Electrochemical skin conductance and heart rate variability in patients with non-dialysis chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) is very common now and associates with high overall and cardiovascular mortality. Numerous studies have reported that Heart rate variability (HRV) could also be used to detect cardiovascular autonomic dysfunction (CAD). We investigated the association of electrochemical skin conductance (ESC) of EZSCAN results with HRV in non-dialysis CKD patients. METHODS: In a cross-sectional study, we enrolled 248 prevalent non-dialysis CKD patients. Patients underwent a 24-h Holter (CB-2302-A, Bio Instrument, China). A time domain analysis of HRV was performed, and the following parameters were obtained: SDNN, SDANN, rMSSD, pNN50. EZSCAN device (Impeto Medical, Paris, France) measures ESC values of each participants. Mean global skin conductance computed as 0.5 * (reflecting (right + left hand)/2 + (right and left foot)/2). Log transforms data into a normal distribution for statistical analysis. RESULTS: There were 142 males and 106 females included in the present study. Patients' age was 56.6±17.08 years. Logarithm(Log) (global ESC) was independently predicted by age (P<0.01), hypertension history, estimated Glomerular filtration rate (eGFR) and log SDNN (P<0.05). While log SDANN, rMSSD and pNN50 were not independent predictors for log (global ESC). CONCLUSION: Increased global ESC significantly associated with elevated HRV, specifically SDNN in non-dialysis CKD patients. This suggested that global ESC may appear to be an important predictor of CAD, and even could be used as a cardiovascular risk factor in non-dialysis CKD patients.

Erchen Decoction Ameliorates the Metabolic Abnormalities of High-Fat Diet-Fed Rats.

Objective: Brown adipose tissue (BAT) dissipates chemical energy to protect against obesity. In the present study, we aimed to determine the effects of Erchen decoction on the lipolysis and thermogenesis function of BAT in high-fat diet-fed rats. Methods: Sprague-Dawley rats were randomly divided into four groups, which were fed a control diet (C) or a high-fat diet (HF), and the latter was administered with high and low doses of Erchen decoction by gavage once a day, for 12 weeks. Body weight, the serum lipid profile, serum glucose, and insulin levels of the rats were evaluated. In addition, the phosphorylation and protein and mRNA expression of AMP-activated protein kinase (AMPK), adipose triglyceride lipase (ATGL), peroxisome proliferator-activated receptor γ coactivator- (PGC-) 1α, and uncoupling protein 1 (UCP-1) in BAT were measured by immunoblotting and RT-PCR. Results: Erchen decoction administration decreased body weight gain and ameliorated the abnormal lipid profile and insulin resistance index of the high-fat diet-fed rats. In addition, the expression of p-AMPK and ATGL in the BAT was significantly increased by Erchen decoction. Erchen decoction also increased the protein and mRNA expression of PGC-1α and UCP-1 in BAT. Conclusion: Erchen decoction ameliorates the metabolic abnormalities of high-fat diet-fed rats, at least in part via activation of lipolysis and thermogenesis in BAT.

MG-132 attenuates cardiac deterioration of viral myocarditis via AMPK pathway.

BACKGROUND: Coxsackievirus B3 (CVB3) is the primary cause of infectious myocarditis. Aggressive immunological activation and apoptosis of myocytes contributes to progressive dysfunction of cardiac contraction and poor prognosis. MG-132, a proteasome inhibitor, regulates mitochondrial-mediated intrinsic myocardial apoptosis and downregulates NF-κB-mediated inflammation. Here, we determined whether AMPK pathway participates in MG-132-mediated myocardial protection in viral-induced myocarditis. METHODS AND RESULTS: Acute viral myocarditis models were established by intraperitoneal inoculation of CVB3 in male BALB/c mice. Myocarditis and age-matched control mice were administered MG-132 and/or BML-275 dihydrochloride (BML) (AMPK antagonist) intraperitoneally daily from the day following CVB3 inoculation. MG-132 improved hemodynamics and inhibited the structural remodeling of the ventricle in mice with myocarditis, while BML largely blunted these effects. TUNEL staining and immunochemistry suggested that MG-132 exerts anti-apoptotic and anti-inflammatory effects against CVB3-induced myocardial injuries. BML attenuated the effects of MG-132 on anti-apoptosis and anti-inflammation. CONCLUSION: MG-132 modulated apoptosis and inflammation, improved hemodynamics, and inhibited the structural remodeling of ventricles in a myocarditis mouse model via regulation of the AMPK signal pathway.

