Impact injuries and probability of survival in a large semiurban endemic pigeon in New Zealand, Hemiphaga novaeseelandiae

The New Zealand Pigeon or kereru (Hemiphaga novaeseelandiae) frequently collides with windows and vehicles. In this study of 146 kereru collected from 1996 to 2009, we used 118 radiographs and 91 necropsies to determine skeletal and soft tissue injuries. Vehicle collisions resulted in more damage to the extremities (wing and femur), whereas collisions with windows resulted in trauma to the head, fractures/dislocations of the coracoids and clavicles, and ruptured internal organs. Soft tissue injuries included damage to the flight muscles and heart ruptures caused by fractured coracoid bones, as well as extensive bruising of pectoral muscles and hemorrhaging of the lungs. Rehabilitation time was not related to number of skeletal injuries sustained, nor was the time until death for those that did not survive. In general, kereru with greater numbers of injuries were less likely to survive rehabilitation. Flight speed and force calculations suggest that a 570-g kereru would collide with 3-70 times the force of smaller birds (5-180 g); this may explain the discrepancies between the injuries characterized here and those reported for North American passerines. The differences in injuries sustained from collisions with windows and cars can be used to inform rehabilitators about the possible nature of injuries if the source of impact is known.     

Impact of food abundance, diet and food quality on the breeding of the fruit pigeon, Parea Hemiphaga novaeseelandiae chathamensis, on Chatham Island, New Zealand

Breeding and diet of Parea Hemiphaga novaeseelandiae chathamensis were studied in relation to food abundance and quality on Chatham Island from 1991 to 1994. Although pairs were found breeding in all months, they nested predominantly during winter and spring (June-November). The timing of the nesting season, the proportion of pairs that bred and the number of chicks reared per pair varied between nesting seasons. During the 1992–1993 and 1994–1995 nesting seasons, all pairs nested, and many pairs reared two chicks, often involving clutch overlap (58% of 12 cases in 1992–1993, 37% of eight cases in 1994–1995). In 1993–1994, when fruit was scarce, nesting began 2 months later, only 44% of pairs nested and no pairs attempted to rear a second chick. Prior to and during the productive nesting seasons (1992–1993, 1994–1995), the diet of Parea consisted mainly of fruit, particularly that of Matipo Myrsine chathamica in autumn (March-May) and Hoho Pseudopanax chathamicus in winter and spring. Nutrient analyses of the main Parea foods showed that the pulp of these fruit were rich in lipids and available carbohydrates compared with those in foliage foods. Heavy fruiting of Matipo and Hoho promoted early nesting and prolonged nesting for 6 months, including nesting during winter.     

Breeding Systems in New Zealand Plants: I. Fuchsia

The three New Zealand Fuchsia species have heteromorphic flowerspreviously described as heterostyled. F. excorticata and F.perscandens are shown to be gynodioecious and F. procumbenstrioecious. The frequencies of the two forms in several populationsof F. excorticata are given.     

Breeding of the bellbird on the Poor Knights Islands,New Zealand

Abstract

The breeding of the bellbird (Anthornis melanura) was studied intensively over three seasons on Aorangi Island, Poor Knights Islands. Adult males defended territories all year but ventured beyond them to exploit localised food resources and to obtain water; some adults defended the same territory for at least 5 years. Adult females shared a territory with a male only during the breeding season. At other times of the year adult females were joined by juveniles and immatures and formed feeding flocks. The breeding season extended from late September to late December. A few nests were built on the ground but most were in dense vegetation, usually near the canopy. Peak egg-laying extended from mid-October to mid-November and only one clutch of two to four eggs was laid. Nest building and incubation were completed by the female alone but both parents fed nestlings. Fledglings stayed in the vicinity of the nest for several days, and were fed by both parents. Incubation and nestling periods were about 15 and 19 days respectively. Comparisons are made with the breeding biology of bellbirds and other native passerines on mainland New Zealand, and the importance of the predator-free enviomment of the Poor Knights Islands is stressed.     

Investigating reasons for socioeconomic inequalities in breast cancer survival in New Zealand

Background: This study investigated the role that demographic and tumour factors play in explaining socioeconomic inequalities in breast cancer survival. Methods: Breast cancer cases notified to the New Zealand Cancer Registry (NZCR) from April 2005 to April 2007 were followed up to April 2009. The New Zealand area-based deprivation index (NZDep) was used as a measure of socioeconomic position. Relative survival rates were estimated using sex-, deprivation- and ethnic-specific life tables. Multiple imputation was used to impute missing data. Excess mortality modelling was used to estimate the contribution of demographic and tumour factors to inequalities in survival. Results: There were 2968 breast cancer cases included and 433 recorded deaths. Relative survival rates at 4 years varied across deprivation groups. Using NZDep deciles 1–4 (least deprived) as the reference group, the age- and ethnicity-adjusted hazard ratio (HR) for NZDep deciles 7–8 was 2.03 (CI 1.36–3.04) and for NZDep deciles 9–10 was 1.93 (CI 1.28–2.92). In the fully adjusted model there remained 50% excess mortality for the two most deprived groups compared to the most affluent. Variables which measured timely access to care (extent/size) accounted for more of the survival disparity than breast cancer subtype variables (ER/PR/HER2). Conclusion: Women from deprived areas in New Zealand who are diagnosed with breast cancer are less likely to survive as long as those from affluent areas. A substantial proportion of these socioeconomic disparities can be attributed to differential access to health care although other factors, currently unknown, are also likely to play an important role.     

