Atherosclerosis is a chronic inflammatory disease of the vascular walls. As the essential mediators of inflammation, cytokines play important roles in atherosclerosis. Through widespread and penetrating studies, many cytokines, such as TNF-, IL-1, IL-6 and IFN-, are found involved in the development of atherosclerosis, as well as the related signal transduction pathways such as the NF- B pathway, the JNK / AP-1 pathway, and the JAK / STAT pathway. This implies that cytokines have a favorable perspective of clinical application. A few cytokines are identified as biomarkers, which help the early diagnosis of the disease and estimation of the risk of the clinical vascular events. Meanwhile, great progress has been made on the cytokine-targeted treatment of atherosclerosis, providing a novel therapy in the treatment of the disease.

Objective To clone the 5′ non-coding region (NCR) of human interferon-?-inducible protein 10(IP-10), and to identify the transcriptional activity of IP-10 promoter induced by lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVEC). Methods Genomic DNA of lymphocytes was isolated from the human blood. With above DNA as the template, the 5'NCR of human IP-10 was amplified by nest polymerase chain reaction (PCR) method. Then, the IP-10 promoter was cloned into luciferase reporter vector, pGL3. The recombined vector was transfected into HUVEC, and then the activity of the luciferase was determined after the cells were stimulated by LPS. Results Human IP-10 promoter was obtained and the pGL3/IP-10 was successfully constructed. Moreover, the activity of luciferase driven by human IP-10 promoter was observed to obviously increase in the HUVEC stimulated by LPS. Conclusion We successfully cloned human IP-10 promoter, constructed luciferase reporter vector driven by the human IP-10 promoter, and confirmed that high transcriptional activity of human IP-10 promoter was induced by LPS in HUVEC. The results supplied an experimental base for the further study of the transcriptional regulation of human IP-10.

AIM: To construct prokaryotic expression vector of His-tagged human IP-10 for further study of its biological function in the inflammatory response. METHODS: The coding sequence of IP-10 lacking signal peptide was amplified from human lung cDNA library by polymerase chain reaction (PCR) and the fragment was cloned into pET-14b plasmid for the construction of His-tagged fusion protein expressing vector, pET-14b/IP-10. After being identified by enzyme digestion and sequencing, the recombinant vector was transformed into a strain of E. coli, BL21 (DE_3). The expression of His-tagged fusion protein was induced with IPTG and purified with Ni+-NTA affinity chromatography. Then the chemotactic activity of IP-10 was determined by transwell migration assay on THP-1 cells. RESULTS: The construction of pET-14b/IP-10 recombinant vector was proved by enzyme digestion and sequencing. The fusion protein IP-10, which was purified by a routine Ni+ affinity method, had an activity on the induction of cell migration of THP-1. CONCLUSION: We successfully construct IP-10 fusion protein expressing vector and get the fusion protein with high bioactivity, which provides essential materials for the future studies on IP-10.

To research the structure-activity relationship (SAR) of glycinamide-bearing compounds that used as inhibitors of dipeptidyl peptidase IV (DPP-IV), P32/98 and compound A were chosen as the leading compounds, heterocycles containing nitrogen atom were introduced to form amide, and different residues on a-position of carbonyl were designed. The nineteen designed compounds were synthesized by a simple route and were evaluated as inhibitors of DPP-IV. All of the structures were characterized by 1H NMR and HRMS. The preliminary SAR result was obtained.

Ulcerative colitis(UC)is a chronic inflammatory bowel disease characterized by continuous inflammation and ulcer formation in the intestinal mucosa.Its pathogenesis involves immune dysfunction,dysbio-sis of gut microbiota,and mucosal damage caused by inflammation.Ferroptosis is an iron-dependent form of cell death regulated by disturbances in iron metabolism,lipid peroxidation,and depletion of glutathione(GSH).Studies have indicated that ferroptosis plays a crucial role in the pathogenesis of UC,particularly in regulating in-flammatory responses and damaging intestinal epithelial cells.This article reviews the regulatory mechanisms and roles of ferroptosis in UC and discusses the potential therapeutic strategies to alleviate UC symptoms by modulating iron metabolism,reducing lipid peroxidation,and maintaining GSH levels,providing new targets and directions for the diagnosis and treatment of UC.