Toxic Effects and Possible Mechanisms of Deoxynivalenol Exposure on Sperm and Testicular Damage in BALB/c Mice.

Deoxynivalenol (DON, vomitoxin) is the most common mycotoxin in cereals and grains. DON contamination can cause a serious health threat to humans and farm animals. DON has been reported to exert significant toxicity effects on the male reproductive system. However, the causes and mechanisms underlying efforts of DON on sperm and testicular damage remain largely unclear. In the present study, we thoroughly investigated this issue. Eighty male BALB/c mice were randomly divided into a control group ( n = 40) and DON treatment group (2.4 mg/kg of body weight, n = 40). The ratio of testes and seminal vesicle to body, sperm survival and motility, and morphology of sperm and testis were observed in DON-treated and control mice. In addition, the concentrations of reactive oxygen species (ROS) and malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and glutathione (GSH), and also the expression levels of JNK/c-Jun signaling and apoptotic factors such as caspase-3, caspase-8, caspase-9, Bim, and Bid were analyzed and compared between the two groups. The results demonstrated that a single topical application of DON significantly increased the percentage of abnormal sperm and decreased the motility of sperm, indicating the sperms are damaged by DON. Additionally, the reduced relative body weight of testis and severe destruction of testicular morphology were observed. Moreover, the increased levels of ROS and MDA levels and decreased activities of SOD and GSH were found in testicular tissues, suggesting that oxidative stress is induced by DON treatment. Furthermore, DON upregulated the expression of stress-induced JNK/c-Jun signaling pathway proteins as well as JNK/c-Jun phosphorylation proteins. In addition, DON could enhance testicular apoptosis by increasing expression levels of apoptotic genes including Bim, cytochrome c, caspase 3, caspase 8, and caspase 9. These results suggest that DON exposure can cause sperm damage, oxidative stress, testicular apoptosis, and phosphorylation of JNK/c-Jun signaling pathway. The underlying mechanisms may be that DON induces sperm damage by exacerbating oxidative stress-mediated testicular apoptosis via JNK/c-Jun signaling pathway.

Serum endocan and circadian heart rate variability in non-dialysis stage 5 chronic kidney disease patients.

BACKGROUND: Chronic kidney disease (CKD) is very common now and is associated with high overall and cardiovascular mortality. Numerous studies have reported that elevated heart rate (HR) is a risk factor for cardiovascular mortality. We investigated the link between serum endocan and circadian heart rate variability in non-dialysis stage 5 CKD patients. METHODS: In a cross-sectional study, we enrolled 54 prevalent n non-dialysis stage 5 CKD patients (32 males, aged 48.2 ± 14.92 years). HR was measured with an automatic system. Serum endocan level was analyzed by ELISA. RESULTS: Night/day HR ratio was independently predicted by serum endocan level (P < 0.01) and hypertension history (P < 0.05). Adjusted R2 of the model was 0.222. CONCLUSION: Increased serum endocan is significantly associated with circadian heart rate variability in non-dialysis stage 5 CKD patients. Further investigation is needed to explore the potential benefits of serum endocan lowering therapy in this patient group.

Induced dural lymphangiogenesis facilities soluble amyloid-beta clearance from brain in a transgenic mouse model of Alzheimer's disease.

Impaired amyloid-ß clearance from the brain is a core pathological event in Alzheimer's disease. The therapeutic effect of current pharmacotherapies is unsatisfactory, and some treatments cause severe side effects. The meningeal lymphatic vessels might be a new route for amyloid-ß clearance. This study investigated whether promoting dural lymphangiogenesis facilitated the clearance of amyloid-ß from the brain. First, human lymphatic endothelial cells were treated with 100 ng/mL recombinant human vascular endothelial growth factor-C (rhVEGF-C) protein. Light microscopy verified that rhVEGF-C, a specific ligand for vascular endothelial growth factor receptor-3 (VEGFR-3), significantly promoted tube formation of human lymphatic endothelial cells in vitro. In an in vivo study, 200 µg/mL rhVEGF-C was injected into the cisterna magna of APP/PS1 transgenic mice, once every 2 days, four times in total. Immunofluorescence staining demonstrated high levels of dural lymphangiogenesis in Alzheimer's disease mice. One week after rhVEGF-C administration, enzyme-linked immunosorbent assay results showed that levels of soluble amyloid-ß were decreased in cerebrospinal fluid and brain. The Morris water maze test demonstrated that spatial cognition was restored. These results indicate that the upregulation of dural lymphangiogenesis facilities amyloid-ß clearance from the brain of APP/PS1 mice, suggesting the potential of the VEGF-C/VEGFR-3 signaling pathway as a therapeutic target for Alzheimer's disease.

