Annual water residence time effects on thermal structure: A potential lake restoration measure?

Innovative methods to combat internal loading issues in eutrophic lakes are urgently needed to speed recovery and restore systems within legislative deadlines. In stratifying lakes, internal phosphorus loading is particularly problematic during the summer stratified period when anoxia persists in the hypolimnion, promoting phosphorus release from the sediment. A novel method to inhibit stratification by reducing residence times is proposed as a way of controlling the length of the hypolimnetic anoxic period, thus reducing the loading of nutrients from the sediments into the water column. However, residence time effects on stratification length in natural lakes are not well understood. We used a systematic modelling approach to investigate the viability of changes to annual water residence time in affecting lake stratification and thermal dynamics in Elterwater, a small stratifying eutrophic lake in the northwest of England. We found that reducing annual water residence times shortened and weakened summer stratification. Based on finer-scale dynamics of lake heat fluxes and water column stability we propose seasonal or sub-seasonal management of water residence time is needed for the method to be most effective at reducing stratification as a means of controlling internal nutrient loading.

Can reductions in water residence time be used to disrupt seasonal stratification and control internal loading in a eutrophic monomictic lake?

Anthropogenic eutrophication caused by excess loading of nutrients, especially phosphorus (P), from catchments is a major cause of lake water quality degradation. The release of P from bed sediments to the water column, termed internal loading, can exceed catchment P load in eutrophic lakes, especially those that stratify during warm summer periods. Managing internal P loading is challenging, and although a range of approaches have been implemented, long-term success is often limited, requiring lake-specific solutions. Here, we assess the manipulation of lake residence time to inhibit internal loading in Elterwater, a shallow stratifying lake in the English Lake District, UK. Since 2016, additional inflowing water has been diverted into the inner basin of Elterwater to reduce its water residence time, with the intention of limiting the length of the stratified period and reducing internal loading. Combining eight years of field data in a Before-After-Control-Impact study with process-based hydrodynamic modelling enabled the quantification of the residence time intervention effects on stratification length, water column stability, and concentrations of chlorophyll a and P. Annual water residence time was reduced during the study period by around 40% (4.9 days). Despite this change, the lake continued to stratify and developed hypolimnetic anoxia. As a result, there was little significant change in phosphorus (as total or soluble reactive phosphorus) or chlorophyll a concentrations. Summer stratification length was 2 days shorter and 7% less stable with the intervention. Our results suggest that the change to water residence time in Elterwater was insufficient to induce large enough physical changes to improve water quality. However, the minor physical changes suggest the management measure had some impact and that larger changes in water residence time may have the potential to induce reductions in internal loading. Future assessments of management requirements should combine multi-year observations and physical lake modelling to provide improved understanding of the intervention effect size required to alter the physical structure of the lake, leading to increased hypolimnetic oxygen and reduced potential for internal loading.

First, do no harm: confronting the myths of psychiatric drugs.

The enduring psychiatric myth is that particular personal, interpersonal and social problems in living are manifestations of 'mental illness' or 'mental disease', which can only be addressed by 'treatment' with psychiatric drugs. Psychiatric drugs are used only to control 'patient' behaviour and do not 'treat' any specific pathology in the sense understood by physical medicine. Evidence that people, diagnosed with 'serious' forms of 'mental illness' can 'recover', without psychiatric drugs, has been marginalized by drug-focused research, much of this funded by the pharmaceutical industry. The pervasive myth of psychiatric drugs dominates much of contemporary 'mental health' policy and practice and raises discrete ethical issues for nurses who claim to be focused on promoting or enabling the 'mental health' of the people in their care.

Mental health nursing and the politics of recovery: a global reflection.

The concept of recovery increasingly dominates mental health policy and practice agendas in most Western countries. However, the many, often conflicting, definitions of recovery have led to theoretical and practical confusion. More importantly, the concept clashes with some of the established assumptions of psychiatric/mental health nursing, especially the traditional notion that the person is "ill" and requires "treatment" or some other active "intervention." The implications of recovery for the further development of person-centered care, especially within a globalized form of mental health nursing, are discussed with specific reference to the Tidal Model, an international midrange theory of mental health nursing.

The tidal model of mental health recovery and reclamation: application in acute care settings.

The development, over the last decade, of the Tidal Model of Mental Health Recovery and Reclamation is described, and a summary of the application of the various Tidal processes of care is provided. Studies of evaluations of the Tidal Model within acute care settings are summarised and the potential contribution that the model makes to the development of person-centred care, within acute settings, is discussed.

p75 NTR expression is induced in isolated neurons of the penumbra after ischemia by cortical devascularization.

