Murine Trophoblast Failure and Spontaneous Abortion

PROBLEM: Infection has been proposed to initiate abortion, and the role of viruses in spontaneous resorption in mice has not been tested. METHOD: The anti-viral drug ribavirin (1-β-D-ribofuranosyl-1,2,4-triazole-3-carboxamide) was fed to CBA/J and C3H/HeJ female mice beginning on the morning after mating with DBA/2J males. RESULTS: Ribavirin treatment increased the rate of abortion (resorption) on day 13.5, and this was associated with retardation of the rate of embryo development and hypoplasia of the trophoblast. There was a reduction in trophoblast-dependent decidua-associated soluble suppressor activity, but there was no maternal mononuclear cell infiltrate of the type reported in association with resorption of semiallogeneic and xenogeneic mouse embryos. This may be due to an immunosuppressive effect of ribavirin. Ribavirin was able to potently suppress proliferation of mouse trophoblast and mastocytoma cell lines in vitro. CONCLUSIONS: There are several drug-induced murine abortion models that provide useful insights into potential mechanisms underlying spontaneous pregnancy failure, but in the ribavirin model, a direct impairment of trophoblast development appears to be responsible.     

Phagolysosomal pH and Location of Particles in Alveolar Macrophages

Phagolysosomal pH and Location of Particles in Alveolar Macrophages.NYBERG, K., JOHANSSON, U., JOHANSSON, A., AND CAMNER, P. (1991).Fundam. Appl. Toxicol. 16, 393–400. Fluorescein-labeledsilica particles (FSP) were instilled into the tracheae of rabbits.Groups of four rabbits were killed after 24 hr, 1 week, 1 month,or 3 months and their lungs were lavaged. Phagolysosomal pHin the alveolar macrophages (AM) was measured using microscopefluorometry with FSP as a probe. Due to the marked decline ofthe fluorescence intensities from the FSP between 1 and 3 monthsafter instillation, it was not possible to measure pH at 3 months,but the values from 24 hr, 1 week, and 1 month were quite similar,with group means of 4.8 and 4.9, respectively. PhagolysosomalpH in AM which phagocytized the FSP in vitro showed values abouthalf a pH unit higher. AM from rabbits lavaged at 1 week hadmore lysosomes in contact with the FSP-containing phagolysosomesand a higher degree of vacuolization between the FSP and thephagolysosomal membrane than AM lavaged at 1 day. The locationof the FSP in the AM appeared to be similar in rabbits lavagedafter 1 week and 3 months. In histologic sections from the lungsthe large majority of the FSP were within cells at all timepoints.     

Creating conditions for good nursing by attending to the spiritual

biro a.l. (2012) Journal of Nursing Management  20, 1002–1011
Creating conditions for good nursing by attending to the spiritual Aim To note similarities, differences, and gaps in the literature on good nursing and spiritual care. Background Good nursing care is essential for meeting patient health needs. With growing recognition of the role of spirituality in health, understanding spiritual care as it relates to good nursing is important, especially as spiritual care has been recognized as the most neglected area of nursing care. Methods Nursing research, reports and discussion articles from a variety of countries were reviewed on the topics of good nursing, spiritual care and spirituality. Key issues A nurse’s spirituality and the nurse–patient relationship are integral to spiritual care and good nursing. Conclusions There are many commonalities between good nursing and spiritual care. Personal attributes of the nurse are described in similar terms in research on spiritual care and good nursing. Professional attributes common to good nursing and spiritual care are the nurse–patient relationship, assessment skills and communication skills. Implications for nursing management Good nursing through spiritual care is facilitated by personal spirituality, training in spiritual care and a culture that implements changes supportive of spiritual care. Further research is needed to address limitations in the scope of literature.     

Intellectual disability: population‐based estimates of the proportion attributable to maternal alcohol use disorder during pregnancy

Aim The aim of this study was to examine the association between maternal alcohol use disorder and intellectual disability in children. Method All mothers with an International Classification of Diseases (ICD) 9 and/or 10 alcohol‐related diagnosis, a proxy for alcohol use disorder, recorded on the Western Australian health, mental health, and drug and alcohol data sets were identified through the Western Australian Data Linkage Unit (n=5614 non‐Aboriginal; n=2912 Aboriginal). A comparison cohort of mothers without an alcohol‐related diagnosis was frequency matched on maternal age within maternal Aboriginal status and year of birth of their children. Linkage with the Western Australian Midwives Notification System (1983–2001) identified all births to these mothers (n=10 664 and 7907 respectively). Linkage to the Western Australian Intellectual Disability Database and Register of Developmental Anomalies identified cases of intellectual disability with no identified genetic origin (intellectual disability) (n=1487) and fetal alcohol syndrome (n=66). Odds ratios (ORs) and 95% confidence intervals (CIs) for intellectual disability were calculated using logistic regression incorporating generalized estimating equations and used to estimate population‐attributable fractions. Results At least 3.8% (95% CI 2.84–4.89%) of cases of intellectual disability could be avoided by preventing maternal alcohol use disorder: 1.3% (95% CI 0.81–1.86%) in non‐Aboriginal and 15.6% (95% CI 10.85–20.94%) in Aboriginal children. We observed a three‐fold increase in the adjusted odds of intellectual disability in children of mothers with an alcohol‐related diagnosis recorded during pregnancy (non‐Aboriginal OR 2.89, 95% CI 1.62–5.18; Aboriginal OR 3.12, 95% CI 2.13–4.56), with a net excess proportion of 3.7% and 5.5% respectively. One‐third (32%) of children diagnosed with fetal alcohol syndrome had intellectual disability. Interpretation Maternal alcohol use disorder is the leading known risk factor for intellectual disability with no identified genetic origin.     

