Survey‐gap analysis in expeditionary research: where do we go from here?

Research expeditions into remote areas to collect biological specimens provide vital information for understanding biodiversity. However, major expeditions to little‐known areas are expensive and time consuming, time is short, and well‐trained people are difficult to find. In addition, processing the collections and obtaining accurate identifications takes time and money. In order to get the maximum return for the investment, we need to determine the location of the collecting expeditions carefully. In this study we used environmental variables and information on existing collecting localities to help determine the sites of future expeditions. Results from other studies were used to aid in the selection of the environmental variables, including variables relating to temperature, rainfall, lithology and distance between sites. A survey gap analysis tool based on ‘ED complementarity’ was employed to select the sites that would most likely contribute the most new taxa. The tool does not evaluate how well collected a previously visited site survey site might be; however, collecting effort was estimated based on species accumulation curves. We used the number of collections and/or number of species at each collecting site to eliminate those we deemed poorly collected. Plants, birds, and insects from Guyana were examined using the survey gap analysis tool, and sites for future collecting expeditions were determined. The south‐east section of Guyana had virtually no collecting information available. It has been inaccessible for many years for political reasons and as a result, eight of the first ten sites selected were in that area. In order to evaluate the remainder of the country, and because there are no immediate plans by the Government of Guyana to open that area to exploration, that section of the country was not included in the remainder of the study. The range of the ED complementarity values dropped sharply after the first ten sites were selected. For plants, the group for which we had the most records, areas selected included several localities in the Pakaraima Mountains, the border with the south‐east, and one site in the north‐west. For birds, a moderately collected group, the strongest need was in the north‐west followed by the east. Insects had the smallest data set and the largest range of ED complementarity values; the results gave strong emphasis to the southern parts of the country, but most of the locations appeared to be equidistant from one another, most likely because of insufficient data. Results demonstrate that the use of a survey gap analysis tool designed to solve a locational problem using continuous environmental data can help maximize our resources for gathering new information on biodiversity. © 2005 The Linnean Society of London, Biological Journal of the Linnean Society, 2005, 85 , 549–567.     

陕西、宁夏部分地区小麦族植物资源调查、收集与分类鉴定

2002年8月对陕西、宁夏部分地区分布的小麦族(Triticeae)植物进行了调查与收集,共收集小麦族植物6属、16种、145个居群,并对每一物种及其居群的分布区、生境、海拔、2n染色体数目等进行了分析。同时,对所收集材料的可利用性、调查收集的基本单元以及小麦族植物的保护进行了讨论。     

大鼠肾近曲小管、远曲小管和集合管壁厚的性别差异

运用光学显微镜对雌、雄大鼠的近曲小管、远曲小管和集合管的壁厚分别进行了测量,结果发现:雌、雄大鼠的近曲小管和集合管存在明显的性别差异(P<0.05);而远曲小管差异不明显(P>0.05).研究结果提示:雌、雄大鼠近曲小管和集合管的功能可能存在显著的性别差异.     

鼎突多刺蚁(Polyrhachis vicina Roger)蚁群的采收与恢复效应

通过对鼎突多刺蚁（Polyrhachis vicina Roger)野生资源的不同采收技术试验,研究采收季节,采收方式、采收强度和人为增加食物源的措施对蚁群恢复程度的影响,结果表明,夏季为最佳采收季节;以采收副巢为主,适当保留主巢有利于蚁群的恢复;在采收中以野生蚁群的25%-35%采收强度采集为宜;人为地在蚂蚁资源较为丰富的山地种植一些能产蜜露昆虫的经济作物,既为蚁群的快速恢复提供了食物保证,也增加额外的经济收入。     

Atmin modulates Pkhd1 expression and may mediate Autosomal Recessive Polycystic Kidney Disease (ARPKD) through altered non-canonical Wnt/Planar Cell Polarity (PCP) signalling

Autosomal Recessive Polycystic Kidney Disease (ARPKD) is a genetic disorder with an incidence of ~1:20,000 that manifests in a wide range of renal and liver disease severity in human patients and can lead to perinatal mortality. ARPKD is caused by mutations in PKHD1, which encodes the large membrane protein, Fibrocystin, required for normal branching morphogenesis of the ureteric bud during embryonic renal development. The variation in ARPKD phenotype suggests that in addition to PKHD1 mutations, other genes may play a role, acting as modifiers of disease severity. One such pathway involves non-canonical Wnt/Planar Cell Polarity (PCP) signalling that has been associated with other cystic kidney diseases, but has not been investigated in ARPKD. Analysis of the Atmin^Gpg6 mouse showed kidney, liver and lung abnormalities, suggesting it as a novel mouse tool for the study of ARPKD. Further, modulation of Atmin affected Pkhd1 mRNA levels, altered non-canonical Wnt/PCP signalling and impacted cellular proliferation and adhesion, although Atmin does not bind directly to the C-terminus of Fibrocystin. Differences in ATMIN and VANGL2 expression were observed between normal human paediatric kidneys and age-matched ARPKD kidneys. Significant increases in ATMIN, WNT5A, VANGL2 and SCRIBBLE were seen in human ARPKD versus normal kidneys; no substantial differences were seen in DAAM2 or NPHP2. A striking increase in E-cadherin was also detected in ARPKD kidneys. This work indicates a novel role for non-canonical Wnt/PCP signalling in ARPKD and suggests ATMIN as a modulator of PKHD1.     