Objective To analyze the distribution of traditional Chinese medicine (TCM) syndromes and characteristics of patients with acute respiratory distress syndrome (ARDS), and to provide reference for further clinical study of ARDS. Methods The clinical data of ARDS patients admitted to the Department of Critical Care Medicine of Affiliated Hospital of Chengdu University of TCM from November 2017 to February 2019 were retrospectively analyzed. The general data (gender and age) and inducing cause of disease, clinical manifestations, intensive care unit (ICU) stay time, total hospitalization time, outcome in ICU, outcome in 28-day follow-up and TCM syndromes were recorded. The different degrees of disease severity, the clinical manifestations and distribution characteristics of TCM syndromes were analyzed. Results A total of 110 patients with ARDS were enrolled, including 2 patients in mild ARDS group, 33 patients in moderate ARDS group and 75 patients in severe ARDS group. In the etiology analysis of ARDS, infection was the commonest cause, including 46 cases of pulmonary infection (41.8%), 27 cases of sepsis (24.5%), 4 cases of abdominal cavity infection (3.6%), 2 case of urinary tract infection (1.9%), and 13 cases had surgical histories (11.8%). The stay in ICU was 9.00 (3.00, 18.00) days and the total hospital stay was 18.00 (10.00, 30.00) days. The mortality in ICU was 32.7% (36/110), and that in 28-day follow-up was 60.0% (66/110). The clinical symptoms of the patients in moderate and severe groups ARDS were mainly dyspnea, cough, fever, sputum, chest tightness, and palpitations, accounting for 75.0% (81/108), 43.5% (47/108), 28.1% (31/108), 26.9% (29/108), 22.2% (24/108) and 25.9% (28/108), respectively. Compared with the ARDS moderate group, the proportions of patients with dyspnea, cough and palpitation in severe ARDS group were significantly higher [80.0% (60/75) vs. 63.6% (21/33), 50.7% (38/75) vs. 27.3% (9/33), 33.3% (25/75) vs. 9.1% (3/33), respectively, all P < 0.05]. The main TCM syndromes were yang deficiency, exuberant heat-toxin, and wind-heat invading lung, accounting for 53.7% (58/108), 28.7% (31/108), and 25.0% (27/108) respectively. The proportion of patients with exuberant heat-toxin syndrome in severe ARDS group was obviously higher than that in the moderate ARDS group [34.7% (26/75) vs. 15.2% (5/33), P < 0.05], while the proportion of patients with wind-heat invading lung syndrome in moderate ARDS group was more than that in the severe ARDS group [42.4% (14/33) vs. 17.3% (13/75), P < 0.05]. Conclusion ARDS is a critical illness with high mortality and various complicated clinical symptoms, the TCM syndromes of ARDS are mainly yang deficiency, exuberant heat-toxin, wind-heat invading lung, and intermingling of deficiency and excess easily leading to collapse syndrome.

Objective:To investigate the clinical, imaging, etiological and prognostic features of patients with infarctions in different locations of the medulla oblongata.Methods:Patients with acute medullary infarction hospitalized at Tianjin Huanhu Hospital from July 2017 to July 2022 were included. The risk factors, clinical manifestation, stroke mechanism and 90-day prognosis of these patients were analyzed retrospectively.Results:Among the 256 patients enrolled, 150 (58.6%) had lateral medullary infarction (LMI), 106 (41.4%) had medial medullary infarction (MMI). The most frequent clinical manifestation of patients with LMI was dizziness (84.7%,127/150). And motor disorders (83.0%,88/106) was the most frequent clinical manifestation of patients with MMI. LMI lesions were mostly located in the middle (42.7%,64/150) and MMI lesions were mostly located in the upper (60.4%,64/106) medulla oblongata, with statistically significant difference (χ 2=47.53, P<0.001). Large artery atherosclerosis (LAA) was the main stroke mechanism in LMI and MMI [57.3%(86/150) vs 56.6%(60/106)]. Early neurological deterioration was more common in MMI (25.5%,27/106) and less common in LMI (7.3%,11/150), with statistically significant difference (χ 2=16.17, P<0.001). At discharge, more patients with MMI showed poor prognosis in short term [45.3% (48/106) vs 24.0% (36/150), with statistically significant difference (χ 2=12.76, P<0.001)] and even long term at 90-day follow-up [33.0% (35/106) vs 12.7% (19/150), also with statistically significant difference (χ 2=15.48, P<0.001)] than those with LMI. A total of 10 patients (4.0%, 10/256) developed respiratory failure during hospitalization, including 7 patients with LMI (4.7%, 7/150) and 3 patients with bilateral MMI (2.8%,3/106). Early neurological deterioration ( OR=3.38, 95% CI 1.25-9.10, P=0.016) and LAA (compared with small artery occlusion) ( OR=3.08, 95% CI 1.13-8.37, P=0.028) were independent risk factors for poor prognosis in MMI. Age ( OR=1.01, 95% CI 1.01-1.17, P=0.026) and early neurological deterioration ( OR=20.19, 95% CI=2.63-155.06, P=0.004) were independently correlated with poor outcome in LMI. Conclusions:LMI and MMI had similar etiology and significant differences in clinical manifestations, early neurological deterioration and prognosis. Further classification of medullary infarction was of great significance for diagnosis, treatment and prognosis evaluation.

Lung cancer, one of the most prevalent cancer types globally, underscores the critical importance of early detection and precise diagnosis in its management. However, conventional pathological diagnostic methods encounter various limitations, including the intricacies of the diagnostic process and the challenges in achieving uniform results. In contrast to traditional pathology, digital pathology integrates digitized pathological information with artificial intelligence, and offers a pathway for rapid and accurate diagnostic assistance. It holds the potential to delve into the tumor characteristics and microenvironment information, thereby supporting precision diagnosis and treatment for lung cancer. This article elucidates the recent applications of digital pathology in lung cancer diagnosis, staging, treatment, and prognosis. Additionally, it addresses the challenges currently faced by digital pathology.