral function

Abstract:Objective To investigate the therapeutic effect of tacrolimus on spinal cord injury rats and its regulation of the NF-κB/ JNK pathway. Methods Rats were randomly divided into three groups ( n = 15): sham group, model group and tacrolimus administration group. The animal model of spinal cord injury was established by Allen’ s method. The rats were given tacrolimus (0. 3 mg / kg) once a day for 21 days. Basso, Beattie and Bresnahan (BBB) scores were tested on days 0, 1, 7, 14 and 21. Hematoxylin and eosin staining was used to observe the state of spinal cord injury in rats; SOD, CAT, and GPX activity and MDA content in spinal cord tissue were measured by a kit; IL-4 and TGF-beta expression in spinal cord tissue was measured by RT-PCR; NF-κB p-p65, NF-κB p-p65, JNK and p-JNK protein expression was measured in spinal cord tissue by western blots. Results Tacrolimus could significantly improve the BBB score of spinal cord injury rats (P < 0. 05), increase SOD, CAT, GPX activity, decrease MDA content, reduce abnormal apoptosis of spinal cord neurons, and decrease the expression of IL-4 and TGF-beta and the NF-κB, p-p65 and p-JNK/ JNK protein ratios. Conclusions Tacrolimus can significantly improve spinal cord injury, and the mechanism may be related to its anti-oxidative, anti-inflammatory response, and anti-apoptosis activities in spinal cord neurons and inhibition of NF-κB/ JNK signaling pathway activation.

Abstract:Objective To investigate the effect and mechanisms of PM2. 5 on atherosclerotic plaques in ApoE- knockout mice. Methods Thirty-two 8-week-old male ApoE^{- / -} mice were divided into two groups, both fed with a high-fat diet: a control group that was treated with normal saline by intratracheal instillation, and an experimental group that was exposed to PM2. 5 (30 mg / kg body weight) saline suspension by intratracheal instillation. We measured PM2. 5 in whole blood using inductively coupled plasma mass spectrometry (ICP-MS), and measured lipids and inflammatory factors using standard method . Echocardiography was used to evaluate cardiac function. The whole descending arteries were stained with Oil Red O, aortic roots were stained with Movat, and descending arteries were investigated using quantitative PCR. Results In the PM2. 5 group,We observed elevated heavy metal components (P < 0.05),but there was no significant change in heart function(P > 0.05),blood glucose and lipid levels(P > 0.05).We also observed elevated serum inflammatory factor levels (P < 0.05). In addition, the PM2. 5 group had larger atherosclerotic plaques (P < 0. 05), elevated levels of the inflammatory factors IL-6, TNF-α, and Lp-PLA2, and elevated levels of the NADPH oxidase subunits p22phox and p47phox (P < 0. 05). Conclusions In ApoE^{- / -} mice, PM2. 5 exposure is associated with increased inflammatory factors and oxidative stress, thus contributing to the progression of atherosclerosis.

Abstract:Objective To investigate the effect of rapamycin on cardiac damage in remote organs after renal ischemia reperfusion (RIR) in rats. Methods A total of 40 rats were randomly divided into four groups: blank group, sham operation group, RIR group and rapamycin treatment group, with 10 rats in each group. Rats in the rapamycin treatment group received gastric administration of rapamycin. Each group of rats was sacrificed 24 hours after surgery, and blood, spleen tissue and heart tissue were collected. The creatine kinase (CK), creatine kinase isoenzyme (CK-MB), serum creatinine (SCr) and blood urea nitrogen (BUN) levels were measured. Semi-quantitative analysis with PAS staining indicated pathological damage to the heart. A TUNEL kit was used to detect apoptosis. The percentage of NKT cells was measured by flow cytometry. The expression levels of CXC chemokine ligand 10 (CXCL10), hypoxia-inducible factoR-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were detected by RT-qPCR. Results The BUN and SCr levels were higher in the RIR group than in the sham group. The serum CK and CK-MB levels were lower in the rapamycin treatment group than in the model group. Semi-quantitative scoring of cardiac pathological lesions showed that the pathological damage score of the rapamycin treatment group was significantly lower than that of the RIR group. The percentage of NKT cells in the heart and peripheral blood was significantly higher in the rapamycin treatment group than in the RIR group. The percentage of spleen NKT cells was lower in the rapamycin treatment group than in the RIR group. The expression of HIF-1α mRNA and VEGF mRNA was lower in the rapamycin treatment group than in the RIR group. The expression level of CXCL10 mRNA was higher in the rapamycin treatment group than in the RIR group. Conclusions Rapamycin can significantly up-regulate the expression level of CXCL10 and promote the migration of NKT cells from the spleen to peripheral blood and the heart. Rapamycin also inhibits HIF-1α expression levels and protects the heart after RIR.

