Abstract:Objective To examine the efficacy and safety (blood?brain barrier permeability) of right hemisphere cerebral perfusion imaging using transcranial ultrasound following skull thinning in the rat. Methods Forty?eight Sprague Dawley rats received local skull?thinning surgery for transcranial ultrasound perfusion imaging (with injection of 0. 15 mL SonoVueTM ). Perfusion findings were compared before and after the skull surgery in six rats, and the brains were examined by magnetic resonance imaging (n = 2) or Evans blue staining (n = 4). The skulls of the rats were also removed for pathological examination to measure the thickness of the remaining skull. Perfusion in the right hemisphere of the brain was analyzed in 48 rats with a time?intensity curve to obtain quantitative transcranial ultrasound perfusion imaging parameters. Results After the surgery, the ultrasound perfusion imaging of the right hemisphere was improved, with typical perfusion patterns including a rapid wash?in and wash?out, and slow clearance of the contrast enhancement. The average peak intensity(PI)value after skull thinning was almost three times higher than that before surgery [(9. 98 ±2. 35) dB vs (3. 24±1. 49) dB, respectively; P < 0. 01], while the time to peak (TTP) was unchanged [(4. 66 ± 0. 45) s vs (3. 86 ±1. 43) s, respectively; P > 0. 01]. The thickness of the thinned skull after grinding was approximately (66.1 ± 11.4)μm. Evans blue staining and magnetic resonance imaging showed no observable blood brain barrier damagses. Conclusions Skull?thinning surgery is safe and can be applied to small animals for quantitative ultrasound imaging without a craniotomy. This minimally invasive and real?time imaging technique may be useful for dynamic studies of cerebral blood flow changes in various animal disease models.

Abstract:Objective To provide a reference for studies of monitoring lung function in mice, this study was aimed to test the indexes of a non?invasive measurement of lung function in mice. Methods Lung function indexes of 460 C57BL/6 mice were detected by whole?body plethysmography. The results were analyzed, and the range of reference values was determined by the percentile method. Results Normal ranges for the following measures were found: inspiration time was 64. 7 (55. 30 -82. 60) ms, expiration time was 83. 4 (71. 70 -109. 20) ms, Rpef was 0. 21 (0. 16 -0. 28) ms, end?inspiratory pause was 2. 19 (1. 96 -3. 76) ms, end?expiratory pause was 1. 67 (0. 12 -9. 15) ms, tidal volume was 0. 44 (0. 25 -0. 58) mL, enhanced pause was 1. 29 (0. 91 -2. 00) ms, pause was 1. 18 (1. 00 -1. 64) ms, expiratory flow?50 was 0. 64 (0. 30 -0. 98) mL/ s, relaxation time was 39. 0 (32. 40 -51. 50) ms, peak inspiratory flow was 9. 74 (5. 33 -12. 83) mL/ s, peak expiratory flow was 9. 86 (5. 12 -13. 47) mL/ s, inspiratory frequency was 412 (331 - 474) BPM, and minute volume was 174. 4 (86. 69 -235. 04) mL. Conclusions The normal reference ranges from non?invasive lung monitoring in C57BL/6 mice can be used as a reference for basic research on respiratory diseases.

Abstract:Objective To determine the optimal technique for establishing a chemically?induced oral ulcer model in rats for future treatment studies. Methods A total of 50 Sprague Dawley rats were randomly divided into five groups; groups 1, 2, 3, and 4 received 40%, 50%, or 60% acetic acid, or sodium hydroxide crystals, respectively, applied to the lower labial mucosa. All animals then received 50% acetic acid applied twice over the same area of the lower labial mucosa after the mucosa ulcer had healed. In the group 5, 50% acetic acid was applied to the buccal mucosa using a similar approach to examine the effects on formation of oral ulcers in different mucosal areas. The gross appearance of the mucosa, the ulcer formation rate, and the healing time were measured. Mucosal specimens were also taken to assess the histological features of the mucosal ulcer. Results Administration of 50% acetic acid to the lower labial mucosa produced the highest rate of ulcer formation, which showed a regular shape that allowed accurate measurement. The healing time and histological features of the ulcers in the groups 2 were similar to humans. By contrast, after the ulcers had healed, there was a low rate of new ulcers when applying 50% acetic acid over the lower labial gingival mucosa. Conclusions Oral ulcer induced by 50% acetic acid at the lower labial mucosa of Sprague Dawley rats is optimal for therapy evaluation. In addition, mucosa previously burnt by chemical regents are unsuitable for repeated establishment of an ulcer model.

