Correlates of Maternal and Paternal Adjustment to Chronic Childhood Disease

This study investigated the correlates of psychosocial adjustment in mothers and fathers of children with chronic disease. Participants were 20 mothers and 15 fathers of children with cystic fibrosis, 11 mothers and 9 fathers of children with muscular dystrophy, 18 mothers and 9 fathers of children with asthma, 13 mothers and 8 fathers of children with Type 1 diabetes and 19 mothers and 11 fathers of healthy children. Questionnaires relating to the variables of interest were used. Poorer levels of adjustment were associated with lower levels of social support and family cohesion for mothers and coping by understanding the child’s medical situation, more family life events and lower family cohesion for fathers. These findings suggest that the correlates associated with maternal and paternal psychological adjustment to chronic childhood disease differ. These differences are important to consider when providing care to children with chronic disease and their families.     

Intrahippocampal administration of A beta(1-40) impairs spatial learning and memory in hyperglycemic mice

Age-related neurodegenerative dementia, particularly Alzheimer's disease (AD), may be exacerbated by several interacting risk factors including genetic predisposition, beta amyloid (A beta) protein accumulation, environmental toxins, head trauma, and abnormal glycolytic metabolism. We examined the spatial learning and memory effects of A beta(1-40) administration on hyperglycemic mice by their performance in the Morris water maze. Chronic hyperglycemia was induced in male C57BL/6J mice to mimic diabetes mellitus by intraperitoneal injection of streptozotocin (STZ), which specifically destroys pancreatic beta-islet cells. Ten days after STZ treatment, intrahippocampal infusion of vehicle, monomer, or oligomer A beta(1-40) was given to these hyperglycemic mice. Our results demonstrate that in comparison with vehicle or monomer A beta(1-40), oligomer A beta(1-40) induced significant deficits of spatial learning and memory in hyperglycemic mice. Apoptotic signals were identified in the CA1 and dentate gyrus of hippocampus in hyperglycemic mice. A beta accumulation, oxidative stress, and apoptosis in the CA1 region were more intensive in hyperglycemic mice than that in normoglycemic mice after acute treatment with oligomer A beta(1-40) peptide treatment. These results indicate that CA1 apoptosis was enhanced by oxidative stress resulting from accumulation of A beta. Considered together, these findings suggest that hyperglycemic mice are more vulnerable to the A beta-induced-oxidative stress than normal subjects. We therefore propose that A beta accumulation would be enhanced by hyperglycemia, and the oxidative stress caused by A beta accumulation would in turn enhance the AD symptoms.     

Contagious Disease and Self-Defence

This paper gives a self-defence account of the scope and limits of the justified use of compulsion to control contagious disease. It applies an individualistic model of self-defence for state action and uses it to illuminate the constraints on public health compulsion of proportionality and using the least restrictive alternative. It next shows how a self-defence account should not be rejected on the basis of past abuses. The paper then considers two possible limits to a self-defence justification: compulsion of the non-culpable and over-inclusive compulsion. The paper claims that objections to compelling the non-culpable do not greatly restrict the scope of the self-defence justification. The over-included are, however, innocent bystanders, and methods such as compulsory quarantine, vaccination, and screening are not justified in self-defence. I am grateful to Julian Lamont, Jeff McMahan and Debbie Tseung for their help with this paper. An earlier version was given at the School of Public Health, the University of Texas at Houston; the Auckland Regional Public Health Service; and a conference at the School of Population Health, the University of Auckland. My thanks to the audiences for their comments.     

The Significance of the Concept of Disease for Justice in Health Care

In this paper, I want to scrutinise the value of utilising the concept of disease for a theory of distributive justice in health care. Although many people believe that the presence of a disease-related condition is a prerequisite of a justified claim on health care resources, the impact of the philosophical debate on the concept of disease is still relatively minor. This is surprising, because how we conceive of disease determines the amount of justified claims on health care resources. Therefore, the severity of scarcity depends on our interpretation of the concept of disease. I want to defend a specific combination of a theory of disease with a theory of distributive justice. A naturalist account of disease, together with sufficientarianism, is able to perform a gate-keeping function regarding entitlements to medical treatment. Although this combination cannot solve all problems of justice in health care, it may inform rationing decisions as well.     

Analyzing feature distinctiveness in the processing of living and non-living concepts in Alzheimer’s disease

The conceptual structure account (CSA) is a model specifying the role of the living and non-living domain dichotomy in the structure of semantic memory. According to this model, feature distinctiveness and the perceptual–functional inter-correlation of concepts are assumed to play a major role in impairing the ability to discriminate between living and non-living concepts in Alzheimer’s disease (AD). The hypothesis was tested in this study by using naming and sorting tasks traditionally considered as assessing distinctiveness, and a property verification task where distinctiveness and perceptual–functional inter-correlation were objectively controlled against norms especially created for this purpose. Alzheimer’s patients (n = 59) with minimal, mild or moderate dementia and normal elderly adults (n = 31) participated in the study. Overall, the findings did not support the CSA predictions. They revealed a distinctiveness effect on response accuracy with shared features dominating distinctive features regardless of domain. They also revealed more difficulties in the tasks involving effortful processes. The results stress the need to consider both cognitive demands of tasks and structural aspects of knowledge in the evaluation of semantic memory in AD.     

