There is an interplay between oncology and mental health, resulting in a high prevalence of mental disorders among cancer patients. Out of the several interventions developed to target cancer specifics, collaborative care is indicated due to its efficacy. The perspective delves into the efficacy of collaborative care models, spotlighting a culturally informed strategy designed to harmonize mental and physical health interventions to bolster the overall wellbeing and resilience of individuals battling cancer. Central to our discussion is a compelling case vignette of Raliat, a patient diagnosed with ovarian cancer whose narrative exemplifies the multifaceted challenges cancer patients face, including stigma, psychological distress, and social isolation. Raliat\'s story illuminates the profound impact of cultural beliefs on patient experiences and the critical importance of a sensitive, holistic approach to care that respects cultural contexts. Through this lens, our analysis reveals that addressing emotional and situational stressors through collaborative care can significantly reduce oxidative stress, potentially decelerating the progression of both cancer and accompanying mental health disorders. We advocate for integrating mental health services into oncological care, drawing on the case vignette to argue for policies that facilitate such merger by employing validated collaborative care models. We conclude with a call for public education to diminish cancer stigma and improve social outcomes, emphasizing the use of a culture-informed PACER (physical, affective, cognitive, environmental, and relationship) strategy in providing comprehensive care for cancer patients and their families.

WHAT IS KNOWN ON THE SUBJECT?: Involuntary detention is a legislative power that allows people to be taken against their will for a mandatory mental health assessment and is known to be a restrictive and traumatizing process for patients. While there is some literature examining police/ambulance and mental health worker co-response models, the conclusions are mixed as to whether they reduce rates of involuntary detentions in mentally ill people. The Police, Ambulance, Clinician Early Response (PACER) model is an example of a tri-response mental health crisis response team whose role is to respond and assess people thought to be experiencing a mental health crisis. There is little literature to determine whether PACER tri-response model reduces incidents of involuntary detention when compared with standard police and/or ambulance responses. WHAT THIS PAPER ADDS TO EXISTING KNOWLEDGE?: This paper describes the outcomes of patients assessed by a PACER team, compared with patients who were assessed by police or ambulance. It demonstrates that PACER may reduce unnecessary involuntary detentions through expert mental health assessment for patients coming to emergency services for assistance. It is one of only two published studies examining a tri-response model. WHAT ARE THE IMPLICATIONS FOR PRACTICE?: The results of this study may support health and policing policymakers to implement PACER models as a means of reducing involuntary detentions, reducing demand for emergency departments, reducing time spent by emergency services responding to people experiencing mental health crisis and improving outcomes for people with mental illness.
UNASSIGNED: BACKGROUND: Involuntary detention is a common method of enforcing mental health assessment and treatment; however, it is associated with poor patient outcomes and high emergency service and hospital demand.
OBJECTIVE: To examine the association between (1) Police, Ambulance, Clinician, Early Response (PACER) model, (2) police or (3) ambulance response and rates of involuntary detention of mentally ill people.
METHODS: A retrospective observational study using routine administrative data in an Australian City, over a 12-month period (2019-2020).
RESULTS: Over a 12-month period, 8577 people received crisis mental health intervention in the study setting. We observed an 18% increase in the relative risk of being involuntarily detained by police, and a 640% increase in the relative risk of being detained by ambulance. The PACER team detained 10% of their total presentations, as compared with 12% by police and 74% by ambulance. Involuntary detentions enacted by PACER were more likely to convert to a post-detention hospitalization (72%), when compared with police (27%) and ambulance (17%).
CONCLUSIONS: PACER was associated with lower rates of involuntary detention and higher rates of post-detention hospitalization when compared to police and ambulance response.
CONCLUSIONS: PACER cohort experience more positive outcomes than with police or ambulance cohorts.

Emergency services are frequently called to attend mental health incidents and are looking for innovative ways to improve their responses and reduce the burden on services. Involuntary detention of people living with mental illness is considered more frequent than necessary, leading to increased pressure on emergency departments, and is often a traumatic experience for patients. The Police, Ambulance, Clinician Early Response (PACER) model was developed in 2019 in Canberra, Australia, and seeks to reduce involuntary detentions by embedding a mental health clinician into emergency services as a mobile mental health crisis response intervention. This protocol details a retrospective cohort study that will examine the association between PACER and involuntary detentions using medical and police records and compare the results to standard ambulance and police responses. We will use relative risk and odds ratio calculations to determine the probability of being involuntarily detained or diverted from hospital; and we will describe the patient characteristics and outcomes in the PACER cohort. Results will be reported using the STROBE checklist for reporting cohort studies. This study was not registered on a publicly accessible registry.

