Oral health‐related quality of life in patients receiving home‐care nursing: associations with aspects of dental status and xerostomia

doi:10.1111/j.1741‐2358.2009.00344.x
Oral health‐related quality of life in patients receiving home‐care nursing: associations with aspects of dental status and xerostomia Objective: To explore the differences in oral status, dental attendance and dry mouth problems between patients with long‐term disease with high and low scores on Oral Health Impact Profile 14 (OHIP 14) and how patients cope with oral problems such as xerostomia and a reduced ability to brush their teeth. Background: There has been a lack of studies of oral health and oral health‐related quality of life in the frail elderly within the community services. Materials and methods: A cross‐sectional questionnaire study was conducted with 137 patients receiving home‐care nursing. Structured interviews were conducted by student nurses using OHIP‐14, items from the Xerostomia Inventory and questions concerning dental visit habits, brushing of teeth and data from medical records. Results: Eighty‐three per cent of patients had natural teeth and 60% had only natural teeth. ‘Natural teeth only’ indicated a low score on OHIP‐14. Problems with brushing and items concerning xerostomia indicated a high score on OHIP‐14. Contrasts in the assessments concerning brushing of teeth and xerostomia indicated low priority from the patients themselves and the nursing staff. Conclusion: Community health services should focus upon oral health. Both patients and nurses should assess the need for regular brushing of teeth carried out by home‐care nurses. Assessment and treatment of dry mouth problems should have higher priority.     

Population persistence in a landscape context: the case of endangered arctic fox populations in Fennoscandia

Anthropogenic fragmentation of habitat and populations is recognized as one of the most important factors influencing loss of biodiversity. Since it is difficult to quantify demographic parameters in small populations, we need alternative methods to elucidate important factors affecting the viability of local populations. The Fennoscandian arctic fox inhabits a naturally fragmented alpine tundra environment, but historic anthropogenic impacts have further fragmented its distribution. After almost 80 yr of protection, the population remains critically endangered. Both intrinsic factors (related to the isolation and size of sub‐populations) and extrinsic factors (related to environmental conditions influencing patch quality and interspecific competition) have been proposed as explanations for the lack of population growth. To distinguish between these hypotheses, we conducted a spatially explicit analysis that compares areas where the species has persisted with areas where it has become locally extinct. We used characteristics of the fragments of alpine tundra habitat and individual arctic fox breeding dens (including both currently active dens and historically active dens) within the fragments to evaluate the importance of habitat characteristics and connectivity in explaining variation in persistence within a fragment. The number of reproductive events in a fragment was related to the size of the fragment, but not more than expected following a 1:1 relationship, suggesting little effect of fragment size on the relative number of reproductions. The likelihood of a den being used for breeding was positively associated with factors minimising interspecific competition as well as increasing within‐fragment connectivity. These results support the idea that the failure of Fennoscandian arctic fox to recover is caused by demographic factors that can be related to fine‐scale Allee or Allee‐like effects, as well as environmental influences related to increased competition and exclusion by red foxes.     

Evaluation of Ki67 Expression across Distinct Categories of Breast Cancer Specimens: A Population-Based Study of Matched Surgical Specimens,Core Needle Biopsies and Tissue Microarrays

Introduction

Tumor cell proliferation in breast cancer is strongly prognostic and may also predict response to chemotherapy. However, there is no consensus on counting areas or cut-off values for patient stratification. Our aim was to assess the matched level of proliferation by Ki67 when using different tissue categories (whole sections, WS; core needle biopsies, CNB; tissue microarrays, TMA), and the corresponding prognostic value.

Methods

We examined a retrospective, population-based series of breast cancer (n = 534) from the Norwegian Breast Cancer Screening Program. The percentage of Ki67 positive nuclei was evaluated by visual counting on WS (n = 534), CNB (n = 154) and TMA (n = 459).

Results

The median percentage of Ki67 expression was 18% on WS (hot-spot areas), 13% on CNB, and 7% on TMA, and this difference was statistically significant in paired cases. Increased Ki67 expression by all evaluation methods was associated with aggressive tumor features (large tumor diameter, high histologic grade, ER negativity) and reduced patient survival.

Conclusion

There is a significant difference in tumor cell proliferation by Ki67 across different sample categories. Ki67 is prognostic over a wide range of cut-off points and for different sample types, although Ki67 results derived from TMA sections are lower compared with those obtained using specimens from a clinical setting. Our findings indicate that specimen specific cut-off values should be applied for practical use.     

