Comparison of leaf transcriptome in response to Rhizoctonia solani infection between resistant and susceptible rice cultivars.

BACKGROUND: Sheath blight (SB), caused by Rhizoctonia solani, is a common rice disease worldwide. Currently, rice cultivars with robust resistance to R. solani are still lacking. To provide theoretic basis for molecular breeding of R. solani-resistant rice cultivars, the changes of transcriptome profiles in response to R. solani infection were compared between a moderate resistant cultivar (Yanhui-888, YH) and a susceptible cultivar (Jingang-30, JG). RESULTS: In the present study, 3085 differentially express genes (DEGs) were detected between the infected leaves and the control in JG, with 2853 DEGs in YH. A total of 4091 unigenes were significantly upregulated in YH than in JG before infection, while 3192 were significantly upregulated after infection. Further analysis revealed that YH and JG showed similar molecular responses to R. solani infection, but the responses were earlier in JG than in YH. Expression levels of trans-cinnamate 4-monooxygenase (C4H), ethylene-insensitive protein 2 (EIN2), transcriptome factor WRKY33 and the KEGG pathway plant-pathogen interaction were significantly affected by R. solani infection. More importantly, these components were all over-represented in YH cultivar than in JG cultivar before and/or after infection. CONCLUSIONS: These genes possibly contribute to the higher resistance of YH to R. solani than JG and were potential target genes to molecularly breed R. solani-resistant rice cultivar.

TIPE2 Inhibits Lung Cancer Growth Attributing to Promotion of Apoptosis by Regulating Some Apoptotic Molecules Expression.

Recent studies found that TIPE2 was involved in cancer development. However, little is known about TIPE2 in lung cancer. Our study aims to clarify the role of TIPE2 in lung carcinogenesis. We examined the expression of TIPE2 in lung squamous cancer (LSC), small cell lung cancer and lung adenocarcinoma (AdC) tissues and found that TIPE2 expression was lost in small cell lung cancer, compared with adjacent non-tumor tissues. Overexpression of TIPE2 significantly inhibited the growth of lung cancer cell H446 in vitro and even suppressed tumor formation in vivo. Flow cytometry analysis found TIPE2 overexpression promoted apoptosis of H446. In TIPE2 over-expression cells, caspase-3, caspase-9, and Bax were significantly up-regulated while Bcl-2 was down-regulated. Moreover, coincident results were shown by immunohistochemistry in tumors from nude mice. TIPE2 inhibited the phosphorylation of Akt, while promoting the phosphorylation of P38, but had no effect on IκBα and ERK pathway. Taken together, TIPE2 promoted lung cancer cell apoptosis through affecting apoptosis-related molecules caspase-3, caspase-9, Bcl-2 and Bax, possibly via regulating P38 and Akt pathways, indicating that TIPE2 might be a novel marker for lung cancer diagnosis and therapy.

[Abnormal semen liquefaction and seminal plasma lipoprotein (a)].

OBJECTIVE: To explore the effect of seminal plasma lipoprotein (a) in abnormal semen liquefaction and its clinical significance. METHODS: According to The WHO Laboratory Manual for the Examination and Processing of Human Semen, we conducted semen routine analyses of 101 patients with abnormal semen liquefaction and 26 normal healthy controls. We added chymotrypsin to the semen for 30 minutes of incubation at 37 degrees C. When there were filaments, we centrifuged the semen and obtained the upper seminal plasma to determine the level of lipoprotein (a). RESULTS: The level of lipoprotein (a) was significantly higher in the 101 patients ([526.2 +/- 243.5] mg/L) than in the 26 normal controls ([296.9 +/- 105.2] mg/L) (P < 0.01) . CONCLUSION: Lipoprotein (a) can inhibit fibrin dissolution, and delayed fibrin dissolution in semen liquefaction may be related to the increased level of seminal plasma lipoprotein (a). The seminal plasma lipoprotein (a) level should be taken into account in the clinical diagnosis of male infertility caused by abnormal semen liquefaction.

[Effect of HOE642 on cardiac myocyte apoptosis in rat non heart-beating donors].

