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Biomedical subjects

E M Allen

Publications and source records attributed to E M Allen.

At least 37 records · Page 2Linked to original sources
PubMed1994

Factors adversely associated with breast feeding in New Zealand.

Control data from 1529 infants studied in a multicentre case-control study of sudden infant death in New Zealand were analysed to identify factors that might hinder the establishment and duration of breast feeding. Although 1300 infants (85%) were exclusively breast-fed at discharge from the obstetric hospital, this fell to 940 (61%) by 4 weeks. Logistic regression was used to identify factors that might adversely influence breast feeding 'at discharge', 'at 4 weeks' and the overall 'duration' of breast feeding. When adjusted for confounding factors, not exclusive breast feeding 'at discharge' was significantly associated with: twin pregnancy, being a Pacific Islander, mother not bedsharing, subsequent dummy use, birthweight less than 2500 g, heavy maternal smoking, not attending antenatal classes and mother less than 20 years old at first pregnancy. Mothers smoking more than 20 cigarettes a day were nearly twice as likely to not exclusively breast feed on discharge compared to those who did not smoke. A 'dose response' was apparent with the heaviest smokers having the least likelihood of establishing exclusive breast feeding. Being exclusively breast-fed at discharge but not 'at 4 weeks' was associated with: twin pregnancy, admission to a neonatal intensive care unit, subsequent dummy use and not being married. A shorter overall 'duration' of breast feeding was associated with maternal smoking, subsequent dummy use, mother not bedsharing, twin pregnancy, mother less than 20 years old at first pregnancy, low occupational status and not attending antenatal classes. These effects persisted when social and demographic factors, including birthweight, were taken into account.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Bed sharing, smoking, and alcohol in the sudden infant death syndrome. New Zealand Cot Death Study Group.

OBJECTIVES: To investigate why sharing the bed with an infant is a not consistent risk factor for the sudden infant death syndrome in ethnic subgroups in New Zealand and to see if the risk of sudden infant death associated with this practice is related to other factors, particularly maternal smoking and alcohol consumption. DESIGN: Nationwide case-control study. SETTING: Region of New Zealand with 78% of all births during 1987-90. SUBJECTS: Home interviews were completed with parents of 393 (81.0% of total) infants who died from the sudden infant death syndrome in the postneonatal age group, and 1592 (88.4% of total) controls who were a representative sample of all hospital births in the study region. RESULTS: Maternal smoking interacted with infant bed sharing on the risk of sudden infant death. Compared with infants not exposed to either risk factor, the relative risk for infants of mothers who smoked was 3.94 (95% confidence interval 2.47 to 6.27) for bed sharing in the last two weeks and 4.55 (2.63 to 7.88) for bed sharing in the last sleep, after other confounders were controlled for. The results for infants of non-smoking mothers were inconsistent with the relative risk being significantly increased for usual bed sharing in the last two weeks (1.73; 1.11 to 2.70) but not for bed sharing in the last sleep (0.98; 0.44 to 2.18). Neither maternal alcohol consumption nor the thermal resistance of the infant's clothing and bedding interacted with bed sharing to increase the risk of sudden infant death, and alcohol was not a risk factor by itself. CONCLUSION: Infant bed sharing is associated with a significantly raised risk of the sudden infant death syndrome, particularly among infants of mothers who smoke. The interaction between maternal smoking and bed sharing suggests that a mechanism involving passive smoking, rather than the previously proposed mechanisms of overlaying and hyperthermia, increases the risk of sudden infant death from bed sharing.

Adult↗
PubMed1993

Ethnic differences in mortality from sudden infant death syndrome in New Zealand.

