DYNAMITE: Dynamic Interplay of Mini-Batch Size and Aggregation Frequency for Federated Learning with Static and Streaming Dataset

Federated Learning (FL) is a distributed learning paradigm that can coordinate heterogeneous edge devices to perform model training without sharing private data. While prior works have focused on analyzing FL convergence with respect to hyperparameters like batch size and aggregation frequency, the joint effects of adjusting these parameters on model performance, training time, and resource consumption have been overlooked, especially when facing dynamic data streams and network characteristics. This paper introduces novel analytical models and optimization algorithms that leverage the interplay between batch size and aggregation frequency to navigate the trade-offs among convergence, cost, and completion time for dynamic FL training. We establish a new convergence bound for training error considering heterogeneous datasets across devices and derive closed-form solutions for co-optimized batch size and aggregation frequency that are consistent across all devices. Additionally, we design an efficient algorithm for assigning different batch configurations across devices, improving model accuracy and addressing the heterogeneity of both data and system characteristics. Further, we propose an adaptive control algorithm that dynamically estimates network states, efficiently samples appropriate data batches, and effectively adjusts batch sizes and aggregation frequency on the fly. Extensive experiments demonstrate the superiority of our offline optimal solutions and online adaptive algorithm.Comment: 20 pages, 12 figure

Septin6 as a new approach for AD treatment

The number of Alzheimer’s disease (AD) patients is increasing and new therapeutic approaches need to be proposed urgently. In recent years, some researchers have focused on the relationship between calcium homeostasis and AD; however, selective regulation of abnormal calcium signaling pathways and related targets of action remain unclear, presenting a challenge. Gerard Griffioen’s team in Belgium has proposed a self-reinforcing amplification between cytoplasmic calcium concentration [Ca 2+ ] cyto and AD pathology in previous studies, discovering a new kind of small-molecule scaffold protein. The protein, ReS19-T, can stabilize the structure of septin filaments and significantly improve the core pathology of AD by inhibiting the pathological activation of store-operated calcium entry (SOCE) and restoring calcium homeostasis, thereby suggesting a new avenue for therapeutic intervention. However, there is still a way to go before clinical application. There are some questions. SEP2/6/7 hexamer plays a role in maintaining immune function, so could ReS19-T affect this function and impact immune responses? Moreover, both Stim1 and Orai (affected by TRPC) contribute to SOCE. The TRPC-specific inhibitor SKF-96365 is highly selective, and its relationship with AD remains to be investigated. Future studies might use SKF-96365 to validate the therapeutic effect of Res19-T. In conclusion, Septin6 as a new approach to AD treatment expects more relevant research to emerge

Development of a sensitive direct competitive chemiluminescent enzyme immunoassay for gentamicin based on the construction of a specific single-chain variable fragment-alkaline phosphatase fusion protein

A sensitive chemiluminescent enzyme immunoassay (CLEIA) was established for the determination of gentamicin (GEN) residue levels in animal tissue. This assay is based on a fusion protein of single-chain variable fragment (scFv) and alkaline phosphatase (AP). Initially, VL and VH derived from anti-gentamicin monoclonal antibody were linked by a short peptide to construct a scFv. Subsequently, the constructed scFv sequence was accessed into the pLIP6/GN vector, and a soluble scFv-AP fusion protein was generated. The scFv-AP fusion protein was used to develop a direct competitive CLEIA (dcCLEIA) for the determination of gentamicin. In the dcCLEIA, the half inhibitory concentration (IC50) and limit of detection (LOD) were 1.073 ng/mL and 0.380 ng/mL, respectively. The average recoveries of gentamicin spiked in animal tissue samples ranged from 78% to 96%. These results showed a strong correlation with ultra performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). The above results suggest that the anti-GEN scFv-AP fusion protein is suitable for detecting gentamicin residues in edible animal tissues

Association between prophylactic hydration volume and risk of contrast-induced nephropathy after emergent percutaneous coronary intervention

Background: Intravenous hydration during percutaneous coronary intervention (PCI) significantly reduces the risk of contrast-induced nephropathy (CIN), but there are no well-defined protocols regard¬ing the optimal hydration volume (HV) required to prevent CIN following emergent PCI. Therefore, this study investigates the association between the intravenous HV and CIN after emergent PCI. Methods: 711 patients were prospectively recruited who had underwent emergent PCI with hydration at routine speed and the relationship was investigated between HV or HV to weight ratio (HV/W) and the CIN risk, which was defined as a ≥ 25% or ≥ 0.5 mg/dL increase in serum creatinine levels from baseline within 48–72 h of exposure to the contrast. Results: The overall CIN incidence was 24.7%. Patients in the higher HV quartiles had elevated CIN rates. Multivariate analysis showed that higher HV/W ratios were not associated with a decreased risk (using the HV) of CIN, but they were associated with an increased risk (using the HV/W) of CIN (Q4 vs. Q1: adjusted odds ratio 1.99; 95% confidence interval 1.05–3.74; p = 0.034). A higher HV/W ratio was not significantly associated with a reduced risk of long-term death (all p > 0.05). Conclusions: The data suggests that a higher total HV is not associated with a decreased CIN risk or beneficial long-term prognoses, and that excessive HV may increase the risk of CIN after emergent PCI

Targeting the BRD4/FOXO3a/CDK6 Axis Sensitizes AKT Inhibition in Luminal Breast Cancer

BRD4 assembles transcriptional machinery at gene super-enhancer regions and governs the expression of genes that are critical for cancer progression. However, it remains unclear whether BRD4-mediated gene transcription is required for tumor cells to develop drug resistance. Our data show that prolonged treatment of luminal breast cancer cells with AKT inhibitors induces FOXO3a dephosphorylation, nuclear translocation, and disrupts its association with SirT6, eventually leading to FOXO3a acetylation as well as BRD4 recognition. Acetylated FOXO3a recognizes the BD2 domain of BRD4, recruits the BRD4/RNAPII complex to the CDK6 gene promoter, and induces its transcription. Pharmacological inhibition of either BRD4/FOXO3a association or CDK6 significantly overcomes the resistance of luminal breast cancer cells to AKT inhibitors in vitro and in vivo. Our study reports the involvement of BRD4/FOXO3a/CDK6 axis in AKTi resistance and provides potential therapeutic strategies for treating resistant breast cancer