Understanding Protective Factors for Men at Risk of Suicide Using the CHIME Framework: The Primacy of Relational Connectedness

Suicide is a global problem, ranking among the leading causes of death in many countries across the world. Most people who die by suicide are “under the radar”, having never seen a mental health professional or been diagnosed with a mental illness. This article describes the protective factors for men experiencing suicidal thoughts, plans, and/or attempts who are “under the radar”. Using in-depth qualitative interviews, we aimed to understand stakeholder perspectives on the protective factors that influence men’s wellbeing. The pervasiveness of relational connectedness in men’s narratives was identified as a central protective factor. Other key protective factors included meaningful activity, empowerment, and hope. These results have the potential to facilitate the development of focused community initiatives. More generally, the current research offers an example of a qualitative inquiry into men’s wellbeing that focuses on strengths and positive factors in their lives and may provide a guide for future community-based suicide prevention research

“A sustained, productive, constructive relationship with someone who can help”—A qualitative exploration of the experiences of help seekers and support persons using the emergency department during a suicide crisis

For Australians experiencing a suicide crisis, the emergency department (ED) is the recommended point of contact for intervention and to ensure personal safety. However, negative ED experiences can deter individuals from returning, thus impacting future suicide risk. In order to improve the ED environment for individuals in suicidal crisis, an in-depth understanding of this experience is needed. In-depth semi-structured interviews with 17 help seekers and 16 support persons were conducted. A grounded theory approach uncovered a core organising concept—all participants wanted a “a sustained, productive, constructive relationship with someone who can help” during the ED visit—which guided analysis. Thematic analysis resulted in two themes and four subthemes exploring the systemic and interpersonal aspects of the ED visit and the roadblocks and pathways to development of the relationship. Interpersonal factors included aspects of staff interaction and presence of a support person. Systemic factors related to aspects controlled by the physical space and internal policies and procedures and included aspects such as the chaotic environment, long waiting times, and access to staff. Overwhelmingly, there were more roadblocks than pathways reported by participants. Improving the ED environment, increasing staff training and encouraging the presence of support persons may help mitigate some of these roadblocks

Synaptic Defects in the Spinal and Neuromuscular Circuitry in a Mouse Model of Spinal Muscular Atrophy

Spinal muscular atrophy (SMA) is a major genetic cause of death in childhood characterized by marked muscle weakness. To investigate mechanisms underlying motor impairment in SMA, we examined the spinal and neuromuscular circuitry governing hindlimb ambulatory behavior in SMA model mice (SMNΔ7). In the neuromuscular circuitry, we found that nearly all neuromuscular junctions (NMJs) in hindlimb muscles of SMNΔ7 mice remained fully innervated at the disease end stage and were capable of eliciting muscle contraction, despite a modest reduction in quantal content. In the spinal circuitry, we observed a ∼28% loss of synapses onto spinal motoneurons in the lateral column of lumbar segments 3–5, and a significant reduction in proprioceptive sensory neurons, which may contribute to the 50% reduction in vesicular glutamate transporter 1(VGLUT1)-positive synapses onto SMNΔ7 motoneurons. In addition, there was an increase in the association of activated microglia with SMNΔ7 motoneurons. Together, our results present a novel concept that synaptic defects occur at multiple levels of the spinal and neuromuscular circuitry in SMNΔ7 mice, and that proprioceptive spinal synapses could be a potential target for SMA therapy

Musculotopic organization of the motor neurons supplying the mouse hindlimb muscles: a quantitative study using Fluoro-Gold retrograde tracing

