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BackgroundPapillary thyroid carcinoma (PTC) concurrent with Hashimoto’s thyroiditis (HT) was associated with a better clinical prognosis. This study aimed to investigate a potential mRNA gene that affects the development of PTC, which helps PTC concurrent with HT patients have a better prognosis.Material/MethodsPTC data were obtained from The Cancer Genome Atlas (TCGA) database. And the validation data of tissue specimens were collected from Guangzhou First People’s Hospital. The thyroid tissue sections were hybridized with deleted in malignant brain tumor 1 (DMBT1) probes by situ hybridization. Survival rates were analyzed using Kaplan-Meier curves, and the log-rank test was used to compare group survival rates. Prognosis clinicopathological factors were analyzed by Cox regression. Gene Ontology (GO) and Kyoto Gene and Genomic Encyclopedia (KEGG) pathway enrichment analyses were performed using single-sample gene set enrichment analysis (ssGSEA). Finally, the correlation of deletion in DMBT1 expression with overall immune status, tumor purity, and human leukocyte antigen (HLA) gene expression profile was analyzed.ResultsHT was significantly associated with sex, tumor foci, extrathyroidal extension (ETE), residual tumor, and tumor stage (T stage). Moreover, PTC concurrent with HT had a lower risk of recurrence versus non-HT groups. A total of 136 differentially expressed mRNAs (DEMs) were identified between HT and non-HT groups. Among them, the expression level of DMBT1 in HT groups was statistically higher than that in non-HT groups. A significant association with ETE and recurrence was revealed in the high expression and the low expression of DMBT1. Furthermore, DMBT1 was an independent predictor of survival. The overall immune activity of high expression of DMBT1 was higher than that of the low-expression group.ConclusionsThe PTC patients with HT had better behavior features and prognosis than those with simple PTC. DMBT1 in PTC-HT patients was a potential possible factor that inhibits tumors. High expression of DMBT1 may improve PTC prognosis by immune-related pathways.

BACKGROUND Asthma accounts for 0.4% of all deaths worldwide, a figure that increases annually. Ketamine induces bronchial smooth muscle relaxation, and increasing evidence suggests that its anti-inflammatory properties might protect against lung injury and ameliorate asthma. However, there is a lack of evidence of the usefulness and mechanism of ketamine in acute asthma exacerbation. This study aimed to analyze the therapeutic effects and mechanism of action of ketamine on acute ovalbumin (OVA)-induced murine asthma. MATERIAL AND METHODS In vivo, BALB/c mice with OVA-induced asthma were treated with or without ketamine (25 or 50 mg/mL). Serum, lung sections, and mononuclear cell suspensions from the lung were collected for histological, morphometric, immunofluorescence, microRNA, quantitative polymerase chain reaction, regulatory T cell identification, cytokine, and Western blotting analyses. In vitro, bronchial epithelial cells were cultured to analyze the effect and mechanism of ketamine on epithelial-mesenchymal transition (EMT) and transforming growth factor-β (TGF-β) signaling. RESULTS The inhalation of ketamine 25 or 50 mg/mL markedly suppressed OVA-induced airway hyper-responsiveness and airway inflammation, significantly increased the percentage of CD4+CD25+ T cells, and significantly decreased OVA-induced up-regulation of TGF-β1 and the EMT. MiR-106a was present at higher amounts in OVA-induced lung samples and was suppressed by ketamine treatment. The in vitro results showed that TGF-β1-induced EMT was suppressed by ketamine via miR-106a level regulation. CONCLUSIONS Ketamine ameliorates lung fibrosis in OVA-induced asthmatic mice by suppressing EMT and regulating miR-106a level, while ketamine inhalation might be a new therapeutic approach to the treatment of allergic asthma.