Breeding and age structure of the population of Macropus parma on Kawau Island,New Zealand

The parma wallaby, Macropus parma, is one of four species of wallaby introduced on to Kawau Island, New Zealand, in ahout 1870. A sample of sixty-four parmas was shot on the island in February 1973 to provide information on breeding activity and age structure of the population. Incidental data were also collected from the tammar wallaby, Macropus eugenii, which is the other common species on the island. Neither the sex ratio of the shot sample of parmas (thirty-seven males to twenty-seven females) nor that of the tammars (eleven males to eleven females) differed significantly from parity. Onset of sexual maturity of female parmas on Kawau I. was delayed when compared with that of captive females. One female was estimated to have bred at 19 months old but most females in the sample were not mature until 2 years old and a few not until 3 years old. In contrast, female tammars became sexually mature at about 12 months. There did not appear to be any delay in the onset of sexual maturity of male parma wallabies. In the shot sample, none of sixteen female parmas capable of having a young were carrying a pouch young whereas nine of ten female tammars had a pouch young. The mean date of birth of these latter young was 30 January (range 18 January - 11 February) which is consistent with the breeding season of tammars in Australia. Among the mature female parmas two had recently mated, six were in pro-oestrus and six were in anoestrus, indicating that the breeding season in 1973 had just commenced. Estimated months of birth for all parmas under 3 years of age suggested that breeding was continuous in 1970–71 but that there had been a defined breeding season in 1972 with births occurring between March and July. There was an excess of 1– and 2–year-old parmas in the sample. This was the result of continuous breeding in 1970–71, presumably due to the provision of pasture on farmland being developed on the island. A sample of thirty-three tammar skulls resulting from a shoot in November 1972 did not show a nmilar excess of 1– and 2–year-old animals as this species has a rigidly defined breeding pattern and the females can produce only one young a year.     

Tolerance defects in New Zealand Black and New Zealand Black X New Zealand White F1 mice

The susceptibility of autoimmune NZB and (NZB X NZW)F1 mice to the induction of tolerance by monomeric BSA was compared with several normal mouse strains. Unresponsiveness in T and B lymphocyte compartments was probed by challenging with DNP8BSA and measuring anti-DNP and anti-BSA antibodies separately. Tolerance induced by monomeric BSA was carrier specific, and there was no evidence of epitope-specific suppression. Normal NZW, NFS, and B10.D2 mice were easily rendered tolerant with monomeric BSA and did not produce anti-DNP or anti-BSA antibodies after challenge with DNP8BSA. By contrast, the lack of anti-DNP antibody response in similarly treated NZB mice was dependent on the dose of monomeric BSA, indicating that the helper T cells were partially resistant to tolerance induction. NZB mice treated with a high dose of monomeric BSA produced anti-BSA, but not anti-DNP, antibodies after immunization. Thus, the anti-carrier B cells in NZB mice may have been primed by monomeric BSA. The presence of the xid gene on the NZB background rendered the mice susceptible to induction of tolerance, suggesting that the tolerance defect in NZB mice involves the B cell compartment. This abnormal antibody response was a dominant trait: (NZB X NFS)F1 and (NZB X B10.D2)F1 mice had the same characteristics as NZB mice. These F1 hybrids do not develop autoimmune disease, indicating that resistance to experimental tolerance induction expressed at a B cell level may not be sufficient for disease development. In contrast to NZB and other NZB F1 hybrids, (NZB X NZW)F1 hybrids treated with monomeric BSA and challenged with DNP8BSA responded to both DNP and BSA. The contribution of a B cell defect to the tolerance abnormality of (NZB X NZW)F1 mice was examined by analyzing the effect of the xid gene on the progeny of (NZB.xid X NZW)F1 mice. Unlike the effect of the xid gene on NZB mice, both phenotypically normal heterozygous female and phenotypically xid hemizygous male mice produced anti-DNP and anti-BSA antibodies after tolerance induction and immunization, demonstrating that a major helper T cell abnormality was present in (NZB X NZW)F1 mice. The (NZW X B10.D2)F1 hybrid was rendered tolerant by this procedure, indicating that the helper T cell defect (NZB X NZW)F1 mice may have resulted from gene complementation with the NZB mice contributing partial resistance of T helper cells to tolerance induction.(ABSTRACT TRUNCATED AT 400 WORDS)