Factors associated with caregivers' perception of children's health and oral health status: a study of 6- to 36-month-olds in Uganda

Background.  The impact of oral diseases on quality of life of children and their families has not been thoroughly investigated.
Aim.   Focusing on Ugandan infants aged 6–36 months and their caregivers, this study examined the degree to which clinical and psychosocial factors were associated with caregivers' overall evaluation of their children's oral health and health status.
Design.  Eight hundred and sixteen children were examined for dental caries and anthropometric status in 2007. A questionnaire was completed by the caregivers.
Results.  Poor child oral health was reported by 40.2% and 17.5% of caregivers who reported their children's health as, respectively, poor and good. Having the least family wealth [odds ratio (OR) = 1.9] and reporting distressed family activities (OR = 2.3) were associated with higher odds of reporting poor child oral health, whereas being a rural resident (OR = 0.4) and reporting no symptoms during tooth eruption (OR = 0.3) were associated with lower odds. Perception of poor child oral health (OR = 2.8) and having the least family wealth (OR = 1.7) were associated with higher odds of reporting poor child health status, whereas no stunting was associated with lower odds (OR = 0.5).
Conclusion.  The results support the growing recognition of oral health as a predictor of health and well-being in early childhood.     

Gastric and oesophageal emptying in insulin-dependent diabetes mellitus

Abstract Gastric emptying of a digestible solid and liquid meal and oesophageal emptying of a solid bolus were measured with scintigraphic techniques in 45 randomly selected insulin-dependent diabetics and in 22 control subjects. In the diabetics, the relationships between oesophageal emptying, gastric emptying, age, duration of diabetes mellitus, upper gastrointestinal symptoms, glycaemic control and the complications, autonomic neuropathy, peripheral neuropathy and retinopathy were examined. The lag period before solid food left the stomach was not significantly different in diabetics compared with control subjects, but the percentage retention of solid food at 100 min was greater ( P < 0.001) in the diabetic subjects. Both the early phase (percentage retention at 10 min) and the 50% emptying time for liquid gastric emptying were delayed ( P < 0.001) in the diabetic subjects. Of the diabetics, 58% had delayed gastric emptying of either the solid and/or the liquid meal; oesophageal emptying was delayed in 42%. Upper gastrointestinal symptoms correlated poorly with both gastric and oesophageal emptying. Oesophageal emptying, solid gastric emptying and the liquid 50% emptying time correlated with the severity of autonomic nerve dysfunction ( P < 0.05). The early phase of liquid emptying (retention at 10 min) was significantly slower ( P < 0.05) in patients with mean plasma glucose concentrations of > 15 mmol/l during the gastric emptying test and the lag period for solid emptying correlated with both the glycosylated haemoglobin and mean plasma glucose concentrations.     

Quantitative electroencephalography during rapid eye movement (REM) and non‐REM sleep in combat‐exposed veterans with and without post‐traumatic stress disorder

Sleep disturbances are a hallmark feature of post‐traumatic stress disorder (PTSD), and associated with poor clinical outcomes. Few studies have examined sleep quantitative electroencephalography (qEEG), a technique able to detect subtle differences that polysomnography does not capture. We hypothesized that greater high‐frequency qEEG would reflect ‘hyperarousal’ in combat veterans with PTSD (n = 16) compared to veterans without PTSD (n = 13). EEG power in traditional EEG frequency bands was computed for artifact‐free sleep epochs across an entire night. Correlations were performed between qEEG and ratings of PTSD symptoms and combat exposure. The groups did not differ significantly in whole‐night qEEG measures for either rapid eye movement (REM) or non‐REM (NREM) sleep. Non‐significant medium effect sizes suggest less REM beta (opposite to our hypothesis), less REM and NREM sigma and more NREM gamma in combat veterans with PTSD. Positive correlations were found between combat exposure and NREM beta (PTSD group only), and REM and NREM sigma (non‐PTSD group only). Results did not support global hyperarousal in PTSD as indexed by increased beta qEEG activity. The correlation of sigma activity with combat exposure in those without PTSD and the non‐significant trend towards less sigma activity during both REM and NREM sleep in combat veterans with PTSD suggests that differential information processing during sleep may characterize combat‐exposed military veterans with and without PTSD.     

Understanding the pathogenesis of type 2 diabetes: can we get off the metabolic merry-go-rounds?

The aetiology of non-insulin-dependent diabetes mellitus (NIDDM) is not known. The concordance of NIDDM in identical twins and differences in the prevalence rate of NIDDM between different racial groups suggest a genetic cause. Hyperglycaemia in established diabetes is caused by a combination of hepatic insulin resistance, impaired peripheral (muscle and fat) glucose uptake and a defect in glucose-mediated insulin secretion. However, it is not known if these defects are all inherited or if one can cause the others. This uncertainty is due to the fact that hyperglycaemia per se can cause defects in insulin action and insulin secretion that resemble those found in NIDDM. Furthermore the elevated free fatty acid (FFA) levels found when NIDDM is associated with obesity are known to cause both peripheral and hepatic insulin resistance. Recently we have demonstrated the mechanism by which elevated FFA levels can cause hepatic insulin resistance. However, we also have evidence that the converse holds in that genetically engineered hepatic insulin resistance in a transgenic rat model leads to obesity. Thus an understanding of the pathogenesis of NIDDM is complicated by the fact that hyperglycaemia and obesity can be both causes and consequences of insulin resistance. To overcome these difficulties, studies in young, euglycaemic diabetes-prone subjects have been conducted. Results suggest that there may be different causes for NIDDM in different racial groups.