Sagittal abdominal diameter and Framingham risk score in non-dialysis chronic kidney disease patients.

BACKGROUND: Chronic kidney disease (CKD) is very common now and is associated with high overall and cardiovascular mortality. Numerous studies have reported that abdominal obesity is a risk factor for cardiovascular mortality. We investigated the link between sagittal abdominal diameter (SAD) and Framingham risk score in non-dialysis CKD patients. METHODS: In a cross-sectional study, we enrolled 307 prevalent non-dialysis CKD patients (175 males, aged 50.7 ± 17.04 years). SAD and Framingham risk score were measured. RESULTS: Framingham cardiovascular disease risk score was independently predicted by SAD (P < 0.01), GFR (P < 0.01) and diabetic history (P < 0.05). Adjusted R2 of the model was 0.178. SAD could be independently predicted by BMI (P < 0.01), diabetic history (P < 0.01), GFR (P < 0.01) and age (P < 0.01). Adjusted R2 of the model was 0.409. Using receiver operating characteristic (ROC) curve, a cutoff SAD value of 16.55 cm was determined with sensitivity of 63.7%, specificity of 58.3%. CONCLUSION: Elevated SAD is significantly associated with increased Framingham risk score in non-dialysis CKD patients. SAD can be predicted by patients' BMI, diabetic history, renal function and age. Further investigation is needed to explore the potential benefits of central obesity lowering therapy in this patient group.

Nucleopolyhedrovirus infection and/or parasitism by Microplitis pallidipes Szepligeti affect hemocyte apoptosis of Spodoptera exigua (Hübner) larvae.

We determined the effects of parasitism by the endoparasitoid Microplitis pallidipes Szepligeti and/or nucleopolyhedrovirus (NPV) infection on hemocyte apoptosis of Spodoptera exigua (Hübner) larvae. Compared to healthy (control) larvae, larvae that were parasitized, virus-infected, or both all showed a significant increase in hemocyte apoptosis during 48-h observation period. The peaks of hemocyte apoptosis in parasitized, virus-infected and parasitized+infected larvae were at 12, 24 and 48 h after treatment, and were 86.7±1.9, 87.4±3.6 and 76.5±1.6%, respectively. Meanwhile, compared to parasitized larvae, hemocyte apoptosis in jointly parasitized and infected larvae increased by 12.9%, 18.7% and 2.8% at 8, 36 and 48 h respectively, and decreased by 39.0% and 9.1% at 12 and 24h. Compared to virus-infected larvae, hemocyte apoptosis in jointly parasitized and infected larvae increased by 13.4%, 2.4% and 15.3% at 8, 36 and 48 h, respectively, and decreased by 4.0% and 29.9% at 12 and 24h. Our study found that joint and separate parasitism and SeNPV infection induced hemocyte apoptosis of S. exigua larvae. It also revealed that NPV infection promoted host hemocyte apoptosis induced by parasitism at early egg and larval stages of M. pallidipes in host larvae, but inhibited the same effect at late egg stage of M. pallidipes in host larvae, and that parasitism promoted host hemocyte apoptosis induced by NPV infection at early egg and larval stages of M. pallidipes in host larvae, but inhibited the same effect at late egg stage of M. pallidipes in host larvae.

Silencing of Cholinergic Basal Forebrain Neurons Using Archaerhodopsin Prolongs Slow-Wave Sleep in Mice.

