Endoplasmic reticulum stress(ERS)is associated with the pathophysiology of various lung diseases.Multiple experiments have confirmed that inhibiting ERS can alleviate inflammatory responses,improve lung function,and possess certain anti-infective effects.ERS inhibitors can positively impact the treatment of respiratory system diseases by targeting the unfolded protein response(UPR)in the ERS pathway and regulating the balance of calcium ions within the endoplasmic reticulum.Most current research on ERS inhibitors is still in the preclinical stage.This article thoroughly reviews the relevant reviews and various experimental research results on ERS in respiratory diseases,systematically examining the potential roles of the main branches of UPR,including inositol requiring enzyme 1 alpha(IRE 1α),protein kinase-like endoplasmic reticulum kinase(PERK),and activated transcription factor 6(ATF6),as well as other ERS inhibitors in respiratory diseases.The aim is to promote clinical trial exploration of ERS inhibitors,with the hope of providing effective drug selection strategies for the treatment and symptom relief of respiratory diseases.

Endoplasmic reticulum stress(ERS)is associated with the pathophysiology of various lung diseases.Multiple experiments have confirmed that inhibiting ERS can alleviate inflammatory responses,improve lung function,and possess certain anti-infective effects.ERS inhibitors can positively impact the treatment of respiratory system diseases by targeting the unfolded protein response(UPR)in the ERS pathway and regulating the balance of calcium ions within the endoplasmic reticulum.Most current research on ERS inhibitors is still in the preclinical stage.This article thoroughly reviews the relevant reviews and various experimental research results on ERS in respiratory diseases,systematically examining the potential roles of the main branches of UPR,including inositol requiring enzyme 1 alpha(IRE 1α),protein kinase-like endoplasmic reticulum kinase(PERK),and activated transcription factor 6(ATF6),as well as other ERS inhibitors in respiratory diseases.The aim is to promote clinical trial exploration of ERS inhibitors,with the hope of providing effective drug selection strategies for the treatment and symptom relief of respiratory diseases.

Objective:To optimize the BALB/c mouse rhinitis model sensitized by Artemisia annua pollen allergen, and explore the humoral and cellular immune indicators that can be used for the evaluation of allergic reactions. Methods:Using BALB/c mice as experimental animals, using Artemisia annua pollen allergen extract as sensitizing protein, through different content of the main allergen Art a1 and different sensitization times, different immunization programs were set to immunize mice subcutaneously, One week and five weeks after the last immunization, Artemisia annua pollen allergen extract containing 50 μg/ml and 500 μg/ml Art a1 was used for nasal stimulation, once a day, for 1 week each time.Observe the allergic reaction of mice, detect the pathological changes of nasal tissues, determine the levels and dynamic changes of antigen-specific IgE, IgG1, IgG2a and other antibodies in the serum of each group of mice. and detect the changes in the number of antigen-specific IL-4, IL-5, IL-2, IFN-γ and other lymphocytes in the spleen of mice. Results:Sensitized mice showed obvious scratching and sneezing reactions after being stimulated by antigen; obvious allergic inflammation appeared in nasal tissue; The increase in serum level of Artemisia annua pollen-specific IgE antibody was significantly correlated with the challenge antigen; The antigen-specific IL-4 lymphocytes in the spleen of the sensitized mice were significantly increased, but the IFN-γ-specific lymphocytes did not change significantly. Conclusions:The successful establishment of a mouse model of Artemisia annua pollen allergen allergy is the first domestic use of ELISPOT technology to detect an increase in the number of antigen-specific IL-4 lymphocytes in Artemisia annua allergy mice, laying a foundation for the subsequent evaluation of the efficacy of preparations for desensitization treatment basis.

