Epidemiologic Analysis of Factors Associated with Local Disappearances of Native Ranid Frogs in Arizona

Abstract:  We examined factors that may independently or synergistically contribute to amphibian population declines. We used epidemiologic case–control methodology to sample and analyze a large database developed and maintained by the Arizona Game and Fish Department that describes historical and currently known ranid frog localities in Arizona, U.S.A. Sites with historical documentation of target ranid species ( n = 324) were evaluated to identify locations where frogs had disappeared during the study period (case sites) and locations where frog populations persisted (control sites). Between 1986 and 2003, 117 (36%) of the 324 sites became case sites, of which 105 were used in the analyses. An equal number of control sites were sampled to control for the effects of time. Risk factors, or predictor variables, were defined from environmental data summarized during site surveys and geographic information system data layers. We evaluated risk factors with univariate and multifactorial logistic-regression analyses to derive odds ratios (OR). Odds for local population disappearance were significantly related to 4 factors in the multifactorial model. Disappearance of frog populations increased with increasing elevation (OR = 2.7 for every 500 m, p < 0.01). Sites where disappearances occurred were 4.3 times more likely to have other nearby sites that also experienced disappearances (OR = 4.3, p < 0.01), whereas the odds of disappearance were 6.7 times less (OR = 0.15, p < 0.01) when there was a source population nearby. Sites with disappearances were 2.6 times more likely to have introduced crayfish than were control sites (OR = 2.6, p = 0.04). The identification of factors associated with frog disappearances increases understanding of declines occurring in natural populations and aids in conservation efforts to reestablish and protect native ranids by identifying and prioritizing implicated threats.     

Molecular taxonomy of vestimentiferans of the western Pacific and their phylogenetic relationship to species of the eastern Pacific

The nucleotide sequence of part (624 bp) of a mitochondrial gene for cytochrome oxidase I was determined for 46 escarpiid vestimentiferans collected from seven sites in the western Pacific and 49 individual specimens of Arcovestia ivanovi from two sites in the Manus Basin. Phylogenetic analysis, based on the newly obtained and previously reported sequences, indicated that escarpiids in the western Pacific can be divided into two tentative species, as we proposed in a previous report. While members of the first tentative species have been collected exclusively from a seep area at a depth of 300 m off the coast of central Japan, the members of the second species inhabit some sites at depths greater than 1,100 m, namely, seep areas in Japanese and Papua-New Guinean waters as well as hydrothermal vent fields in the Okinawa Trough and the Manus Basin. We detected no genetic structure among populations of the second tentative species. The first tentative species was more closely related to a species in the eastern Pacific, Escarpia spicata, and to a species in the Gulf of Mexico, Escarpia laminata, than to the second tentative species in the western Pacific. Sequences obtained from all arcovestiids were identical with the exception of those from three individuals, each of which included a single synonymous nucleotide substitution relative to the dominant haplotype, and no genetic differences were detected between specimens from the two sites in the Manus Basin.     

Prenatal diagnosis of mosaicism for triploidy and trisomy 13

Mosaicism for trisomy 13 and triploidy was detected by amniocentesis performed at 18 weeks' gestation because of fetal anomalies. Pregnancy continued and a live-born male was delivered vaginally at 37 weeks. The infant had features common to both trisomy 13 and triploidy: intrauterine growth retardation (IUGR), small abnormal ears, cleft palate, and a small jaw. In addition, he had complete cutaneous syndactyly of fingers 3 and 4 and partial syndactyly of the toes, as seen in triploidy. Mixoploidy for trisomy 13 and triploidy was confirmed postnatally in blood, skin, and placenta. Examination of chromosome heteromorphisms and DNA markers suggested the presence of two maternal contributions in the triploid cell line. In addition, the extra chromosome 13 in the trisomic cell line was derived from the mother. Copyright © 2001 John Wiley & Sons, Ltd.     

Prenatal diagnosis of a 45,X male with a SRY-bearing chromosome 21

Male phenotype associated with a 45,X karyotype is an infrequent finding. We present a case diagnosed prenatally on amniocentesis performed for maternal age. The male phenotype was associated with a translocation of a distal part of Yp including the pseudoautosomal SHOX gene and SRY gene on the short arm of a chromosome 21. By DNA analysis we could show that the X chromosome was of maternal origin and that the breakpoint was in interval 3 of the Y chromosome. Mechanisms and genetic counselling are discussed based on a review of published cases of 45,X and XX males. Copyright © 2002 John Wiley & Sons, Ltd.     

Total quality practitioner. Improving environmental process

Quick fix. Putting out firs. Do it over. Fix it again. Bottlenecks. Come back to it later. Out of stock. Back order. Not what we ordered. Is that the best you can do? It's the contractor's fault. Not within specs. Defective. Nobody's perfect. Lost in the system. Over budget. Delayed. Late penalities. Fines.     

Role of vitamin A in the haematotoxicity of hexachlorocyclohexane (HCH) in the rat.

The haematotoxicity of technical hexachlorocyclohexane (HCH) (1000 ppm) was investigated in male albino rats fed with diet free of vitamin A or containing vitamin A at 2000 or 10(5) I.U./kg. Assessment of HCH-induced haematotoxicity at the end of the 7 weeks feeding period was done on the basis of haemoglobin content, total count of red blood cells and white blood cells and the differential counts of the white blood cells as well as by parameters such as packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin, mean corpuscular haemoglobin content, prothrombin time and clotting time. In the rats fed with vitamin A-free diet containing HCH, significant reductions were noticed in the total white blood cells count, clotting time and prothrombin time indicating severe haematotoxicity. Differential count of the white blood cells of these rats revealed a non-significant reduction in the lymphocyte count. The only indication of haematotoxicity caused by hexachlorocyclohexane in the vitamin A supplemented rats was a slight but statistically significant reduction of the total count of white blood cells. These results demonstrate that the haematotoxicity of hexachlorocyclohexane in the rats is enhanced by vitamin A-deficiency and its supplementation particularly in excess but not at hypervitaminotic level is protective against the toxicity.