The basal forebrain (BF) plays a crucial role in cortical activation. Our previous study showed that activation of cholinergic BF neurons alone is sufficient to suppress slow-wave sleep (SWS) and promote wakefulness and rapid-eye-movement (REM) sleep. However, the exact role of silencing cholinergic BF neurons in the sleep-wake cycle remains unclear. We inhibitied the cholinergic BF neurons genetically targeted with archaerhodopsin (Arch) with yellow light to clarify the role of cholinergic BF neurons in the sleep-wake cycle. Bilateral inactivation of cholinergic BF neurons genetically targeted with archaerhodopsin prolonged SWS and decreased the probability of awakening from SWS in mice. However, silencing these neurons changed neither the duration of wakefulness or REM sleep, nor the probability of transitions to other sleep-wake episodes from wakefulness or REM sleep. Furthermore, silencing these neurons for 6 h within the inactive or active period increased the duration of SWS at the expense of the duration of wakefulness, as well as increasing the number of prolonged SWS episodes (120-240 s). The lost wakefulness was compensated by a delayed increase of wakefulness, so the total duration of SWS and wakefulness during 24 h was kept stable. Our results indicate that the main effect of these neurons is to terminate SWS, whereas wakefulness or REM sleep may be determined by co-operation of the cholinergic BF neurons with other arousal-sleep control systems.

Reduction of heart failure rehospitalization using a weight management education intervention.

BACKGROUND: Previous investigators have demonstrated that patient adherence to optimal weight monitoring resulted in fewer heart failure (HF)-related rehospitalizations. OBJECTIVE: The aim of this study was to determine whether a weight management (WM) intervention can improve patients' WM ability and cardiac function and reduce HF-related rehospitalizations. METHODS: Heart failure patients were randomly assigned to an intervention group (n = 32) or a control group (n = 34). The intervention group received the WM intervention, including education about regular daily weight monitoring and coping skills when detecting sudden weight gain, with a WM booklet and scheduled telephone visits. Patients' WM ability was measured by the Weight Management Questionnaire (WMQ). We compared scores on the WMQ, New York Heart Association (NYHA) classification, and HF-related rehospitalizations between the 2 groups at enrollment and at 6 months. We also analyzed the association of adherence to weight monitoring and rehospitalization in the intervention group during the 6-month follow-up. RESULTS: There were no significant differences in weight monitoring adherence, WM ability, and NYHA classification between the 2 groups at baseline. At 6 months, scores on all 4 subscales of the WMQ significantly increased within the intervention group, and the WM-practice subscale significantly improved within the control group. Adherence to weight monitoring was significantly improved in the intervention group compared with the control group (81.25% vs 11.76%; P < .01). At 6 months, there was a significant improvement in NYHA class in the intervention group compared with the control group (P = .03). Rehospitalizations related to HF were also fewer in the intervention group (0.28 ± 0.63 vs 0.79 ± 1.18; P = .03) during the follow-up duration. In the intervention group, those who weighed themselves regularly reported less HF-related rehospitalizations than did those who did not (0.23 ± 0.43 vs 0.50 ± 1.23; P = .62). CONCLUSION: This study demonstrates that the WM intervention had a positive impact on patients' adherence to weight monitoring, WM ability, and NYHA classification and reduced HF-related rehospitalization.

[Preparation and performance of controlled-release tablets of sasanquasaponin-casein].

The controlled-release tablets of sasanquasaponin (SQS)-casein were prepared by using SQS, casein and guar gum as the main drug and accessory materials respectively. The method of determination of SQS in the controlled-release tablets of SQS-casein, and the effects of release media on the release rate and IR spectra of the controlled-release tablets of SQS-casein were studied, respectively. The release rate curve of the controlled-release tablets of SQS-casein was fitted as zero order, one order and Higuchi equation. The recovery was 98.59% when the content of SQS in the controlled-release tablets of SQS-casein in phosphate buffer solution (pH 6.8) as release media was determined with chromogenic reaction of vanillin- sulfuric acid. The release rates are 23.80%, 51.26% and 94.77% at release times 3, 6 and 12 h, respectively in phosphate buffer solution (pH 6.8) as release media. The controlled-release tablets of SQS-casein release SQS by slowness and constant in 12 h. The chemical bonds are formed among SQS, casein and guar gum.

