OBJECTIVES: To explore the mechanism of Pingchuanning Formula (PCN) for inhibiting airway inflammation in rats with asthmatic cold syndrome. METHODS: A total of 105 SD rats were randomized equally into 7 groups, including a control group, an asthmatic cold syndrome model group, 3 PCN treatment groups at high, medium and low doses, a Guilong Kechuanning (GLCKN) treatment group, and a dexamethasone (DEX) treatment group. In all but the control rats, asthma cold syndrome models were established and daily gavage of saline, PCN, GLCKN or DEX was administered 29 days after the start of modeling. The changes in general condition, lung function and lung histopathology of the rats were observed, and inflammatory factors in the alveolar lavage fluid (BALF), oxidative stress, lung tissue ultrastructure, cytokine levels, and expressions of the genes related to the HMGB1/Beclin-1 axis and autophagy were analyzed. RESULTS: The rat models had obvious manifestations of asthmatic cold syndrome with significantly decreased body mass, food intake, and water intake, reduced FEV_0.3, FVC, and FEV_0.3/FVC, obvious inflammatory cell infiltration in the lung tissue, and increased alveolar inflammation score and counts of neutrophils, eosinophils, lymphocytes, macrophages, and leukocytes in the BALF. The rat models also had significantly increased MDA level and decreased SOD level and exhibited obvious ultrastructural changes in the lung tissues, where the expressions of HMGB1, Beclin-1, ATG5, TNF-α, IL-6,IL-1β, and IL-13 and the LC3II/I ratio were increased, while the levels of Bcl-2 and IFN-γ were decreased. PCN treatment significantly improved these pathological changes in the rat models, and its therapeutic effect was better than that of GLKCN and similar to that of DEX. CONCLUSIONS PCN can effectively alleviate airway inflammation in rat models of asthmatic cold syndrome possibly by modulating the HMGB1/Beclin-1 signaling axis to suppress cell autophagy, thereby attenuating airway inflammatory damages.
Animals ; Rats ; Autophagy/drug effects* ; Rats, Sprague-Dawley ; Asthma/pathology* ; Beclin-1 ; HMGB1 Protein/metabolism* ; Drugs, Chinese Herbal/therapeutic use* ; Disease Models, Animal ; Male ; Lung/pathology* ; Inflammation

Objective To explore the mechanism of Pingchuanning Formula(PCN)for inhibiting airway inflammation in rats with asthmatic cold syndrome.Methods A total of 105 SD rats were randomized equally into 7 groups,including a control group,an asthmatic cold syndrome model group,3 PCN treatment groups at high,medium and low doses,a Guilong Kechuanning(GLCKN)treatment group,and a dexamethasone(DEX)treatment group.In all but the control rats,asthma cold syndrome models were established and daily gavage of saline,PCN,GLCKN or DEX was administered 29 days after the start of modeling.The changes in general condition,lung function and lung histopathology of the rats were observed,and inflammatory factors in the alveolar lavage fluid(BALF),oxidative stress,lung tissue ultrastructure,cytokine levels,and expressions of the genes related to the HMGB1/Beclin-1 axis and autophagy were analyzed.Results The rat models had obvious manifestations of asthmatic cold syndrome with significantly decreased body mass,food intake,and water intake,reduced FEV0.3,FVC,and FEV0.3/FVC,obvious inflammatory cell infiltration in the lung tissue,and increased alveolar inflammation score and counts of neutrophils,eosinophils,lymphocytes,macrophages,and leukocytes in the BALF.The rat models also had significantly increased MDA level and decreased SOD level and exhibited obvious ultrastructural changes in the lung tissues,where the expressions of HMGB1,Beclin-1,ATG5,TNF-α,IL-6,IL-1β,and IL-13 and the LC3II/I ratio were increased,while the levels of Bcl-2 and IFN-γ were decreased.PCN treatment significantly improved these pathological changes in the rat models,and its therapeutic effect was better than that of GLKCN and similar to that of DEX.Conclusion PCN can effectively alleviate airway inflammation in rat models of asthmatic cold syndrome possibly by modulating the HMGB1/Beclin-1 signaling axis to suppress cell autophagy,thereby attenuating airway inflammatory damages.