The p75 neurotrophin receptor (p75(NTR)) is involved in neuronal functions ranging from induction of apoptosis and growth inhibition to the promotion of survival. p75(NTR) expression is induced in the central nervous system (CNS) by a range of pathological conditions, where it seems to have a role in neuronal death and axonal growth inhibition. The cellular mechanisms driving p75(NTR) expression in cell lines and primary neurons is Sp1 dependent (Ramos et al. [2007] J. Neurosci. 27:1498). In this study, we analyzed the spatiotemporal profile of p75(NTR) expression after an ischemic lesion induced by cortical devascularization (CD). Our results show that p75(NTR) expression occurs in isolated neurons of the ischemic lesion site. The p75(NTR+) neurons presented morphological alterations and active caspase-3 staining. Some p75(NTR+) neurons were also positive for sortilin. The peak of p75(NTR) expression was localized 3 days postlesion (3DPL) in the penumbra. Sp1 transcription factor nuclear localization was observed in p75(NTR+) neurons. The overall level of Sp1 expression was increased until 14DPL on the ipsilateral hemisphere. With primary cortical neurons, we demonstrated that p75(NTR) expression is induced by excitotoxic stress and correlated with increased Sp1 abundance. We conclude that p75(NTR) expression is localized in selected neurons of the ischemic lesion and that these neurons are probably condemned to apoptotic cell death. In primary neuronal culture, it is clear that excitotoxicity and Sp1 are involved in induction of p75(NTR) expression, although, in vivo, some additional mechanisms are likely to be involved in the control of p75(NTR) expression in specific neurons in vivo.

ApTrkl, a Trk-like receptor, mediates serotonin- dependent ERK activation and long-term facilitation in Aplysia sensory neurons.

The Trk family of receptor tyrosine kinases plays a role in synaptic plasticity and in behavioral memory in mammals. Here, we report the discovery of a Trk-like receptor, ApTrkl, in Aplysia. We show that it is expressed in the sensory neurons, the locus for synaptic facilitation, which is a cellular model for memory formation. Serotonin, the facilitatory neurotransmitter, activates ApTrkl, which, in turn, leads to activation of ERK. Finally, inhibiting the activation of ApTrkl with the Trk inhibitor K252a or using dsRNA to inhibit ApTrkl blocks the serotonin-mediated activation of ERK in the cell body, as well as the cell-wide long-term facilitation induced by 5-HT application to the cell body. Thus, transactivation of the receptor tyrosine kinase ApTrkl by serotonin is an essential step in the biochemical events leading to long-term facilitation in Aplysia.

'Veiling sexualities': a grounded theory of mental health nurses responses to issues of sexuality.

AIM: This paper is a report of a study to develop a grounded theory explaining how mental health nurses respond to issues of sexuality in clinical practice. BACKGROUND: The history of sexuality and people with mental health problems has largely been a history shrouded in misunderstanding, stigma, myth and negativity. However, individuals with mental health problems may experience sexuality and relationship difficulties related to their life experiences, mental illness, or its treatment. METHODS: Grounded theory was the methodology used for the study. Interviews were conducted in 2005-2006 with 27 mental health nurses working an urban area in the Republic of Ireland. Data were analysed using the concurrent processes of constant comparative analysis, data collection, theoretical sampling and memo writing. FINDINGS: The core category to emerge from the data was 'veiling sexualities'. This refers to participants' accounts of how they responded to the sexuality dimension of clients' lives. Participants' main concerns about sexuality were related to feelings of personal and professional vulnerability, due to a lack of competence, comfort and confidence in this area. The theory highlights the manner in which nurses perpetuate practices that marginalize, discriminate and socially exclude clients as 'sexual citizens'. CONCLUSION: The theory of Veiled Sexualities may facilitate acknowledgement of the presence of sexuality in all nurse-client encounters, and promote a discourse on the sexual rights of people experiencing mental distress among mental health nurses and all involved in the delivery of mental health services.

Words of wisdom.

When we feel that something is not right or is unsatisfactory in our lives, counselling can help us come to an understanding of the problem and its personal meaning.

Stay in touch.

Touch is used in many cultures as a means of relating directly with another person. In this seventh article in our Heart of Nursing series, we look at how touch, used judiciously, can be a priceless form of doing.

The p75 neurotrophin receptor can induce autophagy and death of cerebellar Purkinje neurons.

