The effect of illness perception on psychosocial adjustment of patients with breast cancer and their spouses: actor-partner independence model.

OBJECTIVE: With the increase in the prevalence rate and improvements in the survival of breast cancer patients, there is a growing interest in understanding the level of psychosocial adjustment in these patients. The study aimed to describe the illness perception and psychosocial adjustment levels of both breast cancer patients and their spouses, to use the Actor-Partner Interdependence Model (APIM) to clarify the actor-partner relationships between spouses, and to explore the impact of illness perception on psychosocial adjustment to the disease within the joint actions of both spouses. METHODS: A total of 216 female patients with breast cancer and their spouses participated in the study. They were selected from two tertiary hospitals in Guangdong Province, China from October 2022 to May 2023 using a convenience sampling method. The participants were assessed using the Brief Illness Perception Questionnaire and the Psychosocial Adjustment to Illness Scale to examine the relationship between illness perception and psychosocial adjustment. AMOS24.0 was used to test and analyze the actor-partner interdependence model. RESULTS: The illness perception score (57.75 ± 10.91) was slightly higher than that of the spouse (57.10 ± 11.00), and the psychosocial adjustment score (64.67 ± 6.33) was slightly lower than that of the spouse (64.76 ± 7.49). The results of the actor-partner interdependence model indicated that there was a couple partner between breast cancer patients and their spouses: the spouse's illness perception significantly affected the patient's psychosocial adjustment (ß = 0.095, p = 0.015); the patient's illness perception also significantly affected the spouse's psychosocial adjustment (ß = 0.106, p = 0.033). Among them, the patient's psychosocial adjustment was found to be related to the patient's illness comprehensibility or coherence of illness (ß = 0.433, p = 0.009), the spouse's emotional illness representation (ß = 0.218, p = 0.037), and the spouse's illness comprehensibility or coherence of illness (ß = 0.416, p = 0.007), while the spouse's psychosocial adjustment was only related to the spouse's illness comprehensibility or coherence of illness (ß = 0.528, p = 0.007). CONCLUSIONS: The psychosocial adjustment of breast cancer patients is affected by both their own and spouse's illness perception. Therefore, in the future, the healthcare staff can implement early psychological interventions for patients diagnosed with breast cancer and their spouses as a unit to promote the psychosocial adjustment of them.

Illness perception profile among cancer patients and its influencing factors: A cross-sectional study.

PURPOSE: The purpose of this study was to explore latent profiles of illness perception among cancer patients and its influencing factors. METHODS: This study was a cross-sectional study adopting convenience sampling to select cancer patients from two hospitals in China. A total of 286 patients completed Brief Illness Perception Questionnaire, Post-traumatic Growth Inventory, Fear of Disease Progression Questionnaire and Psychosocial Adjustment to Illness Scale. Latent profile analysis and multiple linear regression were performed to explore the subgroups and factors influencing classification. RESULTS: Three subgroups were identified, which were labelled as "Moderate Illness Perception Group" (16.8%; C1), "High Illness Perception with Heightened Concerns Group" (68.5%; C2) and "High Resilience and Low Symptomatic Impact Group" (14.7%; C3). Specifically, "Normal", "Mild symptom" and "Bed time during the day <50%" of "Functional Status" were more associated with C3. "Worker", "Farmer" and "Self-employed" were more associated with C1 and C2. Patients who had more "knowledge of the disease" were more associated with C2 and C3, who had less "post-traumatic growth" were more associated with C1, and who had less "fear of disease progression" and more "psychosocial adjustment" were more associated with C3 (all P < 0.05). CONCLUSIONS: There was significant variability of illness perception among three subgroups of cancer patients, which emphasized the complexity of psychological condition. The insights derived from these distinct profiles enables tailored interventions and patient-centered communication strategies. However, integrating objective measures or biomarkers is needed to complement self-reported data.

A 16-gene signature associated with homologous recombination deficiency for prognosis prediction in patients with triple-negative breast cancer.