OBJECTIVES: To examine the factors which might explain the higher mortality from sudden infant death syndrome in Maori infants (7.4/1000 live births in 1986 compared with 3.6 in non-Maori children). DESIGN: A large nationwide case control study. SETTING: New Zealand. 485 infants who died of sudden infant death syndrome were compared with 1800 control infants. There were 229 Maori and 240 non-Maori cases of sudden infant death syndrome (16 cases unassigned) and 353 Maori and 1410 non-Maori controls (37 unassigned). RESULTS: Maori infants had 3.81 times the risk (95% confidence interval 3.06 to 4.76) of sudden infant death syndrome compared with non-Maori infants. The risk factors for sudden infant death syndrome within groups were remarkably similar. When Maori and non-Maori controls were compared the prevalence of many of the known risk factors was higher in Maori infants. In particular, mothers were socioeconomically disadvantaged, younger, and more likely to smoke and their infants were of lower birth weight and more likely to share a bed with another person. Multivariate analysis controlling for potential confounders found that simply being Maori increased the risk of sudden infant death syndrome by only 1.37 (95% CI = 0.95 to 2.01), not statistically significantly different from 1. Population attributable risk was calculated for prone sleeping position, maternal smoking, not breast feeding, and infants sharing a bed with another person. In total these four risk factors accounted for 89% of deaths from sudden infant death syndrome in Maori infants and 79% in non-Maori infants. CONCLUSION: The high rate of sudden infant death syndrome among Maori infants is based largely on the high prevalence in the Maori population of the major risk factors. Other risk factors, not related to ethnicity, probably explain remaining differences between Maori and non-Maori children.

Birth Weight↗
PubMed1993

Pilot study of computerised differentiation of Huntington's disease, schizophrenic, and Parkinson's disease patients using the contingent negative variation.

In this study a potential known as the contingent negative variation was used to differentiate between schizophrenic, Parkinson's disease (PD), Huntington's disease (HD) patients and normal control subjects. The aim was to assist diagnosis and the avoidance of false diagnosis. 20 schizophrenic, 16 PD, 11 HD and 43 normal control subjects were enrolled for this study. The discriminatory variables were generated by applying spectral analysis to pre- and post-stimulus sections of the CNV responses. The patient differentiation was achieved by using the measured variables in a discriminant analysis program. It was possible to accurately differentiate between HD, schizophrenic, PD patients and normal control subjects. It was also attempted to differentiate between HD and schizophrenic patients, HD and PD patients, and schizophrenic and PD patients. The test results indicated that the method is useful in differentiating between these patients. This study had a number of limitations. It was based on a limited number of individuals, and an analysis of medication effects on the test results and the test-retest reliability assessment could not be carried out.

Diagnosis, Computer-Assisted↗
PubMed1993

Acute iodine ingestion increases intrathyroidal glutathione.

In genetically predisposed individuals, autoimmune lymphocytic thyroiditis (LT) is potentiated by excess dietary iodine (I). There have been data which suggest that oxidative stress may have a role in iodine-induced LT. These in vivo studies were undertaken to examine the effect of iodine on intrathyroidal levels of the potent antioxidant glutathione (GSH) and see if the thyroids of LT-prone BB/Wor rats have aberrant GSH responses after iodine-loading. LT-prone BB/Wor, non LT-prone BB/Wor and Wistar rats were randomized to receive either 0.05% I (as Nal) or tap water. Thyroid and liver homogenates were assayed individually for GSH. Following the administration of 0.05% iodine water overnight, all of the animals demonstrated a rise in intrathyroidal GSH regardless of LT-proneness. To determine whether this was a dose-dependent response, Wis rats were randomized to receive tap, 0.0125%, 0.025%, 0.05%, or 0.075% I, overnight. Intrathyroidal GSH levels rose with increasing iodine concentrations peaking at 0.025% I. Hepatic GSH levels were unaltered by iodine treatment. Ten days of 0.05% I water did not result in any difference between the GSH levels of thyroids from treated and control rats. Frozen sections of the thyroids and livers from iodine-treated rats were compared to tap-water controls after staining with Mercury Orange for GSH and Schiff's reagent for evidence of lipid peroxidation. Iodine-treated thyroids had an apparent shift of GSH staining from the apical border to the cytoplasm. However, there was no Schiff's staining indicative of lipid peroxidation in the iodine-treated thyroids.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Breastfeeding and the risk of sudden infant death syndrome.