The efficacy of a low-protein diet (LPD) on diabetic nephropathy is controversial. We aimed to investigate the renoprotective effects of an LPD and the underlying molecular mechanism in a rat model of type 2 diabetes and obesity.Diabetic male Wistar fatty (fa/fa) rats (WFRs) were treated with a standard diet (23.84% protein) or an LPD (5.77% protein) for 20 weeks from 24 weeks of age. We investigated the effect of the LPD on renal function, fibrosis, tubular cell damage, inflammation, mitochondrial morphology of proximal tubular cells (PTCs), apoptosis, autophagy and activation of mammalian target of rapamycin complex 1 (mTORC1).Kidney weight, albuminuria, excretion of urinary liver-type fatty acid binding protein, levels of plasma cystatin C and changes in renal histology, including fibrosis, tubular cell damage and inflammation, were aggravated in WFRs compared with non-diabetic Wistar lean rats (WLRs). Fragmented and swelling mitochondria accumulated in PTCs and apoptosis were enhanced in the kidney of WFRs. Immunohistochemical staining of p62 and p-S6 ribosomal protein (p-S6RP) in the tubular lesions of WFRs was increased compared with WLRs. The LPD intervention clearly ameliorated damage as shown by the assessment of renal function and histology, particularly tubulointerstitial damage in diabetic kidneys. Additionally, the 5.77% LPD, but not the 11.46% LPD, significantly suppressed p-S6RP levels and increased microtubule-associated protein light chain 3-II levels in the renal cortex. The LPD intervention partially decreased HbA1c levels in WFRs, and no differences in mean BP were observed among any of the groups.A very-low-protein diet improved advanced diabetic renal injuries, including tubulointerstitial damage, by restoring autophagy through the suppression of the mTORC1 pathway.

Ovarian cancer is one of the most common types of solid carcinoma diagnosed during pregnancy. Taxane plus a platinum derivative is a combination therapy that is predominantly used in the treatment of ovarian cancer in non-pregnant women. Pregnancy adds various complexities to a course of treatment. In pregnant patients diagnosed with cancer during the first trimester, the risks of fetal malformations and fetal loss increase following the administration of cytotoxic drugs, and this is higher with multi-agent vs. single-agent chemotherapy (~ 25 vs. 10%). Exposure during the second and third trimester has little influence on teratogenic effects but increases the risk of intrauterine growth retardation, prematurity, low birth weight, and bone marrow toxicity. The present study aimed to review the maternal and fetal safety of treatment with taxane plus platinum derivatives for ovarian cancer during pregnancy. Relevant literature was retrieved from the Embase and PubMed databases using the search terms "ovarian cancer", "pregnancy", "taxane", "paclitaxel", "docetaxel", "platinum", "cisplatin", and "carboplatin". All available data up until September 2016 was synthesized, with no language restrictions. A total of 11 articles (including 13 pregnancies and 14 newborns) were retrieved that reported on the use of standard-dose taxane and platinum chemotherapy, including 9 cases treated with paclitaxel and carboplatin, 3 cases treated with paclitaxel and cisplatin, and 1 case treated with docetaxel and cisplatin. In 13 of the 14 (92.9%) births included, a healthy neonate was born, with follow-up ranging from 2 to 160 months. The average weight of the neonates at the time of delivery was 2,442.1 g. In 7 of 9 the case reports that provided survival data, the mother was alive and disease-free at the end of follow-up (ranging from 2 to 40 months). In conclusion, combination therapy with taxanes and a platinum derivative may play a significant role in the management of pregnant patients with ovarian cancer during the second and third trimester. Exposure to this combination of agents during the second and third trimester does not appear to have a significant bearing on fetal mortality and abortion. .

DEAD (Asp-Glu-Ala-Asp) box helicase 5 (DDX5) is an ATP-dependent RNA helicase that is overexpressed in various malignancies. Increasing evidence suggests that DDX5 participates in carcinogenesis and cancer progression via promoting cell proliferation and metastasis. However, the functional role of DDX5 in gastric cancer is largely unknown. In this study, we observed that DDX5 was significantly up-regulated in gastric cancer tissues compared with the paired adjacent normal tissues. The expression of DDX5 correlated strongly with Ki67 index and pathological stage of gastric cancer. In vitro and in vivo studies suggested that knockdown of DDX5 inhibited gastric cancer cell proliferation, colony formation and xenografts growth, whereas ectopic expression of DDX5 promoted these cellular functions. Mechanically, DDX5 induced gastric cancer cell growth by activating mTOR/S6K1. Treatment of everolimus, the specific mTOR inhibitor, significantly attenuated DDX5-mediated cell proliferation. Interestingly, the expression of DDX5 and p-mTOR in gastric cancer tissues demonstrated a positive correlation. Taken together, these results revealed a novel role of DDX5 in gastric cancer cell proliferation via the mTOR pathway. Therefore, DDX5 may serve as a therapeutic target in gastric cancer.

