Screening and Referral for Behavioral Health Symptoms in Collegiate Athletes.

OBJECTIVE: We aim to investigate the prevalence of behavioral health symptoms in collegiate athletes and the frequency of referrals prompted by a preparticipation behavioral health screener. DESIGN: Athletes completed a screening battery to detect behavioral health symptoms and sports psychology clinicians designed criteria for intervention based on the severity of symptoms reported. Data from the screener was retrospectively de-identified and analyzed. SETTING: National Collegiate Athletic Association Division-I university. PARTICIPANTS: All athletes on active rosters were required to complete the screener as a component of the preparticipation examination. INTERVENTIONS: Sports psychology clinicians created a protocol for intervention based on the number and severity of symptoms reported on the screener. MAIN OUTCOME MEASURES: Communication with athletes and referrals made to behavioral health services. RESULTS: Of the 1126 surveys completed, 39% had behavioral health symptoms necessitating behavioral health referral. Twelve percent required a safety check-in, given the severity of their symptoms. Seven percent of the respondents were newly established with behavioral health services. CONCLUSIONS: Symptoms of behavioral health disorders are common among athletes and yet, for a myriad of reasons, many choose to forgo treatment. By implementing a behavioral health screening battery, the prevalence of behavioral health symptoms among athletes at our institution was elucidated and many athletes were newly established with behavioral health services. The tiered intervention protocol in this study allowed for appropriate assessment and triage of high-risk individuals, while simultaneously providing lower-risk individuals with appropriate resources. Surveillance for behavioral health symptoms among college athletes using a screening battery with a tiered intervention protocol can ensure at-risk athletes are identified, contacted, and referred to behavioral health services, potentially improving their athletic performance and overall well-being, while averting poor outcomes.

Behavioral and Physiologic Effects of a Single Dose of Oral Gabapentin in Rabbits (Oryctolagus cuniculus).

Stress in rabbits (Oryctolagus cuniculus) may influence veterinarians' ability to assess their health and can lead to complications such as gastrointestinal hypomotility and poor anesthetic outcomes. Gabapentin has been used as an anxiolytic in various species, but little information is available on its use in rabbits. To assess the effect of gabapentin on stress in rabbits, 5 female and 3 male New Zealand white rabbits, aged 8-12 months, weighing 3-4.5 kg, were administered a single dose (25 mg/kg) of oral compounded gabapentin. Effects on individual behaviors and selected physiologic parameters were assessed by a blinded observer using a human intruder test and tractability score (summed total 0-8, most to least tractable). Heart and respiratory rate, rectal temperature, body weight, and fecal output were also recorded. Baseline measurements for each rabbit were assessed immediately prior to gabapentin administration, and at 1, 2, and 4 hours post-administration. With this method rabbits acted as their own concurrent control group. Rabbits were assessed at 7 AM, 11 AM, and 3 PM. Data were analyzed as continuous, binary, and continuous nonparametric (P ≤ .05). No significant differences in physiologic parameters were observed between baseline and the post-administration timepoints. Fecal output was reduced similar to baseline measurements. Behaviors pressing down decreased (at 2 and 4 hours; P = .05 and P = .013, respectively) and approaching human increased (at 2 hours; P = .022) post-gabapentin compared to baseline. Tractability scores were improved at the 2-hour timepoint compared to baseline (Friedman P = .0461; Wilcoxon P = .0413). These results suggest gabapentin 25 mg/kg orally decreased reactivity with a peak effect at 2 hours, without significant effects on measured physiologic parameters. Oral gabapentin in rabbits should be considered to reduce stress in the presence of humans and to facilitate handling.

Obesity and Fatty Acids Promote Mitochondrial Translocation of STAT3 Through ROS-Dependent Mechanisms.

Obesity promotes the onset and progression of metabolic and inflammatory diseases such as type 2 diabetes. The chronic low-grade inflammation that occurs during obesity triggers multiple signaling mechanisms that negatively affect organismal health. One such mechanism is the persistent activation and mitochondrial translocation of STAT3, which is implicated in inflammatory pathologies and many types of cancers. STAT3 in the mitochondria (mitoSTAT3) alters electron transport chain activity, thereby influencing nutrient metabolism and immune response. PBMCs and CD4+ T cells from obese but normal glucose-tolerant (NGT) middle-aged subjects had higher phosphorylation of STAT3 on residue serine 727 and more mitochondrial accumulation of STAT3 than cells from lean subjects. To evaluate if circulating lipid overabundance in obesity is responsible for age- and sex-matched mitoSTAT3, cells from lean subjects were challenged with physiologically relevant doses of the saturated and monounsaturated fatty acids, palmitate and oleate, respectively. Fatty acid treatment caused robust accumulation of mitoSTAT3 in all cell types, which was independent of palmitate-induced impairments in autophagy. Co-treatment of cells with fatty acid and trehalose prevented STAT3 phosphorylation and mitochondrial accumulation in an autophagy-independent but cellular peroxide-dependent mechanism. Pharmacological blockade of mitoSTAT3 either by a mitochondria-targeted STAT3 inhibitor or ROS scavenging prevented obesity and fatty acid-induced production of proinflammatory cytokines IL-17A and IL-6, thus establishing a mechanistic link between mitoSTAT3 and inflammatory cytokine production.

HISTOLOGIC LESIONS IN PLACENTAS OF NORTHERN FUR SEALS (CALLORHINUS URSINUS) FROM A POPULATION WITH HIGH PLACENTAL PREVALENCE OF COXIELLA BURNETII.