Abstract:Objective To examine the incidence and pathological characteristics of spontaneous liver bile duct hyperplasia in aging rats. Methods Rats were divided into three groups: Group 1, 30 imported Sprague Dawley (SD) male rats and 30 imported SD females; Group 2, 60 domestic SD males and 60 domestic SD females; and Group 3, 60 domestic Wistar males and 60 domestic Wistar females. The animals were euthanized after feeding for 104 weeks. The livers were collected for conventional histopathological and immunohistochemical analyses. Results Bile duct hyperplasia was observed in all groups, with an overall incidence rate of 32. 33%. However, the incidence rate of bile duct hyperplasia in domestic SD rats was higher than that in the imported SD rats (26. 67% vs 1. 67%, respectively), the incidence rate was higher in domestic Wistar rats than that in domestic SD rats (53. 33% vs 26. 67%, respectively), and the incidence rate was higher in the male rats than that in the female rats (20% vs 12. 33%, respectively). Multiple morphological bile duct hyperplasia findings with fibrosis were seen by pathological examination. We defined three hyperplasia grades to evaluate the pathological lesions. The incidence rate of lesions in grade I and grade II was 84. 5%, while the incidence of lesions in grade III was 15. 5%. Hyperplasia of oval cells was observed in cases with bile duct hyperplasia, with differentiation to bile duct epithelium. Conclusions The incidence rate of liver bile duct hyperplasia in aging rats varies by species and sex. These data provide a reference for studies on liver bile duct hyperplasia in ageing animals and humans.

Abstract:Objective The aim of this study was to develop a transgenic rat model of Parkinson’s disease by lentiviral vector?mediated overexpression of human α?synuclein in the substantia nigra of rats. Methods Lentiviral expression vectors were constructed by inserting the normal α?synuclein gene (WT) or the α?synuclein gene with an A30P mutation (A30P) downstream of the Cytomegalovirus (CMV) promoter (pLKO?CMV?α?SYN?WT?P2A?GFP and pLKO2?CMV?α?SYN?A30P?P2A?GFP). The vectors were transduced into 293FT cells, and α?synuclein protein levels were detected by western blotting after transient transfection for 24 h. Following the packaging, enrichment, the viral suspension with control, and normal or mutated forms of α?synuclein, were stereotaxically injected into the substantia nigra. After 21 days, the rats were euthanized, and the substantia nigra harvested and processed for immunofluorescence to detect α?synuclein and tyrosine hydroxylase (TH) expression, and changes in numbers of neurons. Motor performance was also assessed in the A30P rats using the rotating rod test. Results Each lentiviral vector induced equivalent levels of normal or A30P mutated α?synuclein expression. Compared with the control group, both the wild type and A30P mutant groups showed an obvious reduction in numbers of dopaminergic neurons in the substantia nigra, with significantly greater injury in the A30P group. Immunofluorescence staining experiments in the injured region of A30P mutant rats showed largely absent TH staining, but abundant α?synuclein immunoreactive aggregation. The human α?synuclein group was also associated with a marked reduction in TH expression, indicating that A30P mutant overexpression caused neuronal degeneration. In addition, A30P mutant rats showed a progressive decline in motor performance. Conclusions We have established a human α?synuclein A30P transgenic rat model of Parkinson’ s disease, which may be useful for understanding the pathogenesis and developing treatments for this disorder.

