Is there evidence for factorial invariance of the COVID Stress Scales? an analysis of North American and cross-cultural populations.

The COVID-19 pandemic impacted the mental health of more citizens globally than any previous modern viral outbreak. In response to the psychological challenges associated with COVID-19, the COVID Stress Scales (CSS) were developed to assess the presence and severity of COVID-related distress. The initial North American validation study of the CSS identified that the scale comprised five factors: danger and contamination fears, fear of socioeconomic consequences, xenophobia, checking and reassurance seeking, and traumatic stress symptoms. The CSS have since been validated across a multitude of international populations. However, findings support a five- and six-factor model. Methodological issues make interpreting most studies supporting a five-factor model challenging. The purpose of this study was to re-evaluate the factor structure of the CSS using data from North American samples, to assess for potential factorial invariance, and compare these results to cross-cultural findings. Multiple confirmatory factor analyses (mCFA) were conducted across 28 different groups (e.g., age, ethnicity/race, sex) from two large independent North American samples from 2020 (n = 6827) and 2021 (n = 5787), assessing the fit indices of the five-, six-, and alternative-factor model of the CSS. The current results provide evidence for factorial invariance of the six-factor model of the CSS across different North American demographics and highlight potential challenges in interpreting the results of studies that have supported a five-factor model of the CSS.

Factor structure and factorial invariance of the PTSD checklist for DSM-5 in public safety personnel: Results from a large and diverse sample.

OBJECTIVE: Public safety personnel (PSP; e.g., correctional workers, firefighters, paramedics, and police officers) are frequently exposed to potentially psychologically traumatic events (PPTEs) and report posttraumatic stress disorder (PTSD) difficulties more frequently than the general population. The PTSD checklist for DSM-5 (PCL-5) is a commonly used measure to screen PSP for PTSD. A single previous study assessed PCL-5 factorial invariance among PSP but used a small homogenous sample. The current study evaluated factorial invariance with a large (n = 5,855) and diverse PSP sample. METHOD: Multigroup confirmatory factor analyses (mCFAs; n = 98) were conducted using six competing factor models of the PCL-5 across seven PSP sectors, five age groups, and two gender groups. RESULTS: The seven-factor hybrid model of PTSD (i.e., reexperiencing, avoidance, negative alterations in cognitions and mood, hyperarousal, intrusion, emotional numbing, dysphoria, dysphoric arousal, anxious arousal, anhedonia, negative affect) produced consistently superior fit across all sectors assessed and produced marginally better absolute values than the six-factor anhedonia model, supporting PCL-5 factorial invariance among PSP. CONCLUSIONS: The current study is the first to use a large and diverse PSP sample to assess PCL-5 factorial invariance. The results support the PCL-5 as invariant across PSP sectors, age groups, and men and women. Consistent with other studies, the seven-factor hybrid model of PTSD produced the best fit, followed closely by the six-factor anhedonia model. Future research could use structured clinical interviews to further investigate the factorial structure and invariance of PTSD symptoms among PSPs. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

How does COVID stress vary across the anxiety-related disorders? Assessing factorial invariance and changes in COVID Stress Scale scores during the pandemic.

BACKGROUND: No studies have examined whether levels of COVID stress vary across anxiety-related disorders. Likewise, no studies have assessed structural invariance of the COVID Stress Scales (CSS) across clinical diagnoses. We sought to address these issues in the present study. Given the dynamic nature of pandemics, we also assessed whether COVID stress changed from the first to third wave in those with clinical diagnoses and those with no mental health conditions. METHOD: Data were collected during COVID-19 from two independent samples of adults assessed about a year apart (early-mid in 2020, N = 6854; and early-mid 2021, N = 5812) recruited from Canada and the United States through an online survey. Participants provided demographic information, indicated the presence of current (i.e., past-year) anxiety-related or mood disorder, and completed the CSS. RESULTS: The five CSS were reliable (internally consistent), and the five-factor structure was stable across samples. Scores tended to be highest in people with anxiety-related or mood disorders, particularly panic disorder. As expected, scores fluctuated over time, being higher during the early phases of the pandemic when threat was greatest and lower during the later phases, when vaccines were deployed and the COVID-19 threat was reduced. CONCLUSION: The findings add to the growing number of studies supporting the psychometric properties of the CSS. The results encourage further investigations into the utility of the scales, such as their ability to detect treatment-related changes in COVID-19-related distress. The scales also show promise for studies of future pandemics or outbreaks because the CSS can be modified, with minor wording changes, to assess distress associated with all kinds of disease outbreaks.

