Objective The purpose of this study was to explore the effect of nursing intervention on xerostomia in patient with AIDS. Methods From October 2010 to April 2012, nursing interventions were administered in 53 AIDS patients with xerostomia during treatment. The self-designed evaluation form was used to evaluate the oral dryness of patients before and after nursing intervention. Results There were significant changes on oral dryness of patients before and after nursing invention ( < 0.01) . There was a progressive decrease in the occurrence degree of oral dryness from level 0 to level 4. The number of patients decreased by 11.4%in level 4, but increased by 9.4% in level 0. There was a positive correlation between the intervention time and treatment effect. Establishment of an effective oral care hygiene behavior intervention could help patients create a healthy lifestyle. Conclusion Nursing intervention is important to relieving xerostomia of AIDS patients.

To improve tryptophan production in Escherichia coli, key genes in the tryptophan biosynthesis pathway -aroG, trpED, trpR and tnaA were manipulated. TrpR gene was knocked out to eliminate the repression on the key genes controlling tryptophan biosynthesis and transportation on bacteria chromosome, and the tryptophan degradation was blocked by tnaA gene knockout. Then the bottleneck in tryptophan biosynthesis pathway was removed by co-expressing aroGfbr gene and trpEDfbr gene. Compared with the MG1655, the tryptophan production of trpR knockout and double-genes knockout strains was improved 10-folds and about 20-folds, respectively. After the trpEDfbr was expressed, the tryptophan production increased to 168 mg/L, and when the aroGfbr and trpEDfbr were co-expressed, the tryptophan production increased to 820 mg/L. This work laid the foundation for further construction of higher-efficient engineered strain for tryptophan production.
3-Deoxy-7-Phosphoheptulonate Synthase ; metabolism ; Amino Acid Transport Systems ; genetics ; Bacterial Proteins ; genetics ; Cloning, Molecular ; Escherichia coli ; genetics ; metabolism ; Escherichia coli Proteins ; genetics ; Gene Knockout Techniques ; Genetic Engineering ; Repressor Proteins ; genetics ; Tryptophan ; biosynthesis

Traumatic brain injury (TBI)-induced coagulopathy has increasingly been recognized as a significant risk factor for poor outcomes, but the pathogenesis remains poorly understood. In this study, we aimed to investigate the causal role of acrolein, a typical lipid peroxidation product, in TBI-induced coagulopathy, and further explore the underlying molecular mechanisms. We found that the level of plasma acrolein in TBI patients suffering from coagulopathy was higher than that in those without coagulopathy. Using a controlled cortical impact mouse model, we demonstrated that the acrolein scavenger phenelzine prevented TBI-induced coagulopathy and recombinant ADAMTS-13 prevented acrolein-induced coagulopathy by cleaving von Willebrand factor (VWF). Our results showed that acrolein may contribute to an early hypercoagulable state after TBI by regulating VWF secretion. mRNA sequencing (mRNA-seq) and transcriptome analysis indicated that acrolein over-activated autophagy, and subsequent experiments revealed that acrolein activated autophagy partly by regulating the Akt/mTOR pathway. In addition, we demonstrated that acrolein was produced in the perilesional cortex, affected endothelial cell integrity, and disrupted the blood-brain barrier. In conclusion, in this study we uncovered a novel pro-coagulant effect of acrolein that may contribute to TBI-induced coagulopathy and vascular leakage, providing an alternative therapeutic target.

Traumatic brain injury (TBI) triggers the activation of the endogenous coagulation mechanism, and a large amount of thrombin is released to curb uncontrollable bleeding through thrombin receptors, also known as protease-activated receptors (PARs). However, thrombin is one of the most critical factors in secondary brain injury. Thus, the PARs may be effective targets against hemorrhagic brain injury. Since the PAR1 antagonist has an increased bleeding risk in clinical practice, PAR4 blockade has been suggested as a more promising treatment. Here, we explored the expression pattern of PAR4 in the brain of mice after TBI, and explored the effect and possible mechanism of BMS-986120 (BMS), a novel selective and reversible PAR4 antagonist on secondary brain injury. Treatment with BMS protected against TBI in mice. mRNA-seq analysis, Western blot, and qRT-PCR verification in vitro showed that BMS significantly inhibited thrombin-induced inflammation in astrocytes, and suggested that the Tab2/ERK/NF-κB signaling pathway plays a key role in this process. Our findings provide reliable evidence that blocking PAR4 is a safe and effective intervention for TBI, and suggest that BMS has a potential clinical application in the management of TBI.