Diabetes is a serious metabolic disease that causes multiple organ dysfunctions. Recent evidence suggests that diabetes could contribute to the initiation and progression of certain cancers in addition to the classic diabetic complications. Furthermore, some of the drugs used clinically to treat patients with diabetes might affect cancer initiation, progression and mortality. The recent discovery of the possible anticancer effects of metformin, a classic antidiabetic drug, has led physicians and scientists to reconsider the interaction between diabetes and cancer. In the present review, we analyze recent reports in this field, and explore possible mechanistic links between diabetes and cancer biology.

Fluctuating hyperglycemia exerts a more deleterious effect than constant hyperglycemia on cardiovascular outcome in diabetic patients. We investigated the inflammatory responses of human coronary artery endothelial cells (HCAECs) to constant and periodic high glucose in vitro.HCAECs were incubated for 72 h continuously either in normal glucose (5.5 mmol/L), constant high glucose (25 mmol/L glucose), periodic high glucose (5.5 and 25 mmol/L glucose alternating every 6 h) or mannitol.Concentrations of interleukin (IL)-6, tumor necrosis factor (TNF)-α and intercellular adhesion molecule (ICAM)-1 in the supernatants of cell culture were measured using ELISA kits. The mRNAs of IL-6, TNF-α and ICAM-1 were evaluated by real-time quantitative PCR.Periodic high glucose caused a more intense inflammatory response than normal glucose and constant high glucose in HCAECs, with a marked increase in IL-6, TNF-α and ICAM-1 in supernatants of cell culture (P0.05). The concentrations of the three pro-inflammatory cytokine mRNAs were higher in cells exposed to periodic high glucose than those exposed to constant high glucose and normal glucose (P0.05).In cultured HCAECs, periodic high glucose evoked a more intense inflammatory response than constant high glucose.

Objective: To investigate the effects of ligustrazine (Li) on myocardial fibrosis in rats with pressure overload.Methods: Pressure overload rat models were established by constricting the abdominal aorta. Sixty-three SD rats were divided into 3 groups: Sham operated group (SOG, n = 21), operated group (OG,n = 21) and operated combined with ligustrazine group (OG+Li,n = 21). Each group was randomly assigned to seven time points: The 1st, 2nd, 4th, 7th, 14th, 21st and 30th day after operation. Three rats were included in each time point. Serial sections of cardiac tissues were examined and the morphological or morphometric analysis of the SOG, OG and OG+Li done by histopathological and computer image analyzer technique.Results: (1) It showed that there were reactive fibrosis (from the 4th day on after operation) and reparative fibrosis (from the 21st day on after operation) in the OG, while myocardial fibrosis in the OG+Li was alleviated. Though reactive fibrosis (from the 21st day on after operation) was shown, reparative fibrosis wasn’t seen. (2) Perivascular collagen area (PVCA) in the OG (2. 09 ± 0. 45) was significantly higher than SOG (0.83 ± 0.06) from the 1st day on after operation and then steadily increased, while in the OG+Li (1.16 ± 0.06), it was significantly lower than OG at the same time; collagen volume fraction (CVF) in the OG (3.08 ± 0. 56) significantly increased compared with the SOG (2. 78 ± 0. 64) from the 2nd day on after operation and showed a trend of rapid ascending from the 21st day on after operation; and in the OG + Li (4.69 ± 0.85), it was significantly decreased compared with the OG (7.56 ± 0.88) from the 21st day on after operation, with allP

CHF is a common cardiovascular complication, and also is a result of all kinds of cardiopathies. Common cardiotonic and diuretic treatment don’t have a good effect and patients could easily get digitalism because of poor tolerance of digitalis. Recently, good curative effects have been achieved by the therapy of integrative Chinese and western medicine. Especially in recent few years, Chinese medicine has reached a fairly depth and achieved positive results in studying CHF with the raising level of medical research. Even so, because of lacking n a great many controlled observation, further research of the effect on CHF with Chinese medicine is remained to be studied from biochemical and biomolecular level, or from clinical practice.

