海南东寨港发现斑胸滨鹬

正2013年11月15日上午,在海南省海口市东寨港国家级自然保护区周边一片农田(19°53'51.80″N,116°37'01.78″E)观察到1只斑胸滨鹬(Calidris melanotos)(图1),该片农田用作种植蔬菜和饲养水蚤。发现斑胸滨鹬的同时,也记录到林鹬(Tringa glareola)、泽鹬(T.stagnatilis)、白腰草鹬(T.ochropus)、黑尾塍鹬(Limosa     

湖北武汉发现长嘴半蹼鹬

正2014年4月7至25日,在湖北省武汉市江夏区汤逊湖千亩塘(30°26'48″N,114°24'27″E)观测到长嘴半蹼鹬(Limnodromus scolopaceus)1只,隶属于鸻形目鹬科半蹼鹬属。该鹬被发现于一大型荷塘内,同域分布有扇尾沙锥(Gallinago gallinago)、林鹬(Tringa glareola)、鹤鹬(T.erythropus)、泽鹬(T.stagnatilis)等鹬科鸟种。借助蔡司60倍单筒望远镜观察,并拍摄下图片及视频后发现,该鹬中等体型,与扇尾沙锥近似,但比鹤鹬小。具长而粗的嘴,全嘴色深。白色眉纹明显。上体体羽深褐色,具浅色羽缘。尾上覆羽具横斑。下体色浅,胸     

山东省滨州市发现极危鸟类——勺嘴鹬

正2017年5月18日中午12时,在山东省滨州贝壳堤岛与湿地国家级自然保护区大口河监管站外围滨海湿地(117°52'5″E,38°15'52″N)观测到勺嘴鹬Calidris pygmaea1只。勺嘴鹬隶属于鸻形目Charadriiformes鹬科Scolopacidae滨鹬属Calidris(GibsonAllan,2012;郑光美,2017),被列为世界自然保护联盟(IUCN)红色名录极危(CR)物种(BirdL ife International,2018; IUCN,2018)。该鸟种发现之处为保护区内退潮后的淤泥质滩涂,贝类等底栖生物资源丰     

陕西省鸟类新纪录——小滨鹬

正2017年10月3日,笔者在陕西省定边县苟池(107°30'48″E,34°15'46″N)观察到8只小滨鹬Calidris minuta。经查阅《中国鸟类野外手册》(约翰·马敬能等,2000)、《中国鸟类志》(赵正阶,2001)、《中国鸟类分类与分布名录(第三版)》(郑光美,2017)等相关学术著作及网络数据库,确认其为陕西省鸟类新纪录。小滨鹬属鸻形目Charadriiformes鹬科Scolopacidae。观察时,其在苟池(咸水)的水边觅食,进食时快速跑动,用嘴快速啄食     

云南蒙自长桥海发现秃鹳和翻石鹬

正2013年9月4日,云南省红河州蒙自市长桥海(23°25'42″N,103°23'20″E,海拔1 282 m)发现秃鹳(Leptoptilos javanicus)1只和翻石鹬(Arenaria interpres)4只。其中后者经查阅《中国鸟类分类与分布名录》、《云南鸟类志(上卷)》、《中国鸟类野外手册》等资料,确定为云南鸟类新纪录。秃鹳为体型硕大(体长110 cm)的鸟,比同域分布的钳嘴鹳(Anastomus oscitans)、苍鹭(Ardea     

陕西省鸟类新纪录——红颈瓣蹼鹬和尖尾滨鹬

正2012—2015年在对陕西省蒲城卤阳湖国家湿地公园(109°23'24″~109°35'09″E,34°47'41″~34°50'07″N)进行鸟类调查期间陆续发现了一些陕西省新分布鸟类,其中有2种于2014年8月23日和2015年8月11日拍摄到了清晰的照片,根据其外部形态特征,经查阅《中国鸟类野外手册》(马敬能等,2000)和《中国鸟类志》(赵正阶,2001),分别确定为红颈瓣蹼鹬Phalaropus lobatus和尖尾滨鹬Calidris acuminata。据《中国鸟类分类与分布名录(第二版)》(郑光美,2011)以及相关文献,并检索中国     

