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Of the 10,272 currently recognized reptile species, the trade of fewer than 8% are regulated by the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES) and the European Wildlife Trade Regulations (EWTR). However, the International Union for Conservation of Nature (IUCN) Red List has assessed 45% of the world's reptile species and determined that at least 1390 species are threatened by “biological resource use”. Of these, 355 species are intentionally targeted by collectors, including 194 non-CITES-listed species. Herein we review the global reptile pet trade, its impacts, and its contribution to the over-harvesting of species and populations, in light of current international law. Findings are based on an examination of relevant professional observations, online sources, and literature (e.g., applicable policies, taxonomy [reptile database], trade statistics [EUROSTAT], and conservation status [IUCN Red List]). Case studies are presented from the following countries and regions: Australia, Central America, China, Galapagos Islands (Ecuador), Germany, Europe, India, Indonesia (Kalimantan), Islamic Republic of Iran, Japan, Madagascar, Mexico, New Zealand, the Philippines, South Africa, Sri Lanka, Vietnam, Western Africa, and Western Asia. The European Union (EU) plays a major role in reptile trade. Between 2004 and 2014 (the period under study), the EU member states officially reported the import of 20,788,747 live reptiles. This review suggests that illegal trade activities involve species regulated under CITES, as well as species that are not CITES-regulated but nationally protected in their country of origin and often openly offered for sale in the EU. Further, these case studies demonstrate that regulations and enforcement in several countries are inadequate to prevent the overexploitation of species and to halt illegal trade activities.

Introduction. Recent studies have shown that CADM1/MAL-methylation testing detects high-grade CIN lesions with a high short-term progression risk for cervical cancer. Women treated for CIN2/3 are at risk of post-treatment disease, representing either persistent (incompletely treated) or incident (early onset) lesions. Here, we evaluated CADM1/MAL-methylation analysis as potential tool for detecting recurrent high-grade CIN lesions (rCIN2/3). Methods and materials. A multicenter prospective clinical cohort study was conducted among 364 women treated for CIN2/3. Cervical scrapes were taken prior to treatment, and six and 12 months post-treatment and tested for cytology, hrHPV (plus genotype) and CADM1/MAL-methylation. When at six months either of these tests was positive, a colposcopy-directed biopsy was obtained. At 12 months, all women underwent an exit-colposcopy with biopsy. In case of rCIN2/3, re-treatment was done. Results. We found 28 rCIN2 (7.7%) and 14 rCIN3 (3.8%), resulting in a total recurrence rate of 11.5%. All 14 women with rCIN3 and 15/28 (54%) with rCIN2 showed hrHPV type-persistence. Of these, 9/14 ( 64%) rCIN3 and 8/15 (53%) rCIN2 were CADM1/MAL-methylation positive. All incident rCIN2, characterized by hrHPV genotype-switch, were CADM1/MAL-methylation negative. All three carcinomas found after re-treatment were CADM1/MAL-methylation positive. CADM1/MAL-methylation positivity at both baseline and follow-up significantly increased the risk of >= rCIN3 (from 0.7% to 18.4%), and >= rCIN2 (from 82% to 36.8%), compared to a consistently CADM1/MAL-methylation negative result (p-value

Exotic predators can have detrimental impacts on indigenous fauna. Lethal predator control is commonly used to reduce predator impacts, but is not always feasible, effective or ethical. A promising non-lethal alternative is refuge supplementation for prey. We conducted a Before–After Control–Impact (BACI) experiment over 3 years to determine the relative effects of predator removal (by exclosure fencing) and artificial refuge supplementation on survival of McCann’s skink (Oligosoma maccanni) in duneland on Kaitorete Spit (South Island, New Zealand). Skink populations on 0.0625 ha-grids were randomly assigned to four treatment groups, each replicated four times: (a) predator exclosure only; (b) artificial retreats only; (c) exclosure + artificial retreats, and (d) control (no exclosure or artificial retreats), and monitored annually by pitfall trapping. Capture–recapture analysis was used to estimate the difference in annual survival probability between pre- and post-treatment periods. On average, survival increased only at grids that received the exclosure-only treatment (effect size of 0.03 (0.017–0.043; unconditional 95% CI)). Reduction in predator abundance (by lethal predator control or predator exclusion), but not artificial refuge supplementation, is predicted to benefit McCann’s skink. Our findings add to other studies highlighting the detrimental impacts of exotic predators on indigenous prey and calls for improved means of reducing predator impacts.