Background Coronary atherosclerosis, the most common form of coronary artery disease (CAD), is characterized by accumulation of lipid in the walls of coronary arteries. Recent data from clinical trials have showed that high-density lipoprotein cholesterol (HDL-C) has causal role in the pathogenesis and development of coronary atherosclerosis. Cholesteryl ester transfer protein (CETP) is an important regulator of plasma HDL-C. Several genetic mutations in the CETP gene were found to be associated with HDL-C levels. The aim of the present study is to evaluate the association of HDL-C-related CETP polymorphisms and risk of coronary atherosclerosis. Methods We investigated the association of seven single nucleotide polymorphisms (SNP) (rs1800775, rs708272, rs5882, rs1532624, rs1864163, rs7499892, and rs9989419) in the CETP gene with the risk of coronary atherosclerosis and levels of HDL-C in a case–control study in China. Included in the study were 420 patients with coronary atherosclerosis and 424 healthy controls. SNP genotyping was performed by TaqMan allelic discrimination assay and serum lipid levels were measured by standard laboratory methods. Results Carriers of the AA and GA + AA genotypes of rs708272 had significant lower risks of coronary atherosclerosis (OR = 0.55, 95% CI: 0.36-0.85, p = 0.003; OR = 0.67, 95% CI: 0.50-0.90, p = 0.007, respectively) compared to those with GG genotype. These relations remained significant after adjustment for confounding effects of age, smoking, diabetes and hypertension. The rs1800775 polymorphism was significantly associated with serum levels of HDL-C in healthy controls (p = 0.04). Besides, rs708272 was in close linkage disequilibrium (LD) with rs1800775 in this study. Conclusions Our findings indicated that CETP rs708272 may be associated with the risk of coronary atherosclerosis and rs1800775 may influence serum HDL-C levels in healthy controls in Chinese.

Purpose: This study was to investigate whether high pericardial adipose tissue (PAT) volume is related to the presence and severity of coronary artery disease (CAD). Methods: Consecutive patients (310 patients) who underwent both dual-source 64-slice CT and percutaneous coronary angiography were recruited into this study. Waist circumference (WC), body mass index (BMI), blood biochemical variables, coronary artery calcium (CAC) score and Gensini score were measured. Pericardial adipose tissue (PAT) volume was determined by dual-source CT. Results: PAT volume was positively correlated with BMI, WC, gender (male), hypertension, diabetes, age, total cholesterol and low-density lipoprotein-cholesterol. PAT volume in CAD patients was significantly higher than that in patients without CAD (238.36 ± 81.21 cm3 vs. 200.13±72.34 cm3). PAT volumes in patients with multi-vessel lesions were significantly higher than those with one-vessel lesions (P < 0.001). A significant correlation between PAT volume and CAC score (r=0.305, P < 0.001) was found. PAT volume was an independent factor affecting Gensini score. Conclusion: PAT volume was significantly correlated with traditional cardiovascular risk factors, the severity of coronary atherosclerosis and the number of stenotic coronary vessels. Thus, PAT volume may be a reliable marker to evaluate the presence and severity of CAD.

Objective: To describe a case with acute myocardial infarction caused by gastric carcinoma-associated thrombotic thrombocytopenic purpura. Clinical Presentation and Intervention: A 79-year-old man was admitted with abdominal pain and pyrexia. He later developed cardiac complications and microangiopathy that indicated worsening progression. Manifold evidence confirmed the diagnosis of myocardial infarction caused by thrombotic thrombocytopenic purpura. The patient was treated mainly with plasma transfusion incorporated with steroids. Conclusion: This case should remind physicians to consider microangiopathy as a differential diagnosis in patients with unexplained cardiac symptoms or atypical presentation. Early diagnosis and treatment are helpful in decreasing the sequelae of this syndrome.

Background: Dual-source CT coronary angiography (CTCA) has been used to detect coronary artery disease; however, the factors with potential to affect its diagnostic accuracy remain to be defined. Purpose: To prospectively evaluate the accuracy of dual-source CTCA in diagnosing coronary artery stenosis according to conventional coronary angiography (CAG), and the effect of average heart rate, heart rate variability, and calcium score on the accuracy of CTCA. Material and Methods: A total of 113 patients underwent both dual-source CTCA and CAG. The results were used to evaluate the findings in dual-source CTCA to assess the accuracy in the diagnosis of ≥50% (significant stenosis) and >75% (severe stenosis) of coronary artery according to those by CAG. Patients were divided into subgroups according to their heart rate (HR), HR variability (HRV), and calcium score, and the accuracy of CTCA was further evaluated. The chi-square test was used to analyze the difference in sensitivity and specificity for the detection of ≥50% and >75% coronary stenosis among subgroups. The generalized estimation equation method was used in per-vessel analysis to adjust for within-patient correlation. Results: In all, 113 patients had 338 vessels and 1661 segments evaluated by CAG. Dual-source CTCA displayed 1527 segments (91.9%). Among them, 1468 segments (calcium score by CAG score 1, n=1018; score 2, n=270; score 3, n=180) were assessable in CTCA. On a per-patient analysis, the sensitivity and specificity of CTCA were 93.9% and 93.5% for significant stenosis and 86.9% and 98.1% for severe stenosis. On a per-vessel basis, the sensitivity and specificity were 90.2% and 97.1% for significant and 83.3% and 98.1% for severe stenosis. On a per-segment analysis, the sensitivity and specificity were 90.2% and 97.1% for significant and 83.3% and 98.1% for severe stenosis. Average HR had no effect on the sensitivity and specificity of CTCA ( P>0.05); whereas HRV and calcium score had some effect on the sensitivity and specificity of CTCA ( P Conclusion: On a per-patient, per-vessel, and per-segment basis, dual-source CTCA has a high sensitivity and specificity for the diagnosis of coronary artery stenosis. Average HR has no effect on the diagnostic accuracy of CTCA, while HRV and calcium score have a statistically significant effect on the sensitivity and specificity of CTCA.