四川省鸟类新纪录——灰尾漂鹬

<正>2013年9月26日14∶00左右,笔者在四川省雅安市天全县向阳村五组(30°03'11″N,102°45'23″E,海拔736 m)发现并拍摄水鸟一只。经鉴定,确认为鸻形目Charadriiformes鹬科Scolopacidae的灰尾漂鹬Heteroscelus brevipes,为四川省鸟类一新纪录。该鸟嘴粗且直,鼻沟为嘴长的一半;过眼纹黑色,眉纹白;颏近白,上体体羽全灰,胸浅灰,腹白;脚较短而粗,黄色(马敬能等,     

西藏札达发现印度寿带

正在开展西藏第二次陆生野生动物资源调查工作过程中,于2015年6月18、19日在西藏自治区札达县底雅乡什布奇村(78°44'45.6″E,31°48'33.8″N,3110 m)、6月19日在底雅乡底雅村(78°52'5.1″E,31°46'55.5″N,2977 m)观察并拍摄到雌性印度寿带各1只。经鉴定,为印度寿带印巴亚种Terpsiphone paradisi leucogaster(图1)。     

河北沿海发现小凤头燕鸥

正2017年7月25日,在河北省唐山市海港开发区金沙岛一季节性水塘(39°10′26″N,118°58′16″E)观察到1只小凤头燕鸥(Thalasseus bengalensis),该鸟停歇约10 min后飞离该地。至8月7日,在该地点多次记录到单只小凤头燕鸥停歇洗浴。附近亦有普通燕鸥(Sterna hirundo)、白额燕鸥(S.albifrons)、反嘴鹬(Recurvirostra avosetta)、环颈鸻(Charadrius alexandrinus)、青脚滨鹬(Calidris temminckii)等水鸟在此停歇或觅食。所发现的小凤头燕鸥     

东北地区鸟类新纪录——长嘴半蹼鹬

<正>笔者于2012年5月5日11∶48,在黑龙江省大庆市龙凤湿地自然保护区(51°23'28.2″N,122°03'32.9″E)拍摄到1只长嘴半蹼鹬Limnodromus scolopaceus,经查阅《黑龙江省鸟类志》《东北鸟类》《东北鸟类图鉴》《中国鸟类区系纲要》《吉林省野生动物图鉴(鸟类)》《辽宁省动物志(鸟类)》《中国鸟类分布与分布名录(第2版)》等文献资料后认定,长嘴半蹼鹬为东北地区的鸟类新纪录。拍摄时该鸟正在觅食。该鸟体长约30 cm。嘴长而直,约9 cm,黑色,嘴基部较前端颜色略淡一些。具白色眼圈、黑棕色贯眼纹。背部呈黑、褐色     

水稻小穗轴维管系统网络结构探讨

对籼型、粳型或其不育系与保持系代表品种小穗解剖观察表明：水稻小穗轴维管系统网络由中央维管束和各分枝维管束复合而成。来自小穗柄的１条大的中央主束和几条边围维管束经数次分枝、联结,不断产生新的分枝维管束进入相应的结构。一般颖片中维管束１－２条,第一稃片中１－３条,第二稃片中１－４条,第二朵退化小花残余结构中０－３条,顶生可孕小花的外稃中５条,内稃中３条,浆片中各２条,雄蕊中各１条,雌蕊中３条,主束与支     

miR-34a expression,epigenetic regulation,and function in human placental diseases

Preeclampsia (PE) is the major pregnancy-induced hypertensive disorder responsible for maternal and fetal morbidity and mortality that can be associated with intrauterine growth restriction (IUGR). PE and IUGR are thought to be due to a placental defect, occurring early during pregnancy. Several placental microRNAs (miRNAs) have been shown to be deregulated in the context of placental diseases and could thus play a role in the pathophysiology of PE. Here, we show that pri-miR-34a is overexpressed in preeclamptic placentas and that its placental expression is much higher during the first trimester of pregnancy than at term, suggesting a possible developmental role. We explored pri-miR-34a regulation and showed that P53, a known activator of miR-34a, is reduced in all pathological placentas and that hypoxia can induce pri-miR-34a expression in JEG-3 cells. We also studied the methylation status of the miR-34a promoter and revealed hypomethylation in all preeclamptic placentas (associated or not with IUGR), whereas hypoxia induced a hypermethylation in JEG-3 cells at 72 h. Despite the overexpression of pri-miR-34a in preeclampsia, there was a striking decrease of the mature miR-34a in this condition, suggesting preeclampsia-driven alteration of pri-miR-34a maturation. SERPINA3, a protease inhibitor involved in placental diseases, is elevated in IUGR and PE. We show here that miR-34a overexpression in JEG-3 downregulates SERPINA3. The low level of mature miR-34a could thus be an important mechanism contributing to SERPINA3 upregulation in placental diseases. Overall, our results support a role for miR-34a in the pathophysiology of preeclampsia, through deregulation of the pri-miRNA expression and its altered maturation.     

