Sweeping cluster algorithm for quantum spin systems with strong geometric restrictions

Quantum spin systems with strong geometric restrictions give rise to rich quantum phases such as valence bond solids and spin liquid states. However, the geometric restrictions often hamper the application of sophisticated numerical approaches. Based on the stochastic series expansion method, we develop an efficient and exact quantum Monte Carlo "sweeping cluster" algorithm which automatically satisfies the geometrical restrictions. Here we use the quantum dimer model as a benchmark to demonstrate the reliability and power of this algorithm. Comparing to existing numerical methods, we can obtain higher accuracy results for a wider parameter region and much more substantial system sizes

Primer: Fast Private Transformer Inference on Encrypted Data

It is increasingly important to enable privacy-preserving inference for cloud services based on Transformers. Post-quantum cryptographic techniques, e.g., fully homomorphic encryption (FHE), and multi-party computation (MPC), are popular methods to support private Transformer inference. However, existing works still suffer from prohibitively computational and communicational overhead. In this work, we present, Primer, to enable a fast and accurate Transformer over encrypted data for natural language processing tasks. In particular, Primer is constructed by a hybrid cryptographic protocol optimized for attention-based Transformer models, as well as techniques including computation merge and tokens-first ciphertext packing. Comprehensive experiments on encrypted language modeling show that Primer achieves state-of-the-art accuracy and reduces the inference latency by 90.6% ~ 97.5% over previous methods.Comment: 6 pages, 6 figures, 3 table

TrojViT: Trojan Insertion in Vision Transformers

Vision Transformers (ViTs) have demonstrated the state-of-the-art performance in various vision-related tasks. The success of ViTs motivates adversaries to perform backdoor attacks on ViTs. Although the vulnerability of traditional CNNs to backdoor attacks is well-known, backdoor attacks on ViTs are seldom-studied. Compared to CNNs capturing pixel-wise local features by convolutions, ViTs extract global context information through patches and attentions. Na\"ively transplanting CNN-specific backdoor attacks to ViTs yields only a low clean data accuracy and a low attack success rate. In this paper, we propose a stealth and practical ViT-specific backdoor attack $TrojViT$. Rather than an area-wise trigger used by CNN-specific backdoor attacks, TrojViT generates a patch-wise trigger designed to build a Trojan composed of some vulnerable bits on the parameters of a ViT stored in DRAM memory through patch salience ranking and attention-target loss. TrojViT further uses minimum-tuned parameter update to reduce the bit number of the Trojan. Once the attacker inserts the Trojan into the ViT model by flipping the vulnerable bits, the ViT model still produces normal inference accuracy with benign inputs. But when the attacker embeds a trigger into an input, the ViT model is forced to classify the input to a predefined target class. We show that flipping only few vulnerable bits identified by TrojViT on a ViT model using the well-known RowHammer can transform the model into a backdoored one. We perform extensive experiments of multiple datasets on various ViT models. TrojViT can classify $99.64\%$ of test images to a target class by flipping $345$ bits on a ViT for ImageNet.Comment: 10 pages, 4 figures, 11 table

Immunity of replicating Mu to self-integration: a novel mechanism employing MuB protein

We describe a new immunity mechanism that protects actively replicating/transposing Mu from self-integration. We show that this mechanism is distinct from the established cis-immunity mechanism, which operates by removal of MuB protein from DNA adjacent to Mu ends. MuB normally promotes integration into DNA to which it is bound, hence its removal prevents use of this DNA as target. Contrary to what might be expected from a cis-immunity mechanism, strong binding of MuB was observed throughout the Mu genome. We also show that the cis-immunity mechanism is apparently functional outside Mu ends, but that the level of protection offered by this mechanism is insufficient to explain the protection seen inside Mu. Thus, both strong binding of MuB inside and poor immunity outside Mu testify to a mechanism of immunity distinct from cis-immunity, which we call 'Mu genome immunity'. MuB has the potential to coat the Mu genome and prevent auto-integration as previously observed in vitro on synthetic A/T-only DNA, where strong MuB binding occluded the entire bound region from Mu insertions. The existence of two rival immunity mechanisms within and outside the Mu genome, both employing MuB, suggests that the replicating Mu genome must be segregated into an independent chromosomal domain. We propose a model for how formation of a 'Mu domain' may be aided by specific Mu sequences and nucleoid-associated proteins, promoting polymerization of MuB on the genome to form a barrier against self-integration

Icariin stimulates differentiation of bone marrow-derived mesenchymal stem cells (BM-MSCs) through activation of cAMP/PKA/CREB

Icariin, a prenylated flavonol glycoside isolated from Epimedium, has been considered as a potential alternative therapy for osteoporosis. The present study aimed to clarify the detailed molecular mechanisms of action of icariin on osteoblast function, using bone marrow-derived mesenchymal stem cells (BM‑MSCs). BM-MSCs were first stimulated by icariin. Then, gene and protein expression of cAMP/ PKA/CREB signaling molecules were analyzed by RT-PCR and western blotting (WB), and alkaline phosphatase (ALP) was analyzed in cell lysates by ELISA. MTT assays indicated that icariin did not have significant effects on cell viability up to 1 μM. Icariin showed a dose-dependent effect on the alkaline phosphatase activity of BM-MSCs. WB analysis showed that icariin treatment of BM-MSCs significantly enhanced the protein expression of protein kinase A (PKA) and cAMP-responsive element binding protein (CREB), while RT-PCR results showed that icariin dose-dependently increased the mRNA levels of PKA and CREB. Icariin induced BM-MSC differentiation by BMP2, Smad1, and Runx2. RT‑PCR and WB results indicated that icariin significantly increased the expression of BMP2, Smad1, and Runx2 in BM‑MSCs. These results suggest that icariin is an agonist of the cAMP/PKA/CREB pathway in BM-MSC differentiation, raising the possibility that it could be used in the treatment of osteoporosis