Abstract:Objective Osteoclast numbers and activity are directly related to bone turnover and metabolism. This study aimed to investigate the effects of sheep bone marrow peptides (MP) and calcium?chelated MP (MP?Ca) on the formation and activity of RANKL?induced osteoclasts. Methods MP?Ca was prepared by a chelating reaction between MPs and CaCl ₂. RAW264. 7 cells were induced to osteoclasts by RANKL treatment, and cell proliferation was examined using the MTT assay. Induction was intervened by MP and MP?Ca to determine optimal concentrations and to investigate their effects on induction curves, TRAP activity, and the number of lacunae formed in bone slices. Results Under the induction system, on day 5, cultured cells were took on typical morphology of mature osteoclasts, TRAP staining was positive, resorptive pits formed, and the peak OD ₄₉₀value was achieved. The lowest OD ₄₉₀value was achieved when 10³μg/ mL MP or MP?Ca were added into the induction system on day 5. When 10³ μg/ mL MP or MP?Ca was added to the induction system, except on day 1, OD ₄₉₀values from days 2 - 8 were significantly lower than the blank group ( P <0. 05). In addition, the OD490 value and TRAP activity of the MP?Ca group were markedly lower than the MP group ( P <0. 05). Pit numbers in the intervention groups were notably lower than the blank group, and the number of lacunae in the MP group was significantly lower than the MP?Ca group ( P < 0. 05). All indices checked in the 17?β?estradiol group were lower than the intervention groups ( P <0. 05). Conclusions Although inferior to estrogen, both MP and MP?Ca inhibite the RANKL?induced formation and the resorptive activity of osteoclasts. Moreover, MP?Ca was more effective at inhibiting osteoclast formation than MP.

Abstract:Objective To explore the regulation of mammalian embryo implantation, we investigated the expression of Lysozyme 1 ( LYZ1 ) in normal hatching murine blastocysts and dormant embryos before and after superovulation. Methods Normal hatched blastocysts were obtained from day 5 pregnant mice, while dormant embryos were collected from delayed implantation models on day 8. LYZ1 protein expression in the embryos was detected by immunofluorescence and western blot. Results LYZ1 protein was expressed in both hatching blastocysts and dormant embryos before and after superovulation, where it was mainly concentrated in the inner cell mass. LYZ1 was rarely distributed in trophoblasts or in their cytoplasm. Compared with untreated mice, LYZ1 protein expression in superovulation embryos was significantly upregulated; moreover, LYZ1 protein expression in the dormancy model was significantly upregulated. Conclusions LYZ1 protein was expressed in the inner cell mass of embryos, where it may be involved in regulating early development. The high LYZ1 protein expression in dormant embryos after superovulation indicated that LYZ1 protein is upregulated in embryos experiencing adverse environmental conditions, such as the dual effects of dormancy and superovulation.

Abstract:Objective Upregulation of miR34 in the liver has been found in numerous liver diseases, from fatty liver disease to hepatocellular carcinoma. In the present study, we examined the protective actions of anti?miR34c polyamidoamine (PAMAM) dendrimer nanoparticles on hepatic fibrosis in nude mice. Methods Fifteen clean nude mice were randomly divided into the normal control, model control, and anti?miR34c PAMAM dendrimer nanoparticles groups (n =5 per group). Hepatic fibrosis was induced by intraperitoneal injection of 100 μL of 20% carbon tetrachloride twice weekly for 6weeks. Hepatic pathology, serum biochemical indicators, and transforming growth factor?β(TGF?β) / α?smooth muscle cell actin (α?SMA) immunohistochemistry were examined. Results Anti?miR34c delivered by the PAMAM dendrimer decreased inflammatory cell infiltration, collagen deposition, and TGF?β and α?SAM expression in the liver, and improved serum biochemical factors. Conclusions Anti?miR34c PAMAM dendrimer nanoparticles can improve hepatic fibrosis by reducing activation of HSC and incidence of liver injury in nude mice.