Objectives:This study aimed to compare the clinical characteristics between light-chain cardiac amyloidosis(AL-CA)and transthyretin cardiac amyloidosis(ATTR-CA). Methods:A retrospective analysis was conducted in patients diagnosed with AL-CA and ATTR-CA at Peking University Third Hospital from January 2011 to October 2023.There were 35 patients diagnosed with AL-CA(AL-CA group)and 21 patients diagnosed with ATTR-CA(ATTR-CA group).Clinical manifestations,ECG,echocardiography and cardiac magnetic resonance(CMR)results were compared between patients with AL-CA and ATTR-CA. Results:Compared to the AL-CA group,the ATTR-CA group has a higher proportion of males(54.3%vs.90.5%,P=0.005),the proportion of patients with hypertension was lower(42.9%vs.9.5%,P=0.009).In terms of clinical manifestations,edema,proteinuria,renal insufficiency and serous effusion were more common in the AL-CA group,while the incidence of limb numbness was higher in the ATTR-CA group(all P＜0.05).There were significant differences in the incidence of limb lead low voltage(57.1%vs.28.6%,P=0.038)and conduction block(14.3%vs.61.9%,P=0.001)between the AL-CA group and ATTR-CA group on ECG.Although the AL-CA group had a shorter time interval from initial symptoms to diagnosis(6.0[2.0,15.0]months vs.35.0[14.0,56.5]months,P=0.002)and less pronounced left ventricular thickening on echocardiography(interventricular septum thickness:[13.3±2.0]mm vs.[15.7±2.2]mm,P=0.001;left ventricular mass:[198.4±67.8]g vs.[246.6±53.5]g,P=0.009)and CMR(interventricular septum thickness:[16.0±2.1]mm vs.[18.9±3.8]mm,P=0.033;left ventricular mass:[132.9±45.3]g vs.[194.7±50.8]g,P=0.011),the proportion of patients with NYHA grades Ⅲ-Ⅳ(48.6%vs.19.0%,P=0.027)was higher,the levels N-terminal B-type natriuretic peptide precursor and cardiac troponin T levels were higher(both P＜0.05),and the 1-year survival rate was lower in the AL-CA group than in the ATTR-CA group(65.7%vs.100%,P=0.001). Conclusions:AL-CA and ATTR-CA had differences in clinical and ECG manifestations.While the severity of left ventricular hypertrophy was less pronounced in AL-CA compared to ATTR-CA,cardiac function and prognosis were worse in AL-CA than in ATTR-CA.

ObjectiveTo investigate the effect of Mashao Pingchuan decoction （MSPC） on lipopolysaccharides （LPS）-induced autophagy in human bronchial airway epithelial cells （16HBE） via the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway. Method16HBE cells were selected for the study， and cell counting kit-8 （CCK-8） was used to detect the activity of of LPS-induced 16HBE cells and the effect of MSPC-containing serum on the cells. Suitable LPS-induced 16HBE cells were screened by the CCK-8 method， and the content of tumor necrosis factor-α （TNF-α） was measured to identify the established model. And MSPC-containing serum was prepared. The cells were divided into normal group， LPS group， LPS+MSPC group， LY294002+LPS group and LY294002+LPS+MSPC group. Transmission electron microscopy was performed to observe the changes in autophagic vesicles and ultrastructure of the cells. Western blot was performed to detect the protein expressions of PI3K， phosphorylated PI3K （p-PI3K）， Akt， phosphorylated Akt （p-Akt）， mTOR， phosphorylated mTOR （p-mTOR） and microtubule-associated protein 1 light chain 3B （LC3B）， and enzyme-linked immunosorbent assay （ELISA） was used to detect the expressions of inflammatory factors interleukin-5 （IL-5）， IL-6， TNF-α and IL-10 in the five groups. ResultLPS inhibited the 16HBE cells in a dose-dependent manner. Compared with the normal group， the LPS group （150 mg·L^-1 of LPS） increased the expression of pro-inflammatory factor TNF-α after 24 h of treatment （P<0.05） and facilitated the autophagosome formation， and MSPC-containing serum exerted a concentration-dependent promotion effect on the 16HBE cells， inhibited the autophagy to a certain degree and enhanced the cell status. Western blot revealed that the protein expressions of p-PI3K， p-Akt and p-mTOR in the model group were lower （P<0.05） and the protein expression of LC3B was higher （P<0.01） than those in the normal group. Compared with the conditions in the LPS group， the protein expressions of p-PI3K， p-Akt and p-mTOR in the LPS+MSPC group were elevated （P<0.05） and that of LC3B was reduced （P<0.05）. Compared with the LPS+LY294002 group， the LY294002+LPS+MSCP group had up-regulated protein expressions of p-PI3K， p-Akt and p-mTOR （P<0.05） and down-regulated protein expression of LC3B （P<0.05）. ELISA showed that the LPS group had higher levels of IL-5， IL-6， TNF-α and IL-10 than the normal group， while the levels of TNF-α， IL-6 and IL-8 were decreased （P<0.01） and the level of IL-10 was increased （P<0.01） after treatment with MSCP. ConclusionMSCP may lower the LPS-induced autophagy in 16HBE cells and improve the inflammatory response through activating the PI3K/Akt/mTOR signaling pathway.