BACKGROUND: The vibration of high speed handpiece during tooth preparation may have adverse effect on the continuous force of the bonding interfaces among the cement, dentin, and post core. OBJECTIVE: To find the effect of different types of cements on the coronal microleakage of fiber post under different tooth preparation timings, and to provide evidence for the clinical operation. METHODS: The extracted mandibular premolars were divided into 3 groups, and they were cemented by Rely X luting, Panavia F and Paracora 5 mL, respectively. Each group was averagely divided into 3 subgroups: A, B, C groups which were prepared 15 minutes, 45 minutes, and 90 minutes after the cements mixed. All roots were then dyed and transparented. The teeth were observed under stereoscopic microscope and the dyeing scores were also recorded. RESULTS AND CONCLUSION: Rely X luting caused the highest coronal microleakage of fiber post, followed by Panavia F, while Paracore 5 mL, brought about the lowest under the same tooth preparation timing. Different tooth preparation timing caused no significant effect on the coronal microleakage of fiber post when the cement had been completely set.

OBJECTIVE To explore the effect of plasma endotoxin on the prognosis of multiple organ dysfunction syndrome(MODS).METHODS Retrospective analysis was carried out on 60 patients of MODS.They were 23 patients in survival group and 37 patients in death group,compared the level of plasma endotoxin on the dd 1,3,5,and 7 after admitted in both groups,and analyzed the relationship between the plasma endotoxin and lethal outcome.RESULTS The level of plasma endotoxin in death group was higher than that of survival group on the dd 1,3,5,and 7(P

Objective: To determine the potency of QN-2013, a derivative of quinoxaline 1,4-N-oxide, as a hypoxia-selective cytotoxin or a radiosensitizer. Methods: In vitro cytotoxicity and radiosensitization, as well as in vivo antitumor activity were determined by colony formation and tumor growth delay respectively. The changes in the cell cycle, DNA damage and repair of damaged DNA were assayed by FCM and “comet” assay, separately. Results: ICN250 and ICair50 of QN-2013 for HeLa-S3 cells were 0.08 and 1.7 mmol*L－1 respectively, namely, HCR=21. This suggested that QN-2013 was a fairly hypoxic cytotoxin, but inferior to SR-4233. QN-2013 had an evident radiosensitization either in vitro or in vivo. It was noted, however, that the value of in vitro SERs increased exponentially with increasing concentration of the drug, but the in situ antitumor activity seemed to be independent of doses of the drug. The systemic toxicity of QN-2013 was superior to an LD50 of 265　mg*kg－1 compared with 80　mg*kg－1 for SR-4233. In hypoxic condition QN-2013 induced S retension effect and G2M block in HeLa-S3 cells, caused DNA double strand break, and inhibited the repair of radiation-induced DNA damages. All of these reactivenesses might be involved in the action mechanism of QN-2013. Conclusion: QN-2013 is a fair hypoxia-selective cytotoxin, and has shown improved antitumor activity in vivo in combination with radiation. In general, These results suggest that the series of quinoxaline di-N-oxide derivatives hold out bright prospect for the development of novel bioreductive antitumor drugs.

Objective To investigate the expression of apoptosis-related neuclosome assembly protein-1(NAP-1) gene in related brain region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) treated mice and beta-amyloid treated rats. Methods The animal models with central nervous system degeneration were established by consecutive administration of MPTP to C57BL mice and injection of beta-amyloid to brain ventricular of SD rats. The RNA in striatum and substantia nigra of mice and the RNA in cortex and hippocampus of rats were extracted. The levels of NAP-1 mRNA in these samples were estimated by RT-PCR. Results For mice, the expression of NAP-1 were decreased after MPTP treatment in substantia nigra, while its expression showed no significant change in striatum. In contrast, no effect on NAP-1 gene expression by beta-amyloid injection can be detected in cortex and hippocampus of rats. Conclusions The apoptosis of dopaminergic neurons in nigrostriatal pathway after MPTP treatment may be related to the expression of NAP-1 gene. But the mechanism of neurodegeneration after beta-amyloid injection in rats may be different.