Rab27a regulates the peripheral distribution of melanosomes in melanocytes

Rab GTPases are regulators of intracellular membrane traffic. We report a possible function of Rab27a, a protein implicated in several diseases, including Griscelli syndrome, choroideremia, and the Hermansky-Pudlak syndrome mouse model, gunmetal. We studied endogenous Rab27a and overexpressed enhanced GFP-Rab27a fusion protein in several cultured melanocyte and melanoma-derived cell lines. In pigmented cells, we observed that Rab27a decorates melanosomes, whereas in nonpigmented cells Rab27a colocalizes with melanosome-resident proteins. When dominant interfering Rab27a mutants were expressed in pigmented cells, we observed a redistribution of pigment granules with perinuclear clustering. This phenotype is similar to that observed by others in melanocytes derived from the ashen and dilute mutant mice, which bear mutations in the Rab27a and MyoVa loci, respectively. We also found that myosinVa coimmunoprecipitates with Rab27a in extracts from melanocytes and that both Rab27a and myosinVa colocalize on the cytoplasmic face of peripheral melanosomes in wild-type melanocytes. However, the amount of myosinVa in melanosomes from Rab27a-deficient ashen melanocytes is greatly reduced. These results, together with recent data implicating myosinVa in the peripheral capture of melanosomes, suggest that Rab27a is necessary for the recruitment of myosinVa, so allowing the peripheral retention of melanosomes in melanocytes.     

Vasopressin 1a receptor knockout mice have a subtle olfactory deficit but normal aggression

Two receptors for vasopressin (Avp) are expressed in the brain, the Avp 1a receptor (Avpr1a) and the Avp 1b receptor (Avpr1b). To investigate the role of Avpr1a in behaviors in mice more extensively, we generated a line of mice lacking a functional Avpr1a (knockout, Avpr1a(-/-)). We first performed a baseline phenotypic screen of the Avpr1a knockouts followed by a more detailed analysis of their circadian rhythms and olfactory function. When free-running in constant darkness, the Avpr1a(-/-) mice have a longer circadian tau than the wild types. There are also subtle olfactory deficits in Avpr1a(-/-) mice as measured in an olfactory habituation/dishabituation test and in the discrimination of female urine from male urine using an operant testing paradigm. An extensive body of research has shown that manipulation of the Avpr1a alters behavior, including aggression and social recognition. Therefore, we expected profound behavioral deficits in mice lacking the Avpr1a gene. Contrary to our expectations, social aggression, anxiety-like behavior and social recognition are unaffected in this line of Avpr1a knockout mice. These data suggest either that the Avpr1a is not as critical as we thought for social behavior in mice or, more likely, that the neural circuitry underlying aggression and other social behaviors compensates for the life-long loss of the Avpr1a. However, the olfactory deficits observed in the Avpr1a(-/-) mice suggest that Avp and Avpr1a drugs may affect behavior, in part, by modulation of chemosensory systems.     

Cocaine decreases expression of neurogranin via alterations in thyroid receptor/retinoid X receptor signaling

The molecule responsible for the enzyme activity plasma membrane (PM) aminophospholipid translocase (APLT), which catalyzes phosphatidylserine (PS) translocation from the outer to the inner leaflet of the plasma membrane, is unknown in mammals. A Caenorhabditis elegans study has shown that ablation of transbilayer amphipath transporter-1 (TAT-1), which is an ortholog of a mammalian P-type ATPase, Atp8a1, causes PS externalization in the germ cells. We demonstrate here that the hippocampal cells of the dentate gyrus, and Cornu Ammonis (CA1, CA3) in mice lacking Atp8a1 exhibit a dramatic increase in PS externalization. Although their hippocampi showed no abnormal morphology or heightened apoptosis, these mice displayed increased activity and a marked deficiency in hippocampus-dependent learning, but no hyper-anxiety. Such observations indicate that Atp8a1 plays a crucial role in PM-APLT activity in the neuronal cells. In corroboration, ectopic expression of Atp8a1 but not its close homolog, Atp8a2, caused an increase in the population (V(max) ) of PM-APLT without any change in its signature parameter K(m) in the neuronal N18 cells. Conversely, expression of a P-type phosphorylation-site mutant of Atp8a1 (Atp8a1*) caused a decrease in V(max) of PM-APLT without significantly altering its K(m) . The Atp8a1*-expressing N18 cells also exhibited PS externalization without apoptosis. Together, our data strongly indicate that Atp8a1 plays a central role in the PM-APLT activity of some mammalian cells, such as the neuronal N18 and hippocampal cells.     

