COMPUTERIZED SOFTWARE QUALITY EVALUATION WITH NOVEL ARTIFICIAL INTELLIGENCE APPROACH

Software quality assurance has grown in importance in the fast-paced world of software development. One of trickiest parts of creating and maintaining software is predicting how well it will perform. The term "computer evaluation" refers to use of advanced AI techniques in software quality assurance, replacing human evaluations and paving the way for a new era in software evaluation. We proposed Hybrid Elephant herding optimized Conditional Long short-term memory (HEHO-CLSTM) to estimate Software Quality Prediction. Software quality prediction and assurance has grown in importance in ever-changing world of software development. Software quality prediction encompasses a wide range of activities aimed at improving the quality of software systems via the use of data-driven approaches for prediction, evaluation and enhancement. We have collected Software Defects data and we feature extracted the attributes using linear discriminant Analysis (LDA). The suggested system improves the accuracy, AUC and Buggy instance compared with the current methods

Designing a Renewable Energy System for Industrial IoT with Artificial Intelligence

This paper reviews the integration of renewable energy systems with Industrial IoT (IIoT) through Artificial Intelligence (AI). It examines various studies focusing on the design and monitoring of solar-powered wireless sensor nodes in diverse IIoT settings, particularly outdoors. A proposed distributed network architecture, underpinned by open-source technologies, aims for efficient solar power harvesting and data acquisition on solar radiation and ambient parameters. This data aids in devising estimation techniques to predict solar panel voltage outputs, optimizing energy utilisation of solar-powered sensor nodes. The discourse extends to photovoltaic plants, emphasising continuous monitoring and fault detection for operational safety and reliability. Reviewed works advocate embedding AI and IoT for remote sensing, fault detection, and diagnosis, addressing challenges posed by undetectable faults. Furthermore, the paper explores AI’s transformative potential in the broader energy sector, impacting electricity production, distribution, energy storage, and efficiency. The synergy of AI, IIoT, and renewable energy systems is underscored as a conduit for enhancing energy management, operational transparency, and deploying cost-effective solutions for complex industrial challenges, significantly bolstering the efficiency and intelligence of industrial production and services

Defective Molecular Timer in the Absence of Nucleotides Leads to Inefficient Caspase Activation

In the intrinsic death pathway, cytochrome C (CC) released from mitochondria to the cytosol triggers Apaf-1 apoptosome formation and subsequent caspase activation. This process can be recapitulated using recombinant Apaf-1 and CC in the presence of nucleotides ATP or dATP [(d)ATP] or using fresh cytosol and CC without the need of exogenous nucleotides. Surprisingly, we found that stored cytosols failed to support CC-initiated caspase activation. Storage of cytosols at different temperatures led to the loss of all (deoxy)nucleotides including (d)ATP. Addition of (d)ATP to such stored cytosols partially restored CC-initiated caspase activation. Nevertheless, CC could not induce complete caspase-9/3 activation in stored cytosols, even with the addition of (d)ATP, despite robust Apaf-1 oligomerization. The Apaf-1 apoptosome, which functions as a proteolytic-based molecular timer appeared to be defective as auto-processing of recruited procaspase-9 was inhibited. Far Western analysis revealed that procaspase-9 directly interacted with Apaf-1 and this interaction was reduced in the presence of physiological levels of ATP. Co-incubation of recombinant Apaf-1 and procaspase-9 prior to CC and ATP addition inhibited CC-induced caspase activity. These findings suggest that in the absence of nucleotide such as ATP, direct association of procaspase-9 with Apaf-1 leads to defective molecular timer, and thus, inhibits apoptosome-mediated caspase activation. Altogether, our results provide novel insight on nucleotide regulation of apoptosome

Combination therapy induces unfolded protein response and cytoskeletal rearrangement leading to mitochondrial apoptosis in prostate cancer

Development of therapeutic resistance is responsible for most prostate cancer (PCa) related mortality. Resistance has been attributed to an acquired or selected cancer stem cell phenotype. Here we report the histone deacetylase inhibitor apicidin (APC) or ER stressor thapsigargin (TG) potentiate paclitaxel (TXL)‐induced apoptosis in PCa cells and limit accumulation of cancer stem cells. TXL‐induced responses were modulated in the presence of TG with increased accumulation of cells at G1‐phase, rearrangement of the cytoskeleton, and changes in cytokine release. Cytoskeletal rearrangement was associated with modulation of the cytoplasmic and mitochondrial unfolded protein response leading to mitochondrial dysfunction and release of proapoptotic proteins from mitochondria. TXL in combination with APC or TG enhanced caspase activation. Importantly, TXL in combination with TG induced caspase activation and apoptosis in X‐ray resistant LNCaP cells. Increased release of transforming growth factor‐beta (TGF‐β) was observed while phosphorylated β‐catenin level was suppressed with TXL combination treatments. This was accompanied by a decrease in the CD44+CD133+ cancer stem cell‐like population, suggesting treatment affects cancer stem cell properties. Taken together, combination treatment with TXL and either APC or TG induces efficient apoptosis in both proliferating and cancer stem cells, suggesting this therapeutic combination may overcome drug resistance and recurrence in PCa

