Pancreatic cancer is characterized by nerve invasion and a high mortality rate， and its pathological process depends on the complex interaction network between tumor and the nervous system. Based on the concept of “pancreatic cancer neuroecology”， this article analyzes the mechanism of action of peripheral motor nerve， sensory nerve， and central nerve in tumorigenesis， pain regulation， and cachexia formation and emphasizes the synergistic regulatory role of immune cells， Schwann cells， and extracellular matrix in the microenvironment of perineural invasion. At the same time， this article further elaborates on the metabolic interaction and chemotaxis between neuraxis and tumor， the effect on promoting chemotherapy resistance， and the dynamic relationship between neuroplasticity and tumor adaptability. In clinical practice， this article summarizes the key value of perineural invasion in prognostic evaluation， preoperative evaluation， and the selection of surgical strategy. In addition， this article reviews the basic research advances in the biomarkers and potential targets associated with perineural invasion in pancreatic cancer and points out the limitations of current model and transformation research. In the future， systematically analyzing the nerve-tumor-immune network and targeting its key nodes may provide multi-dimensional strategies and new breakthroughs for the precise intervention of pancreatic cancer， the reversal of drug resistance， and the relief of symptoms.

OBJECTIVE To create a highly effective algorithm for automatically generating easily confused drug catalogs （ECDC）， as well as to develop a management system for ECDC based on this algorithm， in order to improve the management efficiency of ECDC. METHODS This study， based on Levenshtein distance algorithm， delved deeply into the automatic identification mechanism of easily confused drugs and the screening method for determining similarity thresholds， ultimately leading to the development of an algorithm for automatically generating ECDC. Besides a management system was designed and developed， using SQL Server 2008 R2 Express as the data storage platform and Visual Basic.NET as the programming language. RESULTS The similarity threshold δ played a crucial role in the algorithm for automatically generating ECDC. As the value of δ gradually increased， the total count of easily confused drugs decreased gradually， while the count of drug groups exhibited a pattern of initially increasing and then decreasing. Practically， ECDC could be created using either the generic or varietal names of drugs， with corresponding similarity thresholds of 0.75 and 0.83. Furthermore， ECDC management system had significantly reduced the time required to establish a catalog from about one week to less than one hour， resulting in a substantial enhancement in work efficiency. CONCLUSIONS The algorithm used to automatically generate ECDC is highly efficient and rapid， offering robust technical assistance for the management of easily confused drugs. Implementing the ECDC system can greatly reduce the time cost related to building and maintaining the catalogs， thus significantly improving the efficiency of managing ECDC.

OBJECTIVE To investigate a method for dynamic monitoring of drug consumption （DMDC） based on statistical process control （SPC）， aiming to improve the macro-supervisory capacity in the process of drug utilization. METHODS The lists of key monitoring drug varieties in our hospital were established based on drug cost and relevant national documents. Monthly consumption data of key monitoring drug varieties in the entire hospital， outpatient pharmacy and inpatient pharmacy were taken as monitoring objects，and the DMDC model was established using SPC’s X control chart， moving range control chart， and exponentially weighted moving-average control chart， monitoring from three dimensions： single-month consumption， range variation， and consumption trend. Rosuvastatin， metoprolol and meropenem were taken as examples to demonstrate the monitoring capabilities of the DMDC model. RESULTS Lists of key monitoring drug varieties were established for entire hospital， outpatient pharmacy and inpatient pharmacy， containing 203， 167 and 200 varieties， respectively. After excluding drug varieties that could not be modeled and for which modeling failed， 179， 116 and 172 DMDC models were successfully established for these three drug consumption areas， respectively. During the first four months of 2024， these three groups of model separately warned 54， 32 and 62 drug varieties. The DMDC model successfully monitored the monthly consumption of drugs，such as rosuvastatin throughout the hospital， metoprolol in outpatient pharmacy， and meropenem in inpatient pharmacy. Compared with the previously used floating rate ranking method in our hospital， the application of the DMDC model significantly improved the scope and depth of drug monitoring， with the monitored drug varieties greatly expanded from about 50 to 179， and the monitoring dimensions increased from a single dimension to three. CONCLUSIONS The DMDC model based on SPC is effective and feasible，suitable for monitoring drug varieties with stable monthly consumption.

In order to understand the evolution of the diagnosis and treatment plans of corona virus disease 2019 (COVID-19), and provide convenience for medical staff in actual diagnosis and treatment, this paper uses the 9 diagnosis and treatment plans of COVID-19 issued by the National Health Commission during the period from January 26, 2020 to August 19, 2020 as research data to perform comparative analysis and visual analysis. Based on text mining, this paper obtained the text similarity and summarized its evolution law by expressing and measuring the similarity of the overall diagnosis and treatment plans of COVID-19 and the same modules, which provides reference for clinical diagnosis and treatment practice and other diagnosis and treatment plan formulation.
COVID-19 ; Data Mining ; Humans ; SARS-CoV-2

Pyroptosis is a form of new programmed cell death which is dependent on Caspase-1 in recent years.When it' s stimulated by various dangerous signals from hepatic ischemia-reperfusion injury,the intracellular pattern recognition receptors are assembled into inflammasomes and Caspase-1 which was transformed into active form.Activated Caspase-1 promotes the maturation and secretion of pro-inflammatory cytokines IL-1β and IL-18,initiates the innate immunity rapidly and then induces severe inflammatory reaction.In addition,Caspase-1 can also cleave Gasdermin D and release its N-terminal domain triggering pyroptosis.Many studies showed that pyroptosis play a crucial role in hepatic ischemia-reperfusion injury.In this review,we discussed the activation mechanism and research progress of pyroptosis in hepatic ischemia-reperfusion injury.