Homologous recombination deficiency (HRD) commonly occurs in breast cancer, which is the second cause of cancer death in women with a high rate of relapse and poor outcomes. Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. Thus, we aim to develop a prognostic signature based on HRD expecting to help improve outcomes in TNBC. The Cancer Genome Atlas (TCGA)-TNBC cohort was divided into the training set and the testing set randomly. Sixteen genes were filtered from the prognostic HRD-associated genes to establish a prognostic model in the training set. Patients were divided into high-risk and low-risk groups based on the median value of the risk score. Prognosis analysis showed that the high-risk group was associated with a worse prognosis in the training set, the testing set, the entire TCGA-TNBC cohort, and the METABRIC-TNBC cohort. The time-dependent receiver operating characteristic curve showed that our model had very good accuracy in the prediction of 1-5-year overall survival in the TCGA-TNBC cohort. Besides, a comparison of the area under curve value and C-index between our model and four published models showed that our model had the best predictive efficiency compared to other models. Subsequently, a nomogram was established. Finally, our finding also indicated that our model was associated with immunoregulation in TNBC and had the potential to be the target for TNBC treatment. Therefore, our findings not only provided a new strategy in the personalized prognosis management of TNBC but also offered new insight into precision treatment in TNBC.

The effect of miR-21 on SWOZ2 glioma cells and its biological mechanism.

PURPOSE: To investigate the role of micro RNA-21 (miR- 21) in human glioma cells and its potential disease-causing mechanism. METHODS: jetPRIME was used to transfect the miR-21- mimics and its negative control into SWOZ2 human glioma cells. Real-time fluorescence quantitative PCR assay was used to measure differences in the expression of miR-21 in SWOZ2 glioma cells, SWOZ2-miR-21-mimics cells, and control cells. Cell counting kit-8 assay was used to measure the activity of SWOZ2 glioma cells and SWOZ2-miR-21- mimics cells, and Western blot was used to measure PTEN, p-Akt, and P-glycoprotein (P-gp). RESULTS: The level of miR-21 in SWOZ2-miR-21-mimics cells was significantly higher than in SWOZ2 cells and the negative control group. Compared with SWOZ2 cells, the expression of PTEN protein in SWOZ2-miR-21 cells decreased significantly, and the expression of p-Akt and P-gp protein were significantly increased. Compared with SWOZ2 cells and the negative control group, the proliferation rate of SWOZ2-miR-21-mimics cells was significantly increased (p<0.05).The rate of apoptosis as determined by flow cytometry showed that the number of apoptotic SWOZ2-miR-21- mimics cells decreased significantly (p<0.05). Transwell assay found that the invasive ability of SWOZ2-miR-21-mimics cells increased significantly, suggesting that miR-21 can mediate the biological functions of SWOZ2 cells by inhibiting the expression of PTEN. CONCLUSION: miR-21 may regulate the proliferation and apoptosis of human glioma cells by downregulating the expression of the PTEN protein, and miR-21 may represent a potential therapeutic target for the treatment of glioma.

Sex differences in behavior and expression of CGRP-related genes in a rodent model of chronic migraine.