Mitochondrial dysfunction-mediated apoptosis resistance associates with defective heat shock protein response in African-American men with prostate cancer

African-American (AA) patients with prostate cancer (PCa) respond poorly to current therapy compared with Caucasian American (CA) PCa patients. Although underlying mechanisms are not defined, mitochondrial dysfunction is a key reason for this disparity. Cell death, cell cycle, and mitochondrial function/stress were analysed by flow cytometry or by Seahorse XF24 analyzer. Expression of cellular proteins was determined using immunoblotting and real-time PCR analyses. Cell survival/motility was evaluated by clonogenic, cell migration, and gelatin zymography assays. Glycolytic pathway inhibitor dichloroacetate (DCA) inhibited cell proliferation in both AA PCa cells (AA cells) and CA PCa cells (CA cells). AA cells possess reduced endogenous reactive oxygen species, mitochondrial membrane potential (mtMP), and mitochondrial mass compared with CA cells. DCA upregulated mtMP in both cell types, whereas mitochondrial mass was significantly increased in CA cells. DCA enhanced taxol-induced cell death in CA cells while sensitising AA cells to doxorubicin. Reduced expression of heat shock proteins (HSPs) was observed in AA cells, whereas DCA induced expression of CHOP, C/EBP, HSP60, and HSP90 in CA cells. AA cells are more aggressive and metastatic than CA cells. Restoration of mitochondrial function may provide new option for reducing PCa health disparity among American men

Stored cytosols require exogenous nucleotides to support CC-initiated caspase activation.

<p><b>A</b>, GM701 cytosols (250 µg) either freshly purified or stored at 4°C for 5 days were incubated with CC (15 µg/ml) for 150 min at 37°C. At the end of incubation, reaction mixtures were subjected to Western blotting for caspase-9 and caspase-3. <b>B and C</b>, GM701 cytosols (250 µg) either freshly purified or stored at 4°C for 5 days were incubated with CC in the absence or presence of dATP (200 µM). Some reaction mixtures were supplemented with recombinant Apaf-1 (A1) or procaspase-9 (C9) or procaspase-3 (C3) to assess if these molecules were inactivated during storage. <b>D and E</b>, HCT116 cytosols either freshly purified or stored at 4°C for 5 days were incubated with CC. At the end of incubation, aliquots were used in activity assays for caspase-9 and caspase-3. Procasp-9, procaspase-9; procasp-3, procaspase-3; CC, cytochrome c.</p

Exogenous dATP restores CC-initiated caspase activation.

<p><b>A</b>, GM701 cytosols stored at 4°C for 5 days were incubated with increasing amounts of CC in the absence (lanes 1–6) or presence (lanes 7–11) of dATP (1 mM). <b>B,</b> Cytosol stored at −20°C for 15 days were incubated with CC in the absence or presence of ATP (1 mM). At the end of incubation, samples were subjected to Western blotting for caspase-9 or caspase-3. <b>C,</b> Cytosols stored at 4°C for 5 days were subjected to Western blotting to detect the levels of indicated proteins. Procasp-9, procaspase-9; Procasp-3, procaspase-3; CC, cytochrome c.</p

Changes in nucleotide levels during storage at different temperatures^*.

<p>*Cytosols obtained from GM701 cells were stored at different temperatures for the time intervals indicated and then nucleotides levels were measured using HPLC. Values represent the mean (nmoles/mg protein) derived from two independent measurements (values in the parentheses represent percentage changes compared to the fresh cytosol).</p

Oligomerized Apaf-1 in stored cytosol fails to activate caspase-3.

<p><b>A–B</b>, GM701 cytosols either freshly prepared or stored at −20°C for 15 days were incubated with CC in the absence (for fresh cytosol) or presence (for stored cytosol) of dATP. At the end of incubation, samples were fractionated on superose-6 gel filtration column on AKTA FPLC machine. 20 µl of fractions 10–14 were used for caspase processing activity (CPA) measurement (<b>A</b>) by incubating with 100 nM recombinant procaspase-3 (C3) and 100 nM of procaspase-9 (C9) for 90 min at 30°C followed by DEVDase activity measurement. (<b>B</b>) CPA measurement in fractions 11–13. Shown are the mean ± S.D (n = 2). CPA activities are presented as arbitrary unit.</p

Procaspase-9 interacts with Apaf-1 in the absence of ATP, whereas physiological levels of ATP disrupt Apaf-1-procaspase-9 interaction, and prior incubation of Apaf-1 with procaspase-9 leads to defective apoptosome.

<p><b>A</b>, 500 ng of recombinant Apaf-1 or bovine serum albumin (BSA) were immobilized on PVDF membrane. Membrane was then incubated with procaspase-9 (500 ng) in the absence or presence of physiological levels of ATP (2 mM) followed by Western blotting for caspase-9. Left panel represents coomassie stained gel image. <b>B,</b> To induce defective apoptosome formation, recombinant Apaf-1 was pre-incubated with procaspase-9 for 30 min at 4°C followed by the addition of procaspase-3, CC, and ATP (200 µM). Caspase-3 activity presented as DEVDase activity. Control, Apaf-1+procaspase-9+procaspase-3; apoptosome, Apaf-1+procaspase-9+procaspase-3+CC+ATP. Apopto, apoptosome.</p