Force: Making 4PC > 4 × PC in Privacy Preserving Machine Learning on GPU

Tremendous efforts have been made to improve the efficiency of secure Multi-Party Computation (MPC), which allows n ≥ 2 parties to jointly evaluate a target function without leaking their own private inputs. It has been confirmed by previous researchers that 3-Party Computation (3PC) and outsourcing computations to GPUs can lead to huge performance improvement of MPC in computationally intensive tasks such as Privacy-Preserving Machine Learning (PPML). A natural question to ask is whether super-linear performance gain is possible for a linear increase in resources. In this paper, we give an affirmative answer to this question. We propose Force, an extremely efficient 4PC system for PPML. To the best of our knowledge, each party in Force enjoys the least number of local computations and lowest data exchanges between parties. This is achieved by introducing a new sharing type X -share along with MPC protocols in privacy-preserving training and inference that are semi-honest secure with an honest-majority. Our contribution does not stop at theory. We also propose engineering optimizations and verify the high performance of the protocols with implementation and experiments. By comparing the results with state-of-the-art researches such as Cheetah, Piranha, CryptGPU and CrypTen, we showcase that Force is sound and extremely efficient, as it can improve the PPML performance by a factor of 2 to 1200 compared with other latest 2PC, 3PC and 4PC syste

HSPA12A Unstabilizes CD147 to Inhibit Lactate Export and Migration in Human Renal Cell Carcinoma

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. Background: Metastasis accounts for 90% of cancer-associated mortality in patients with renal cell carcinoma (RCC). However, the clinical management of RCC metastasis is challenging. Lactate export is known to play an important role in cancer cell migration. This study investigated the role of heat shock protein A12A (HSPA12A) in RCC migration. Methods: HSPA12A expression was examined in 82 pairs of matched RCC tumors and corresponding normal kidney tissues from patients by immunoblotting and immunofluorescence analyses. The proliferation of RCC cells was analyzed using MTT and EdU incorporation assays. The migration of RCC cells was evaluated by wound healing and Transwell migration assays. Extracellular acidification was examined using Seahorse technology. Protein stability was determined following treatment with protein synthesis inhibitor cycloheximide and proteasome inhibitor MG132. Mass spectrometry, immunoprecipitation, and immunoblotting were employed to examine protein-protein interactions. Results: RCC tumors from patients showed downregulation of HSPA12A, which was associated with advanced tumor node metastasis stage. Intriguingly, overexpression of HSPA12A in RCC cells inhibited migration, whereas HSPA12A knockdown had the opposite effect. Lactate export, glycolysis rate, and CD147 protein abundance were also inhibited by HSPA12A overexpression but promoted by HSPA12A knockdown. An interaction of HSPA12A with HRD1 ubiquitin E3 ligase was detected in RCC cells. Further studies demonstrated that CD147 ubiquitination and proteasomal degradation were promoted by HSPA12A overexpression whereas inhibited by HSPA12A knockdown. Notably, the HSPA12A overexpression-induced inhibition of lactate export and migration were abolished by CD147 overexpression. Conclusion: Human RCC shows downregulation of HSPA12A. Overexpression of HSPA12A in RCC cells unstabilizes CD147 through increasing its ubiquitin-proteasome degradation, thereby inhibits lactate export and glycolysis, and ultimately suppresses RCC cell migration. Our results demonstrate that overexpression of HSPA12A might represent a viable strategy for managing RCC metastasis

PDRPS7 protects cardiac cells from hypoxia/reoxygenation injury through inactivation of JNKs

Myocardial ischemia/reperfusion (I/R) injury is a major complication of reperfusion therapy in myocardial infarction. Ischemic myocardium produces a variety of peptides. We recently identified PDRPS7 as a novel peptide in cardiomyocytes that can be induced by hypoxia. However, the role of PDRPS7 is unknown. Here, we investigated the effects of PDRPS7 on hypoxia/reoxygenation (H/R)‐induced injury in rat cardiomyoblast H9c2 cells and NRCMs. We found that PDRPS7 improved cell survival and attenuated lactate dehydrogenase leakage following H/R in H9c2 cells and NRCMs. PDRPS7 also alleviated H/R‐induced pulsation reduction in NRCMs. Moreover, H/R‐induced cell apoptosis was decreased in the presence of PDRPS7. H/R‐induced reactive oxygen species generation was reduced by PDRPS7; in addition, PDRPS7 did not impact H2O2‐induced cell injury. Signaling analysis demonstrated that H/R increased the phosphorylation levels of JNKs, ERKs, and p38 mitogen‐activated protein kinases. However, PDRPS7 only attenuated H/R‐induced JNK phosphorylation, but not phosphorylation of ERKs and p38. PDRPS7 protected cardiomyocytes from apoptosis by inhibiting JNK phosphorylation and c‐Jun phosphorylation pathways, markedly upregulating anti‐apoptotic Bcl‐2 expression and inhibiting that of pro‐apoptotic Bax and cleaved caspase‐3. Importantly, pharmacological activation of JNKs diminished the protective effect of PDRPS7 in terms of cell survival against H/R stimulation. In summary, our study identified PDRPS7 as a novel cardioprotective peptide against H/R challenge and this action was mediated, at least in part, through inactivation of JNKs