Regulation of Alr1 Mg transporter activity by intracellular magnesium

Mg homeostasis is critical to eukaryotic cells, but the contribution of Mg transporter activity to homeostasis is not fully understood. In yeast, Mg uptake is primarily mediated by the Alr1 transporter, which also allows low affinity uptake of other divalent cations such as Ni(2+), Mn(2+), Zn(2+) and Co(2+). Using Ni(2+) uptake to assay Alr1 activity, we observed approximately nine-fold more activity under Mg-deficient conditions. The mnr2 mutation, which is thought to block release of vacuolar Mg stores, was associated with increased Alr1 activity, suggesting Alr1 was regulated by intracellular Mg supply. Consistent with a previous report of the regulation of Alr1 expression by Mg supply, Mg deficiency and the mnr2 mutation both increased the accumulation of a carboxy-terminal epitope-tagged version of the Alr1 protein (Alr1-HA). However, Mg supply had little effect on ALR1 promoter activity or mRNA levels. In addition, while Mg deficiency caused a seven-fold increase in Alr1-HA accumulation, the N-terminally tagged and untagged Alr1 proteins increased less than two-fold. These observations argue that the Mg-dependent accumulation of the C-terminal epitope-tagged protein was primarily an artifact of its modification. Plasma membrane localization of YFP-tagged Alr1 was also unaffected by Mg supply, indicating that a change in Alr1 location did not explain the increased activity we observed. We conclude that variation in Alr1 protein accumulation or location does not make a substantial contribution to its regulation by Mg supply, suggesting Alr1 activity is directly regulated via as yet unknown mechanisms.     

Lack of the DNA glycosylases MYH and OGG1 in the cancer prone double mutant mouse does not increase mitochondrial DNA mutagenesis

Reactive oxygen species (ROS) are formed as natural byproducts during aerobic metabolism and readily induce premutagenic base lesions in the DNA. The 8-oxoguanine DNA glycosylase (OGG1) and MutY homolog 1 (MYH) synergistically prevent mutagenesis and cancer formation in mice. Their localization in the mitochondria as well as in the nucleus suggests that mutations in mitochondrial DNA (mtDNA) contribute to the carcinogenesis in the myh^?/?/ogg1^?/? double knockout mouse.In order to test this hypothesis, we analyzed mtDNA mutagenesis and mitochondrial function in young (1 month) and adult (6 months) wt and myh^?/?/ogg1^?/? mice. To our surprise, the absence of OGG1 and MYH had no impact on mtDNA mutation rates in these mice, even at the onset of cancer. This indicates that mtDNA mutagenesis is not responsible for the carcinogenesis of myh^?/?/ogg1^?/? mice. In line with these results, mitochondrial function was unaffected in the cancerous tissues liver and lung, whereas a significant reduction in respiration capacity was observed in brain mitochondria from the adult myh^?/?/ogg1^?/? mouse. The reduced respiration capacity correlated with a specific reduction (?25%) in complex I biochemical activity in brain mitochondria.Our results demonstrate that mtDNA mutations are not associated with cancer development in myh^?/?/ogg1^?/? mice, and that impairment of mitochondrial function in brain could be linked to nuclear DNA mutations in this strain. OGG1 and MYH appear to be dispensable for antimutator function in mitochondria.     

Problems in physiological experimental animal models investigated with factorial design

In the present study we investigated four variables using factorial design to decide if any of these could explain the variations in the control measurements of interstitial fluid pressure (P_if) in rat trachea that were experienced. This approach requires only a fraction of the animals normally needed when studying each factor separately. P_if in tracheal tissue was measured with the servocontrolled counterpressure system using sharpened micropipettes. The measurements were performed over a period of 60 min and are presented as mean for every 15 min period. The factors investigated in the study were: three strains of female rats (Strain) two brands of diets (Food); two breeder companies (Source); and finally two batches of the same set of animals to repeat the experiment twice (Week), using a total of 48 animals. There was a highly significant effect within Strain the first week (p=0.007), but this response was not observed the second week. The interaction between Strain×Week was significant (p=0.007) while the main effects Strain or Week alone were not significant. The response pattern for Strain and Food was inconsistent for the two experimental weeks studied. These experiments made it possible for us to simultaneously test several factors and exclude these factors as the reason for the observed changes in our experiments since the experiments did not allow the conclusion that one or several of these factors could explain the variation in P_if.