OBJECTIVE: The objectives of this study were to develop a preclinical rodent model that produces migraine-like behaviors based on International Headache Society diagnostic criteria, to determine whether sex differences are present, and to determine whether expression of calcitonin gene-related peptide (CGRP) and the genes encoding its receptor in trigeminal ganglion or medulla correlates with those behaviors. BACKGROUND: Few animal studies of migraine have tested behaviors associated with migraine diagnostic criteria. In this study, changes in activity and in mechanical sensitivity of facial regions following application of inflammatory soup (IS) or vehicle (phosphate-buffered saline [PBS]) to the dura were measured to model changes in routine activity and allodynia. CGRP, an important mediator of migraine pathogenesis, and the 3 components of its receptor, calcitonin-like receptor (CLR), receptor activity-modifying protein 1 (RAMP1), and receptor component protein (RCP) mRNAs were quantified in the trigeminal ganglion and medulla to identify baseline sex differences and changes associated with application of IS or PBS to the dura. METHODS: Male and female Sprague-Dawley rats were implanted with a dural cannula. Groups of rats were treated with 10 or 20 µL volumes of IS or PBS. Baseline behavioral testing was conducted prior to surgery and again at 7 days postsurgery, and dural application of IS or PBS was performed repeatedly for a total of 8 applications. Locomotor activity was assessed using force plate actimetry during and following application to provide information on distance traveled, bouts of low mobility, spatial confinement, and focused energy. Periorbital and perimasseter sensory testing was performed 20 minutes post-application to measure allodynia. The rats were sacrificed 30 minutes following the final dural treatment, tissue was dissected and total RNAs were isolated from ipsilateral trigeminal ganglia and ipsilateral medulla. Quantitative real-time polymerase chain reactions were used to measure the expression of amplified constructs using gene-specific primers for CGRP, RAMP1, CLR, and RCP. RESULTS: Both males and females showed behavioral effects of IS application, but there were pronounced sex differences. Females showed effects at the lower dose, and activity changes were present for a longer duration, but males required fewer applications of IS to exhibit behavioral changes. Females showed increased withdrawal responses for periorbital and perimasseter mechanical testing (10 µL IS groups), and males showed increased perimasseter withdrawal responses (20 µL IS group). In the trigeminal ganglion, there were no baseline sex differences in CGRP-encoding mRNA, but females had lower baseline expression of RAMP1, CLR, and RCP-encoding mRNAs. In the medulla, females had higher baseline levels of CGRP-encoding mRNAs and lower baseline levels of RAMP1, CLR, and RCP-encoding mRNAs than males. Both IS and PBS increased expression of mRNAs encoding CGRP, RAMP1, RCP, and CLR in the trigeminal ganglion in males, but in females, only CLR and RCP were increased. In the medulla both IS and PBS increased expression of CGRP, CLR in males and CLR and RCP in females. Thus, expression of CGRP-related genes did not mirror the behavioral differences between IS and PBS groups. Instead, CGRP-related genes were upregulated by both IS and PBS applications. CONCLUSIONS: This study demonstrates significant changes in locomotor activity and facial allodynia associated with application of IS to the dura as well as significant sex differences, demonstrating that International Headache Society diagnostic criteria can be used to design a rodent behavioral model of migraine. In addition, there were prominent baseline sex differences in expression of CGRP and its receptor in both the trigeminal ganglion and medulla, but the majority of changes in expression of CGRP and its receptor were present in both the IS and PBS treated rats. This suggests that the CGRP pathway responds to changes in intracranial pressure or meningeal stretch, while migraine-like behaviors occur after meningeal inflammation.

Upregulation of inflammatory mediators in a model of chronic pain after spinal cord injury.

Chronic neuropathic pain is a disabling condition observed in large number of individuals following spinal cord injury (SCI). Recent progress points to an important role of neuroinflammation in the pathogenesis of central neuropathic pain. The focus of the present study is to investigate the role of proinflammatory molecules IL-1ß, TNF-α, MCP-1, MMP-9 and TIMP-1 in chronic neuropathic pain in a rodent model of SCI. Rats were subjected to spinal cord contusion using a controlled linear motor device with an injury epicenter at T10. The SCI rats had severe impairment in locomotor function at 7 days post-injury as assessed by the BBB score. The locomotor scores showed significant improvement starting at day 14 and thereafter showed no further improvement. The Hargreaves' test was used to assess thermal hyperalgesia for hindpaw, forepaw and tail. A significant reduction in withdrawal latency was observed for forepaw and tail of SCI rats at days 21 and 28, indicating the appearance of thermal hyperalgesia. Changes in expression of mRNAs for IL-1ß, TNF-α, MCP-1, MMP-9 and TIMP-1 were assessed using real-time polymerase chain reaction in spinal cord including the injury epicenter along with regions above and below the level of lesion at day 28 post-injury. A significant increase was observed in the expression of MCP-1, TNF-α, TIMP-1 and IL-1ß in the injury epicenter, whereas only TIMP-1 was upregulated in the area below the injury epicenter. The results of the study suggest that prolonged upregulation of inflammatory mediators might be involved in chronic neuropathic pain in SCI, and that TIMP-1 may play a role in maintenance of chronic below level pain.

Detrimental effects of aging on outcome from traumatic brain injury: a behavioral, magnetic resonance imaging, and histological study in mice.

