Annual report of the Australian National Poliovirus Reference Laboratory, 2006

The Australian National Poliovirus Reference Laboratory (NPRL), located within the Victorian Infectious Diseases Reference Laboratory, is the national laboratory for Australia, the Pacific Islands and Brunei Darussalam, and is accredited by the World Health Organization (WHO) as the Regional Reference Laboratory for the WHO Western Pacific Region. The NPRL, in collaboration with the Australian Paediatric Surveillance Unit, co-ordinates surveillance for acute flaccid paralysis (AFP), the major clinical presentation of poliovirus infection. After classification of AFP cases by the Polio Expert Committee, the non-polio AFP rate for Australia in 2006 was 1.1, meeting the WHO surveillance requirement of detecting more than one AFP case per 100,000 children aged less than 15 years. During 2006, 80 specimens were referred to the NPRL, 59 from AFP cases and 21 from other sources. Poliovirus type 3 was isolated from two patients without AFP and the isolates were characterised as Sabin-like using WHO accredited methodologies. Echovirus 30 was isolated from two cases of AFP and coxsackievirus B5 and adenovirus were isolated from individual cases. During 2006, 1,998 cases of poliomyelitis due to wild poliovirus infection were reported world-wide, of which, only 6.8% (127) were due to importation of wild poliovirus.     

Correlates of Positive Parenting Behaviors

The present study examined the influence of maternal and child characteristics on parenting behaviors in a genetically informative study. The participants were 976 twins and their mothers from the Colorado Longitudinal Twin Study and the Twin Infant Project. Indicators of positive parenting were coded during parent–child interactions when twins were 7–36 months old. Child cognitive abilities and affection were independent correlates of positive parenting. There were significant gender differences in the magnitude of genetic and environmental influences on positive parenting, with shared environmental influences on parenting of girls and additive genetic influences on parenting of boys. Girls received significantly more positive parenting than boys. Differences in etiology of positive parenting may be explained by developmental gender differences in child cognitive abilities and affection, such that girls may have more rewarding interactions with parents, evoking more positive parenting.     

Exploring the relationship between β-adrenergic receptor kinase-1 and physical symptoms in heart failure

Background

The relationship between physical heart failure (HF) symptoms and pathophysiological mechanisms is unclear.

Changes in Alcohol Use and Drinking Context due to the COVID-19 Pandemic: A Multimethod Study of College Student Drinkers

Background

In spring 2020, U.S. universities closed campuses to limit the transmission of COVID-19, resulting in an abrupt change in residence, reductions in social interaction, and in many cases, movement away from a heavy drinking culture. The present mixed-methods study explores COVID-19-related changes in college student drinking. We characterize concomitant changes in social and location drinking contexts and describe reasons attributed to changes in drinking.

Methods

We conducted two studies of the impact of the COVID-19 pandemic on drinking behavior, drinking context, and reasons for both increases and decreases in consumption among college students. Study 1 (qualitative) included 18 heavy-drinking college students (M_age = 20.2; 56% female) who completed semi-structured interviews. Study 2 (quantitative) included 312 current and former college students who reported use of alcohol and cannabis (M_age = 21.3; 62% female) and who completed an online survey.

Results

In both studies, COVID-19-related increases in drinking frequency were accompanied by decreases in quantity, heavy drinking, and drunkenness. Yet, in Study 2, although heavier drinkers reduced their drinking, among non-heavy drinkers several indices of consumption increased or remained stable . Both studies also provided evidence of reductions in social drinking with friends and roommates and at parties and increased drinking with family. Participants confirmed that their drinking decreased due to reduced social opportunities and/or settings, limited access to alcohol, and reasons related to health and self-discipline. Increases were attributed to greater opportunity (more time) and boredom and to a lesser extent, lower perceived risk of harm and to cope with distress.

Conclusion

This study documents COVID-19-related changes in drinking among college student drinkers that were attributable to changes in context, particularly a shift away from heavy drinking with peers to lighter drinking with family. Given the continued threat of COVID-19, it is imperative for researchers, administrators, and parents to understand these trends as they may have lasting effects on college student drinking behaviors.

     

Defective “pacemaker” current (Ih) in a zebrafish mutant with a slow heart rate

At a cellular level, cardiac pacemaking, which sets the rate and rhythm of the heartbeat, is produced by the slow membrane depolarization that occurs between action potentials. Several ionic currents could account for this pacemaker potential, but their relative prominence is controversial, and it is not known which ones actually play a pacemaking role in vivo. To correlate currents in individual heart cells with the rhythmic properties of the intact heart, we have examined slow mo (smo), a recessive mutation we discovered in the zebrafish Danio rerio. This mutation causes a reduced heart rate in the embryo, a property we can quantitate because the embryo is transparent. We developed methods for culture of cardiocytes from zebrafish embryos and found that, even in culture, cells from smo continue to beat relatively slowly. By patch-clamp analysis, we discovered that a large repertoire of cardiac currents noted in other species are present in these cultured cells, including sodium, T-type, and L-type calcium and several potassium currents, all of which appear normal in the mutant. The only abnormality appears to be in a hyperpolarization-activated inward current with the properties of I_h, a current described previously in the nervous system, pacemaker, and other cardiac tissue. smo cardiomyocytes have a reduction in I_h that appears to result from severe diminution of one kinetic component of the I_h current. This provides strong evidence that I_h is an important contributor to the pacemaking behavior of the intact heart.     