长白山地区不同采集土样方式筛菌效率比较

目的对随机采样和田字格定点采样两种取样方式筛菌效率进行比较分析。方法利用随机采样和定点采样两种不同方式,采集了长白山地区的土样,取来自不同植物根际的土样,制成菌悬液后煮沸,涂布无氮平板以分离固氮芽胞杆菌。对分离的菌株进行菌落16S rDNA PCR,从中筛选鉴别巨大芽胞杆菌。结果定点采集土样分离出无晶体芽胞菌和有晶体芽胞菌分别是261株和76株,随机采集土样分离出无晶体芽胞菌和有晶体芽胞菌分别是279株和94株。经16S rDNA法鉴定分离巨大芽胞杆菌共19株。结论随机采样的取土方式与定点采样的取土方式差异度小,两种采集土样的方式在筛菌效率上并未表现出明显差异。     

Keep collecting: accurate species distribution modelling requires more collections than previously thought

Aim Species distribution models (SDMs) use the locations of collection records to map the distributions of species, making them a powerful tool in conservation biology, ecology and biogeography. However, the accuracy of range predictions may be reduced by temporally autocorrelated biases in the data. We assess the accuracy of SDMs in predicting the ranges of tropical plant species on the basis of different sample sizes while incorporating real‐world collection patterns and biases. Location Tropical South American moist forests. Methods We use dated herbarium records to model the distributions of 65 Amazonian and Andean plant species. For each species, we use the first 25, 50, 100, 125 and 150 records collected and available for each species to analyse changes in spatial aggregation and climatic representativeness through time. We compare the accuracy of SDM range estimates produced using the time‐ordered data subsets to the accuracy of range estimates generated using the same number of collections but randomly subsampled from all available records. Results We find that collections become increasingly aggregated through time but that additional collecting sites are added resulting in progressively better representations of the species’ full climatic niches. The range predictions produced using time‐ordered data subsets are less accurate than predictions from random subsets of equal sample sizes. Range predictions produced using time‐ordered data subsets consistently underestimate the extent of ranges while no such tendency exists for range predictions produced using random data subsets. Main conclusions These results suggest that larger sample sizes are required to accurately map species ranges. Additional attention should be given to increasing the number of records available per species through continued collecting, better distributed collecting, and/or increasing access to existing collections. The fact that SDMs generally under‐predict the extent of species ranges means that extinction risks of species because of future habitat loss may be lower than previously estimated.     

Synthesis of an endogeneous lectin, galectin-1, by human endothelial cells is up-regulated by endothelial cell activation

The pattern of expression of an endogenous lectin, galectin-1, was examined in human lymphoid tissue. Galectin-1 was detected in the endothelial cells lining specialized vessels, termed high endothelial venules, in activated lymphoid tissue, but not in a resting lymph node. Cultured endothelial cells (human aortic and umbilical vein endothelial cells (HAECs and HUVECs)) expressed galectin-1. Activation of the cultured endothelial cells increased the level of galectin-1 expression, as determined by ELISA, Northern blot analysis and high throughput cDNA sequencing. These results suggest that galectin-1 expressed by endothelial cells may bind to and affect the trafficking of cells emigrating from blood into tissues.     

Urea transport in freshly isolated and cultured cells from rat inner medullary collecting duct

Summary Regulation of urea transport by vasopressin in inner medullary collecting duct (IMCD) cells is thought to be important for the urinary concentrating mechanism. Isolated tubule perfusion studies suggest the existence of a saturable urea carrier. We have measured¹⁴C-urea efflux in IMCD cells which were freshly isolated and grown in primary culture. Cells were isolated from rat papilla by collagenase digestion and hypotonic shock. In suspended cells,¹⁴C-urea efflux (J _urea from loaded cells was exponential with time constant 59±3 sec (sem,n=6, 23°C).J _urea had an activation energy of 4.1 kcal/mole and was inhibited 42±7% by 0.25mm phloretin and 30–40% by the high affinity urea analogues dimethylurea and phenylurea.J _urea was increased 40–60% by addition of vasopressin (10^–8 m) or 8-bromo-cAMP (1mm); stimulatedJ _urea was inhibited 55±8% by the kinase A inhibitor H-8. Phorbol esters and epidermal growth factor did not alterJ _urea. IMCD cells grown in primary culture were homogeneous in appearance with>fivefold stimulation of cAMP by vasopressin. The exponential time constant for urea efflux was 610±20 sec (n=3).J _urea was not altered by vasopressin, cAMP or phloretin. Another function of in vivo IMCD cells, vasopressin-dependent formation of endosomes containing water channels, was absent in the cultured cells. These results demonstrate presence of a urea transporter on suspended IMCD cells which is activated by cAMP and inhibited by phloretin and urea analogues. The urea transporter and its regulation by cAMP, and cAMP-dependent apical membrane endocytosis, are lost after growth in primary culture.