Publications by authors named "Jay Campisi"

Purpose: Mental health disorders continue to increase and are the leading cause of disability among adults living in the United States. While there are well documented racial disparities among many physical health conditions, the association between race, ethnicity and depression is complicated and not well understood. Utilizing data obtained from the 2022 version of the Behavioral Risk Factors Surveillance System (BRFSS) survey, we examined the relation between the diagnosis of depression and race and ethnicity with a particular focus on how income levels play a role in such disparities.

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Group work is essential in professional settings to encourage effective communication and optimize outcomes. Stress can reduce teamwork effectiveness and aromatherapy might be able to reduce feelings of stress/anxiety in individuals. However, it is unclear if aromatherapy impacts stress levels or performance during group activities.

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The use of lipid nanoparticles as biodegradable shells for controlled drug delivery shows promise as a more effective and targeted tumor treatment than traditional treatment methods. Although the combination of target therapy with nanotechnology created new hope for cancer treatment, methodological issues during in vitro validation of nanovehicles slowed their application. In the current work, the effect of methotrexate (MTX) encapsulated in different matrices was evaluated in a dynamic microfluidic platform.

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Increased access to electronic devices and the ubiquity of social media has resulted in a rapid rise in the prevalence of students "multitasking" while in a classroom setting. While some data indicate the use of electronic devices in class can improve the classroom environment, other studies demonstrate the opposite finding. Moreover, it remains unclear if using social networking sites such as Instagram impacts performance on cognitive tasks when students are presented new material and, if so, what features of Instagram modulate this response.

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Recent evidence indicates that social network use (e.g., Facebook) prior to exposure to an acute stressor can buffer the physiological response to that stressor.

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Cardiovascular disease (CVD) remains the leading cause of disease burden globally and chronic stress is associated with increased risk of CVD. Recognition of chronic occupational stressors as a potential contributor to CVD highlights the need to recognize and prevent stress during work. The ubiquity of wearable technology devices to monitor health provides a new opportunity to noninvasively examine the cardiovascular system throughout a work shift.

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While the number of individuals participating in internet-based social networks has continued to rise, it is unclear how participating in social networks might influence quality of life (QOL). Individuals differ in their experiences, motivations for, and amount of time using internet-based social networks, therefore, we examined if individuals differing in social network user experiences, motivations and frequency of social network also differed in self-reported QOL. Two-hundred and thirty-seven individuals (aged 18-65) were recruited online using the online platform Mechanical Turk (MTurk).

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Having a large social network is generally beneficial to health. However, it is unclear how Internet-based social networks might influence health. Chronic stress can have negative health consequences, and some data suggest that Facebook could be a new source of psychological stress.

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Undergraduate students routinely experience acute psychosocial stress when interviewing for post-collegiate employment. While numerous studies have demonstrated that acute stress can increase release of immune-relevant molecules in blood, fewer studies have examined if acute stress also increases immune-relevant molecules into saliva. Saliva, and the biomolecules found in saliva often serve important immune defense roles and can be used to non-invasively screen for many systemic diseases.

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Activation of the in vivo stress response can facilitate antibacterial host defenses. One possible mechanism for this effect is stress-induced release of heat shock protein 72 (Hsp72) into the extracellular environment. Hsp72 is a ubiquitous cellular protein that is up-regulated in response to cellular stress, and modulates various aspects of immune function including macrophage inflammatory/bactericidal responses and T-cell function when found in the extracellular environment.

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To increase student engagement, active participation, and performance, personal response systems (clickers) were incorporated into six lecture-based sections of four required courses within the Health Sciences Department major curriculum: freshman-level Anatomy and Physiology I and II, junior-level Exercise Physiology, and senior-level Human Pathophysiology. Clickers were used to gather anonymous student responses to questions posed within the class period after individual thought and peer discussion. Students (n = 293, 88% of students completing the courses) completed a perceptual survey on clicker effectiveness inserted into the Student Assessment of Learning Gains online instrument.

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Background: The role of histocompatibility and immune recognition in stem cell transplant therapy has been controversial, with many reports arguing that undifferentiated stem cells are protected from immune recognition due to the absence of major histocompatibility complex (MHC) markers. This argument is even more persuasive in transplantation into the central nervous system (CNS) where the graft rejection response is minimal.