Two novel mutations of the MYBPC3 gene identified in Chinese families with hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiovascular disorders. Mutations in the MYBPC3 gene are one of the most frequent genetic causes of HCM. OBJECTIVES: To screen MYBPC3 gene mutations in Chinese patients with HCM, and analyze the correlation between the genotype and the phenotype. METHODS: The 35 exons of the MYBPC3 gene were amplified by polymerase chain reaction in the 11 consecutive unrelated Chinese pedigrees. The sequences of the products were analyzed and the mutation sites were determined. The clinical data of genotype-positive families were collected, and the correlation between genotype and phenotype was analyzed. RESULTS: Two mutations of the MYBPC3 gene were confirmed among 11 pedigrees. A frameshift mutation (Pro459fs) was identified in exon 17 in family H8, and a splice mutation (IVS5+5G−>C) was identified in intron 5 in family H3. These two mutations were first identified in Chinese patients with familial HCM and were absent in 110 chromosomes of healthy controls. Seven known polymorphisms were found in the cohort. CONCLUSIONS: Compared with what was reported abroad, the MYBPC3 gene is a common pathogenic gene responsible for HCM in Chinese patients, and the phenotypes of these two mutations in their respective families may have their own clinical characteristics.

[Novel Val606Met mutation in beta myosin heavy chain gene in Chinese pedigrees with familiar hypertrophic cardiomyopathy].

OBJECTIVE: To screen the disease-causing gene mutation in Chinese patients with familiar hypertrophic cardiomyopathy (HCM) and to analyse the correlation between the genotype and phenotype. METHODS: Eight Chinese pedigrees with HCM and 80 age-matched normal control subjects were studied. The exons in the functional regions of the beta myosin heavy chain gene (beta-MHC) were amplified with PCR and the products were sequenced. The relation between the genotype and phenotype was analyzed. RESULT: Val606Met mutation was identified in exon 16 in one family and Val606Met mutation was identified in 4 out of 8 family members in this pedigree and 3 out of 4 Val606Met carriers suffered from HCM. No similar mutation was identified in controls. CONCLUSION: The Val606Met mutation located at the actin-binding region of the cardiac beta-MHC gene is involved in the pathogenesis of HCM in this Chinese pedigree.

Mutation of Arg723Gly in beta-myosin heavy chain gene in five Chinese families with hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a form of cardiomyopathy with an autosomal dominant inherited disease, which is caused by mutations in at least one of the sarcomeric protein genes. Mutations in the beta-myosin heavy chain (beta-MHC) are the most common cause of HCM. This study was to reveal the disease-causing gene mutations in Chinese population with HCM, and to analyze the correlation between the genotype and phenotype. METHODS: The exons 3 to 26 of MYH7 were amplified by PCR, and the PCR products were sequenced in five non-kin HCM patients. A 17-year-old patient was detected to be an Arg723Gly mutation carrier. Then his family was gene-screened, and the correlation between genotype and phenotype was analyzed. RESULTS: The mutation of Arg723Gly in a Chinese family with HCM was detected for the first time. With a C-G transversion in nucleotide 13,619 of the MYH7 gene, located at the essential light chain interacting region in S1, the replacement of arginine by glycine took place at amino acid residue 723. A two-dimensional echocardiogram showed moderate asymmetrical septal hypertrophy with left atria enlargement. There was no obstruction in the left ventricular outflow tract. In his family, a total of 13 individuals were diagnosed HCM and 5 of them were dead of congestive heart failure at a mean age of 66-year-old. Eight living members were all detected to carry the mutation, in which 3 developed progressive heart failure. Moreover, the heart function of the people evidently deteriorates when their age are older than 50. The mutation and the disease show co-separated. CONCLUSION: The Arg723Gly mutation is a malignant type. In Chinese the mutation has the similar characters to the former report but has low degree malignant.

[Malignant hypertrophic cardiomyopathy caused by the Arg723Gly mutation in beta-myosin heavy chain gene in a Chinese pedigree].

OBJECTIVE: Hypertrophic cardiomyopathy (HCM) is a genetically and phenotypically heterogeneous disease and an Arg723Gly mutation in beta-myosin heavy chain (beta-MHC) gene was found in 3 Spanish families with malignant HCM. We detected this gene mutation in 5 Chinese pedigrees with hypertensive cardiomyopathy. METHODS: Five Chinese pedigrees with HCM and 80 age-matched normal control subjects were chosen for the study. The exons in the functional regions of the beta-MHC gene were amplified with PCR and the products were sequenced, genotype and phenotype analyzed. RESULTS: Arg723Gly mutation was identified in exon 20 in one pedigree. In this pedigree, 13 out of 25 family members were diagnosed as HCM, 5 died of heart failure, all HCM patients in this pedigree had Arg723Gly mutation and 3 of them had NYHA III and 2 of them were diagnosed as HCM before the age of 20. CONCLUSIONS: Arg723Gly mutation was also one of the main disease-causing genes in Chinese familial HCM. The mutation of Arg723Gly is a malignant phenotype as shown by early progressive heart failure development and poor prognosis in this pedigree with Arg723Gly mutation.

