Objective To explore the incidence and severity of diverse clinical symptoms in patients with severe acute pancreatitis (SAP), construct a symptom correlation network model, accurately identify core symptoms within the network, and classify symptom clusters. MethodsA convenience sampling method was adopted. A total of 211 patients with SAP admitted to the First Affiliated Hospital with Nanjing Medical University (Jiangsu Provincial People’s Hospital) from January 2024 to December 2025 were enrolled. The memorial symptom assessment scale was used for evaluation to investigate the composition of clinical symptoms in SAP patients. Exploratory factor analysis was performed to extract symptom clusters. R 4.4.2 software was applied to construct symptom clusters network. Centrality indicators including strength, betweenness and closeness were analyzed to identify core symptoms and core symptom clusters. ResultsA total of three symptom clusters were extracted in this study, including the gastrointestinal symptom cluster (abdominal pain, abdominal distension, dyspnea, dry mouth, nausea, vomiting, diarrhea, constipation, dizziness), the fatigue symptom cluster (lack of energy, difficulty concentrating, drowsiness), and the psychological symptom cluster (anxiety, sleep disturbance, irritability, sadness, distress). Among them, anxiety [95.7% (202/211)], difficulty concentrating [94.8% (200/211)], lack of energy [92.4% (195/211)], and abdominal pain [90.0% (190/211)] were identified as core symptoms. Symptoms with high strength values included anxiety (rs=2.2), difficulty concentrating (rs=1.2), and dyspnea (rs=1.0); symptoms with high closeness centrality values included drowsiness (rc=1.8), difficulty concentrating (rc=1.7), and anxiety (rc=1.1); symptoms with high betweenness centrality values included difficulty concentrating (rb=2.3), anxiety (rb=2.0), and drowsiness (rb=1.5). ConclusionsAnxiety, difficulty concentrating, lack of energy, and abdominal pain were identified as the core symptoms within the symptom clusters of SAP patients, with the fatigue symptom cluster being the core symptom cluster. It is recommended that medical staff pay close attention to the manifestations of core symptoms in SAP patients during treatment and formulate targeted symptom management plans.
Objective To explore the activity of Ca2 + -activated K+ ( KCa) inairwaysmoothmuscle cells( ASMCs) in a rat model of chronic obstructive pulmonary disease( COPD) , and to observe the effect of 11, 12-Epoxyeicosatrienoic acid( 11, 12-EETs) on the KCa channel of ASMCs. Methods Forty male Sprague-Dawley rats were randomly assigned to a COPD group and a normal control group. The rats in the COPD group were exposed to cigarette smoking in a relatively closed chamber to induce COPD. The ASMCs were isolated from small bronchi using an acute enzymatic digestion method. In the symmetrical high K+ solution,the KCa currents were separated with inside-out configuration using the patch clamp technique. The activity of KCa currents in ASMCs between the COPD group and the normal group were compared and the effect of 11, 12-EETs on KCa channel was recorded. The opening probability( Po) , opening time( To) and closing time ( Tc) of the KCa were measured. Results Compared with the normal group, Po of KCa in the COPD rats was much shorter ( 0. 084 ±0. 028 vs 0. 198 ±0. 029, P lt; 0. 01) , To was shorter [ ( 0. 732 ±0. 058) ms vs ( 1. 648 ±0. 152) ms, P lt; 0. 01] and Tc was longer[ ( 12. 259 ±2. 612) ms vs ( 6. 753 ±1. 237) ms, P lt;0. 01] . 11, 12-EETs can evoke the activity of KCa currents of ASMCs in the COPD rats while Po was increased( 0. 227 ±0. 059 vs 0. 084 ±0. 028, P lt; 0. 01) , To was much longer[ ( 2. 068 ±0. 064) ms vs ( 0. 732 ±0. 058) ms, P lt; 0. 01] , and Tc was shorter [ ( 4. 273 ±0. 978) ms vs ( 12. 259 ±2. 612) ms, P lt;0. 01] .Conclusions The results suggest that the decreasing of KCa activity plays an important role in the development of COPD. 11,12-EETs can directly evoke the activity of KCa channel in COPD rats, thus relax the airway smooth muscles.
Objective To investigate the role of Kv1. 5 in the pathogenesis of pulmonary hypertension simulated by hypobaria and hypoxia, and the effects of dichloroacetate ( DCA) on the Kv1. 5 expression in pulmonary arterial smooth muscle cells ( PASMCs ) and mean pulmonary arterial pressure ( mPAP) . Methods Twenty-four SD rats were randomly divided into a normal group ( N group) , a high altitude group ( HA group) , and a DCA treated group ( DCA group) . The N group were fed in normalconditions, the HA group and DCA group were fed in a hypobaria and hypoxia chamber simulated to an altitude of 5000 meters. In addition, the DCA group rats were gastric gavaged with DCA ( 70 mg · kg - 1 · d - 1 ) .Twenty-one days later, percentage of wall thickness ( WT% ) and percentage of wall area ( WA% ) of the pulmonary arteriole, mPAP, and the ratio of right ventricle / left ventricle and septum ( RV/ LV + S) were evaluated. Real-time PCR, immunohistochemistry and Western blot were carried out to detect the Kv1. 5 expression in PASMCs. Results In the HA group, WT% , and WA% of pulmonary arteriole, mPAP and RV/ ( LV + S) all increased significantly compared with the N group ( P lt;0. 01) . These changes in the DCA group were significantly lower than those in the HA group( P lt; 0. 01) . Furthermore, the protein and mRNA expression of Kv1. 5 in the PASMCs deceased significantly in the HA group compared with the N group( P lt;0. 01) , but recovered in the DCA group ( P lt;0. 01) . Conclusions The expression of Kv1. 5 in PASMCs is tremendously inhibited in rats fed in high altitude, which might be a important role of pulmonaryhypertension. DCA can inhibit the remodeling of pulmonary arterials probably by recovering Kv1. 5 expression.