Introduction In recent years, intravascular ultrasound (IVUS) has evolved as a valuable adjunct to angiography. IVUS allows precise tomographic measurement of lumen area and plaque size, distribution and, to some extent, composition. It is essential in clinic decision making. Myocardial fractional flow reserve (FFR myo ) is a special index of the functional severity of coronary stenosis. Although the application of FFR myo to assess intermediate coronary lesion is widely performed in some centers in developed countries, its use in China was lagged. Because it is relatively expensive to measure FFR myo , it will be beneficial to save the expenses and to short operation time if CAG and IVUS criteria could be clinically used as tools to discriminate functional significant of intermediate stenosis. Materials and Methods In 46 lesions of intermediate severity (eg, 40%–60% diameter stenosis) we assessed 1. by pressure wire: myocardial fractional flow reserve (FFR myo , index of functional significance), and 2. by IVUS: minimal lumen cross-sectional area (MLA) and percent area stenosis at the lesion site. Receiver operating characteristic (ROC) curve analysis was performed to establish the best cut-off values of IVUS indexes (ie, MLA and percent area stenosis) that were most predictive of FFR myo Results FFRmyo in 46 lesions of angiographic intermediate stenosis (49±11%) was significantly lower than it was in angiographic normal artery (0.83±0.15 vs 0.97±0.02, p myo myo (r=−0.68, p myo (r=0.63, p 2 (sensitivity 93%, specificity 77%) to be the best cut-off values to fit with FFR myo Conclusion IVUS area stenosis ≥65% and minimal lumen cross-sectional area ≤4 mm 2 reliably identified functionally critical intermediate coronary stenosis.

Rationale: MicroRNAs are released by cultured cells and can be detected in the blood. Recent studies reported that circulating microRNAs profile could be the biomarker of coronary artery disease. Objective: To address the regulation of circulating microRNAs in patients with myocardial bridging. Methods and results: To determine the regulation of microRNAs, we performed a microRNA profile using RNA isolated from n=15 healthy volunteers and n=33 patients with myocardial bridging that diagnosed by the invasive coronary angiography. Low density chip initially screened the almost 30 suspected microRNAs differentially expressed in the mixed serum from patients and volunteers. To prospectively confirm these data, we detected selected microRNAs in serum among each donator by quantitative PCR. Staticstical analysis demonstrated that seven microRNAs' expression level were significantly different between the myocardial bridging patients and healthy volunteers. Consistent with the data obtained by the profile, microRNA-92a/487a/503/201/126 were obviously higher, while microRNA-29b/339 were remarkably lower in the patient group compared with healthy control. These results were demanded to be validated by more cohort of patients with documented myocardial bridging from other cardiological centers. Likewise, bioinfromatics database shown that microRNA-92a/503/126 were involved in the cellular hypoxia/ischemia, miR-29b may regulated the process of angiogenesis, collagen remodelling. In addition miR-339 takes part in the mesenchymal cell differentiation and embryonic development, while miR-487a is associated with vascular constriction/dilation. The specific regulatory function and mechanism are required further research in the future. Conclusions: Circulating levels of vascular development and cellular hypoxia/ischemia -associated microRNAs are significantly detectable in serum and discrepantly expressed in patients with myocardial bridging.