In contrast to most expectations, we showed previously that dietary fructooligosaccharides (FOS) stimulate intestinal colonization and translocation of invasive Salmonella enteritidis in rats. Even before infection, FOS increased the cytotoxicity of fecal water, mucin excretion, and intestinal permeability. In the present study, we tested whether FOS has these effects in humans. A double-blind, placebo-controlled, crossover study of 2 x 2 wk, with a washout period of 2 wk, was performed with 34 healthy men. Each day, subjects consumed lemonade containing either 20 g FOS or placebo and the intestinal permeability marker chromium EDTA (CrEDTA). On the last 2 d of each supplement period, subjects scored their gastrointestinal complaints on a visual analog scale and collected feces and urine for 24 h. Fecal lactic acid was measured using a colorimetric enzymatic kit. The cytotoxicity of fecal water was determined with an in vitro bioassay, fecal mucins were quantified fluorimetrically, and intestinal permeability was determined by measuring urinary CrEDTA excretion. In agreement with our animal studies, FOS fermentation increased fecal wet weight, bifidobacteria, lactobacilli, and lactic acid. Consumption of FOS increased flatulence and intestinal bloating. In addition, FOS consumption doubled fecal mucin excretion, indicating mucosal irritation. However, FOS did not affect the cytotoxicity of fecal water and intestinal permeability. The FOS-induced increase in mucin excretion in our human study suggests mucosal irritation in humans, but the overall effects are more moderate than those in rats.

Background & aims: In several rat infection experiments, we have shown that dietary calcium inhibits intestinal colonization and translocation of invasive salmonella. The aim of the present study was to find out whether calcium is also protective against enterotoxigenic Escherichia coli (ETEC) infection. This was first tested in our rat model and subsequently verified in a human infection study. Methods: Rats were fed a purified diet with either a low or a high amount of calcium phosphate and orally infected with ETEC. In addition, a parallel, double-blind, placebo-controlled intervention study of 3 weeks was performed with 32 healthy men. Subjects largely maintained their habitual diet and consumed either regular milk products (calcium supply, 1100 mg/day) or placebo milk products (calcium supply, 60 mg/day). On day 10, subjects ingested a live but attenuated ETEC strain (strain E1392/75-2A), able to induce mild although short-lived symptoms. Primary outcomes studied were infection-induced diarrhea (total fecal output and relative fecal dry weight) and fecal mucin excretion. Results: In humans, ETEC induced diarrhea in both groups, in that total fecal output doubled and mean relative fecal dry weight dropped from 25% to 20%. Additionally, fecal mucin excretion was increased in both groups. All these fecal parameters were completely normalized in the calcium group on the second infection day, in contrast to the placebo group, which recovered on the third infection day. Likewise, supplemental calcium inhibited ETEC colonization and diarrhea in rats. Conclusions: Calcium in milk products improves human resistance to ETEC infection as it inhibits infectious diarrhea.

Prebiotics, such as fructo-oligosaccharides (FOS), stimulate the protective gut microflora, resulting in an increased production of organic acids. This may result in increased luminal killing of acid-sensitive pathogens. However, host defense against invasive pathogens, like salmonella, also depends on the barrier function of the intestinal mucosa. Rapid fermentation of prebiotics leading to high concentrations of organic acids may impair the barrier function. Therefore, we determined the dose-dependent effect of dietary FOS on the resistance of rats to Salmonella enteritidis. Male Wistar rats were fed restricted quantities of a "humanized" purified diet supplemented with 0, 3 or 6 g/100 g of FOS (n = 7 in the 6% FOS group and n = 8 in the other diet groups). After an adaptation period of 2 wk, rats were orally infected with 1.7 x 10(10) colony-forming units of S. enteritidis. Supplement-induced changes in the intestinal microflora and fecal cation excretion were determined before and after infection. Cytotoxicity of fecal water was determined with an in vitro bioassay, and fecal mucins were quantified fluorimetrically. Colonization of S. enteritidis was determined by quantification of salmonella in cecal contents and mucosa. Translocation of S. enteritidis was quantified by analysis of urinary nitric oxide metabolites in time. Before infection, FOS decreased cecal and fecal pH, increased fecal lactic acid concentration and increased bifidobacteria and enterobacteria. FOS also increased cytotoxicity of fecal water and fecal mucin excretion, indicating mucosal irritation. Remarkably, FOS dose-dependently increased salmonella numbers in cecal contents and mucosa and caused a major increase in infection-induced diarrhea. In addition, FOS enhanced translocation of salmonella. Thus, in contrast to most expectations, FOS dose-dependently impairs the resistance to salmonella infection in rats. These results await verification by other controlled animal and human studies.