Abstract:Objective To investigate the microbial composition of different intestinal segments of wild and captive tree shrews. Methods Seven samples of gastrointestinal segments of three healthy wild and captive tree shrews were collected to extract total bacterial DNA and adopt high-throughput sequencing technology. The V3-V4 hypervariable region of the 16SrRNA gene was sequenced, and the structure and diversity of the flora were analyzed. Results The diversity of the alpha index in different intestinal segments revealed significant differences between the wild and captive groups in the cecal and stomach segments (P< 0. 05). The microbial compositions of the intestines in the wild and captive groups were significantly different. At the gate level, the average proportion of Firmicutes in the rectum, colon, cecum, and stomach of the wild group was significantly higher than that of the captive group (P< 0. 05). In contrast, the average proportion of Spirochetes in the rectum, colon, cecum, and ileum of the captive group was significantly higher than that of the wild group (P< 0. 05). The average proportion of Bacteroidetes in the rectum was significantly higher in the wild group than in the captive group (P < 0. 05). At the genus level, the intestinal diversity of the wild group was significantly higher than the main genus of the captive group: the Weissella genus in the ileum, jejunum, and stomach; Bacteroides in the rectum; and Lactococcus in the ileum. The main breeding genus of the captive group was significantly higher than that of the wild group: Brachyspira in the rectum, colon, cecum, and ileum; Prevotella_9 in the cecum and stomach; Streptococcus in the cecum and jejunum; and Lactobacillus in the ileum. The functional gene prediction of the different intestinal segments revealed statistically significant differences among the 17 gene types in the wild and captive groups (P< 0. 05). Conclusions The intestinal flora composition in the intestines of wild and captive tree shrews is quite different. The bacterial function of each intestine is different, and is related to its physiological function and dietary structure. When studying intestinal flora, it is therefore necessary to consider whether the composition of the microbial sample microorganisms fully represents the composition of the gut microbes.

Abstract:Objective Myocardial ischemia caused by coronary atherosclerotic cardiopathy is a serious disease that can cause death. This study describes the effects of ursolic acid on autophagy and apoptosis caused by serum deprivation of cardiomyocytes at the cellular level. Methods Rat H9c2 cardiomyocytes were cultured in vitro. The cells were divided into the control group, serum deprivation group, ursolic acid treatment group, autophagy inhibitor 3- methyladenine (3-MA) pretreatment combined with ursolic acid group, and rapamycin pretreatment combined with ursolic acid group. Apoptosis was detected using flow cytometry. Expression of the autophagy-related proteins LC3, Beclin1, and ATG5, and the apoptosis-related proteins cleaved-caspase3, BcL-2, and Bax, were detected by western blotting. Results 10 μM ursolic acid was the optimal concentration for H9c2 cells. Serum deprivation increased the expression of Beclin1 and ATG5 as well as the ratio of LC3II/ I in H9c2 cells (P< 0. 01), and these levels decreased after ursolic acid treatment (P< 0. 05). Serum deprivation caused an increase in the apoptosis rate of H9c2 cells (P< 0. 001), and ursolic acid treatment reduced the rate of apoptosis (P< 0. 01). The 3-MA pretreatment group had a further reduced apoptosis rate (P< 0. 001), while the rapamycin pretreatment group had an increased apoptosis rate (P< 0. 001). Serum deprivation increased the expression of cleaved-caspase3 and the ratio of Bax / BcL-2 ( P < 0. 001). Following treatment with ursolic acid, the expression of cleaved-caspase3 and the ratio of Bax / BcL-2 was decreased (P< 0. 01), and pretreatment with 3-MA further reduced the expression of cleaved-caspase3 and the ratio of Bax / BcL-2 (P< 0. 001). The ratio of Bax / BcL-2 was increased in the rapamycin pretreatment group (P< 0. 05). Conclusions The anti-apoptotic effect of ursolic acid on serum-deprived H9c2 cells is related to the inhibition of autophagy.