Abstract:Objective In this study, we tested the therapeutic efficacy and mechanisms of action of Du Zhong injection in a mouse mastitis model. Methods The mastitis mouse model was produced by injection of lipopolysaccharide (LPS) into the breast duct. At 12 h post LPS injection, mice were split into six groups and administered different concentrations of Eucommia ulmoides (Du Zhong) into the abdominal cavity. After a further 12 h recovery, mice were killed and the mammary glands collected. Pathological changes in each group were observed using hematoxylin and eosin staining. Changes in tumour necrosis factor?α(TNF?α), interleukin?6(IL?6) and interleukin?1(IL?1) cytokines in breast tissue were detected by enzyme?linked immunosorbent assay. Results The mouse mastitis model was successfully constructed using 50 μL of 0. 2 mg/ ml LPS. Pathological examination revealed that, increasing doses of Du Zhong injection were associated with decreased mammary gland injury in the model mice, with the greatest effect observed at 20 mg/ kg and 27 mg/ kg. By enzyme?linked immunosorbent assay, Du Zhong injection also reduced pro?inflammatory cytokine expression in the breast tissue, with greatest effects observed at 27 mg/ kg ( P < 0. 01). Conclusions Du Zhong injection can significantly reduce pathological damages, pro?inflammatory cytokine release, and neutrophil invasion in mammary gland tissue in a mouse model of mastitis, with an optimal dosing of 27 mg/ kg.

Abstract:Objective To compare the histopathological changes of large intestinal mucosa between a rat ulcerative colitis (UC) model induced by dextran sulfate sodium (DSS) and human UC, and examine the pathological mechanisms. Methods Twenty healthy Sprague Dawley male rats (specific?pathogen?free grade)were divided into normal control and model (free access to 5% DSS solution) groups (n =10 per group). The general condition, appearance of the large intestine, and histopathological changes of the mucosa in rats were compared with nine cases of human UC admitted in our hospital. Results The most common lesions involved large intestinal cryptitis, crypt abscesses, crypt atrophy and structural disorder, and erosion and ulcer formation in the rat and human UC cases. In the majority of rats, early lesions showed atrophy of ~1/3 of crypts in the inferior lamina propria, which gradually developed to the entire layer. Interstitial inflammation predominantly involved macrophages, with no plasma cells. The surface epithelia then degenerated, with necrosis and shedding, and formation of a mucosal ulcer, followed by multiple intravascular thrombosis, individual thrombus organization, and occasional glandular dysplasia. By contrast, early stage human UC typically involved acute inflammation of surface epithelia and the upper 1/3 of crypts, while glandular destruction and atrophy were associated with crypt abscesses. All of the human cases were accompanied by basic pathological changes involving chronic enteritis and atypical gland hyperplasia, and occasional thrombosis with/ without organization. Conclusions The common pathogenesis of UC in human ulcerative colitis and DSS?induced rat UC involves injury of large intestinal crypt stem cells. However, DSS?treated rats showed initial lower 1/3 crypt damage expanding into whole crypt destruction, with secondary inflammation, while human UC showed the opposite pattern. These differences should be considered when using this model to study the efficacy and mechanism of drugs for treatment of Ulcerative colitis.

Abstract:Objective The objective of this study was to isolate, characterize, and differentiate ferret adipose?derived stem cells (ADSCs). Methods Subcutaneous fat tissues from ferret abdomens were obtained via germ?free procedures, mechanically minced into 0. 5 mm3 pieces, and digested with 0. 075% collagenase. Subsequently, ADSCs were cultured in high?glucose DMEM medium containing 10% FBS, antibiotics, and 4 ng/ mL β?FGF. Then, analyses of cell morphology and cell surface antigen expression were made by flow cytometry. Finally, osteogenic, adipogenic, chondrogenic, and neural differentiation were examined using different method. Results We isolated and identified ADSCs from fresh fat tissues of ferrets, which demonstrated a more fibroblast?like morphology. FACS analysis show high expression of CD29 (53. 1%), CD90 (99. 6%) and CD105 (93. 7%), but low expression of CD11b (36. 3%) and CD44 (28. 3%). The ADSCs could be differentiated into adipocytes, osteoblasts, chondrocytes, and neurons by in vitro induction. Conclusions ADSCs can be isolated from the subcutaneous fat tissue of ferrets, and these cells have multi?directional differentiation ability.

