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In recent years, grid-connected multifunctional photovoltaic (PV) systems have proven to be highly efficient. This system integrates PV panels with a DC-DC boost converter (DC-DC-BC) and the electrical distribution grid (DEG). Linking the PV to the AC-DEG is accomplished through a three-level multifunctional voltage source inverter (MVSI). The DC-DC-BC component in this study is engineered to perform maximum power point tracking (MPPT) irrespective of normal or abnormal conditions. The conventional MPPT technique poses several challenges and constraints on system usage. Hence, the suggestion is to adopt synergetic control (SC) and sliding mode control (SMC) to enhance the MPPT technique's performance within the proposed system framework. Moreover, predictive direct power control is applied to the MVSI-based shunt active power filter, utilizing a phase-locked loop technique to achieve multiple objectives: minimizing energy fluctuations, injecting active power, correcting power factors, compensating reactive power, and mitigating harmonic currents. To implement the proposed system, the MATLAB is used for this purpose, with several tests used to study the behavior of the controls proposed in this work. Numerical results indicate significant reductions in active and reactive power fluctuations, with estimated rates of 38.46% and 15.30%, respectively, compared to traditional strategies. Moreover, the total harmonic distortion (THD) of the source current after filtering is reduced by 31.88% under solar irradiation of G = 1000 Wm 2 . Before filtering, the THD of current experiences a reduction estimated at 97.65%. These findings underscore the superior performance of the proposed control technique across all evaluated aspects., (© 2024. The Author(s).)

Diets rich in saturated fats may contribute to the loss of pancreatic β-cells in type 2 diabetes. JunB, a member of the activating protein 1 (AP-1) transcription factor family, promotes β-cell survival and mediates part of the beneficial effects of GLP-1 agonists. In this study we interrogated the molecular mechanisms involved in JunB-mediated β-cell protection from lipotoxicity. The saturated fatty acid palmitate decreased JunB expression, and this loss may contribute to β-cell apoptosis, as overexpression of JunB protected cells from lipotoxicity. Array analysis of JunB-deficient β-cells identified a gene expression signature of a downregulated endoplasmic reticulum (ER) stress response and inhibited AKT signaling. JunB stimulates XBP1 expression via the transcription factor c/EBPδ during ER stress, and forced expression of XBP1s rescued the viability of JunB-deficient cells, constituting an important antiapoptotic mechanism. JunB silencing inhibited AKT activation and activated the proapoptotic Bcl-2 protein BAD via its dephosphorylation. BAD knockdown reversed lipotoxic β-cell death potentiated by JunB siRNA. Interestingly, XBP1s links JunB and AKT signaling as XBP1 knockdown also reduced AKT phosphorylation. GLP-1 agonists induced cAMP-dependent AKT phosphorylation leading to β-cell protection against palmitate-induced apoptosis. JunB and XBP1 knockdown or IRE1 inhibition decreased AKT activation by cAMP, leading to β-cell apoptosis. In conclusion, JunB modulates the β-cell ER stress response and AKT signaling via the induction of XBP1s. The activation of the JunB gene network and the crosstalk between the ER stress and AKT pathway constitute a crucial defense mechanism by which GLP-1 agonists protect against lipotoxic β-cell death. These findings elucidate novel β-cell-protective signal transduction in type 2 diabetes.

Destruction of insulin-producing pancreatic β-cells by local autoimmune inflammation is a hallmark of type 1 diabetes. Histochemical analysis of pancreases from non-obese diabetic mice indicated activation of the transcription factor JunB/AP-1 (activator protein-1) after autoimmune infiltration of the islets. In vitro studies demonstrated that the cytokines tumor necrosis factor (TNF)-α and interferon (IFN)-γ induce JunB expression as a protective mechanism against apoptosis in both human and rodent β-cells. The gene network affected was studied by microarray analysis showing that JunB regulates nearly 20% of the cytokine-modified β-cell genes, including the transcription factor ATF3. Direct transcriptional induction of ATF3 by JunB is a key event for β-cell survival after TNF-α+IFN-γ treatment. Moreover, pharmacological upregulation of JunB/ATF3 via increased cAMP protected rodent primary β-cells and human islet cells against pro-inflammatory mediators. These results were confirmed in genetically modified islets derived from Ubi-JunB transgenic mice. Our findings identify ATF3 as a novel downstream target of JunB in the survival mechanism of β-cells under inflammatory stress.