Abstract:Objective To investigate the effects of carbon tetrachloride ( CCl4 )-induced acute liver injury on brown adipose tissue at different time points and to evaluate the related mechanisms. Methods Eighteen 8-week-old C57BL/ 6 male mice were randomly divided into a control group, CCl4 2-week group, and CCl4 4-week group, with 6 rats in each group.CCl4 group was injected with CCl4 twice, and the control group was given the same dose of olive oil. Brown adipose tissue was then weighed, and HE staining was used to observe pathological changes in the liver and brown adipose tissue. Immunohistochemistry and real-time quantitative PCR were used to detect the expression of uncoupling protein 1 (UCP1) in brown adipose tissue. The enzyme-linked immunosorbent assay (ELISA) method was used to evaluate levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-α(TNF-α) in serum. The Pearson method was used to test the relationship between Ucp1 mRNA levels and TNF-α content. Results Compared with the control group, the serum content of ALT and AST in the CCl4 2-week group were increased (P< 0. 01), the weight of brown adipose tissue in the CCl4 2-week group was decreased (P< 0. 05), the expression of UCP1 protein in brown adipose tissue in the CCl4 2-week group was decreased (P< 0. 05), the expression of Ucp1 mRNA in the CCl4 2-week group was decreased (P< 0. 05), and the serum content of TNF-α in the CCl4 2-week group was increased (P< 0. 001). Compared with the CCl4 2-week group, the serum content of ALT and AST in the CCl4 4-week group was decreased (P< 0. 05), the weight of brown adipose tissue in the CCl4 4-week group was increased (P< 0. 05), the expression of Ucp1 mRNA in the CCl4 4-week group was increased (P< 0. 01), and the serum content of TNF-α in the CCl4 4-week group was decreased (P < 0. 001). There was a significant negative correlation between Ucp1 mRNA levels and TNF-α content in the CCl4 2-week group and the CCl4 4-week group (r = -0. 950, P< 0. 01; r = -0. 859, P< 0. 05). Conclusions Acute liver injury can lead to the decrease of brown adipose tissue function and the decrease of body heat production, thus affecting the metabolic homeostasis. The mechanism may be related to increased TNF-α content.

Abstract:Objective To explore the role of vascular endothelial growth factor imbalance and abnormal complement immune activation in decidua and placenta formation during early pregnancy, and to clarify its relationship with preeclampsia. Methods Inbred BPH-5 mice were selected as preeclampsia model animals, and C57 mice were selected as control animals. The day of pregnancy was defined as day E0. 5 d. Tissues from uterine implantation sites were collected on day E5. 5 d and E7. 5 d, and placental tissues were collected from pregnant rats on day E10. 5 d. The following complement components were detected in the uterus and placenta by real-time quantitative PCR, immunohistochemistry, immunofluorescence and western blots: C3, C9, C1qa, and CfB. Additionally the expression of the following vascular endothelial growth factor (VEGF) family members was detected: VEGF, VEGFR1, VEGFR2, and sFlt-1. Results The expression of specific complement components in the uterus of BPH-5 mice was significantly increased on day E7. 5 d, during the peak period of decidualization, and the deposition of C3 and C9 was detected in the trophoblast giant cell layer of the placenta on day E10. 5 d, in the second trimester of pregnancy. On day E5. 5 d after implantation, VEGFa mRNA was significantly up-regulated, VEGFR1 and VEGFR2 mRNA levels were down-regulated, and the expression of VEGF protein was significantly increased in pregnant BPH-5 mice. The histopathological examination result showed that the decidual ratio of BPH-5 mice was significantly decreased on day E7. 5 d, and decidual angiogenesis was significantly inhibited after implantation. Conclusions In the pathogenesis of preeclampsia, the imbalance of VEGF occurs earlier than the increase in complement components at the maternal-fetal interface, and this change in maternal pregnancy precedes the occurrence of the placenta, which promotes the progression of maternal preeclampsia.

Abstract:Objective To investigate whether the protective mechanism by which intrathecal injection of dexmedetomidine improves neuromotor function in rats with spinal cord ischemia-reperfusion injury is based on the CXCR4-FAK signaling pathway. Methods Sixty SPF-grade SD male rats aged 10-12 weeks were randomly divided into four groups ( n = 15 per group): the sham group, model group, DHI group, and DPA group. The SCIRI model was constructed in the model, DHI, and DPA groups by opening the thoracic clipped aortic arch for 15 min. In the sham group, the thoracic free aortic arch was only opened, without clamping. After successful establishment of the model, each rat was fed in a single cage with conventional feed and a standard diet. The DHI and DPA groups were injected in the sheath 72 h before ischemia with DHI and Diprotin A, respectively, with a dose of 30 μL at a concentration of 5 μmol / L. The sham and model groups were injected with the same volume of normal saline, with a fixed point injection once daily for 3 consecutive days. On day 4 after modeling, the neuromotor function score, blood-spinal cord barrier structural integrity, water content, ultrastructural changes, apoptosis, oxidative stress response, and the expression levels of CXCR4 and p-FAK were detected using the improved Tarlov scoring method , Evans blue ( EB) staining, wet / dry weight method , electron microscopy, TUNEL staining, DCFH-DA staining kit, and western blot techniques, respectively. Results Compared with the sham group, the neuromotor function score and SOD activity of the model group were significantly decreased. In contrast, the water content of the spinal cord, EB red fluorescence intensity, apoptosis rate, ROS green fluorescence intensity, MDA content, and CXCR4 and pFAK expression levels were significantly increased. Compared with the model group, the neuromotor function score, SOD activity, and CXCR4 and pFAK expression levels in the spinal cord were significantly increased in the DHI and DPA groups. In contrast, the water content of the spinal cord, EB red fluorescence intensity, apoptosis rate, the green fluorescence intensity of ROS, and MDA content were significantly lower, and these differences were statistically significant (P< 0. 05). There were no significant differences between the DHI and DPA groups ( P> 0. 05). Conclusions The protective effect of dexmedetomidine on SCIRI rats may be caused by the activation of the CXCR4-FAK signaling pathway, thus reducing oxidative stress injury in cells, and playing a protective role in the spinal cord of SCIRI rats.