The New Zealand Cot Death Study, a multicentre case-control study, was set up to identify risk factors associated with sudden infant death syndrome (SIDS). In the 3 years of the study there were 485 infant deaths classified as SIDS in the study areas and 1800 infants who were randomly selected as controls. Data were collected by parent interviews and from obstetric notes. A full set of data for this analysis was available from 356 cases and 1529 control infants. The relationship between length of any breastfeeding and SIDS was examined: 92% of the controls were initially breastfed compared to 86% of the cases. As time went by, cases stopped breastfeeding sooner than controls: by 13 weeks, 67% controls were breastfed versus 49% cases. A reduced risk for SIDS in breastfed infants persisted during the first 6 months after controlling for confounding demographic, maternal and infant factors. Infants exclusively breastfed 'at discharge from the obstetric hospital' (odds ratio [OR] = 0.52, 95% confidence interval (CI): 0.35-0.71) and during the last 2 days (OR = 0.65, 95% CI: 0.46-0.91) had a significantly lower risk of SIDS than infants not breastfed after controlling for potential confounders. We have shown a substantial association of breastfeeding with a lowered risk for SIDS. This supports the need for more positive promotion and active community support to further enhance the level and length of exclusive breastfeeding.

Breast Feeding↗
PubMed1993

Subclass reactivity of pemphigus foliaceus autoantibodies with recombinant human desmoglein.

Pemphigus foliaceus (PF) and its endemic form, Fogo Selvagem (FS), are autoimmune disorders characterized by subcorneal vesicles and IgG4 subclass autoantibodies that recognize a surface antigen of normal epidermal cells. FS and PF autoantibodies have been shown to bind desmoglein (DGI), a desmosomal glycoprotein classified as a member of the cadherin family of calcium-dependent cell adhesion molecules. In the present study we report the isolation of three overlapping cDNA clones representing greater than 90% of the extracellular domain of human DGI. Recombinant proteins encoded by these clones, designated DGI-1, DGI-2, and DGI-3, were produced in bacteria and analyzed for immunoblot (IB) reactivity with a panel of FS, PF, and control sera. FS and PF autoantibodies possessing reactivity with each of the three recombinant fusion proteins (FPs) were identified. FP DGI-3 (containing 123 amino acids of the membrane proximal region of the DGI ectodomain) showed reactivity with the largest number of patient sera--seven FS and one PF. IB reactivity with the DGI-1 FP (encoding 205 amino acids of the N-terminal region of DGI) could be eliminated by truncation of the C-terminal portion of this protein, indicating that autoantibodies were not binding the R-A-L motif. Autoantibodies reactive with two of the three FPs were predominantly restricted to IgG4, the subclass shown to be pathogenic in the passive transfer mouse model. The findings of this study demonstrate that the extracellular domain of DGI contains at least three antigenic sites recognized by FS and PF autoantibodies. The region near the membrane-spanning domain of DGI appears to contain an immunodominant site. This study is the first to document immunoblot reactivity of FS and PF autoantibodies with recombinant forms of DGI. The use of such molecular tools should facilitate the identification and characterization of relevant antigen/antibody systems in FS and PF.

Autoantibodies↗
PubMed1993

Dummies and the sudden infant death syndrome.

The association between dummy use and sudden infant death syndrome (SIDS) was investigated in 485 deaths due to SIDS in the postneonatal age group and compared with 1800 control infants. Parental interviews were completed in 87% of subjects. The prevalence of dummy use in New Zealand is low and varies within New Zealand. Dummy use in the two week period before death was less in cases of SIDS than in the last two weeks for controls (odds ratio (OR) 0.76, 95% confidence interval (CI) 0.57 to 1.02). Use of a dummy in the last sleep for cases of SIDS or in the nominated sleep for controls was significantly less in cases than controls (OR 0.44, 95% CI 0.26 to 0.73). The OR changed very little after controlling for a wide range of potential confounders. It is concluded that dummy use may protect against SIDS, but this observation needs to be repeated before dummies can be recommended for this purpose. If dummy sucking is protective then it is one of several factors that may explain the higher mortality from SIDS in New Zealand than in other countries, and may also explain in part the regional variation within New Zealand.

Case-Control Studies↗
PubMed1993

Smoking and the sudden infant death syndrome.