Considerable evidence indicates that outcomes from traumatic brain injury (TBI) are worse in the elderly, but there has been little preclinical research to explore potential mechanisms. In this study, we examined the age-related effects on outcome in a mouse model of controlled cortical impact (CCI) injury. We compared the responses of adult (5-6 months old) and aged (21-24 months old) male mice following a moderate lateral CCI injury to the sensorimotor cortex. Sensorimotor function was evaluated with the rotarod, gridwalk and spontaneous forelimb behavioral tests. Acute edema was assessed from hyperintensity on T2-weighted magnetic resonance images. Blood-brain barrier opening was measured using anti-mouse immunoglobulin G (IgG) immunohistochemistry. Neurodegeneration was assessed by amino-cupric silver staining, and lesion cavity volumes were measured from histological images. Indicators of injury were generally worse in the aged than the adult mice. Acute edema, measured at 24 and 48 h post-injury, resolved more slowly in the aged mice (p < 0.01). Rotarod recovery (p < 0.05) and gridwalk deficits (p < 0.01) were significantly worse in aged mice. There was greater (p < 0.01 at 3 days) and more prolonged post-acute opening of the blood-brain barrier in the aged mice. Neurodegeneration was greater in the aged mice (p < 0.01 at 3 days). In contrast, lesion cavity volumes, measured at 3 days post-injury, were not different between injured groups. These results suggest that following moderate controlled cortical impact injury, the aged brain is more vulnerable than the adult brain to neurodegeneration, resulting in greater loss of function. Tissue loss at the impact site does not explain the increased functional deficits seen in the aged animals. Prolonged acute edema, increased opening of the blood-brain barrier and increased neurodegeneration found in the aged animals implicate secondary processes in age-related differences in outcome.

A mouse model of sensorimotor controlled cortical impact: characterization using longitudinal magnetic resonance imaging, behavioral assessments and histology.

The present study establishes a new mouse model for traumatic brain injury (TBI), using an electromechanically driven linear motor impactor device to deliver a lateral controlled cortical impact (CCI) injury to the sensorimotor cortex. Lesion cavity size was measured, and inter-animal consistency demonstrated, at 14 days post injury. Qualitative information regarding damage progression over time was obtained by scanning with high field magnetic resonance imaging (MRI) at five time points following injury. Functional impairment and recovery were measured with the Rotarod, gridwalk and cylinder tests, and lesion cavity volume was measured post mortem with thionin-stained tissue sections. The study establishes the reliability of a linear-motor based device for producing repeatable damage in a CCI model, demonstrates the power of longitudinal MRI in studying damage evolution, and confirms that a simple battery of functional tests record sensorimotor impairment and recovery.

Electrical stimulation of cortex improves corticospinal tract tracing in rat spinal cord using manganese-enhanced MRI.

Following bilateral injection of manganese (Mn) into the rat's motor cortex, electrical stimulation of the cortex is shown to increase the transport, uptake and accumulation of Mn in the corticospinal tract (CST), as assessed by manganese-enhanced magnetic resonance imaging (MEI). T(1)-weighted gradient echo images were acquired in 3-D and displayed in different orientations to anatomically delineate the CST pathway from cortex to spinal cord (SC) at the thoracic level. T(1)-maps of the SC were produced from spin-echo based image data to demonstrate the distribution of the T(1) properties of the SC tissue and to quantitatively assess the T(1)-change occurring in the CST due to the presence of Mn therein. Implications for improving the tract tracing ability with the proposed in vivo approach and its application to spinal cord injury (SCI) research are discussed in terms of aiding future experimental investigations of neuroplasticity following an injury.

Manganese-enhanced MRI of rat spinal cord injury.

The potential of the manganese-enhanced MRI (MEI) technique in labeling the intact neuronal circuitry of rat spinal cord was examined. Experiments were conducted on normal and injured cords at 9.4-T magnetic field strength using an implantable rf coil. The contrast agent manganese (Mn) was locally delivered within the parenchyma at a dose of 25 mmol/L in 10 nL. The transport, uptake and accumulation of Mn in tissue were then followed remotely on T1-weighted images that were acquired serially from the cord. In MEIs of normal cord, Mn was observed to be transported in directions both rostral and caudal to the site of injection. In the cord that was subjected to hemisection, signal enhancement was on the contralesional side of the cord, but not at the ipsilesional side. The sensitivity and specificity of the MEI technique in labeling the neurons that are functional were also validated with a traditional track-tracing method using biotinylated dextran amine.

Magnetic resonance angiography of rat spinal cord at 9.4 T: a feasibility study.

In this study we investigated the feasibility of performing 3D time-of-flight magnetic resonance angiography to remotely image the arteries of rat spinal cord. Using a custom-designed implantable radiofrequency coil, we acquired angiograms from normal and injured cords. The potential of the approach was evaluated in terms of longitudinally monitoring the vascular reorganization of spinal cord following an injury.