The cellular mechanisms underlying Purkinje neuron death in various neurodegenerative disorders of the cerebellum are poorly understood. Here we investigate an in vitro model of cerebellar neuronal death. We report that cerebellar Purkinje neurons, deprived of trophic factors, die by a form of programmed cell death distinct from the apoptotic death of neighboring granule neurons. Purkinje neuron death was characterized by excessive autophagic-lysosomal vacuolation. Autophagy and death of Purkinje neurons were inhibited by nerve growth factor (NGF) and were activated by NGF-neutralizing antibodies. Although treatment with antisense oligonucleotides to the p75 neurotrophin receptor (p75ntr) decreased basal survival of cultured cerebellar neurons, p75ntr-antisense decreased autophagy and completely inhibited death of Purkinje neurons induced by trophic factor withdrawal. Moreover, adenoviral expression of a p75ntr mutant lacking the ligand-binding domain induced vacuolation and death of Purkinje neurons. These results suggest that p75ntr is required for Purkinje neuron survival in the presence of trophic support; however, during trophic factor withdrawal, p75ntr contributes to Purkinje neuron autophagy and death. The autophagic morphology resembles that found in neurodegenerative disorders, suggesting a potential role for this pathway in neurological disease.

The Tidal Model: psychiatric colonization, recovery and the paradigm shift in mental health care.

Psychiatric research and practice involves the colonization of the personal experience of problems of human living. From a Western perspective, this process shares many similarities with the subjugation of women, people of colour and people embracing non-Christian faiths and cultures. The Tidal Model is a mental health recovery and reclamation model, developed to provide the framework for discrete alternatives to the colonizing approach of mainstream psychiatric practice. The Model asserts the intrinsic value of personal experience and the centrality of narrative in the development of contextually bound, personally appropriate, mental health care. This paper summarizes the features of the Model, which attempt to address the foci of the more significant critiques of psychiatric practice (and psychiatric nursing), against a background sketch of psychiatric colonization.

The tidal model. The healing potential of metaphor within a patient's narrative.

1. The human experience of growth and development is a fluid phenomenon, occurring in small, barely visible changes. 2. The Tidal Model embraces a patient's expression of his or her experience by focusing on the lived experience of the narrative and its personally meaningful metaphors and symbols. 3. To re-empower a patient, the Tidal Model assessment is written in the patient's own voice and all care planning is conducted conjointly. 4. The Tidal Model was developed from empirical studies of the perceived need for nursing and the process of empowerment in clinical nursing practice.

The proinflammatory RAGE/NF-κB pathway is involved in neuronal damage and reactive gliosis in a model of sleep apnea by intermittent hypoxia.

Sleep apnea (SA) causes long-lasting changes in neuronal circuitry, which persist even in patients successfully treated for the acute effects of the disease. Evidence obtained from the intermittent hypoxia (IH) experimental model of SA has shown neuronal death, impairment in learning and memory and reactive gliosis that may account for cognitive and structural alterations observed in human patients. However, little is known about the mechanism controlling these deleterious effects that may be useful as therapeutic targets in SA. The Receptor for Advanced Glycation End products (RAGE) and its downstream effector Nuclear Factor Kappa B (NF-κB) have been related to neuronal death and astroglial conversion to the pro-inflammatory neurodegenerative phenotype. RAGE expression and its ligand S100B were shown to be increased in experimental models of SA. We here used dissociated mixed hippocampal cell cultures and male Wistar rats exposed to IH cycles and observed that NF-κB is activated in glial cells and neurons after IH. To disclose the relative contribution of the S100B/RAGE/NF-κB pathway to neuronal damage and reactive gliosis after IH we performed sequential loss of function studies using RAGE or S100B neutralizing antibodies, a herpes simplex virus (HSV)-derived amplicon vector that induces the expression of RAGEΔcyto (dominant negative RAGE) and a chemical blocker of NF-κB. Our results show that NF-κB activation peaks 3 days after IH exposure, and that RAGE or NF-κB blockage during this critical period significantly improves neuronal survival and reduces reactive gliosis. Both in vitro and in vivo, S100B blockage altered reactive gliosis but did not have significant effects on neuronal survival. We conclude that both RAGE and downstream NF-κB signaling are centrally involved in the neuronal alterations found in SA models, and that blockage of these pathways is a tempting strategy for preventing neuronal degeneration and reactive gliosis in SA.

Myth of mental health nursing and the challenge of recovery.

Although the concept of 'mental health nursing' has grown in popularity over the past 35 years, it remains a myth. People believe that they know what it is and value it highly, but cannot describe or define it other than in vague terms. This paper briefly charts the rise of 'mental health nursing', emphasizing its political implications, and in particular, the drive towards an embrace of a person-centred, recovery-focused approach to care. If nurses are to realize such ambitions, they must resolve their historical association with psychiatric nursing. The concept of the 'mental health nurse' might signal the emergence of a new vision for human services, but might also signal the need for 'mental health nurses' to negotiate a formal separation from the traditional 'psychiatric' family.