Coxiella burnetii is an intracellular bacterial pathogen that can be associated with significant reproductive disease or acute mortality in livestock and wildlife. A novel marine mammal-associated strain of C. burnetii has been identified in pinnipeds of the northwestern Pacific Ocean. Little is known about C. burnetii infection in regard to reproductive success or population status. Our objective was to characterize the severity and extent of histologic lesions in 117 opportunistically collected placentas from presumed-normal northern fur seals (Callorhinus ursinus) in July 2011 on St. Paul Island, Alaska, US, where a high placental prevalence of C. burnetii had been reported. Sections were examined by histology and immunohistochemistry and impression smears with modified acid-fast stain. The nature and frequency of histologic changes were compared with target COM1 PCR-confirmed C. burnetii positive and negative placentas. Overall, histologic changes were similar to placental lesions described in aborting ruminants; however, changes were variable within and between placentas. Vasculitis and occasional intracellular bacteria were seen only in C. burnetii PCR-positive placentas. Dystrophic mineralization, edema, and inflammation were seen in PCR-positive and negative placentas, although they were statistically more common in PCR-positive placentas. Results suggest that C. burnetti and associated pathologic changes are multifocal and variable in placentas from these presumably live-born pups. Therefore, multiple sections of tissue from different placental areas should be examined microscopically, and screened by PCR, to ensure accurate diagnosis as the genomes per gram of placenta may not necessarily represent the severity of placental disease. These limitations should inform field biologists, diagnosticians, and pathologists how best to screen and sample for pathogens and histopathology in marine mammal placental samples.

Regulation of immune cell function by nicotinamide nucleotide transhydrogenase.

Redox homeostasis is elemental for the normal physiology of all cell types. Cells use multiple mechanisms to tightly regulate the redox balance. The onset and progression of many metabolic and aging-associated diseases occur due to the dysregulation of redox homeostasis. Thus, it is critical to identify and therapeutically target mechanisms that precipitate abnormalities in redox balance. Reactive oxygen species (ROS) produced within the immune cells regulate homeostasis, hyperimmune and hypoimmune cell responsiveness, apoptosis, immune response to pathogens, and tumor immunity. Immune cells have both cytosolic and organelle-specific redox regulatory systems to maintain appropriate levels of ROS. Nicotinamide nucleotide transhydrogenase (NNT) is an essential mitochondrial redox regulatory protein. Dysregulation of NNT function prevents immune cells from mounting an adequate immune response to pathogens, promotes a chronic inflammatory state associated with aging and metabolic diseases, and initiates conditions related to a dysregulated immune system such as autoimmunity. Although many studies have reported on NNT in different cell types, including cancer cells, relatively few studies have explored NNT in immune cells. This review provides an overview of NNT and focuses on the current knowledge of NNT in the immune cells.

Establishing a reference interval for acute phase proteins, cytokines, antioxidants and commonly measured biochemical and hematologic parameters in the northern fur seal (Callorhinus ursinus).

Over the past several decades there has been a precipitous decline of northern fur seals (Callorhinus ursinus; NFS) at their breeding grounds on the Pribilof Islands in the Bering Sea. The cause of this decline is likely multifactorial and could include changes in environmental parameters, prey abundance and distribution as well as exposure to pathogens and pollutants. Evaluation of inflammatory markers and antioxidant levels of the current population of fur seals in addition to hematologic and biochemical profiles could provide important information regarding health and subclinical or clinical disease in this population. Serum and plasma samples were obtained from clinically healthy adult female NFS and references intervals were determined for multiple parameters that can be altered in response to the presence of disease and environmental stressors. We established a reference interval for cytokines involved in acute inflammation and infection (TNFa, IL1, IL6, IL8, KC, IL10, C-reactive Protein) by utilizing commercially available canine cross-reactive antibodies. Reference intervals were also established for reactive oxygen species (hydrogen peroxide and malondialdehyde), as well as antioxidant levels (vitamin E and selenium) and acute phase proteins evaluated by serum electrophoresis. To improve the ability to compare and interpret indicators of health and disease in this species, we developed reference intervals for commonly utilized hematologic and biochemical tests in addition to the aforementioned markers of oxidative stress and inflammatory biomarkers. There were several animals identified as outliers indicating that they may have had subclinical illness or inflammation. Further investigation utilizing these tests in clinically ill animals and comparison to animals that exhibit normal behavior and no overt signs of illness could increase our understanding of the utility of measuring these parameters in this species.

Selective Autophagy in Hyperglycemia-Induced Microvascular and Macrovascular Diseases.

Dysregulation of autophagy is an important underlying cause in the onset and progression of many metabolic diseases, including diabetes. Studies in animal models and humans show that impairment in the removal and the recycling of organelles, in particular, contributes to cellular damage, functional failure, and the onset of metabolic diseases. Interestingly, in certain contexts, inhibition of autophagy can be protective. While the inability to upregulate autophagy can play a critical role in the development of diseases, excessive autophagy can also be detrimental, making autophagy an intricately regulated process, the altering of which can adversely affect organismal health. Autophagy is indispensable for maintaining normal cardiac and vascular structure and function. Patients with diabetes are at a higher risk of developing and dying from vascular complications. Autophagy dysregulation is associated with the development of heart failure, many forms of cardiomyopathy, atherosclerosis, myocardial infarction, and microvascular complications in diabetic patients. Here, we review the recent findings on selective autophagy in hyperglycemia and diabetes-associated microvascular and macrovascular complications.