Radicular cysts are characterized by significant levels of changes in inflammatory biomarkers. Among them, interleukins and growth factors have been reported to be deregulated in radicular cyst tissues. Moreover, long non-coding RNAs are recently discovered non-coding RNA molecules that regulate various intracellular stimuli to keep homeostasis in balance. A growing body of evidence suggests that lncRNAs are significantly involved in the regulation of inflammation by targeting various inflammatory biomarkers. Accordingly, the present study was aimed to investigate the gene expression levels of inflammation-related lncRNAs in radicular cysts and show their possible roles in the development of radicular cysts. For the study, a total of 25 patients with a radiologically and pathologically confirmed radicular cyst were enrolled. For the determination of non-coding RNA expression levels, real-time qPCR was used. As a result of the current study, expression levels of PACER and THRIL were found to be significantly elevated in radicular cyst tissues compared to control tissue samples. However, MALAT1, ANRIL, and NEAT1 expression levels were not significantly altered in radicular cyst tissues compared to control tissue samples. In conclusion, long non-coding RNAs, PACER and THRIL, seem to have significant pathophysiological roles by acquiring molecular changes during inflammation and might be involved in the development and formation of radicular cysts.

BACKGROUND: Necroptosis is a controlled form of necrosis which can be stimulated in cases where the apoptosis signal is absent. Necroptosis can be induced by DR family ligands and by various intracellular and extracellular stimuli that triggers the activation of DR family ligands. Necrostatins, which are specific RIP1 antagonists, prevent necroptosis by inhibiting RIP1 kinase, allowing survival and propagation of cells in the presence of DR ligands. Furthermore, there is a mounting evidence that long non-coding RNA (lncRNA) molecules accomplish vital functions in cell death processes such as apoptosis, autophagy, pyroptosis, and necroptosis. Accordingly, here we aimed to decipher the lncRNAs that are involved in the control and maintenance of necroptosis signaling.
RESULTS: Colon cancer cell lines, HT-29 and HCT-116 were used for the study. For the chemical modulation of necroptosis signaling, 5-Fluorouracil, TNF-α and/or Necrostatin-1 were used. Gene expression levels were determined by quantitative real-time PCR. Remarkably, lncRNA P50-associated COX-2 extragenic RNA (PACER) was identified to be suppressed in necroptosis-induced colon cancers, whereas the expression of PACER was restored when necroptosis was suppressed. In addition, no detectable change was observed in HCT-116 colon cancer cells, as these cells lack the expression of RIP3 kinase.
CONCLUSIONS: Collectively, current findings clearly imply that PACER have key regulatory roles in the control of necroptotic cell death signaling circuitry. Notably, the tumor promoter activity of PACER might be responsible for the lack of necroptotic death signal in cancer cells. Also, RIP3 kinase seems to be essential component in PACER-associated necroptosis.

Bipolar disorder (BD) is a severe condition characterized by periods of mania and depression. Despite advances in the neurobiology of bipolar disorder, the exact etiology of the disease remains unclear. There is evidence that Inflammation is associated with bipolar disorder. COX-2 and NF-κB are two critical mediators in the inflammatory pathways. Long non-coding RNAs (lncRNAs) are a new class of non-coding RNAs that play a wide range of roles, especially in developing and maintaining normal brain functions. Two lncRNAs called PACER and NKILA control the expression of COX-2 and NF-κB genes, respectively. In this study, Expression levels of PACER and NKILA lncRNAs, as well as, COX-2 and NF-κB genes were measured in fifty patients with bipolar disorder and 50 healthy individuals by real-time PCR. Expression levels of NKILA and COX2 were considerably reduced in BD patients compared with healthy controls. Such significant downregulation in the expression of NKILA and PACER was only observed in male patients with BD compared with male healthy subjects. Also, according to the results of the ROC curve, the area under curve values for NKILA and COX2 were 0.68 and 0.52 respectively. Consequently, the NKILA gene could be considered a biomarker. By examining the degree of pairwise correlation between genes, all genes had a significant positive correlation with each other. Taken together, these results revealed a function for NKILA and PACER lncRNAs in the pathogenesis of BD.

