High-resolution 3.0 T MR imaging of esophageal carcinoma with histopathological findings / 中华放射学杂志

Objective To prospectively determine the feasibility of high-resolution in vivo MR imaging in the evaluation of esophageal carcinoma invasion at 3.0 T.Methods One hundred and eighteen patients with esophageal carcinoma,proven by the gastroscopic biopsy,were prospectively studied using 3.0 T MR.The esophageal specimens were sectioned transversely to keep consistent in the orientation with the MR images,the histopathological stage was made and the thickness of the tumor on the largest diameter of the slice were measured.The MR images were reviewed in the transverse plane.According to the seventh American joint committee on cancer,the MR stage was made and the tumor's thickness was measured.The MR images and the histopathological slices were matched.The staging diagnostic efficacy of the MR imaging was evaluated with the histopathological results as the standard reference,Kappa test was used to compare the stage of MR imaging with that at the histopathological analysis.Bland-Altman scatterplots were used to compare the thickness of tumor measured on the MR images with that at the histopathological measurement.Results Ninety seven cases(82.2％,97/118) of MR stage were accurately made,including 7 T1a,15 T1b,18 T2,25 T3 and 32 T4a cases,furthermore,14 cases were over staged and 7 cased were underestimated.The MR stage was highly consistent with the histopathological stage (Kappa=0.772).The sensitivity for the staging of high-resolution MR imaging at 3.0 T was 58.3％(7/12) to 100.0％(32/32),the specificity was 95.3％ (82/86) to 98.1％ (104/106),and the accuracy was 91.5％ (108/118) to 96.6％ (114/118),respectively.Bland-Altman scatterplots demonstrated that the discrepancy of the mean thickness between the value obtained by three radiologists respectively and the histopathological analysis were 2.0,2.6 and 2.1 mm,which demonstrated a good consistency.Conclusion High-resolution MR images obtained at 3.0 T can be used to evaluate the depth of carcinoma invasion and provide excellent diagnostic accuracy for preoperative staging.

Down-regulation of miR-221-3p/222-3p inhibits cell proliferation and promotes chondrogenic differentiation of human bone marrow mesenchymal stem cells / 中国组织工程研究

BACKGROUND:The use of mesenchymal stem cels in the field of tissue engineering for osteoarticular injury repair is a very promising tool since these cels are readily expandable and able to differentiate into chondrocytes. Abundant evidence suggests that microRNAs play critical roles in chondrogenic differentiation of mesenchymal stem cels. OBJECTIVE:To observe the chondrogenic effect of human bone marrow mesenchymal stem cels transfected with lentiviral vectors bearing miR-221-3p/222-3p inhibition, thereby provding new strategies for cartilage injury. METHODS: miRNA microarray technology was applied to detect microRNAs expression profiles at three different stages of chondrogenic differentiation induction after transforming growth factor-β3 treatment and verified by real-time fluorescence quantitative PCR (RT-qPCR). Human bone marrow mesenchymal stem cels were infected with lentivirus bearing miR-221-3p/222-3p inhibition. After co-suppressing the expression of miR-221/222-3p, cel counting kit-8 was used to determine the cel proliferation, the differentiation of bone marrow mesenchymal stem cels towards chondrocytes was verified by type II colagen protein expression through immunohistochemistry and glycosaminoglycan accumulation was also elevated by sarranine O staining. RT-PCR was used to detect type II colagen and aggrecan mRNA expression at 21 days of chondrogenic induction. RESULTS AND CONCLUSION: The expression of miR-221-3p/222-3p was inhibited after Lv-miR221-3p/222-3p inhibition co-transfected into bone marrow mesenchymal stem cels. microRNA microarray and RT-qPCR results showed that the expression of miR-221-3p/222-3p was declined significantly at the anaphase of chondrogenic differentiation. The expression levels of chondrogenic markers, Aggrecan and type II colagen were significantly increased in the miR-221-3p/222-3p inhibition group and cel proliferation was also inhibited significantly compared with non-transduced cels or transduced with the empty lentiviral vector group. miR-221-3p/222-3p knockdown in bone marrow mesenchymal stem cels could inhibit proliferation but promote chondrogenic differentiation of bone marrow mesenchymal stem cels.

Role of neuropeptide Y and peroxisome proliferator-activated receptor γ coactivator-1α in stress cardiomyopathy / 华中科技大学学报（医学）（英德文版）

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.

Role of neuropeptide Y and peroxisome proliferator-activated receptor γ coactivator-1α in stress cardiomyopathy / 华中科技大学学报（医学）（英德文版）

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.

Role of reactive oxygen species in triptolide-induced apoptosis of renal tubular cells and renal injury in rats / 华中科技大学学报（医学）（英德文版）

This study investigated the role of reactive oxygen species (ROS) in the pathogenesis of triptolide-induced renal injury in vivo. Rats were randomly divided into 4 groups (n=5 in each): triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8; control group in which the rats received a single intraperitoneal injection of 0.9% physiological saline on day 8; vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8; triptolide+vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days, and then to the same treatment as the triptolide group on day 8. All the rats were sacrificed on day 10. Blood samples were collected for detection of plasma creatinine (Pcr) and plasma urea nitrogen (PUN) concentrations. Both kidneys were removed. The histological changes were measured by haematoxylin-eosin (HE) staining. The production of ROS was determined by detecting the fluorescent intensity of the oxidation-sensitive probe rhodamine 123 in renal tissue. Renal malondialdehyde (MDA) content was measured to evaluate lipid peroxidation level in renal tissue. TUNEL staining was performed to assess apoptosis of renal tubular cells. Renal expression of apoptosis-related proteins Bcl-2, Bax, Bid, Bad, Fas and FasL, as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR. The results showed that triptolide treatment promoted the generation of a great amount of ROS, up-regulated the expression of Bax, Bid, Bad, Fas and FasL at both protein and mRNA levels, as well as the ratio of Bax to Bcl-2, and caused the apoptosis of renal tubular cells and renal injury. However, pretreatment with an antioxidant, vitamin C, significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury. It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury. The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.

Multiple keratoacanthoma centrifugum marginatum: first case report in China / 中华皮肤科杂志

A case of multiple keratoacanthoma centrifugum marginatum is first reported in China. A 37-year-old woman was admitted to the hospital for papules and plaques on her face, which had been increasing in number for 4 months. Cutaneous examination revealed dozenes of well-marginated, pale-red or skin-colored crateriform papules of variant size, and plaques in a geographic pattern on her face. The papules presented with a central umbilication filled with grey-brown corneous material. The plaques were surrounded by dyke-like borders, covered with thick, crusted brown corneous material, and partly depressed in the center. Histopathology showed hyperkeratosis, parakeratosis, irregular strip-like extension of epidermis into dermis, keratinous cysts and squamous eddies. The tumor cells had eosinophilic and glassy cytoplasm characteristic of keratoacanthoma.Given both the clinical and histologic evidence, a diagnosis of multiple keratoacanthoma centrifugum marginatum was made. After more than 3 months of treatment with oral acitretin and topical tretinoin, the lesions faded,leaving rugosity scars. No relapse was noted during 3-year follow-up.