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release.

Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colony-stimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release. Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 microM-100 microM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5-5 nM) and SLIGKV (100 and 400 microM). The cells were then stimulated with interleukin (IL)-1beta and/or tumour necrosis factor (TNF)-alpha (10 ng.mL(-1)) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E(2) measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1beta-induced GM-CSF release and markedly reduced TNF-alpha-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE(2) release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect. In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.

Mechanisms of serum potentiation of GM-CSF production by human airway smooth muscle cells.

Inflammation and vascular leakage are prevalent in asthma. This study aimed to elucidate the mechanisms involved in serum potentiation of cytokine-induced granulocyte macrophage colony stimulating factor (GM-CSF) production by human airway smooth muscle cells and to identify possible factors responsible. Serum-deprived cells at low density were stimulated with TNF-alpha and IL-1beta for 24 h. Human AB serum (10%), inhibitors of RNA and protein synthesis or specific signaling molecules, or known smooth muscle mitogens were then added for 24 h. Culture supernatants were analyzed for GM-CSF levels, and cells were harvested to assess viability, cell cycle progression, GM-CSF-specific mRNA content, and p38 phosphorylation. Serum potentiated GM-CSF release when added before, together with (maximal), or after the cytokines. The potentiation involved both new GM-CSF-specific mRNA production and protein synthesis. The mitogens IGF, PDGF, and thrombin all potentiated GM-CSF release, and neutralizing antibodies for EGF, IGF, and PDGF reduced the serum potentiation. Inhibitor studies ruled as unlikely the involvement of p70(S6kinase) and the MAPK p42/p44, two signaling pathways implicated in proliferation, and the involvement of the MAPK JNK, while establishing roles for p38 MAPK and NF-kappaB in the potentiation of GM-CSF release. Detection of significant p38 phosphorylation in response to serum stimulation, through Western blotting, further demonstrated the involvement of p38. These studies have provided evidence to support p38 being targeted to interrupt the cycle of inflammation, vascular leakage and cytokine production in asthma.

Prediction of ifosfamide/mesna associated encephalopathy.

Ifosfamide and mesna were administered to 77 patients with advanced malignancies. Seven (9%) experienced a severe but reversible encephalopathy. In 56% of patients in whom EEG data was available, characteristic changes were seen with or without mild clinical toxicity. Discriminant analysis identified low serum albumin concentration, high serum creatinine concentration and the presence of pelvic disease as variables which predispose patients to the development of severe encephalopathy. A nomogram has been constructed which can be used to determine the probability that an individual patient may be given ifosfamide and mesna safely. This has important implications for the clinical use of a highly active chemotherapy regimen.

Distribution of fibronectin in the rectal mucosa.

Fibronectin is a glycoprotein of high molecular weight present in tissues, plasma, and tissue fluids. Its distribution in the rectal mucosa was studied by immunofluorescent and immunoperoxidase techniques using a monospecific antiserum. Immunofluorescent reactivity for fibronectin was present in the normal rectal mucosa of control subjects in epithelial cells, on basement membranes, and as a loose cribriform network of extracellular reactivity in the lamina propria that codistributed with histochemically demonstrable reticulin. Fibronectin was demonstrated immunoelectromicroscopically on collagen fibres, on smooth muscle cells and within and between columnar epithelial cells. In the rectal mucosa of patients with colitis with marked inflammatory changes, fibronectin appeared thickened and more prominent when present on basement membranes and as sparse strands between inflammatory cells infiltrating the lamina propria. In patients with longstanding colitis and less inflammatory cell infiltration there was a diffuse increase in fibronectin which was densely and uniformly present throughout the lamina propria. Fibronectin is a structural component of the rectal mucosa and changes in its distribution may form an important part of the local reaction to inflammatory bowel disease.