Abstract:Objective To study the regulatory effect and mechanism of silencing microRNA-16 on immune function in mice with pulmonary tuberculosis. Methods Forty CD2F1 female mice were divided into the control group, model group, overexpression group, and silent group (n = 10 per group). In the model group, overexpression group, and silent group, the pulmonary tuberculosis model was established. After successful modeling, the overexpression group and silent group were aseptically injected with 10 μL microRNA-16 lentivirus suspension. T lymphocyte subsets, thymus index, lung inflammatory factors and toll like receptor (TLRs) signaling pathway factors were detected in lung tissues. Results The levels of CD3+, CD4+, CD4+ / CD8+, thymus index and IL-10 in the overexpression group were lower than those in the model group, while the levels of CD8+, IL-6, TNF-α, TLR2, TLR4 and NF-κB in the overexpression group were higher than those in the model group (P < 0. 05).The levels of CD3+, CD4+, CD4+ / CD8+, thymus index and IL-10 in the silence group were higher than those in the model group, while the levels of CD8+, IL-6, TNF-α, TLR2, TLR4 and NF-κB in the silence group were lower than those in the model group (P < 0. 05).The levels of CD3+, CD4+, CD4+/ CD8+, thymus index and IL-10 in the silence group were higher than those in the over expression group, and the levels of CD8+, IL-6, TNF-α, TLR2, TLR4 and NF-κB were lower than those in the over expression group (P < 0. 05). Conclusions Silencing microRNA-16 may play a role in regulating the immune function in mice with tuberculosis, by acting on TLR signaling pathways and inhibiting abnormal expression of pathway factors, thus regulating the immune response and improving immune disorders.

Abstract:Objective To provide a multifunctional animal behavior experimental system based on open-source sharing protocol, which can be used to observe, train, and test the behavior of conditioned fear and active avoidance. Methods The system was composed of a box, a camera, a stimulus circuit, and control software, which can be used to record and quantitatively analyze the behavior of various experimental animals under unattended conditions. Results After the system was set up separately in two universities, typical animal behavior experiments, including conditioned fear and active avoidance, were tested using Sprague-Dawley rats. The data were statistically analyzed, and result demonstrated that both conditioned fear behavior and active avoidance behavior could be stably analyzed. Conclusions An open-source multifunctional animal behavior experimental system was successfully developed. The overall design of the system is open,from hardware to software, and is therefore feasible and scalable. This system should be extensively promoted to lower the threshold of experimental access, as well as to benefit all animal laboratory staff.

Abstract:Individual ventilation cages ( IVCs) are currently widely used in animal facilities. Maintaining the normal function and cleaning status of IVCs has thus become a crucial task, but it is difficult for facilities without large washing quipmentto thoroughly clean IVCs. This lack of thorough cleaning brings a risk of cross-contamination of facilities, and in turn may affect the health status of laboratory animals. In this article, the author introduces some useful method for keeping functional and clean IVCs.

Abstract:Objective To study method for testing the technical parameters of individually ventilated cages (IVCs) and evaluating the stability of IVC parameters. Methods In accordance with the method of GB 14925-2010 and DB32 / T 972 - 2006, IVCs that were placed in the conventional and barrier environments were tested respectively. Correlations between the micro- and macro-environments were analyzed. Two method for testing air changes per hour (ACH) were compared. The relative deviation ( based on 5 diagonal cages) of IVC and cage leakage rates were also calculated. Results The temperature and humidity of the micro-environment were positively correlated with those of the macro-environment. The ACH was significantly higher when tested using the method of GB 14925 - 2010 compared with using the flowmeter method . The relative deviations of ACH, noise, and airflow velocity were smaller than that of the hydrostatic pressure difference. Cage leakage rates were high, at 75%. Conclusions Use of IVCs was limited to the macro-environment. The hydrostatic pressure difference showed a low stability, which was correlated with cage leakage rates. The result of this study provide a reference for formulating national or trade standards.