Enhanced optical response of crystalline silicon photovoltaic devices with integration of silver nanoparticles and ultrathin TiO2 dielectric layer

Silver nanoparticles (Ag NPs) and the titanium dioxide (TiO2) dielectric layer produced by magnetron sputtering and subsequent annealing treatment, were integrated at the front side of crystalline silicon (c-Si) solar cells. A photovoltaic device was realized based on the c-Si substrate and stacked Ag NPs/TiO2/n/p/Ag layer. The results show that the energy conversion efficiency (ECE) can be improved by 9.9% with the introduction of well-sized Ag NPs and an ultrathin TiO2 dielectric layer to the c-Si solar cells. The presence of the dielectric layer enables Ag NPs to fully exert the advantage of localized surface plasmon resonance (LSPR) and light scattering, and the recombination of the photogenerated carriers originating from Ag NPs is effectively avoided at the surface or in the vicinity of Ag NPs. Moreover, COMSOL Multiphysics simulations were performed to investigate the reflection and absorption of incident light in the c-Si. The simulation results match well with the experimental data

Effects of VK2 on LPS-induced inflammation.

(A) TNF-α, (B) IL-6 and (C) IL-10 were measured with ELISA in mouse serum. (D) The protein expression levels of TLR4, p-P38 MAPK, and P38 MAPK were evaluated by western blotting. (E, F) Quantitative analysis of TLR4 and the ratio of p-P38/P38 normalized with GAPDH were performed using Image J software. (G) The protein expression levels of iNOS and IL-6 were evaluated by western blotting. (H, I) Quantitative analysis of iNOS and IL-6 normalized with GAPDH. Values represent means ± SEM, *p p p p < 0.0001.</p

VK2 attenuated LPS-induced acute lung injury.

(A) Mice were pre-administered intragastrically solvent or VK2 (0.2 and 15 mg/kg respectively) and subsequent intraperitoneal injection of LPS (7 mg/kg). (B) Histological analysis of lung tissue sections by HE staining (original multiples: 200 ×, scale = 75 μm). (C) Lung tissue injury was assessed by histological scores in all groups. (D) Determination of the myeloperoxidase (MPO) activity in lung homogenates. Values represent means ± SEM, *p p p p < 0.0001.</p

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Acute lung injury (ALI) is a life-threatening disease that has received considerable critical attention in the field of intensive care. This study aimed to explore the role and mechanism of vitamin K2 (VK2) in ALI. Intraperitoneal injection of 7 mg/kg LPS was used to induce ALI in mice, and VK2 injection was intragastrically administered with the dose of 0.2 and 15 mg/kg. We found that VK2 improved the pulmonary pathology, reduced myeloperoxidase (MPO) activity and levels of TNF-α and IL-6, and boosted the level of IL-10 of mice with ALI. Moreover, VK2 played a significant part in apoptosis by downregulating and upregulating Caspase-3 and Bcl-2 expressions, respectively. As for further mechanism exploration, we found that VK2 inhibited P38 MAPK signaling. Our results also showed that VK2 inhibited ferroptosis, which manifested by reducing malondialdehyde (MDA) and iron levels, increasing glutathione (GSH) level, and upregulated and downregulated glutathione peroxidase 4 (GPX4) and heme oxygenase-1 (HO-1) expressions, respectively. In addition, VK2 also inhibited elastin degradation by reducing levels of uncarboxylated matrix Gla protein (uc-MGP) and desmosine (DES). Overall, VK2 robustly alleviated ALI by inhibiting LPS-induced inflammation, apoptosis, ferroptosis, and elastin degradation, making it a potential novel therapeutic candidate for ALI.</div

VK2 inhibits apoptosis in LPS-induced ALI.

(A) The protein expression levels of Caspase-3 and Bcl-2 were evaluated by western blotting. (B, C) Quantitative analysis of Caspase-3 and Bcl-2 normalized with GAPDH were performed using Image J software. Values represent means ± SEM, *p p < 0.01.</p

VK2 alleviates LPS-induced lung elastin degradation.

(A) uc-MGP levels in serum. (B) DES levels in lung tissues. Values represent means ± SEM, *p p < 0.01.</p