Abstract:Objective To determine the specific targets for spleen?kidney yang?deficiency ulcerative colitis (UC). Methods Ninety?six Wistar rats were randomly divided into the model, high dose, middle dose, and low dose sulfasalazine (SASP) groups. Then, next?generation sequencing was performed on colon lesions from the blank and model groups. Real?time quantitative PCR was performed to detect the mRNA expression of screened chemokines. Results Compared with the model group, differentially expressed genes in the blank group were screened according to a q?value of 0. 05 and fold?change of 1. 5. According to Gene Ontology classification analysis, the differentially expressed genes mainly functioned in three pathways: biological process, cellular component, and molecular function. Kyoto Encyclopedia of Genes and Genomes enrichment analysis of the differentially expressed genes showed alterations in the chemokine signaling pathway, and real?time quantitative PCR confirmed that CXCL1, CXCL2, CXCR2, CXCL6, CCL7, CCL12, and CCL7were significantly unregulated. Thus, the expression of the above factors was consistent with sequencing, and levels of these factors were decreased following treatment. Conclusions CCL12 expression was significantly unregulated along with the chemokine signaling pathway involving CXCL1, CXCL2, CXCR2, CXCL6, CCL7, and CCL12 in spleen?kidney yang?deficiency UC. Thus, this panel can be used as an objective index of inflammation for UC mucosa. Warming the spleen and kidney with Lizhong decoction and Sishen pills can effectively downregulate the expression of these factors, which restrained inflammatory reactions and promoted the repair of injured colonic mucosa.

Abstract:Objective This study is aimed to validate whether Chinese rare minnows (Gobiocypris rarus) are applicable for the juvenile fish growth test as a test fish, and to lay a foundation for the national standards of chemical testing. Methods According to “OECD Guidelines for the Testing of Chemicals No. 215: Fish, Juvenile Growth Test”, juvenile fish growth tests were performed using G. rarus that were exposed to two reference substances ( potassium bichromate and 3,4?dichloroaniline). To evaluate the repeatability of the testing method using G. rarus, the toxic effects of each substance were determined three times in our testing facility, while other domestic laboratories were involved in the ring test program to evaluate the reproducibility of the method. Results Regarding the repeated tests, the mean estimates of the concentration that would cause a 20% reduction in growth relative to controls (EC₂₀ ) were 30. 9 mg/ L and 163 μg/L for potassium bichromate and 3,4?dichloroaniline, respectively. For both, the coefficients of variance were < 15%.Although higher coefficients of variance for the datasets of the two substances were reported in the ring test, EC₂₀ values from all laboratories varied within a range of (x ± 2s). Conclusions Evaluating the repeatability and reproducibility of this test using G. rarus has presented promising result, and the level of sensitivity of this native fish species is comparable to that of Oncorhynchus mykiss in relation to the exposure of 3,4?dichloroaniline. Therefore, G. rarus can serve as standard test fish for toxicity studies.

Abstract:Objective To investigate the protective effect of mild hypothermia on radiation?induced lung injury, and to compare the differences with the clinically used drug amifostine. Methods Seventy?five male Sprague Dawley rats were randomly divided into control, irradiation, amifostine, mild hypothermia prevention, and mild hypothermia treatment groups. All groups (except the control group) received a single?dose 20 Gy electron?beam full?chest irradiation. The amifostine group received an intraperitoneal amifostine injection(150 mg/ kg)at 30 min before irradiation. The hypothermia prevention group received mild body cooling initiated prior to irradiation(34 ±1℃)and continued for 6 h. The hypothermia treatment group received mild body cooling immediately after irradiation and continued for 6 h. Lung tissues were examined by histopathology and for collagen content. Serum levels of malondialdehyde and glutathione, and superoxide dismutase (SOD) activity, were examined at 14 d and 35 d after irradiation. Tumor necrosis factor α levels in the lung tissue homogenates, and apoptosis in the lung tissues, were also examined. Results Serum SOD activity decreased immediately after irradiation, and was significantly recovered in the mild hypothermia treatment group at 14 d recovery compared with the irradiation group ( P < 0. 05). Malondialdehyde content in the amifostine group and mild hypothermia intervention group were lower than the irradiation group at 14 d recovery ( P < 0. 05). TNF?α levels in the irradiation group were significantly increased at 6 h after irradiation, but were significantly reduced in the amifostine group and mild hypothermia treatment group ( P < 0. 05). Numbers of apoptotic cells in the irradiation group were significantly increased and widely distributed in the irradiation group, but were reduced in all intervention groups (there were no differences between the intervention groups). Conclusions Mild hypothermia can provide antioxidant, anti?inflammatory, and anti?apoptotic effects following radiation?induced lung injury in rats, to levels similar to that using the clinical drug amifostine.