OBJECTIVE: Maternal smoking has been shown to be a risk factor for sudden infant death syndrome (SIDS). The effect of smoking by the father and other household members has not previously been examined. METHODS: A large nationwide case-control study. Four hundred eighty-five SIDS deaths in the postneonatal age group were compared with 1800 control infants. RESULTS: Infants of mothers who smoked during pregnancy had a 4.09 (95% confidence interval [CI] = 3.28, 5.11) greater risk of death than infants of mothers who did not smoke. Infants of mothers who smoked postnatally also had an increased risk of SIDS compared with infants of nonsmokers and, furthermore, the risk increased with increasing levels of maternal smoking. Smoking by the father and other household members increased the risk (odds ratio [OR] = 2.41, 95% CI = 1.92, 3.02 and OR = 1.54, 95% CI = 1.20, 1.99, respectively). Smoking by the father increased the risk of SIDS if the mother smoked, but had no effect if she did not smoke. In analyses controlled for a wide range of potential confounders, smoking by the mother and father was still significantly associated with an increased risk of SIDS. CONCLUSION: Passive tobacco smoking is causally related to SIDS.

Case-Control Studies↗
PubMed1992

Disruption of social circadian rhythms in major depression: a preliminary report.

While dysregulations of physiological circadian rhythms are common findings in depression and have been posited to be involved in the mediation of depressive episodes, only recently has the role of social circadian rhythms in the pathogenesis of depression been a focus of interest. The Social Rhythm Metric (SRM), designed to describe the regularity of a human subject's social circadian rhythms, was used in this study to compare the social rhythms of depressed patients with those of normal controls and to determine the relationship between SRM scores and depression severity. Depressed patients' SRM scores were significantly lower than those of normal controls. The SRM negatively correlated with scores on the Hamilton Rating Scale for Depression. Overall social activity was negatively correlated with a Hamilton item, social activity impairment. The results of this preliminary study support the hypothesis that social zeitgebers are disrupted in major depression.

Activities of Daily Living↗
PubMed1992

Postnatal depression and SIDS: a prospective study.

This study was carried out in response to reports from nurses to a post-neonatal mortality review committee that a number of mothers of infants dying from sudden infant death syndrome (SIDS) appeared to be depressed before the child's death. The New Zealand Cot Death Study was a 3 year multicentre case-control study for SIDS. There were 485 SIDS cases in the post-neonatal age group in the study regions, and these were compared with 1800 control infants. Infants of mothers with either a self-reported use of medication for psychiatric disorders, a history of hospitalization for psychiatric illness or a family history of postnatal depression had a significantly increased risk of SIDS compared with infants of mothers who were either not using medication (odds ratio (OR) = 1.45; 95% confidence interval (CI) = 1.03, 2.04) or were without a history of hospitalization for psychiatric illness (OR = 1.80; 95% CI = 1.03, 3.11) or a family history of postnatal depression (OR = 1.61; 95% CI = 1.06, 2.43). All mothers of infants born in the study areas over a 1 year period were eligible to complete a questionnaire measuring maternal depression when the infant was 4 weeks of age. Thirty-three infants subsequently died from SIDS, and they were compared with 174 controls. Fifteen (45.5%) of the mothers of cases were depressed, compared with 28 (16.1%) of the mothers of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗
PubMed1992

Four modifiable and other major risk factors for cot death: the New Zealand study.

New Zealand's high mortality rate from sudden infant death syndrome (SIDS) prompted the development of the New Zealand Cot Death Study. A report of the analysis of the data from the first year has been published. This report now gives the major identified risk factors from the full 3 year data set. In this case-control study there were 485 infants who died from SIDS in the post-neonatal age group, and 1800 control infants, who were a representative sample of all hospital births in the study region. Obstetric records were examined and parental interviews were completed in 97.5% and 86.9% of subjects, respectively. As expected many risk factors for SIDS were confirmed including: lower socio-economic status, unmarried mother, young mother, younger school-leaving age of mother, younger age of mother at first pregnancy, late attendance at antenatal clinic, non-attendance at antenatal classes, Maori, greater number of previous pregnancies, the further south the domicile, winter, low birthweight, short gestation, male infant and admission to a special care baby unit. In addition, however, we identified four risk factors that are potentially amenable to modification.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1992

Further evidence supporting a causal relationship between prone sleeping position and SIDS.

