CheapNET: Improving Light-weight speech enhancement network by projected loss function

Noise suppression and echo cancellation are critical in speech enhancement and essential for smart devices and real-time communication. Deployed in voice processing front-ends and edge devices, these algorithms must ensure efficient real-time inference with low computational demands. Traditional edge-based noise suppression often uses MSE-based amplitude spectrum mask training, but this approach has limitations. We introduce a novel projection loss function, diverging from MSE, to enhance noise suppression. This method uses projection techniques to isolate key audio components from noise, significantly improving model performance. For echo cancellation, the function enables direct predictions on LAEC pre-processed outputs, substantially enhancing performance. Our noise suppression model achieves near state-of-the-art results with only 3.1M parameters and 0.4GFlops/s computational load. Moreover, our echo cancellation model outperforms replicated industry-leading models, introducing a new perspective in speech enhancement

Heating control strategy for variable refrigerant flow air conditioning system with multi-module outdoor units

The heating control strategy is key technology for stable and reliable heating operation of variable refrigerant flow air conditioning system with multi-module outdoor units. The synoptic control strategy is that the host module coordinates the system operation and adjusts the operation frequency of every module based on equal frequency allocation principle for suction pressure balance among modules. The heating control model including heating frequency adjustment, module switching condition and frequency allocation model has been built. Considering the discharge pressure disturbance, a certain discharge pressure region is taken as the control objective to adjust the frequency. And considering the lag between pressure and frequency, the restriction condition of discharge pressure and a certain judgment time are introduced into the model to avoid frequent module switching. Furthermore, different frequency allocation models have been built for increase and decrease of module number. In the model, when the module number increases and evenly allotted frequency to every module is less 70 Hz, one or two certain frequencies 70 Hz are distributed to the pre-existing thermo-on module(s) and the remaining frequency is distributed to ensuing thermo-on module so as to avoid sharp frequency fluctuation and inferior heating effect. Experiments demonstrate the feasibility of the control strategy. (C) 2010 Elsevier B.V. All rights reserved

Education Assistance to Africa: We Can Do More and Better

Education Assistance to Africa, Global governance, One harmonious world, I21,

Peptides derived from the integrin β cytoplasmic tails inhibit angiogenesis

Abstract Background Integrins are essential regulators of angiogenesis. However, the antiangiogenic potential of peptides derived from the integrin cytoplasmic tails (CT) remains mostly undetermined. Methods Here we designed a panel of membrane-penetrating peptides (termed as mβCTPs), each comprising a C-terminal NxxY motif from one of the conserved integrin β CTs, and evaluated their antiangiogenic ability using both in vitro and in vivo approaches. Results We found that mβ3CTP, mβ5CTP and mβ6CTP, derived respectively from the integrin β3, β5 and β6 CTs, but not others, exhibit antiangiogenic ability. Interestingly, we observed that the integrin β3, β5 and β6 CTs but not others are able to interact with β3-endonexin. In addition, the antiangiogenic core in mβ3CTP is identical to a previously identified β3-endonexin binding region in the integrin β3 CT, indicating that the antiangiogenic mβCTPs may function via their binding to β3-endonexin. Consistently, knockdown of endogenous β3-endonexin in HUVECs significantly suppresses tube formation, suggesting that β3-endonexin is proangiogenic. However, neither treatment with the antiangiogenic mβCTPs nor knockdown of endogenous β3-endonexin affects integrin-mediated HUVEC adhesion and migration, indicating that their antiangiogenic effect may not rely on directly regulating integrin activity. Importantly, both treatment with the antiangiogenic mβCTPs and knockdown of endogenous β3-endonexin in HUVECs inhibit VEGF expression and cell proliferation, thereby providing mechanistic explanations for the functional consequences. Conclusion Our results suggest that the antiangiogenic mβCTPs can interact with β3-endonexin in vascular endothelial cells and suppress its function in regulating VEGF expression and cell proliferation, thus disclosing a unique pathway that may be useful for developing novel antiangiogenic strategies

Additional file 1: of Peptides derived from the integrin β cytoplasmic tails inhibit angiogenesis

Figure S1. mβ3CTP is membrane-permeable. The peptides of mβ3CTP (a) and β3CTP (b) were Nterminally conjugated with FITC and used to incubate with HUVECs, and the signal of FITC in HUVECs was evaluated under fluorescent microscopy. Scale bar, 15 μm. Figure S2. The antiangiogenic peptides do not suppress RM1 cancer cell proliferation. RM1 cancer cells were treated with mβ3CTP or mβ5CTP (each at 20 μM) and their effects on cell proliferation were evaluated using CCK-8 cell proliferation assay. Cells without treatment were used as a control. Figure S3. Both mβ3CTP and mβ5CTP suppress in vivo tumor growth. RM1 cancer cells were subcutaneously injected into BALB/c nude mice. Mice were treated with mβ3CTP and mβ5CTP as described in Methods. PBS alone was used as a control. Mice were sacrificed at the end point and tumor tissues were isolated and photographed. Figure S4. mβ3CTP and mβ5CTP fail to affect VEGF-induced HUVEC adhesion and migration on vitronectin. a HUVECs were treated with the indicated mβCTPs (20 μM) and allowed to adhere to immobilized vitronectin for 30 min in the absence or presence of VEGF (20 ng/ml). b HUVECs were treated with the indicated mβCTPs (20 μM) and allowed to migrate on Transwell membrane coated with vitronectin for 8 h in the presence of VEGF (20 ng/ml). The adhered and migrated cells were fixed, stained, photographed and counted (*, p < 0.05; **, p < 0.01). Figure S5. The antiangiogenic mβCTPs and siRNA against β3-endonexin suppress HUVEC proliferation. HUVECs were treated with the indicated mβCTPs (a) or siRNA against β3-endonexin (b). Their effects on cell proliferation were evaluated using the MTT assay (**, p < 0.01). (PDF 230 kb