Sex and season influence behaviour and physiology of lake trout following angling.

Catch-and-release angling exposes fish to challenges that may result in sub-lethal effects or mortality. Lake trout (Salvelinus namaycush) undergo high rates of release because of size-based harvest regulations or voluntary angler behaviour. Here, we examine short-term impairment in lake trout angled during the summer (n = 74) and fall spawning period (n = 33) to inform best practices for angling. Immediately following capture or 0.5 h post-capture, fish underwent reflex and barotrauma assessments, and a small blood sample was collected. Fish were also fitted with an externally mounted biologger equipped with depth, temperature and tri-axial acceleration sensors, that was tethered to allow retrieval of the logger after 14 min. In the summer, reflex impairment and barotrauma at 0 and 0.5 h were significantly correlated. Loss of orientation and bloating were the most observed indicators. Larger fish and those captured at increased depth had higher barotrauma scores, while prolonged fight times decreased the barotrauma score regardless of sampling time. Plasma cortisol, lactate and glucose increased 0.5 h after capture, and extracellular and intracellular pH decreased, all signs that angling was inducing a metabolic response. However, no relationships were found between blood indices and mortality (18.9%). The time required to reach maximum depth after release was longer for fish with increased air exposure but shorter for those with longer fight times. During the fall, fish displayed no mortality or reflex impairment. Anal prolapse was the most observed indicator of barotrauma but only observed in females. Blood indices were most altered 0.5 h after capture, with increased cortisol values for fish that were female, particularly large or captured at deeper depth. Locomotor activity was highest for males and increased with depth. Together, our findings suggest that the effects of catch-and-release angling may be dependent on several factors, including sex, season and angling depth.

Are the effects of catch-and-release angling evident in changes to mRNA abundances related to metabolism, acid-base regulation and stress in lake trout (Salvelinus namaycush) gills?

Catch-and-release (C&R) angling is a conservation-oriented practice intended to reduce the impact recreational angling has on fish populations. Even though most recreationally angled fish are released, little is known about how C&R angling impacts fish at the cellular or tissue level. As the first to explore the impacts of C&R angling on mRNA abundances, our study aimed to identify how the stress of angling influenced metabolism, acid-base regulation and cellular stress in the gills of lake trout (Salvelinus namaycush). Because gills are responsible for metabolic gas exchange, are crucial sites of acid-base homeostasis and respond to stressors quickly, we hypothesized that the relative mRNA abundance of genes related to these three physiological processes would be altered after angling. We took gill samples of live lake trout at 0, 2 or 48 h after fish were angled by rod and reel, and then used quantitative PCR (qPCR) to measure the relative abundance of nine candidate mRNA transcripts. Heat shock protein 70 (hsp70) mRNA levels significantly increased over 5-fold 2 h after angling, indicating a potential activation of a cytoprotective response. However, contrary to our hypothesis, we observed no change in the relative mRNA abundance of genes related to metabolism or acid-base regulation in response to C&R angling within a 48-h period. As C&R angling can negatively impact fish populations, further use of transcript-level studies will allow us to understand the impact C&R has on specific tissues and improve our knowledge of how C&R influences overall fish health.

Neurological monitoring in ECMO patients: current state of practice, challenges and lessons.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) in critically ill patients serves as a management option for end-stage cardiorespiratory failure in medical and surgical conditions. Patients on ECMO are at a high risk of neurologic adverse events including intracranial hemorrhage (ICH), acute ischemic stroke (AIS), seizures, diffuse cerebral edema, and hypoxic brain injury. Standard approaches to neurological monitoring for patients receiving ECMO support can be challenging for multiple reasons, including the severity of critical illness, deep sedation, and/or paralysis. This narrative literature review provides an overview of the current landscape for neurological monitoring in this population. METHODS: A literature search using PubMed was used to aid the understanding of the landscape of published literature in the area of neurological monitoring in ECMO patients. RESULTS: Review articles, cohort studies, case series, and individual reports were identified. A total of 73 varied manuscripts were summarized and included in this review which presents the challenges and strategies for performing neurological monitoring in this population. CONCLUSION: Neurological monitoring in ECMO is an area of interest to many clinicians, however, the literature is limited, heterogenous, and lacks consensus on the best monitoring practices. The evidence for optimal neurological monitoring that could impact clinical decisions and functional outcomes is lacking. Additional studies are needed to identify effective measures of neurological monitoring while on ECMO.

Clinical Reasoning: A 43-Year-Old Man With Subacute Onset of Vision Disturbances, Jaw Spasms, and Balance and Sleep Difficulties.

A brainstem syndrome is recognizable in patients presenting with a combination of visual disturbances, incoordination, gait problems, speech and swallowing difficulties, and new-onset sleep symptomatology. Brainstem disorders of subacute onset (onset and progression with accumulation of disabling deficits in 6-12 weeks) are generally of autoimmune, infectious, inflammatory, or infiltrative neoplastic cause. An autoimmune or infectious brainstem disorder may be referred to as brainstem encephalitis or rhombencephalitis. We describe a patient with paraneoplastic autoimmune rhombencephalitis, in whom diagnostic clues included the following: diverse visual and sleep symptoms, trismus, and choking in the history; see-saw nystagmus, opsoclonus, dysarthria, jaw dystonia, and episodic laryngospasm on examination; subtle but longitudinal and nonenhancing T2 MRI abnormalities in the brainstem and upper cervical cord; and oligoclonal bands in the CSF. His movement disorder-specific neural IgG profile revealed ANNA-2 (anti-Ri) and KLHL-11-IgG. Both are biomarkers of paraneoplastic brainstem encephalitis. KLCHL-11-IgG has been reported to accompany germ cell tumors, which was found in a solitary metastasis to the left inguinal lymph node in our patient, along with an atrophic left testis. Multidisciplinary treatment (autoimmune neurology, sleep medicine, ophthalmology, and physiatry) led to significant clinical improvements. This case provides a framework for the evaluation of patients with subacute-onset brainstem syndromes and the investigation and management of those with paraneoplastic and other autoimmune diseases.

Dysfunction of central control of breathing in amyotrophic lateral sclerosis.

Dysfunction in central control of breathing in some amyotrophic lateral sclerosis (ALS) patients is not adequately detected with standard evaluation for respiratory dysfunction. Nocturnal oximetry reveals periodic desaturations despite normal respiratory muscle movements. Continuous diaphragmatic electromyography has provided in vivo data consistent with impaired central control of diaphragm motor units. Current understanding of central control of breathing identifies the pre-Botzinger complex as the inspiratory rhythm generator. Animal models of pre-Botzinger complex neurodegeneration demonstrate rapid eye movement-related central sleep apneas progressing to loss of rapid eye movement sleep, also apparent in some ALS patients. Evidence supports the hypothesis that dysfunction in central control of breathing in some ALS patients may be related to pre-Botzinger complex degeneration. As the impact dysfunction of central control of breathing has on ALS becomes better defined the current standard of evaluating respiratory dysfunction in ALS patients may need updating. Muscle Nerve 56: 197-201, 2017.