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Amer, T.

Publications and source records attributed to Amer, T..

2 recordsLinked to original sources

Early Diagnosis of Parkinson via Transient Beta Frequencies in a Delayed Van der Pol Model

Biological motor circuits are shaped by pathway-specific delays that generate history-dependent oscillations and short-lived transients not captured by memoryless models. We develop a delayed Van der Pol in which the delay ratio r acts as a control parameter for Hopf bifurcation and internal resonance and we pair it with an auditable, short-window signal-processing pipeline tailored to early beta activity. The pipeline combines Short-Time Fourier Transform (STFT), Continuous Wavelet Transform (CWT) ridge tracking, kernel-density estimates (KDE) of the dominant frequency, and algorithmic beta-burst detection under fixed, shared parameters. Transient burden is quantified by a metric triplet with a software-implementable attenuation rule and complemented by an early-detection index-the Transient Persistence Time. Across methods, we observe a monotonic attenuation of short-lived beta transients as r approaches a critical band. A reliable observation window of 0 - 0.35 s captures compact early packets at low r, progressive ridge stabilization in CWT, KDE narrowing over time, and near-elimination of bursts for near critical r, consistent with a transition to sustained narrowband rhythm. Clinically, these measures enable stage inference, a bedside Move-Stop protocol for rapid readout, and actionable policies for adaptive DBS and medication titration that minimize transient burden without inducing rigid locking. The fixed parameterization and audit-ready outputs support reproducibility and multi-center deployment. This framework advances data-driven, precision neuromodulation by targeting early transients before pathological synchrony becomes entrenched.

neuroscience↗

The Second Mitochondrial Activator of Caspases (SMAC) regulates growth, inflammation and mitochondrial integrity in cancer cells

SMAC is a mitochondrial intermembrane space protein, which is released during apoptosis and whose known function is antagonism of inhibitor of apoptosis proteins in the cytosol, to facilitate caspase activation. Recent data suggest that SMAC can also be released by sub-lethal signals in the apoptosis pathway, in the absence of cell death. We here explored potential functions of SMAC in non-apoptotic cells. We found that a portion of SMAC is spontaneously released into the cytosol in the absence of apoptosis, regulated by the BCL-2-family proteins BAX and BAK and the fission GTPase DRP1. In cancer cell lines, SMAC was required for the activation of caspases in lethal and non-lethal conditions, while this contribution to caspase-activation was much smaller in non-malignant fibroblast lines. In cells with high levels of cytosolic SMAC, SMAC deficiency reduced in vitro migration, invasion and anchorage-independent growth. SMAC-deficient cells further showed a reduced activity in interferon signalling, associated with reduced cytosolic presence of mitochondrial DNA and activation of the stimulator of interferon genes (STING), and SMAC expression levels correlated with interferon-induced genes in cancer data sets. We further found that SMAC can regulate mitochondrial morphology and integrity. Finally, high gene-expression of SMAC was associated with poor prognosis in patients of several cancer types. These results identify SMAC as a regulator of inflammation and growth behaviour of cancer cells. They further report a mitochondrial function of SMAC and demonstrate a role of SMAC in human cancer biology across several cancer entities.

cell biology↗