Abstract:Objective To develop a rat model of battleship fire?related smoke inhalation?induced acute lung injury using combustion of composite materials with a controllable temperature. Methods We designed a smoke?generating chamber and a test chamber. Sober rats were restricted to cages located inside the chamber during the experiments. In aim one, we investigated the survival rates at different inhalation times (15, 30, and 50 min). In aim two, we evaluated blood gas values, lung pathological scores, pro?inflammatory molecules, and protein concentrations in the bronchoalveolar lavage fluid, circulating white cells, and liver and renal functions at 1 h, 6 h, and 24 h after 30 min smoke inhalation. Results The survival rates at the different inhalation periods were 84. 21% (15 min), 25% (30 min), and 0% (50 min). There was a significant increase in carboxyhaemoglobin (COHB), lactate, and partial pressure of carbon dioxide (PCO2 ) at 1 h post injury ( P < 0. 05), which then gradually returned to normal. In the bronchoalveolar lavage fluid (BALF), the protein concentration and lung injury were score increased immediately after smoke inhalation, and persisted until 24 h. In the BALF, the total number of leukocytes cells significantly increased after smoke inhalation, while the proportion of macrophages significantly decreased at 6 h, then slightly recovered at 24 h; neutrophils showed the opposite trend. By western blot, there was a significant increase in signal pathway factors and inflammatory factors at 6 h recovery. There were no changes in the liver or renal functions after smoke inhalation. Conclusions This stable and reliable rat smoke inhalation injury model induced using our novel smoke generators is characterized by activation of inflammatory signaling pathways, inflammatory cell changes, and lung injury. This model may be useful for studies examining acute and chronic lung injury.

Abstract:Objective To study the effect of NF?E2 related factor 2 (Nrf?2) pathway activation on particulate matter 2. 5 (PM_2.5 )?induced reproduction injury in female rats. Methods Thirty Sprague Dawley rats were randomly divided into control (normal saline), low dose exposure (1. 5 mg/ kg PM_2.5 ), and high dose exposure (37. 5 mg/ kg PM_2.5) groups. The levels of tumor necrosis factor?α (TNF?α), interleukin 1?β (IL?1β), and interleukin?6 (IL?6) were measured by enzyme?linked immunosorbent assay. The mRNA and protein expression of Nrf?2 and heme oxygenase?1 (HO?1) were also examined by qPCR and western blot. Results There was a significant increase in TNF?α, IL?1β, and IL?6 expression in the low dose and high dose exposure groups compared with the control groups ( P < 0. 05). The expression levels were also increased with increasing dose of PM_2.5 (r = 0. 870, 0. 847, and 0. 855, respectively). Both the Mrna and protein expressions of Nrf?2 and HO?1 were also significantly increased in the low dose and high dose exposure groups compared with controls ( P <0. 05). Conclusions The Nrf?2 signaling pathway is activated following exposure of PM2. 5 in female rats, although PM2. 5 can still induce uterine inflammation and injury.