Methodology/principal Findings: In this study, we evaluate graft survival and neuron production in perfectly matched vs.

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Many undergraduate institutions offer individual research opportunities for upper-level students in independent study courses and summer undergraduate research programs. These are necessarily limited to a small number of students. Greater numbers of students can benefit from incorporating student-directed investigative experiences into laboratories in standard courses.

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Heat-shock protein concentrations in the blood increase after exposure to a variety of stressors, including trauma and psychological stress. Although the physiological function of extracellular heat shock protein remains controversial, there is evidence that extracellular heat shock protein 72 (Hsp72) can facilitate immunologic responses. The signal(s) that mediate(s) the in vivo elevation of extracellular Hsp72 in the blood after stressor exposure remain(s) unknown.

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The present experiments examined the role of spinal proinflammatory cytokines [interleukin-1beta (IL-1)] and chemokines (fractalkine) in acute analgesia and in the development of analgesic tolerance, thermal hyperalgesia, and tactile allodynia in response to chronic intrathecal morphine. Chronic (5 d), but not acute (1 d), intrathecal morphine was associated with a rapid increase in proinflammatory cytokine protein and/or mRNA in dorsal spinal cord and lumbosacral CSF. To determine whether IL-1 release modulates the effects of morphine, intrathecal morphine was coadministered with intrathecal IL-1 receptor antagonist (IL-1ra).

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It has become clear that spinal cord glia (microglia and astrocytes) importantly contribute to the creation of exaggerated pain responses. One model used to study this is peri-spinal (intrathecal, i.t.

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Heat-shock proteins (Hsp) play an important role in stress physiology. Exposure to a variety of stressors will induce intracellular Hsp72, and this induction is believed to be beneficial for cell survival. In contrast, Hsp72 released during stress (extracellular Hsp72; eHsp72) activates pro-inflammatory responses.

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Extracellular heat-shock proteins (eHsp) such as those belonging to the 70-kDa family of Hsp (eg, Hsp72) have been hypothesized to act as a "danger signal" to immune cells, promote immune responses, and improve host defense. The current study tested this hypothesis. Adult male F344 rats were exposed to an acute laboratory stressor (100, 5-second, 1.

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Serotonin (5-HT) neurons in the dorsal raphe nucleus (DRN) are implicated in mediating learned helplessness (LH) behaviors, such as poor escape responding and expression of exaggerated conditioned fear, induced by acute exposure to uncontrollable stress. DRN 5-HT neurons are hyperactive during uncontrollable stress, resulting in desensitization of 5-HT type 1A (5-HT1A) inhibitory autoreceptors in the DRN. 5-HT1A autoreceptor downregulation is thought to induce transient sensitization of DRN 5-HT neurons, resulting in excessive 5-HT activity in brain areas that control the expression of learned helplessness behaviors.

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Habitual, moderate exercise is associated with improved health, including reductions in illness. These benefits may stem, in part, from immune function improvements. We have previously reported that daily wheel running increases serum and peritoneal natural IgM (nIgM) in pathogen-free Sprague-Dawely rats.

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Exposure to acute stress modulates immune function. Most research regarding stress and immunity has described the deleterious effects of stress. Recent studies, however, indicate that acute stress enhances many features of innate immunity.

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The mechanism(s) for how physically active organisms are resistant to many damaging effects of acute stressor exposure is unknown. Cellular induction of heat-shock proteins (e.g.

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Moderate, habitual physical activity improves health, possibly because of beneficial changes in immune function. For example, physical activity can increase natural killer cell cytotoxicity, T cell proliferation, and macrophage function but has minimal impact on antigen-driven B-2-mediated immunoglobulin (Ig) responses. The following studies tested whether physical activity selectively impacts nonantigen-driven B-1-natural IgM (nIgM) but not antigen-driven B-2 Ig.

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Acute stressor exposure can facilitate innate immunity and suppress acquired immunity. The present study further characterized the potentiating effect of stress on innate immunity, interleukin-1beta (IL-1beta), and demonstrated that stress-induced potentiation of innate immunity may contribute to the stress-induced suppression of acquired immunity. The long-term effect of stress on IL-1beta was measured by using an ex vivo approach.

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