Objective:To explore the pupil size distribution of the Chinese myopic population under different mesopic conditions, and to analyze the possible influencing factors.Methods:A cross-sectional study was conducted.Two hundred and fourteen myopic patients (428 eyes) who underwent refractive surgery in Tianjin Eye Hospital from December 2018 to April 2019 were randomly selected.The patients were 17 to 45 years old, with an average age of (22.62±4.88) years old.The patients were divided into astigmatism <-1.5 D group (372 eyes) and astigmatism ≥-1.5 D group (56 eyes) according to their astigmatism measurements.The low mesopic pupil size (LMPS) (0.2 lx) was measured with the infrared Colvard pupillometer, and the high mesopic pupil size (HMPS) (6-12 lx) was obtained through the anterior Pentacam segment analyzer.The pupil size was compared between both eyes, different sexes and different astigmatism measurements.The relationship between pupil size and possible influencing factors, such as age, sex, spherical equivalent, spherical diopter, cylinder diopter, axis, mean keratometry(Km), and central cornea thickness was analyzed.This study adhered to the Declaration of Helsinki.The study protocol was approved by the Ethics Committee of Tianjin Eye Hospital (No.201912). Written informed consent was obtained from each subject or their guardians.Results:The pupil sizes measured by the Colvard pupillometer and Pentacam were (6.806±0.776)mm and (3.312±0.540)mm, respectively.The pupil size of male subjects was (6.692±0.754)mm, which was larger than (6.668±0.792)mm of females, showing a statistically significant difference ( t=2.935, P=0.004). Under the high mesopic condition, the pupil size of astigmatism ≥-1.5 D group was lower than that of astigmatism <-1.5 D group, with a statistically significant difference ( t=2.611, P=0.009). Under the low mesopic condition, pupil size was negatively correlated with age and Km ( r=-0.213, -0.210; both at P<0.001). Under the high mesopic condition, pupil size was weakly positively correlated with cylinder power ( r=0.124, P=0.010) and was weakly negatively correlated with Km ( r=-0.142, P=0.003). The multiple linear regression analysis revealed that the LMPS=0.659×HMPS-0.019×age-0.084×Km+ 8.662.About 28% of pupil size under low mesopic conditions could be predicted by Pentacam.LMPS of ≤7 mm could be better predicted when the results were below 3.6 mm. Conclusions:Age and corneal curvature are influencing factors of mesopic pupil size.Older people with steep curvature have a smaller pupil.At high mesopic conditions, astigmatism affects pupil size.Pentacam measurements can predict LMPS to some degree but are not a substitute for dark-adapted pupil diameter.

Circular RNA is a kind of single-stranded RNA ring without 5'capping and 3'polyadenylation.As a new member of non-coding RNA, circular RNA is evolutionally conserved, relatively stable,highly specific and enormously abundant.Instead of liner RNA,circular RNA became the research hotspot.So far,cerebellar degeneration-related protein 1 antisense(CDR1as)is a molecule that has garnered intense research.CDR1as harbors 74 conventional miRNA-7 binding sites.Expression of CDR1as efficiently tethers micro RNA-7, resulting in reduced micro RNA-7 activity and increased levels of micro RNA-7 targeted transcripts consistent with the micro RNA sponge and competing endogenous RNA(ceRNA)hypothesis.Moreover,CDR1as can restore micro RNA-7 and release it at right time.CDR1as can be stabilized in the exosomes.And its level has correlation with many clinical characteristics.

Tumor progression locus 2 (Tpl2) is a crucial three-stage kinase of the mitogen-activited protein kinase (MAPK) family,which plays an important role in MAPK pathway and other signaling pathways.In recent years,a large number of studies have found that aberrant expressing Tpl2 is involved in tumorigenesis and development of various cancers,and is expected to serve as a new biomarker and therapeutic target.Therefore,to reveal the mechanism of Tpl2 will provide a feasible theoretical basis and potential interventional target for the diagnosis and treatment of cancers.

It has been estimated that approximately 75% of the human genome is transcribed into RNA, 74% of which would be transcribed into non-coding RNA (ncRNA).The ncRNA can be divided into 2 major groups including small RNA and long non-coding RNA (lncRNA).There is increasing evidence that the dysregulation of lncRNA is closely associated with the occurrence and progression of many tumors.The lncRNA taurine up-regulated gene 1 (TUG1) is originally detected in a genomic screen for genes in response to taurine treatment of developing mouse retinal cells.According to research reports, dysregulation of TUG1 participates in the progression of a variety of tumors.Therefore, the regulatory effects of lncRNA TUG1 on tumorigenesis are summarized in this article.

With the advance of biology technology, non-coding RNA (ncRNA) has been confirmed to be closely associated with the occurrence and development of the cancer. The ncRNA can be divided into two groups by length, including microRNA (miRNA) and long non-coding RNA (lncRNA). As a member of lncRNA,LINC00152(long intergenic non-protein-coding RNA 152)has been taken into cancer research, which can regulate the activity of miRNA and involve the regulation of gene transcription of gene transcription and protein generation. The characteristics of LINC00152 that correlate with many clinical manifestations and can be detected in liquid biopsies make it becoming new biomarkers of cancer diagnosis. This paper reviews the current progress of LINC00152 in gastrointestinal cancer.

As the crucial member of noncoding RNA family,there is increasing evidence that long noncoding RNA has participated in numerous physiological and pathological processes of organisms.HOXA distal transcript antisense RNA is a long noncoding transcript located at the 5'tip of HOXA.According to research reports,the up-regulation of HOTTIP is closely associated with occurrence and progression of multiple digestive system cancers and promotes the carcinogenesis.The regulatory effect of long noncoding RNA HOXA distal transcript antisense in digestive system neoplasms will be summarized in this article.