Parental disability,parent care,and offspring mental health outcomes

Decades of research supports a widely held view that providing parent care is stressful, and that these stresses are associated with adverse mental health outcomes. However, some recent studies suggest an additional possibility, namely that “noncaregiver stress”—a consequence of having a parent with major care needs, but not being an active caregiver—may be a serious problem as well. This finding emerges in data which permit separate controls for parental needs for care and offspring provision of parent care. We extend these results using Generations and Gender Programme data from five countries—Bulgaria, France, Georgia, Romania, and Russia—for which the necessary variables can be comparably measured. Our outcome variable is a depression score based on a 7-item scale. In country-specific regressions, we find two instances of statistically significant associations of depression with the regular provision of personal care to a parent with care needs, i.e., the usual “caregiver stress” result. However, we also find two instances of statistically significant differences in respondents’ depressive symptoms that are associated with having a parent with care needs, i.e., instances of “noncaregiver stress.” We find limited evidence of gender-specific responses to both forms of stress. Our evidence supports both the typical caregiver stress response and the less-studied noncaregiver stress response, which suggests the need for additional research.     

The role of coherence of mind and reflective functioning in understanding binge-eating disorder and co-morbid overweight

Coherence of mind and reflective functioning may impact negative affect and interpersonal functioning over and above the effects of symptoms of depression and interpersonal problems that contribute to symptoms of binge-eating disorder (BED) and overweight/obesity. Matched samples of overweight women with BED and overweight and normal weight women without BED completed the Adult Attachment Interview, a measure of depressive symptoms, and a measure of interpersonal problems. Greater symptoms of depression distinguished women with BED from the matched comparison samples. Greater interpersonal problems differentiated women with BED from overweight women without BED. Coherence of Mind scores did not differentiate the samples. However, lower Reflective Functioning scores did distinguish both women with BED and overweight women without BED from normal weight women. Lower reflective functioning may lead to binge eating independent of depressive symptoms and interpersonal problems.     

eNOS Deficiency Predisposes Podocytes to Injury in Diabetes

Endothelial nitric oxide synthase (eNOS) deficiency may contribute to the pathogenesis of diabetic nephropathy in both experimental models and humans, but the underlying mechanism is not fully understood. Here, we studied two common sequelae of endothelial dysfunction in diabetes: glomerular capillary growth and effects on neighboring podocytes. Streptozotocin-induced diabetes increased glomerular capillary volume in both C57BL/6 and eNOS^−/− mice. Inhibiting the vascular endothelial growth factor receptor attenuated albuminuria in diabetic C57BL/6 mice but not in diabetic eNOS^−/− mice, even though it inhibited glomerular capillary enlargement in both. In eNOS^−/− mice, an acute podocytopathy and heavy albuminuria occurred as early as 2 weeks after inducing diabetes, but treatment with either captopril or losartan prevented these effects. In vitro, serum derived from diabetic eNOS^−/− mice augmented actin filament rearrangement in cultured podocytes. Furthermore, conditioned medium derived from eNOS^−/− glomerular endothelial cells exposed to both high glucose and angiotensin II activated podocyte RhoA. Taken together, these results suggest that the combined effects of eNOS deficiency and hyperglycemia contribute to podocyte injury, highlighting the importance of communication between endothelial cells and podocytes in diabetes. Identifying mediators of this communication may lead to the future development of therapies targeting endothelial dysfunction in albuminuric individuals with diabetes.One of the earliest features of kidney disease in diabetes is an alteration in the size- and/or charge-selective properties of the glomerular filtration barrier, a trilaminar structure that normally prevents the free passage of macromolecules into the urinary space. Manifested clinically as albuminuria, this disruption in the filtration barrier may result from structural or molecular changes in the fenestrated glomerular endothelial cells, podocytes, and/or the interpositioned glomerular basement membrane (GBM). High glucose-mediated molecular events¹ and flow-mediated stress forces induce endothelial dysfunction in diabetes² and diabetic nephropathy in particular.³ However, the mechanism by which such injury may translate to loss of glomerular permselectivity remains incompletely understood.Endothelial dysfunction in diabetic nephropathy is perhaps most readily observed as “neoangiogenesis” of the glomerular capillaries.^4,5 A number of experimental studies exploiting antiangiogenic therapies would appear, at first glance, to endorse a role for abnormal angiogenesis in the development of diabetic nephropathy.⁶ The proangiogenic growth factor, vascular endothelial growth factor (VEGF), for example, is abundantly expressed by podocytes within the diabetic glomerulus⁷ and strategies to block the activity of VEGF have been reported to attenuate albuminuria,^8–10 despite evidence to the contrary in the nondiabetic setting.^11,12 Podocytes act as the final barrier to macromolecular flow and, over recent years, injury to this specialized epithelial cell type has been acknowledged as playing a pivotal role in the pathogenesis of albuminuria in diabetes. Bidirectional crosstalk between glomerular endothelial cells and neighboring podocytes, accordingly, represents an alternative route via which endothelial injury may translate to urinary leakage of albumin.^13,14One of the major obstacles to the study of pathogenetic mechanisms in diabetic nephropathy has been the lack of an animal model that develops disease analogous to that seen in humans.¹⁵ However, augmented renal injury has recently been described in diabetic mice genetically deficient in endothelial nitric oxide synthase (eNOS), the major NOS isoform responsible for NO generation within the micro- and macrovasculature.^16–20 In this study, we sought to establish the role that eNOS plays in glomerular capillary growth in diabetes and in the paradoxical response to anti-VEGF therapy, as well as the effects of eNOS deficiency on communication with neighboring podocytes and its response to “standard of care” with renin-angiotensin-aldosterone system (RAAS) blockade.