We have mapped the motor neurons (MNs) supplying the major hindlimb muscles of transgenic (C57/BL6J-ChAT-EGFP) and wild-type (C57/BL6J) mice. The fluorescent retrograde tracer Fluoro-Gold was injected into 19 hindlimb muscles. Consecutive transverse spinal cord sections were harvested, the MNs counted, and the MN columns reconstructed in 3D. Three longitudinal MN columns were identified. The dorsolateral column extends from L4 to L6 and consists of MNs innervating the crural muscles and the foot. The ventrolateral column extends from L1 to L6 and accommodates MNs supplying the iliopsoas, gluteal, and quadriceps femoris muscles. The middle part of the ventral horn hosts the central MN column, which extends between L2–L6 and consists of MNs for the thigh adductor, hamstring, and quadratus femoris muscles. Within these longitudinal columns, the arrangement of the different MN groups reflects their somatotopic organization. MNs innervating muscles developing from the dorsal (e.g., quadriceps) and ventral muscle mass (e.g., hamstring) are situated in the lateral and medial part of the ventral gray, respectively.MN pools belonging to proximal muscles (e.g., quadratus femoris and iliopsoas) are situatedventral to those supplying more distal ones (e.g., plantar muscles). Finally, MNs innervatingflexors (e.g., posterior crural muscles) are more medial than those belonging to extensors ofthe same joint (e.g., anterior crural muscles). These data extend and modify the MN maps in the recently published atlas of the mouse spinal cord and may help when assessing neuronal loss associated with MN diseases

Pathogenesis of adolescent idiopathic scoliosis in girls - a double neuro-osseous theory involving disharmony between two nervous systems, somatic and autonomic expressed in the spine and trunk: possible dependency on sympathetic nervous system and hormones with implications for medical therapy

Anthropometric data from three groups of adolescent girls - preoperative adolescent idiopathic scoliosis (AIS), screened for scoliosis and normals were analysed by comparing skeletal data between higher and lower body mass index subsets. Unexpected findings for each of skeletal maturation, asymmetries and overgrowth are not explained by prevailing theories of AIS pathogenesis. A speculative pathogenetic theory for girls is formulated after surveying evidence including: (1) the thoracospinal concept for right thoracic AIS in girls; (2) the new neuroskeletal biology relating the sympathetic nervous system to bone formation/resorption and bone growth; (3) white adipose tissue storing triglycerides and the adiposity hormone leptin which functions as satiety hormone and sentinel of energy balance to the hypothalamus for long-term adiposity; and (4) central leptin resistance in obesity and possibly in healthy females. The new theory states that AIS in girls results from developmental disharmony expressed in spine and trunk between autonomic and somatic nervous systems. The autonomic component of this double neuro-osseous theory for AIS pathogenesis in girls involves selectively increased sensitivity of the hypothalamus to circulating leptin (genetically-determined up-regulation possibly involving inhibitory or sensitizing intracellular molecules, such as SOC3, PTP-1B and SH2B1 respectively), with asymmetry as an adverse response (hormesis); this asymmetry is routed bilaterally via the sympathetic nervous system to the growing axial skeleton where it may initiate the scoliosis deformity (leptin-hypothalamic-sympathetic nervous system concept = LHS concept). In some younger preoperative AIS girls, the hypothalamic up-regulation to circulating leptin also involves the somatotropic (growth hormone/IGF) axis which exaggerates the sympathetically-induced asymmetric skeletal effects and contributes to curve progression, a concept with therapeutic implications. In the somatic nervous system, dysfunction of a postural mechanism involving the CNS body schema fails to control, or may induce, the spinal deformity of AIS in girls (escalator concept). Biomechanical factors affecting ribs and/or vertebrae and spinal cord during growth may localize AIS to the thoracic spine and contribute to sagittal spinal shape alterations. The developmental disharmony in spine and trunk is compounded by any osteopenia, biomechanical spinal growth modulation, disc degeneration and platelet calmodulin dysfunction. Methods for testing the theory are outlined. Implications are discussed for neuroendocrine dysfunctions, osteopontin, sympathoactivation, medical therapy, Rett and Prader-Willi syndromes, infantile idiopathic scoliosis, and human evolution. AIS pathogenesis in girls is predicated on two putative normal mechanisms involved in trunk growth, each acquired in evolution and unique to humans

The size of the langerhans’ islets in infants with severe jaundice of varying etiology

The histological specimens of the pancreas of 33 newborn jaundiced infants were examined and compared to 35 controls. In 4 babies the jaundice was due to Rhesus incompatibility, in 8 to ABO incompatibility, in 13 to G-6-PD deficiency and in 8 the etiology of jaundice could not be ascertained. The Langerhans’ islets were found to be hyperplastic not only in the 4 infants, whose severe jaundice was due to Rhesus incompatibility, but, to a lesser degree, in the majority of the other jaundiced infants’ pancreas as well. The surface of the Langer-hans’ islets was well correlated with the highest bilirubin level in all groups of jaundiced infants. © 1973 S. Karger AG, Basel