Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

OBJECTIVETo find sensitive and specific laboratory examination items for early diagnosing and monitoring liver transplantation reject reaction.

METHODSRandomly investigate 41 liver transplantation patients, among them there were 16 patients with reject reaction (including 12 with acute rejection, 4 with chronic rejection). Plasma soluble thrombomodulin (STM) and von Willebrand factor (vWF) levels were measured before operation and every other day after operation.

RESULTSPlasma STM level increased significantly after operation, two days before rejection and after acute rejection (5.58 ng/ml +/- 0.42 ng/ml, 5.93 ng/ml +/- 0.45 ng/ml, and 7.88 ng/ml +/- 0.29 ng/ml, respectively), so did vWF level (101.2% +/- 4.68%, 104.3% +/- 5.78%, and 127.7% +/- 5.74%, respectively). STM level was much higher in acute rejection than that in chronic rejection (7.88 ng/ml +/- 0.29 ng/ml vs. 6.35 ng/ml +/- 0.54 ng/ml, t = 2.46, P < 0.05), in no reaction group after impacting therapy than in effective group (8.30 ng/ml +/- 0.19 ng/ml vs. 3.82 ng/ml +/- 0.22 ng/ml, t = 12.98, P < 0.01), and in dead group after treatment than in living group (7.98 ng/ml +/- 0.18 ng/ml vs. 6.51 ng/ml +/- 0.41 ng/ml, t = 3.39, P < 0.01).

CONCLUSIONSPlasma STM and vWF can be taken as laboratory items for monitoring liver transplantation rejection. Plasma STM can act as not only an early prognosticating marker, but also suitable to distinguish acute from chronic reject reaction, and as a marker for monitoring impacting therapy effect and judging prognosis.

Adolescent ; Adult ; Biomarkers ; blood ; Female ; Graft Rejection ; Humans ; Liver Transplantation ; adverse effects ; Male ; Middle Aged ; Thrombomodulin ; blood ; von Willebrand Factor ; analysis

OBJECTIVETo retrospectively analyze the curative effects and prognostic factors of HLA-matched sibling donor allogeneic hematopoietic stem cell transplantation (allo-HSCT) for chronic myelogenous leukemia patients (CML).

METHODSOf the 35 CML patients, 26 were males and 9 were females, with a median age of 32 (12 - 50) years. 30 patients were in chronic phase of CML, 5 patients were in accelerated phase. Allo-HSCT from HLA identical siblings was performed for 35 patients, of whom 11 received bone marrow transplantation (BMT) and 24 peripheral blood stem cell transplantation (PBSCT). Conditioning regimens was TBI (total-body irradiation) + CY (CTX) protocol in 8 patients and BU/CY protocol in 27 patients. The average follow-up was 48 months (range 7 - 108 months).

RESULTS34 (97.1%) patients were successfully engrafted. Among them, 21 patients (60.0%) had three years disease-free (DFS) survival. The overall 5-year survival (OS) was 57.1%. Two patients (5.7%) relapsed. Transplant-related mortality occurred in 12 patients. Hemorrhagic cystitis (HC) occurred in 5 patients and HVOD was observed in 1 patient. Acute graft-versus-host disease (aGVHD) occurred in 18 patients (51.4%), among them 7 patients (20.0%) were of grade III-IV. Chronic GVHD was in 17 patients (48.5%). There was no significant difference in 3-years DFS between BMT group and PBSCT group (54.5% vs. 62.5%, P > 0.05). The 3-year disease-free survival (DFS) was 42.9% in TBI/CY group and 55.6% in BU/CY group (P > 0.05). In univariate prognostic analysis model, the DFS at 3 years is 75% and 47.4% for < or =30 years patients and >30 years patients, respectively, P < 0.05. The 3-year DFS of patients with first chronic phase is higher than patients with advanced diseases (61.3% vs. 40%, P < 0. 05). The 3-year DFS in patients of grade I - II GVHD was higher than that in patients of grade III-IV GVHD (81.8% vs. 14.3%, P < 0.05).

CONCLUSIONThe patients who had transplantation done within 1 year after diagnosis during their first chronic phase of disease and who had low-grade GVHD have better prognosis. Those patients who had III-IV acute GVHD are prone to incorporate severe infection, which was a worse prognostic factor of allo-HSCT for chronic myelogenous leukemia.

Adolescent ; Adult ; Age Factors ; Child ; Cystitis ; etiology ; Disease-Free Survival ; Female ; Follow-Up Studies ; Graft vs Host Disease ; etiology ; Hematopoietic Stem Cell Transplantation ; adverse effects ; methods ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; mortality ; therapy ; Male ; Middle Aged ; Recurrence ; Retrospective Studies ; Siblings ; Survival Rate ; Transplantation Conditioning ; Transplantation, Homologous

Background: Children and young refugees often experience negative events that affect their mental health. Their caregivers may also be in the same predicament, implying that the teachers in schools are a potential source of help and support. However, most teachers have little understanding of mental health and are, thus, clueless in helping their students. To address this need, a newly developed one-day mental health literacy programme was conducted among 68 refugee teachers in Malaysia. Methods: Participants learned the symptoms of mental health issues among children and adolescents in the context of post-trauma, provision of early intervention, and channel for professional supports. They also answered a packet of measurements of mental health literacy before and after the programme. Results: The paired sample t-test showed that participants reported higher willingness to contact with people having mental health problems (t = 2.787, P = 0.008, Cohen’s d = 0.394), less stereotypes toward mental illness (t = 4.603, P < 0.001, d = 0.651) and a better understanding of self-help strategies (t = 2.16, P = .036, d = 0.322) than baseline. Conclusion: The results of this study offered preliminary empirical evidence on the effectiveness of the programme as a promising channel for alleviating mental health issues among refugees.

Objective To investigate suitable condition for extraction of the active components from Ajuga nipponensis (A. nipponensis). Methods Orthogonal experimental design was used to determine the optimal extraction parameters for ecdysterones and flavonoids. Finally, the hepatoprotective abilities of A. nipponensis extracts were evaluated by CCl