Abstract:This paper examines a Good Laboratory Practice vivarium, and introduces a design for a cooling and heating source for air conditioning, a ventilation system, airflow distribution and an automatic control system. Through Computational Fluid Dynamics(CFD)simulation technology, the airflow distribution of the vivarium was optimized, and the result show that a ceiling air supply and corner exhaust with auxiliary top exhausts could help to reduce the indoor ammonia concentration. The demand-based variable air volume control mode of the vivarium is highlighted, reflecting the energy savings of the control mode. Finally, future concerns of HVAC design in vivariums are presented.

Abstract:Recent rapid developments in life sciences and biomedical engineering technology, as well as breakthroughs in gene editing technology, an increasing number of rat and mouse models have been established and widely applied in basic research, including oncology, infectious diseases and immunology research. Although the total amount of animal model resources is increasing constantly, there is no unifying standard nomenclature, which makes the management of model animals as well as international exchange and intellectual property protection difficult. This paper is based on the rules of the JAX laboratory in America and summarizes the nomenclature of common model animals ( rat and mouse) in detail. Examples of different types of models are given in order to establish nomenclature and rules that are in compliance with international norms and exchange.

Abstract:Hyperlipidemia is a type of disease involving lipid metabolism disorders. It is also the leading cause of cardiovascular and cerebrovascular diseases, such as coronary heart disease, cerebral infarction and atherosclerosis, which have become one of the most harmful chronic diseases to human health in the word. At present, the development of new, high-efficiency and low-toxicity target, lipid-lowering, hypolipidemic, traditional Chinese medicines is essential for improving hyperlipidemia and its secondary cardiovascular and cerebrovascular diseases. However, because of the complexity and compatibility of traditional Chinese medicine ingredients, it is difficult to conduct in-depth research on the effective components of the therapeutic effect and the specific lipid-lowering mechanism by relying on a single lipid-lowering model. Therefore, the establishment of an ideal high-fat model is a key factor in screening lipid-lowering Chinese medicines and studying the pathogenesis of hyperlipidemia. In this paper, several of the most commonly used lipid-lowering models were reviewed from three aspects: cell models, mammalian models and zebrafish models, and the common modeling method of various models and their respective advantages and disadvantages were summarized. As a result , this work provides references and an experimental basis for selecting reproducible hyperlipidemia models for hyperlipidemia mechanism research and screening of effective lipid-lowering traditional Chinese medicines.

Abstract:Cerebral stroke refers to the damage of brain function caused by ischemic or hemorrhagic lesions of cerebral blood vessels, which can occur for various reasons. In recent years, the number of cerebral stroke patients has increased year by year, and cerebral stroke seriously affects quality of life. Scavenger receptors ( SRs) are a group of scavenging receptors that exist on the surface of phagocytes and can recognize and eliminate pathogens. Recently, a number of studies have reported that SRs are related to cerebral stroke, and have demonstrated that SRs affect the occurrence, development, and prognosis of cerebral stroke by participating in processes such as inflammation, oxidative stress, atherosclerosis, and immunity. Here, we review the related research progress of SRs and cerebral stroke.

Abstract:Primary biliary cholangitis (PBC) is a chronic inflammatory cholestatic liver disease that is mediated by autoimmunity and is characterized by progressive intrahepatic small bile duct non-suppurative inflammation and the appearance of antimitochondrial autoantibodies. At present, the cause and mechanisms of PBC remain unknown, and there is no specific treatment for this disease. Research into the pathogenesis of PBC has therefore become an important target. One of the greatest difficulties in this research has been the establishment of an animal model that is similar to human PBC. This article briefly introduces several commonly used PBC mouse models, compares the advantages and disadvantages of each model, discusses the problems in the construction of PBC animal models, and provides a solid basis for the selection of a research model.

Abstract:Ulcerative colitis is a major type of inflammatory bowel disease. Its pathogenesis and treatment have become a focus of concern because of the increasing number of patients in recent years. A model of ulcerative colitis induced by dextran sodium sulfate has attracted much attention because it is the most similar model to human ulcerative colitis. This paper reviews research progress in recent years, mechanism and influencing factors of dextran sodium sulfate- induced ulcerative colitis animal models.