Abstract:Objective To develop a combined behavioral test for assessment of scopolamine?induced delirium in mice. Methods Two groups of mice were randomly assigned to receive 15 mg/ kg scopolamine (delirium group; n =12) or isovolemic saline (control group; n = 8) via intraperitoneal injection. We developed a novel behavioral experiment in which mice received the light and black box test for 10 min, the open?field test for 10 min, and then the non?selective non?sustained attention test for 10 min, from 30 to 60 min after intervention. Five behavioral indexes were compared between the groups to assess the delirium status. Results Compared with the control group, there were significant differences in all five behavioral indexes in mice in the delirium group mice at 30 min after intervention: time spent in the white box was significantly shorter ( P < 0. 05), the movement speeds were significantly increased ( P < 0. 05), time spent beside the wall area was increased significantly ( P < 0. 05), the freezing time, and the attention level were significantly decreased ( P < 0. 05). Conclusions This combined behavioral experiment can be used to assess the key elements for delirium diagnosis, and with a faster time than conventional tests.

Abstract:Hepatitis B virus (HBV) is a prototype of hepadnavirus, and hepatitis B caused by HBV infection is a serious public health problem. Using the currently available anti?HBV drugs, including nucleotide analogs and interferon?α, it is difficult to achieve a “clinical cure” endpoint. Thus, new anti?HBV drugs and combination therapy strategies are urgently needed, as are appropriate animal models for preclinical evaluations. Woodchuck hepatitis virus (WHV) was first discovered in woodchucks at the Philadelphia Zoo in the United States in 1978, and has been classified as hepadnavirus due to its comparable genomic structure and replication cycle with HBV. Furthermore, the natural history of WHV infection in woodchucks is highly similar to that of HBV infection in humans; therefore the woodchuck model has been used to evaluate HBV DNA vaccines and anti?HBV drugs for decades. In recent years, many cytokines, their receptors, and other immune cell surface markers have been cloned and identified. Additionally, detection method for T cell responses, including lymphocyte proliferation assays and CD107a degranulation assays, have been established and have greatly promoted the woodchuck model for studies of the immune?pathogenesis and immunomodulatory therapy of HBV infection. This review summarizes the immunological features of the WHV?infected woodchuck model and its application for evaluating anti?HBV drugs and immunomodulation therapies.

Abstract:Immunotherapy has shown significant efficacy in the treatment of many tumors. Natural killer cells play a key role in the identification and eradication of tumors and have great potential for tumor treatment. This paper summarizes the progress of research on natural killer cells as well as their mechanism of action and associated clinical treatments, providing a reference for future applications and basic research on the use of natural killer cells in tumor therapy.

Abstract:Growth hormone (GH) is synthesized and released by somatotrophic cells in the pituitary gland. As well as functions in growth and development, GH is also important in many metabolic diseases. The biological functions of GH are initiated by ligand binding to the surface receptor,growth hormone receptor (GHR). Rapid advances in molecular technology have enabled construction of various GHR knockout mice models to examine the mechanisms of action of GH. Using a Cre ?LoxP recombinase system, the mouse GHR has also been successfully knocked out systemically and tissue?specifically, including in the liver, skeletal muscle, adipose tissues, macrophages, and pancreatic islet β?cells. This has provided a unique platform for studying GH/ GHR signal transduction and its interactions with other signaling pathways. In this brief review, we discuss the phenotypic characteristics and applications of these GHR knockout mouse models.

Abstract:Radiation?induced heart damage (RIHD) is unavoidable in the mediastinal heart during radiotherapy for chest and abdominal tumors. This condition has been considered to be important in conventional radiation?induced pulmonary fibrosis. It is a severe side effect of radiotherapy. In recent years, research on RIHD has gradually increased in intensity. At present, many clinical observations are being undertaken in this field, but the basic research is insufficient, the etiological mechanism is not clear, and there is a lack of effective intervention. Therefore, there is an urgent need to carry out animal experiments as basic research on RIHD, to explore the pathomolecular mechanisms of cardiac injury induced by radiation and to actively develop potential intervention measures. This paper reviews the result of basic research on RIHD in terms of animal modeling, index detection, pathological mechanism, drug intervention, and pharmacological action in order to provide a reference for future RIHD research.