OBJECTIVES: To investigate the effect of HOE642 on cardiac myocyte apoptosis of the heterotopic heart transplantation of rat non heart-beating donors. METHODS: Totally 112 male Sprague-Dawley rats were randomly divided into 7 groups (n=16 in each group) C, the control group (normal hearts); S10, S30, and S45 (groups of transplanted hearts after 10, 30, and 45 minutes of asystole); and SH10, SH30, and SH45 (groups of transplanted hearts after 10, 30, and 45 minutes of asystole and infused with HOE642). After rata in the experimental groups were killed by warm ischemia the donators of the S10, S30 and S45 groups were infused with 5TH-1 for 30 minutes, and the dead rats in group SH10, SH30, and SH4 were infused with STH-1 and HOE642 (20 micromol/L) for 30 minutes. Heterotopic heart transplantation were processed by the method of neck Cuff. The heart specimens of S10, SH10, S30, and SH30 groups were taken after 48 hours of transplantation, and the heart specimens of S45 and SH45 groups were taken immediately after transplantation. Then apoptotic myocytes were detected with terminal deoxynucleotide transferase-mediated deoxyuridine-biotin nick end labeling method and the expressions of Bcl-2, Bax, and Caspase-3 proteins were detected by immunohistochemistry. RESULTS: The rats were discerned death when cardiac electric wave vanished after 9-11 minutes of bloodletting by transsection of abdominal aorta. The number of positive cardiac muscle cells in S10 and S30 groups were significantly larger than those in group SH10 and SH30 (P < 0.05). The levels of Bcl-2 protein expression in S10 and S30 groups were significantly lower than those in SH10 and SH30 groups (P < 0.05). The levels of Bax and Caspase-3 protein expression were significantly higher than those in SH10 and SH30 groups (P < 0.05). CONCLUSIONS: The rat model of a heterotopic heart transplantation on the cervical part is a convenient animal model for cardiac muscle protection. HOE642 can suppress rat cardiac muscle cells apoptosis (within 30 min) after death caused by warm ischemia.

[Protection of cadaver lungs of non-heart-beating donor lung transplantation in rats].

OBJECTIVE: To investigate the methods to alleviate lung injury of non-heart-beating donor to attain better structure and function. METHODS: Sixty-four Sprague-Dawley rats were randomly divided into 4 groupsú a heart-beating donor group(HBD group), a non-heart-beating donor group without protective measures(NHBD-N group), a non-heart-beating donor group with continuous mechanical ventilation or with topical cooling on cadaver lung (NHBD-V group and NHBD-I group). After the transplantation, lung compliance,pulmonary function,wet/dry ratio of lung and content of energy metabolism were compared among the 4 groups. RESULTS: Due to the longer warm ischemic period, NHBD lungs suffered more injuries than HBD lungs. However, compared with NHBD-N group, the wet/dry ratio of the lung in NHBD-V group and NHBD-I group was lower(5.28+/-1.24,4.21+/-0.85,4.14+/-1.33,P<0.01),the lung injury index (14.35+/-3.21,11.28+/-3.26,10.41+/-2.85, P<0.01)and the count of white blood cells(425.60+/-86.47,316.30+/-56.24,295.50+/-70.26, P<0.01) were milder, while the lung compliance and preservation of energetic metabolte were better in the NHBD-V group and the NHBD-I group. CONCLUSION: Continuous mechanical ventilation or topical cooling may protect the NHBD lung during the warm ischemic period.

[Surgical treatment of cor triatriatum in 15 patients].

OBJECTIVE: To review the clinical data of pathological morphology, diagnosis, surgical treatment of cor triatriatum in 15 patients. METHODS: Fifteen patients with a mean age of (14.6+/-10.3) years (range from 6 months to 40 years) were performed operations under extracorporeal circulation. Fourteen of the patients had cor triatriatum sinister, and 1 had cor triatriatum dexter; 12 of the 15 patients had other cardiac abnormalities. The excision of the fibromuscular membrane was accomplished through a right atrial incision in all of the 14 cases, and the associated abnormalities were corrected at the same time. RESULTS: One patient died after the operation, and the other survivors had good outcome. CONCLUSION: Operation is necessary if the diagnosis is clear. The patients generally have good prognosis. Surgical results of cor triatriatum depend on the complexity of associated defects and the adequacy of the repair.