Zebrafish ftz-f1a (nuclear receptor 5a2) functions in skeletal muscle organization

Fushi-tarazu factor 1a (Ftz-F1a, Ff1a, Nr5a2) is a nuclear receptor with diverse functions in many tissues. Here, we report the function of ff1a in zebrafish muscle differentiation. In situ hybridization revealed that ff1a mRNA was present in the adaxial and migrating slow muscle precursors and was down-regulated when slow muscle cells matured. This expression was under the control of hedgehog genes, expanded when hedgehog was increased and missing in mutants defective in genes in the Hedgehog pathway like you-too (yot), sonic you (syu), and u-boot (ubo). Blocking ff1a activity by injecting a deleted form of ff1a or an antisense ff1a morpholino oligo into fish embryos caused thinner and disorganized fibers of both slow and fast properties. Transient expression of ff1a in syu, ubo, and yot embryos led to more fibril bundles, even when slow myoblasts were transfated into fast properties. We showed that ff1a and prox1 complemented each other in slow myofibril assembly, but they did not affect the expression of each other. These results demonstrate that ff1a functions in both slow and fast muscle morphogenesis in response to Hedgehog signaling, and this function parallels the activity of another slow muscle gene, prox1.     

Mutation of the maize sbe1a and ae genes alters morphology and physical behavior of wx-type endosperm starch granules

In maize, three isoforms of starch-branching enzyme, SBEI, SBEIIa, and SBEIIb, are encoded by the Sbe1a, Sbe2a, and Amylose extender (Ae) genes, respectively. The objective of this research was to explore the effects of null mutations in the Sbe1a and Ae genes alone and in combination in wx background on kernel characteristics and on the morphology and physical behavior of endosperm starch granules. Differences in kernel morphology and weight, starch accumulation, starch granule size and size distribution, starch microstructure, and thermal properties were observed between the ae wx and sbe1a ae wx plants but not between the sbe1a wx mutants when compared to wx. Starch from sbe1a ae wx plants exhibited a larger granule size with a wider gelatinization temperature range and a lower endotherm enthalpy than ae wx. Microscopy shows weaker iodine staining in sbe1a ae wx starch granules. X-ray diffraction revealed A-type crystallinity in wx and sbe1a wx starches and B-type in sbe1a ae wx and ae wx. This study suggests that, while the SBEIIb isoform plays a dominant role in maize endosperm starch synthesis, SBEI also plays a role, which is only observable in the presence of the ae mutation.     

Complement factor C5a induces atherosclerotic plaque disruptions

Complement factor C5a and its receptor C5aR are expressed in vulnerable atherosclerotic plaques; however, a causal relation between C5a and plaque rupture has not been established yet. Accelerated atherosclerosis was induced by placing vein grafts in male apoE^?/? mice. After 24 days, when advanced plaques had developed, C5a or PBS was applied locally at the lesion site in a pluronic gel. Three days later mice were killed to examine the acute effect of C5a on late stage atherosclerosis. A significant increase in C5aR in the plaque was detectable in mice treated with C5a. Lesion size and plaque morphology did not differ between treatment groups, but interestingly, local treatment with C5a resulted in a striking increase in the amount of plaque disruptions with concomitant intraplaque haemorrhage. To identify the potential underlying mechanisms, smooth muscle cells and endothelial cells were treated in vitro with C5a. Both cell types revealed a marked increase in apoptosis after stimulation with C5a, which may contribute to lesion instability in vivo. Indeed, apoptosis within the plaque was seen to be significantly increased after C5a treatment. We here demonstrate a causal role for C5a in atherosclerotic plaque disruptions, probably by inducing apoptosis. Therefore, intervention in complement factor C5a signalling may be a promising target in the prevention of acute atherosclerotic complications.