In 2019, a Rodent Eradication Project (REP) was implemented on World Heritage listed Lord Howe Island, Australia. Among the species expected to benefit was a burrow-nesting seabird, the Black-winged Petrel Pterodroma nigripennis. Prior to the REP, we assessed causes of Black-winged Petrel nest failure using surveillance cameras. We also measured breeding success before and after the REP and investigated emerging pressures on breeding success from other native species. In 2017, ship rats Rattus rattus were a major cause of Black-winged Petrel nest failure, and breeding success was as low as 2.5%, compared to 47.5% on rodent-free Phillip Island (Norfolk Island Group). In 2020, in the absence of rodents, breeding success on Lord Howe Island increased dramatically to 67% and remained high (50%) in 2021. This result suggests that reproductive output of small seabirds has been heavily supressed by rodents on Lord Howe Island for decades. A subsequent increase in the population of a predatory endemic rail, the Lord Howe Woodhen Hypotaenida sylvestris, combined with burrow competition from Little Shearwaters Puffinus assimilis, indicated that initial high breeding success may not be sustained. However, the surge in successful breeding of Black-winged Petrels is likely to result in a significant increase in fledgling numbers and the recruitment of hundreds of additional birds each year. Given the important role of petrels in global nutrient cycling, and their positive influence on island biodiversity, their expansion should benefit the ecological restoration of Lord Howe Island.

Dysfunctions of glutamatergic and GABAergic neurotransmission are two important hypotheses for the pathogenesis of schizophrenia. Thus, genes in the pathway are candidates for schizophrenia susceptibility. Phosphate-activated glutaminase (GLS), glutamine synthetase (GLUL), glutamic acid decarboxylase (GAD), GABA transaminase (ABAT) and succinic semialdehyde dehydrogenase (ALDH5A1) are five primary enzymes in glutamate and GABA synthetic and degradative pathway. In order to investigate the possible involvement of these genes in the development of paranoid schizophrenia, we genotyped 80 paranoid schizophrenics from northern China and 108 matched controls by polymerase chain reaction (PCR) and restriction fragment length polymorphisms (RFLP) methods or directly sequencing of PCR product. Seven SNPs were found to be polymorphic in the population investigated. No significant differences in the genotype distributions or allele frequencies between patients and controls were found. Therefore, we conclude the polymorphisms studied in the five genes do not play major roles in pathogenesis of paranoid schizophrenia in the population investigated.