Parents play a critical role in emotional socialization and the development of emotion regulation during childhood. The tools to measure how parents assist children\'s emotion regulation are very limited. The Parental Assistance with Child Emotion Regulation (PACER) Questionnaire is a novel scale developed for this purpose with excellent psychometric properties. The aim of this study is to adapt the PACER to Turkish and investigate its psychometric properties in the Turkish cultural setting. The data were collected from 700 parents who have children aged birth to 17 years. In addition to the PACER, participants filled out some scales about their own beliefs and behaviors, also their children\'s psychological symptoms. We confirmed the original ten-factor structures of the PACER in a Turkish sample and the measurement invariance supported the PACER\'s structure across subgroups. The high internal consistencies of factors were achieved; however, the test-retest reliability was lower than expected. The factors of maladaptive emotion regulation strategies (e.g., rumination, expressive suppression, avoidance) were positively associated with parents\' own emotion regulation deficit, symptoms, and child\'s symptoms, while others (e.g., reappraisal, problem-solving) were negatively associated with them. Overall, our results suggest that the Turkish version of the PACER is a psychometrically valid and reliable measurement to assess how parents support their children to regulate their emotions. We believe that this adaptation allows the scale to be used in developmental and clinical psychology studies and will pave the way for cross-cultural studies.

Background: Child weight status is inversely associated with fitness, but less is known about this relationship across fitness domains. This study examined the longitudinal association between weight status and fitness domains in a large, diverse sample of children. Methods: Data were drawn from the New York City Fitnessgram (2010-2011 to 2017-2018). Height and weight were collected annually and converted to weight status using Centers for Disease Control and Prevention growth charts. Aerobic capacity, muscular strength, and endurance were measured as age and sex standardized z-scores based on the fitness performance tests. Repeated-measures multilevel models were run testing the association between weight status and 1-year lagged fitness domains. Results: The sample included 917,554 children (51.8% male, 39.3% Hispanic, 29.9% non-Hispanic Black, 13.9%, 4.7%, and 1.7% class I, II, and III obesity, respectively). For each fitness domain, fitness scores decreased with increasing weight status across all demographic categories, with the lowest fitness scores observed in children with the most severe obesity, and highest magnitude of effects for aerobic capacity, and particularly among boys, non-Hispanic Whites, and older youth. For example, compared with youth with healthy weight, youth with overweight had 0.28 standard deviation lower aerobic capacity performance [confidence interval (95% CI): -0.29 to -0.28], followed by class 1 obesity (β = -0.57, 95% CI: -0.58 to -0.57), class 2 obesity (β = -0.88, 95% CI: -0.88 to -0.88), and class 3 obesity (β = -1.19, 95% CI: -1.20 to -1.18). Conclusions: Compared with youth with healthy weight, youth at every other weight status had lower subsequent fitness, with the magnitude of the relationship increasing as weight status increased. Future research should examine interventions targeting aerobic capacity to reduce fitness disparities.

Alzheimer\'s disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells. However, Rubicon participates in different pathways depending on cell type, and little information is currently available on neuronal Rubicon\'s role in the AD context. Here, we investigated the cell-specific expression of Rubicon in postmortem brain samples from AD patients and 5xFAD mice and its impact on amyloid β burden in vivo and neuroblastoma cells. Further, we assessed Rubicon levels in human-induced pluripotent stem cells (hiPSCs), derived from early-to-moderate AD and in postmortem samples from severe AD patients. We found increased Rubicon levels in AD-hiPSCs and postmortem samples and a notable Rubicon localization in neurons. In AD transgenic mice lacking Rubicon, we observed intensified amyloid β burden in the hippocampus and decreased Pacer and p62 levels. In APP-expressing neuroblastoma cells, increased APP/amyloid β secretion in the medium was found when Rubicon was absent, which was not observed in cells depleted of Atg5, essential for autophagy, or Rab27a, required for exosome secretion. Our results propose an uncharacterized role of Rubicon on APP/amyloid β homeostasis, in which neuronal Rubicon is a repressor of APP/amyloid β secretion, defining a new way to target AD and other similar diseases therapeutically.

Mesenchymal stem cells (MSC) have emerged as a promising tool to treat inflammatory diseases, such as inflammatory bowel disease (IBD), due to their immunoregulatory properties. Frequently, IBD is modeled in mice by using dextran sulfate sodium (DSS)-induced colitis. Recently, the modulation of autophagy in MSC has been suggested as a novel strategy to improve MSC-based immunotherapy. Hence, we investigated a possible role of Pacer, a novel autophagy enhancer, in regulating the immunosuppressive function of MSC in the context of DSS-induced colitis. We found that Pacer is upregulated upon stimulation with the pro-inflammatory cytokine TNFα, the main cytokine released in the inflammatory environment of IBD. By modulating Pacer expression in MSC, we found that Pacer plays an important role in regulating the autophagy pathway in this cell type in response to TNFα stimulation, as well as in regulating the immunosuppressive ability of MSC toward T-cell proliferation. Furthermore, increased expression of Pacer in MSC enhanced their ability to ameliorate the symptoms of DSS-induced colitis in mice. Our results support previous findings that autophagy regulates the therapeutic potential of MSC and suggest that the augmentation of autophagic capacity in MSC by increasing Pacer levels may have therapeutic implications for IBD.