Heart rate variability and drawing impairment in hypoxemic COPD

We studied 54 patients with hypoxemic chronic obstructive pulmonary disease (COPD). The Mini Mental State Examination and the Mental Deterioration Battery were used for neuropsychological assessment. Heart rate variability (HRV) was assessed based on 24-h Holter ECG recording. Mann–Whitney test was used to compare HRV parameters of patients performing normally or abnormally on individual neuropsychological tasks. Spearman’s rho was used to investigate the correlations between HRV parameters and neuropsychological scores, indexes of health status or COPD severity. Patients with defective performance at copying drawings with landmarks (CDL) test (N = 23) had lower very low frequency (VLF) power with respect to patients with normal performance (N = 31) (24 h: median 213; interquartile range 120–282 vs. 309; 188–431 ms², p = 0.043; daytime: 202; 111–292 vs. 342; 194–397 ms², p = 0.039). The CDL score correlated with the VLF power (24 h: ρ = 0.27, p = 0.049; daytime: ρ = 0.30, p = 0.028), and the normalized low frequency/high frequency (LF/HF) ratio (24 h: ρ = 0.27, p = 0.05; daytime: ρ = 0.33, p = 0.015). Sympathetic modulation decreased for increasing severity of COPD. In conclusion, drawing impairment correlates with depressed sympathetic modulation in patients with COPD, and both might be indexes of COPD severity.     

Response speed, contingent negative variation and P300 in Alzheimer’s disease and MCI

Background

Decreased speed of information processing is a hallmark of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Recent studies suggest that response speed (RS) measures are very sensitive indicators of changes in longitudinal follow-up studies. Insight into the psycho-physiological underpinnings of slowed RS can be provided by measuring the associated event-related potentials (ERP).

Aims

The current study aims to investigate the relation between RS and its psycho-physiological correlates in AD and MCI.

Methods

Fifteen psychoactive drug-naïve AD patients, 20 MCI patients and twenty age-matched, healthy control subjects participated. Response speed was measured during a simple (SRT) and choice reaction time task (CRT). An oddball and contingent negative variation (CNV) paradigm were used to elicit ERP. To evaluate test-retest reliability (TRR), subjects underwent a similar assessment one week after the first.

Results

The SRT and CRT distinguished the patient groups significantly. The P300 amplitude and latency also distinguished the groups and showed a significant correlation with response speed. The CNV amplitude did not reveal a significant difference between groups and also showed a low TRR.The TRR of the SRT, CRT and P300 amplitude and latency in general was moderate to high.The current study suggests that response speed measures on a behavioural and psycho-physiological level deserve attention as a possible marker in the diagnosis and follow-up of AD.     

Does implicit learning in non-demented Parkinson’s disease depend on the level of cognitive functioning?

We investigated the influence of the level of cognitive functioning on sequence-specific learning in Parkinson's disease (PD). This was done by examining the relationship between the scales for outcomes in Parkinson's disease-cognition [SCOPA-COG, Marinus, J., Visser, M., Verwey, N. A., Verhey, F. R. J., Middelkoop, H. A. M.,Stiggelbout, A., et al. (2003). Assessment of cognition in Parkinson's disease. Neurology, 61, 1222-1228] and the serial reaction time (SRT) task [Nissen, M. J., & Bullemer, P. T. (1987). Attentional requirements for learning: Evidence from performance measures. Cognitive Psychology, 19, 1-32] in a homogeneous sample, consisting of 25 PD patients diagnosed in Stage 3 of the Hoehn and Yahr [Hoehn, M. M., & Yahr, M. D. (1967). Parkinsonism: onset, progression, and mortality. Neurology, 17, 427-442] scale. Six patients in the low scoring cognitive group, 11 patients in the average scoring and eight patients in the high scoring group, conducted a SRT task with a deterministic sequence. Sequence-specific learning was assessed by inserting a random block to determine whether the acquisition of sequence movements differed between groups. Our results indicate an association between cognitive functioning in PD patients and sequence learning. These findings emphasize the use of assessing cognition in addition to the well-known motor aspects in PD.     

MTHFR and ACE gene polymorphisms and risk of vascular and degenerative dementias in the elderly

Focal lacunar infarctions due to cerebral small vessel atherosclerosis or single/multiple large cortical infarcts lead to vascular dementia, and different genes and environmental factors have been implicated in causation or aggravation of the disease. Previous reports suggest that some of the risk factors may be common to both vascular as well as degenerative dementia. Among genetic factors, role of angiotensin converting enzyme (ACE) and methylene-tetrahydrofolate reductase (MTHFR) genes as putative risk factors has been examined but the outcome of these studies remain inconclusive. Present study attempted to see the importance of ACE alu insertion/deletion and MTHFR C677T polymorphisms as genetic predisposers to dementia. The study comprised of 80 vascular dementia patients, 90 degenerative dementia patients and 170 age matched controls. All were genotyped for ACE, MTHFR and APOE polymorphisms using PCR-RFLP method. Frequency of ACE D allele was seemingly high in dementia cases (26.7%) when compared to controls (11.2%). However, after adjusting for age and APOE E4^*, none of the ACE alleles showed good correlation. MTHFR genotypes or alleles also did not show any correlation. Our study suggests no true correlation of ACE or MTHR genes with dementia in elderly.     

防治血管剩留风险的决策探讨

针对冠心病和（或）2型糖尿病患者,已有许多有效的防治措施。然而,尽管接受了当前的标准治疗,这类患者仍会反复发生许多大血管和微血管事件,这种现象称之为血管剩留风险。有许多因素影响血管剩留风险的存在,其中最为重要的是致动脉粥样硬化性血脂异常。因此,采取积极的全面干预措施如改善生活方式、联合降脂以改善所有的脂质异常指标,是最大程度降低血管剩留风险的动向。