THE MAMMALIAN FOSSILS FROM WESTERN TAIWAN STRAIT

本文简要记述了出自台湾海峡西部海域的170件哺乳动物化石，其中的102件分属于urSuSSP，ElEPHASMAXIMuS，dICErOrHInuSSP，CErVuSunICOlOr，CErVuSnIPPOn，SuSSP，和bubAluSbubAluS，时代为更新世晚期；67件属全新世早期，包括CETACEAgEn.ETSP.IdET，ElEPHASSP，SuSSCrOfACErVuSunICOlOr和CErVuSnIPPOn等；属于第三纪晚期的仅有1件鹿超科角化石。台湾海峡西部海域更新世晚期和全新世早期的哺乳动物组合不同于已知的我国海域其他地点的哺乳动物组合，也异于福建中、西部山区的哺乳动物组合。Numerous mammalian Fossils From Western Taiwan Strait were brieFly discri-bed here.Concerning the age, besides an antler of Cervidea dated to late Tertiary,other specimens were suggested to be of late Pleistocene, such as Ursus sp., Elcphasmaximus, Dicerorhinus sp., Sus sp., Cervus unicolor, Cervus nippon and Bubalus bu-balus, and early Holocene, incIuding Cetacea gen.et sp.indet., Elephas sp.Susscrofa, Cervus unicolor and Cervus nippon etc.The Late Pleistocene and Early Holocene Faunal assemblages of Western Tai-wan Strait diFFer From contemporary Faunal assemblages either From other sea areain Cbina or localities at middle-western mountain area in Fujian, they probablyrepresent a local branch of Ailuropoda-Stegodon Fauna occured along the Soutbeasterncoast of China.国家自然科学基

(40(2):209-224)Regional Trial on the Yield Performance and Adaptability of Hybrid Rice Strains

試驗的目的在調整雜種水稻品系之種植適期，利用疑似感光性，探討每年種植單期作條件下，是否可發揮雜種優勢而提高增產潛力，以應稻田轉作政策及改進輪作制度之需。本試驗於民國77年利用氣溫較高之夏秋季於全省七個地點進行，測驗八個秈稻雜種品系之稻穀產量及適應性。試驗結果顯示；參試品系在各地之稻穀產量差異極大，在桃園新屋、花蓮、宜蘭三星三處因種植期較早，臺秈雜育1、7及11號等三品系因抽穗障礙而致產量偏低或全無收穫，僅有臺秈雜育2與6號兩品系的平均稻穀產量比對照品種臺中秈10號稍高；在彰化大村等四處採用一般正常二期作之早植，疑似感光性之臺秈雜育1、7及11號三品系平均稻穀產量較對照品種增產10.1─24.9％。臺秈雜育2號在各試驗地區產量最穩定，不論於五月的中間作或七月的一般二期作早植栽培，其平均產量都超過對照品種臺中秈10號。試驗結果顯示如能適當的調整種植時期及利用雜種品系之疑似感光性，可使雜種水稻品系發揮其高產潛力。Experiments were conducted at 7 locations to study the yield performance, adaptability and response to photoperiod of 8 indica hybrid rice strains, Rice was cultured as a mid-season crop with transplanting dates ranged from May to July in 1988. Experimental results indicated significant yield variation for hybrid strains among locations. At Hsinwu (Taoyuan), Sanhsing (Ilan) and Hualien, early transplanting in May rendered the three photosensitive strains, i. e. Tainung Sen Hybrid (TNSH) Nos. 1,7 and 11, to show difficulties in panicle extrusion. Grain yield was therefore very low, or even no harvest, for these strains. For overall average grain yield of the other 5 photo-insensitive strains, only TNSH Nos. 2 and 6 was higher than the check variety Taichung Sen No. 10. At Tatsun (Changhua), Lutsao (Chiayi), Pingtung and Taitung, late transplanting in June and July was carried out and different results were recorded. The three photo-sensitive strains out yielded the check variety by 10.1-24.9%, and all the photo-insensitive strains. TNSH No.2 showed the best adaptability as its grain yield averaged from 7 locations was 6.3% higher than the check variety. Based on the results of this experiment, it is suggested that by adjusting planting date and utilizing photosensitivity, yield performance of hybrid rice can be improved greatly when cultured under local conditions

Gelsolin (GSN) induces cardiomyocyte hypertrophy and BNP expression via p38 signaling and GATA-4 transcriptional factor activation.

[[abstract]]Cardiomyocyte hypertrophy is an adaptive response of the heart to various types of stress. During the period of stress accumulation, the transition from physiological hypertrophy to pathological hypertrophy results in the promotion of heart failure. Gelsolin (GSN) is a member of the actin-binding proteins, which regulate dynamic actin filament organization by severing and capping. Moreover, GSN also regulates cell morphology, differentiation, movement, and apoptosis. In this study, we used H9c2 and H9c2-GSN stable clones in an attempt to understand the mechanisms of GSN overexpression in cardiomyocytes. These data showed that the overexpression of GSN in H9c2-induced cardiac hypertrophy and increased the pathological hypertrophy markers atrial natriuretic peptide brain natriuretic peptide. Furthermore, we found that E-cadherin expression decreased with the overexpression of GSN in H9c2, but β-catenin expression increased. These data presume that the cytoskeleton is loose. Further, previous studies show that the mitogen-activated protein kinase pathway can induce cardiac hypertrophy. Our data showed that p-p38 expression increased with the overexpression of GSN in H9c2, and the transcription factor p-GATA4 expression also increased, suggesting that the overexpression of GSN in H9c2-induced cardiac hypertrophy seemed to be regulated by the p38/GATA4 pathway. Moreover, we used both the p38 inhibitor (SB203580) and GSN siRNA to confirm our conjecture. We found that both of these factors significantly suppressed gelsolin-induced cardiac hypertrophy through p38/GATA4 signaling pathway. Therefore, we predict that the gene silencing of GSN and/or the downstream blocking of GSN along the p38 pathway could be applied to ameliorate pathological cardiac hypertrophy in the future

Phenethyl isothiocyanate triggers apoptosis in human malignant melanoma A375.S114 cells through reactive oxygen species and the mitochondria-dependent pathways

[[abstract]]We have reported previously that phenethyl isothiocyanate (PEITC) induces apoptosis in human osteosarcoma U-2 OS cells. Cytotoxic activity of PEITC towards other cancer cells such as human malignant melanoma and skin cancer cells has not been reported. In this study, the anticancer activity of PEITC towards human malignant melanoma cancer A375.S2 cells was investigated. To determine the mechanisms of PEITC inhibition of cell growth, the following end points were determined in A375.S2 cells: cell morphological changes, cell cycle arrest, DNA damage and fragmentation assays and morphological assessment of nuclear change, reactive oxygen species (ROS) and Ca(2+) generations, mitochondrial membrane potential disruption, and nitric oxide and 10-N-nonyl acridine orange productions, expression and activation of caspase-3 and -9, B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), Bcl-2, poly (adenosine diphosphate-ribose) polymerase, and cytochrome c release, apoptosis-inducing factor and endonuclease G. PEITC induced morphological changes in time- and dose-dependent manner. PEITC induced G2/M phase arrest and induced apoptosis via endoplasmic reticulum stress-mediated mitochondria-dependent pathway. Western blot analysis showed that PEITC promoted Bax expression and inhibited Bcl-2 expression associated with the disintegration of the outer mitochondrial membrane causing cytochrome c release, and activation of caspase-9 and -3 cascade leading to apoptosis. We conclude that PEITC-triggered apoptotic death in A375.S2 cells occurs through ROS-mediated mitochondria-dependent pathways