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Until the development of HTTP request smuggling in 2005, individual HTTP requests were considered as independent entities and could not be split or merged. This is a security problem caused by inconsistent content length interpretation approach between web servers, or the web server is not fully implemented in accordance with the RFC standard. It is especially dangerous for web services with complex web architectures. It can route the victims to receive malicious responses, amplify the impact of certain low-threat vulnerabilities, steal user credentials, or bypass network devices’ defenses. However, since its concept and implementation are quite difficult to overcome, it is often ignored by many network administrators, making users who browse such websites vulnerable to the HTTP request smuggling attacks. This paper proposes a general solution to deal with various HTTP request smuggling attacks. A reverse proxy implemented by Flask validates and cleans dubious HTTP requests from the client side and ensures that the original requests comply with RFC standards. Therefore, the website administrators no longer need to configure complicated network settings or customize some open-source project codes to resist or minimize the risk of the HTTP request smuggling attacks. A series of experiments demonstrate that this method is effective and practical.

Adipose-derived mesenchymal stem cells (A-MSCs) are promising cellular therapies for the treatment of immune-mediated diseases. Non-gene editing technologies can improve the immune regulatory function of A-MSCs. Our preliminary experiments revealed that an active form of vitamin B6—pyridoxal-5′-phosphate (PLP)—plays an important role in regulating gene expression and cytokine secretion in A-MSCs in vivo. To further clarify the effect of PLP on receptors and cytokines related to the immune regulatory function of A-MSCs, a series of experiments were designed to verify the relationships between PLP and A-MSCs in vitro. Initially, A-MSCs were obtained, and cytokine secretion and the expression of IDO1, NF-κB, and Toll-like receptors in PLP-stimulated A-MSCs were evaluated. In addition, coculture was used to detect A-MSCs-mediated apoptosis of CD3+CD8+ T lymphocytes. These results showed that A-MSCs stimulated with PLP were highly proliferative, consistent with their pluripotent capacity. Further, the surface receptors TLR3, TLR4, IDO1, and NF-κB were upregulated, while TLR6 was downregulated. Concurrently, A-MSCs preconditioned with PLP had the greatest inhibitory effect on CD3+CD8+ T lymphocyte proliferation, indicating that PLP altered the immune regulatory function of A-MSCs through the regulation of TLRs and IDO1 expression.

Zinc finger proteins are associated with hereditary diseases and cancers. To obtain an adequate amount of zinc finger proteins for studying their properties, structure, and functions, many protein expression systems are used. ZNF191(243-368) is a zinc finger protein and can be fused with His-tag to generate fusion proteins such as His6-ZNF191(243-368) and ZNF191(243-368)-His8. The purification of His-tag protein using Ni-NTA resin can overcome the difficulty of ZNF191(243-368) separation caused by inclusion body formation. The influences of His-tag on ZNF191(243-368) properties and structure were investigated using spectrographic techniques and hydrolase experiment. Our findings suggest that insertion of a His-tag at the N-terminal or C-terminal end of ZNF191(243-368) has different effects on the protein. Therefore, an expression system should be considered based on the properties and structure of the protein. Furthermore, the hydrolase activity of ZNF191(243-368)-His8has provided new insights into the design of biological functional molecules.

Objective. To compare and analyze the relevance and applied value of chronic liver disease questionnaire (CLDQ) and Traditional Chinese Medicine liver disease questionnaire (TCMLDQ) in patients with posthepatitic cirrhosis.Methods. The data of 146 patients' scales of CLDQ and TCMLDQ which based on the characteristics of chinese medical symptoms were collected. We made comparative analysis of the relationship between these two scales by the linear regression model and canonical correlation method and evaluated the advantages and disadvantages of two scales about its items setting and dimension definition.Result. There is a negative correlation in total scores between the two scales and the linear regression equation:CLDQ=239.38−1.232TCMLDQ. The further canonical correlation analysis was used to analyze the two extracted canonical correlative variables with significances (P<0.05), and the results showed that the overall negative correlation between the two scales mainly came from contributions of both the four dimensions of TCMLDQ (CS, GSYX, GYPX, and OS) and the five dimensions of CLDQ (AS, FA, SS, AC, and EF).Conclusion. These two scales have good consistency in the evaluation of severity and life quality of liver cirrhosis patients, so we suggested that TCMLDQ can be used to evaluate the severity and life quality of patients with posthepatitic cirrhosis.

Neuronal growth inhibitory factor (GIF), also known as metallothionein (metallothionein-3), impairs the survival and neurite formation of cultured neurons. It is known that theα-βdomain-domain interaction of hGIF is crucial to the neuron growth inhibitory bioactivity although the exact mechanism is not clear. Herein, theβ(MT3)-β(MT3) mutant and the hGIF-truncatedΔ33-35 mutant were constructed, and their biochemical properties were characterized by pH titration, EDTA, and DTNB reactions. Their inhibitory activity toward neuron survival and neurite extension was also examined. We found that theΔ33-35 mutantα-domain containingβ-domain-likeM3S9cluster exhibits the function ofα-domain withM4S11cluster in hGIF. These results showed that the stability and solvent accessibility of the metal-thiolate cluster inβ-domain is very significant to the neuronal growth inhibitory activity of hGIF and also indicated that the particular primary structure ofα-domain is pivotal to domain-domain interaction in hGIF.