Examining the role of perceived stress on learning satisfaction under the influence of academic burnout in the post-COVID world.

BACKGROUND: In the last two years, due to the impact of COVID-19, students were forced to continue their education online because the government imposed restrictions to limit the spread of the virus. However, with the resumption of offline classes, the students seem to be suffering more from stress and isolation as they must face the challenges of the real world, which are quite different from the virtual one to which they have become accustomed. In this study, the effect of stress on students leading to their academic burnout and the influence of burnout on their learning satisfaction was studied. MATERIALS AND METHODS: The data were collected from 343 students of final year postgraduation courses in business management studies in India. The collected data were subject to analysis using PLS-SEM through SmartPLS 4.0 software. RESULT: The results of the study state that the perceived stress significantly increases cynicism, and exhaustion with a coefficient value of 0.481 each and decreases self-efficacy with - 0.03. Additionally, exhaustion acts as a mediator that decreases the effect of perceived stress over learning satisfaction with a positive indirect effect of 0.176. CONCLUSION: The study concludes that not all types of stress are bad for students; hence, increasing perceived stress leads to increased learning satisfaction. Whereas, in the presence of burnout factors, such as exhaustion and cynicism, learning satisfaction decrease. However, self-inefficacy, one of the factors under burnout, doesn't show any effect on learning satisfaction. The present study is widely applicable to industry and academia to deal with burnout to improve students learning satisfaction.

Clonal dominance of CD133+ subset population as risk factor in tumor progression and disease recurrence of human cutaneous melanoma.

Chemotherapeutic refractoriness of advanced cutaneous melanoma may be linked with melanoma-initiating cells, also known as melanoma stem cells. This study aimed to determine relative risk of clonal dominance of the CD133+ phenotype in tissues from melanoma patients with different clinical outcomes that could be applied to early diagnosis, prognosis or disease monitoring. Significant overexpression of CD133 (p<0.02) was observed by immunohistochemical staining in tissues from patients with recurrent disease versus those without disease recurrence. Relative risk analysis between these two groups suggested that the patients with recurrence or metastatic lesion had a greater than 2-fold overexpression of CD133. In addition, immunodetectable CD133 corroborated with upregulation of CD133 RNA levels (14- to 30-fold) as assessed by quantitative real-time reverse transcription-PCR (qRT-PCR) comparison of melanoma cell lines derived from patients with poor clinical outcomes and short overall survival (<10 months), vs. those derived from patients with good clinical outcomes and longer overall survival (>24 months). Further, cells derived from patients, and MACS-sorted according to their CD133 status retained their CD133-positivity (>95%) or CD133-negativity (>95%) for more than 8 passages in culture. CD133+ cells could repopulate and form tumors (p<0.03) in athymic NCr-nu/nu mice within 8 weeks while no tumors were observed with CD133- phenotype (up to 200,000 cells). Taken together, the study demonstrates, for the first time, that there exists a clonal dominance of a CD133+ population within the hierarchy of cells in cutaneous tissues from patients that have undergone successive progressive stages of melanoma, from primary to metastatic lesions. CD133, thus, provides a predictive marker of disease as well as a potential therapeutic target of high-risk melanoma.

Immuno-expression of human melanoma stem cell markers in tissues at different stages of the disease.