[Study on the biological characteristic of Blastocystis hominis: morphology, mode of reproduction and the relation to bacteria].

OBJECTIVE: To observe the reproductive modes of Blastocystis hominis and study the relation between this protozoa and bacteria. METHODS: Using the Iodine and Haematoxylin staining, the morphology of B. h from patients and RPMI 1640 medium were observed. The B. h positive mucous diarrheal specimens were cultured and identified any possible known pathogenic intestinal bacteria. B. h and colibacillus were co-cultured to observe the interaction between them. RESULTS: Four modes of reproduction for B. h were confirmed: binary fission, endodyogeny, multiple fission and budding. The fact that there was no other intestinal pathogens in half of the B. h positive specimens suggested B. h may cause disease independently. B. h and colibacillus were restrained each other. CONCLUSION: B. h reproduces in at least four modes. B. h could be a pathogen and its pathogenesis may be related to micro-ecological changes.

[A pig model of myocardial infarction by intracoronary embolization with gelatin sponge].

OBJECTIVE: We produced a large-animal model of myocardial infarction induced by transcatheter embolization of the left coronary artery using a gelatin sponge. METHODS: Seven pigs underwent transcatheter embolization of the left anterior descending artery (LAD) using gelatin sponge to produce anteroapical myocardial infarction (MI). 4 weeks later, Echocardiography, Coronary angiography and Pathology was performed, and the data were compared with those of the control group (n = 6). RESULTS: The procedure mortality was 1 of 7. In the MI group, the LV end-diastolic dimension increased (control versus MI: 37.0 mm +/- 3.4 mm and 50.8 mm +/- 6.1 mm, P < 0.01), the ejection fraction (EF) decreased (control versus MI: 62.3% +/- 2.9% and 36.6% +/- 2.1%, P < 0.001). Coronary angiography revealed the LAD remained occluded. The postmortem specimen showed a transmural MI scar in the anteroseptal and apical regions in the MI group and the LV volumes at 30 mm Hg were 81.4 ml +/- 4.3 ml, the scar areas were 18.4% +/- 1.6% of total left ventricular free wall and the scar thickness was 3.5 mm +/- 0.8 mm. Histologic samples in the MI group stained with Masson's trichrome showed massive fibrosis in the border zone and patchy fibrosis in the remote region in the LV free wall, whereas the control group showed no fibrosis. CONCLUSION: This pig model of myocardial infarction is reliable, reproducible, and similar to the human condition, amenable to investigate other investigation.

[Experimental infection of mice with Blastocystis hominis].

OBJECTIVE: To seek a better pathway and proper number of parasites for Blastocystis hominis (B.h) infection in normal and immunocompromised ICR mice. METHODS: (1) 10(4), 10(5) and 10(6) B.h, cultured in RPMI 1640 medium from 3 generations were used to infect mice through oral and rectum; (2) 10(6) B.h were used to infect immunocompromised mice through rectum. The reproduction of B.h in gastrointestinal tract and the pathologic changes in the tissues were observed. RESULTS: Mice were infected by B.h through either oral or rectum. The infected immunocompromised mice showed slow locomotion, depressed, lethargy, and descended body weight. Some infected mice discharged mucus feces, a few of them died during the experiment. Parasites were found in the whole gastrointestinal tract. Severe edema, hyperemia and congestion were observed in the tissues of jejunum, ileum, cecum and colon. The epithelia of small intestine and colonic mucous membrane showed exfoliation, inflammatory cell infiltration in submucosa, and structural changes in glands. CONCLUSION: Mice were more susceptible to Blastocystis hominis infection through rectum than orally. The parasites can be found in the whole gastrointestinal tract of mice, and can breed rapidly and cause significant pathological change in the gastrointestinal mucosa in immunocompromised mice.