A 3 year case-control study identifying the risk factors for SIDS was undertaken. Preliminary analysis of the data from the first year suggested that SIDS mortality could fall by 50% if the prevalence of the prone sleeping position changed from 40 to 0%. During the 3 year study the prevalence of the prone sleeping position among infants has fallen from 43% in the first year to 20% in the third year. SIDS mortality has fallen to 3.1/1000 live births, which is very close to that predicted. When considered with other available evidence this strongly supports a causal relationship between the prone sleeping position and SIDS.

Case-Control Studies↗
PubMed1992

The New Zealand Cot Death Study: some legal and ethical issues.

The New Zealand Cot Death Study is a 3 year multicentre case-control study aimed at identifying the risk factors for sudden infant death syndrome (SIDS). The paper describes some of the legal and ethical issues which arose in the planning, implementation and analysis of the study.

Case-Control Studies↗
PubMed1991

Results from the first year of the New Zealand cot death study.

New Zealand's high mortality rate from the sudden infant death syndrome (SIDS) prompted the development of the New Zealand cot death study. This report of the preliminary analysis of the first year of the data gives the major identified risk factors. One hundred and sixty-two infants who died from SIDS were compared with 589 control infants, who were a representative sample of all hospital births in the study region. Obstetric records were examined and parental interviews were completed in 96% and 89% of subjects respectively. Data were available for all the variables in this study in 95% of those interviewed, thus 128 cases and 503 controls make up the subjects of this report. As expected we confirmed many risk factors for SIDS including: lower socioeconomic status, unmarried mother, young mother, younger school leaving age of mother, younger age of mother at first pregnancy, late attendance at antenatal clinic, nonattendant at antenatal classes, Maori, greater number of previous pregnancies, lower birth weight, shorter gestation, male infant, admission to neonatal intensive care unit. In addition, however, we identified three risk factors which are potentially amenable to modification. These were the prone sleeping position of baby (odds ratio = 3.53, 95% confidence interval 2.26, 5.54), maternal smoking (1-9 cigarettes/day OR = 1.87, 95% CI = 0.98, 3.54; 10-19/day OR = 2.64, 95% CI = 1.47, 4.74; 20+/day OR = 5.06, 95% CI = 2.86, 8.95) and breast feeding (OR = 2.93, 95% CI = 1.84, 4.67).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Management of nutritional and infectious complications of postoperative chylothorax in children.

Postoperative chylothorax may occur following any intrathoracic surgical procedure in children. From January 1979 through February 1987, 18 children aged 1 month to 9 years had chylothorax listed among their discharge diagnoses. Initial therapy for all patients consisted of chest tube placement for pleural space drainage and nutritional support with either enteral formulas enriched with medium-chain triglycerides or total parenteral nutrition. Both total parenteral nutrition and medium-chain triglyceride-enriched enteral regimens provided adequate nutritional support in these children. Five of the 18 experienced lymphopenia secondary to chylous lymphocyte loss. Infections were diagnosed in 5 patients during hospitalization; one was a fatal viral pneumonitis. No correlation between infectious complications and lymphocyte count could be demonstrated.

Bacterial Infections↗
PubMed1991

Herpes simplex virus type 1-specific cytotoxic T lymphocytes recognize immediate-early protein ICP27.

The identity of herpes simplex virus type 1 (HSV-1) antigens that serve as targets for cytotoxic T lymphocytes (CTL) and their ability to induce protective immunity remain uncertain. In this article, we report the identification of the immediate-early protein ICP27 as a CTL antigen in H-2d mice but not in H-2k or H-2b mice. Calculation of the frequencies of H-2d-restricted virus-specific CTL demonstrated that approximately one-fourth of the total HSV-1-specific response was directed against ICP27. To define the location of this CTL epitope, four truncated derivatives of the ICP27 gene which place the epitope in a 217-amino-acid region (amino acids 189 to 406) near the central portion of the protein were constructed. Mice immunized with ICP27 were able both to induce HSV-1-specific CTL and to survive a lethal intraperitoneal challenge with virulent HSV-1. However, neither appreciable antibody nor delayed-type hypersensitivity responses were induced in immunized mice, and they were also unable to clear a local epithelial virus challenge. It appears that ICP27, although capable of inducing several aspects of the immune response, is by itself unable to provide complete immunity.

Animals↗