BACKGROUND: Human cutaneous melanoma can be one of the most aggressive tumors and is extremely resistant to all current therapeutic modalities. Immunohistochemistry (IHC) studies were undertaken to assess independent relative frequency on preferential overexpression and simultaneous expression of four stem cell markers; CD133+, ABCB5+, CD166, and Nestin, at different stages of the disease. MATERIAL AND METHODS: Five-micron sections from paraffin blocks from primary melanoma, lymph node (LN) metastases, distant metastases, benign nevi from non-melanoma patients (NMP), and patients with past history of melanoma (MP) were IHC stained with monoclonal antibodies (mAb) to the four stem cell markers. RESULTS: Overexpression of CD133+ was noted in tissues from LN and distant metastases compared to benign nevi (P < 0.0022, P < 0.013, respectively). Overexpression of ABCB5+ was observed comparing primary melanoma, LN, and distant metastases to benign nevi from NMP (P < 0.0063, P < 0.001, P < 0.00058, respectively). Significant overexpression of ABCB5+ was noted in tissues from LN and distant metastases compared with benign nevi from MP (P < 0.0003, P < 0.0068). None of the benign nevi of NMP demonstrated ABCB5+. CONCLUSIONS: This study clearly shows the existence of a distinct hyperpolarized population of stem cells and may implicate genetic factors in human cutaneous melanoma. Simultaneous overexpression of CD133+ and Nestin could reflect on their origin or lineage association with a neural stem cell. These findings may open new perspectives for therapeutic implication of a melanoma stem cell in specific cancer therapy.

Biology of human cutaneous melanoma.

A review of the natural behavior of cutaneous melanoma, clinical and pathological factors, prognostic indicators, some basic research and the present and possible futuristic strategies in the management of this disease are presented. While surgery remains to be the most effective therapeutic approach in the management of early primary lesions, there is no standard adjuvant therapy after surgical resection, or for metastatic disease.

Cytokines and growth factors expressed by human cutaneous melanoma.

Cytokines and growth factors have biologic effects that could stimulate tumor growth, invasion and angiogenesis. The incidence of 24 factors was investigated in 25 cultured human melanoma cell lines and in 62 fixed tissues at different stages of the disease. Over 80% of the human melanoma cell lines expressed TGF-ß, IL-8, IL-6, VEGF, PDGF-AA and OPN. Significantly higher TGF-ß, IGF-1 and IL-15 were determined in primary lesions compared to distant metastases by immunohistochemistry. Illustrating the complexity of the milieu of the tumor microenvironment, some of these factors may have to be considered in targeted therapy.

Stress up-regulates neuronal expression of the herpes simplex virus type 2 large subunit of ribonucleotide reductase (R1; ICP10) by activating activator protein 1.

Herpes simplex virus type 2 (HSV-2) genes expressed in neuronal cells in response to stress stimuli that trigger latency reactivation are largely unknown. Using a chloramphenicol acetyltransferase (CAT) reporter assay we found that stress caused a significant (P < .001) increase in ICP10 expression in neuronal cells. Up-regulation correlated with activator protein (AP)-1 activation, notably c-Jun and c-Fos that bind cognate elements in the ICP10 promoter. It was blocked by mutation of the AP-1 motifs in the ICP10 promoter. ICP10 expression protected neuronal cells from stress-induced apoptosis. The data suggest that ICP10 may contribute to HSV-2 reactivation by increasing neuronal survival.

CD34+ cells in the peripheral blood transport herpes simplex virus DNA fragments to the skin of patients with erythema multiforme (HAEM).

Herpes simplex virus (HSV)-associated erythema multiforme (HAEM) is a recurrent disease characterized by the presence and expression of HSV DNA fragments in lesional skin. Our studies examined the mechanism of viral DNA transport to the skin of HAEM patients. CD34+ cells were isolated from the blood of normal subjects and HSV and HAEM patients during acute lesions and at quiescence. They were cultured with cytokines that favor their differentiation into Langerhans cells (LC) precursors (CD1a+/CD14-) and examined for HSV replication, HSV-induced cellular alterations, viral DNA fragmentation, and clearance. CD34+ cells from all study groups were non-permissive for HSV replication but infection favored their differentiation into CD1a+/CD14- LC precursors and upregulated E-cadherin expression, thereby assisting LC targeting to the skin. Only HAEM patients had CD34+ cells that retained viral DNA fragments, notably polymerase DNA, for at least 7 d of in vitro culture. The percentages of circulating CD34+ (and CD34+/CLA+) cells were significantly higher in HAEM patients at the time of acute lesions. A similar increase was not seen for HSV patients. The data are the first report implicating CD34+ cells in HAEM pathogenesis, likely by transporting HSV DNA fragments to lesional skin.