Objectives To investigate the effect of ligustrazine (tetramethylpyrazine, TMP) in attenuating myocardial apoptosis on rats with myocardial ischaemia reperfusion (IR) injury and to explore its mechanism. Methods The animal model was built by ligation of the left anterior descending artery of rats (35 min of regional ischaemia followed by 120 min of reperfusion). Male Sprague-Dawley rats were randomly divided into sham, IR, TMP pretreated (TMP 10 mg/kg intravenous injection, 5 min before ligation), and TMP+L-NAME group (TMP 10 mg/kg intravenous injection, 5 min before ligation and L-NAME 30 mg/kg intravenous injection, 15 min before reperfusion). Caspase-3 activity and TUNEL staining were used to detect myocardial apoptosis. Nitric oxide production (NO x ) of myocardial tissue was examined using nitric oxide detection kit and expression of eNOS were observed by RT-PCR and western blot. Results There were some TUNEL-positive staining myocardial cells in experimental groups except the sham group. Compared with IR group, TMP reduced apoptosis index (15.0±2.9% vs 25.2±3.3% in the IR group, p x (0.40±0.04 µmol/g vs 0.30±0.03 µmol/g in IR group, p Conclusions Ligustrazine offers antiapoptotic and cardioprotection effects against myocardial IR injury possibly through increasing the expression of eNOS and the level of NO.

Introduction The percentage of angina and cardiac dysfunction and cardiovascular events increased significantly in hypertensive diabetes mellitus compared with essential hypertension and type 2 diabetes mellitus alone. Hypertension and diabetes are often associated with cardiac microvascular abnormalities. The major cardiac microcirculation alterations are the capillary rarefaction and endothelial cell functional impairment, which may be in the development of coronary insufficiency. We presume that the more serious injury in cardiac microvascular structure and function followed by hypertensive diabetes mellitus. Aims The purpose of the present study is to investigate ultrastructural changes and expression of eNOS in rat myocardial capillary endothelial cells as a response to hypertension with diabetes mellitus. Methods The rat model of hypertension with diabetes mellitus (SHDM) and the rat model of diabetes mellitus (DM) alone were induced by an intraperitoneal injection of streptozotocin combined with high fat diet in spontaneously hypertensive rats (SHR) and SD rats, respectively. The groups were as follows: SD, DM, SHR, and SHDM. After 16 weeks, ultrastructure of the myocardial capillaries was examined by transmission electron microscopy and the expression of endothelial nitric oxide synthase (eNOS) was detected by immunohistochemistry. Results Ultrastructural alterations of myocardial capillaries in SHR, DM and SHDM were oedematous endothelial cell, endothelial protrusions into lumen and narrowed /or irregular lumen respectively. These alterations indicate that cell injury was more significant in the myocardium of DM and SHDM. Thickening of basal lamina in myocardial capillaries with SHR was less considerable compared with SD (31.3±4.2 nm vs 28.6±3.6 nm, p>0.05), while thickening was a prominent feature of DM (46.6±5.3) nm and SHDM (51.5±4.6) nm (compared with SD or SHR, p Conclusions These results suggest that a combination of hypertension and diabetes mellitus enhanced the damage of myocardial capillaries endothelial cell ultrastructure and function more than either hypertension or diabetes mellitus alone.

Introduction Pericytes are perivascular cells with multifunctional activities which are now being elucidated. Pericyte alteration or degeneration is linked directly with microangiopathy in diabetes, scleroderma and hypertension. Aims The purpose of the present study is to investigate the pathologic changes of the myocardial capillary pericytes in hypertension with diabetes rats. Methods The rat model of hypertensive with diabetes mellitus (SHDM) and the rat model of diabetes mellitus (DM) were induced by an intraperitoneal injection of streptozotocin combined with high fat diet in spontaneously hypertensive rats (SHR) and SD rats, respectively. The four groups were as follows: SD, DM, SHR and SHDM. The ultrastructure changes were examined by transmission electron microscope and the number of precity was assessed by immunohistochemistry of ventricular sections at 16 weeks. Results Ultramicroscopic analysis of capillaries showed the pericytes on myocardial capillaries of SHR, DM, and SHDM were conspicuously abnormal in shape and were with cytoplasm containing abundant myofilament and organelle. In addition, pericytes seemed to be loosely associated with the endothelium. The number of pericytes in SHR, DM and SHDM were significantly increased than that in SD. The number of pericytes in SHDM were much higher than that in SHR (11.8±3.6 vs 3.9±1.1, p 0.05). Conclusion These results suggest the phenotype changes and increase of myocardial capillary pericytes in response to hypertension with diabetes. These changes may contribute to arterialisations of myocardial capillary and pericapillary fibrosis.