Objective To explore the effects of hepatocyte nuclear factor 1 homeobox A(HNF1A) on drug resistance of PANC1 cells to gemcitabine plus abaraxane and explore the potential mechanism. Methods 78 pancreatic cancer patients with locally advanced or distant metastasis who received gemcitabine plus abaraxane chemotherapy after surgery in Biliary and Pancreatic Surgery Department of Sun Yat-sen Memorial Hospital from March 2012 to May 2017 were enrolled. qPCR was used to detect HNF1A mRNA levels in pancreatic cancer tissue. The patients were divided into high-expression group ( n=39 ) and low-expression group (n=39) according to the median expression level of HNF1A, and the correlation of HNF1A expression with cancer clinicopathologic parameters and survival was analyzed. qPCR was used to detect HNF1A mRNA of 3 drug-sensitive cell lines (BxPC-3, CFPAC-1 and L3. 6pl) and 4 drug-resistant pancreatic cancer cell lines (PANC1, MIA PaCa-2, Hs766T and Mpanc96). Lentivirus with plasmids carrying HNF1AcDNA infection was used to establish HNF1A overexpressing PANC1 cells ( HNF1A group), and lentivirus with empty plasmids were used to infect PANC1 cells to construct the control group. The mRNA and protein expression of HNF1A and ATP binding cassette transporter family ABCC1 in HNF1A group and control group were measured by qPCR and Western Blot, respectively. The half inhibition concentration ( IC50 ) of gemcitabine plus abaraxane was detected by MTT, and cell apoptosis was examined by flow cytometry. Results Pancreatic cancer patients with high HNF1A expression had a better overall survival than those with low HNF1A expression (17. 9 months vs 12.4 months), and the difference was statistically significant (P<0.001). HNF1A low expression in pancreatic cancer tissue was significantly associated with advanced TNM stage, perineural invasion ( PNI) and short overall survival. The expression level of HNF1A was significantly down-regulated in drug-resistant PANC1 cells compared to drug-sensitive BxPC-3 cells by an average fold change of 6. 73, and the difference was statistically significant ( P<0. 001 ). In HNF1A group, the mRNA and protein levels of ABCC1 were significantly decreased compared with those in control group (0. 012 ± 0. 004vs 0. 047 ± 0. 008,0. 281 ± 0. 040 vs 0. 832 ± 0. 046,P=0. 003,P <0. 001). IC50 of HNF1A group to gemcitabine plus abraxane was decreased compared with that of control group [(26. 31 ± 2. 91)μmol/L vs (72. 63 ± 4. 07) μmol/L], and the cell apoptosis rate of HNF1A group was increased compared with that of control group [(40. 18 ± 1. 64)％ vs (21. 31 ± 1. 98)％], and the differences were statistically significant (P<0. 01). Conclusions HNF1A may induce resistance of pancreatic cancer cell to gemcitabine plus abraxane by downregulating ABCC1.

Objective To evaluate the effect of autophagy inhibitor 3-methyladenine (3-MA) on phenotype transformation and proliferation of rat pulmonary arterial smooth muscle cells (PASMCs).Methods Cultured PASMCs were treated with different concentrations of 3-MA (low-dose group,2.0 mmol/L;middle-dose group,4.0 mmol/L;high-dose group,8.0 mmol/L;control group,0 mmol/L).The protein expression of LC3 Ⅱ,OPN and Vimentin was detected by Western blotting.Cell proliferation was detected by MTT assay.Results The autophagy of PASMCs was decreased with the increase of the concentration of 3-MA.Compared with the control group,significantly down-regulated protein expression of LC3 Ⅱ,OPN and Vimentin was observed in 3-MA-treated cells,with significantly lower proliferation activity.Conclusion The autophagy inhibitor 3-MA significantly down-regulated the expression of LC3 Ⅱ,OPN and Vimentin in PASMCs,with inhibiting the proliferation of PASMCs.

Objective To evaluate the effects of the serum of patients with obstructive jaundice on myogenic differentiation of human pulmonary microvascular endothelial cells (PMVECs). Methods Hu?man PMVECs were isolated and then subcultured. The cultured PMVECs were incubated with the serum of patients with obstructive jaundice or with the serum of healthy volunteers. At 24, 48 and 72 h of incubation (T1?3), the inverted microscope was used to observe the morphology of primary PMVECs. The expression of muscular proteins ( alpha?smooth muscle actin [α?SMA ] , smooth muscle?mysion heavy chain [ SM?MHC] , capolnin) in PMVECs was detected using Western blot analysis. Results The expression of cal?ponin andα?SMA was negative, and a few SM?MHC proteins were expressed when PMVECs were incubated with the serum of healthy volunteers; the expression of calponin, α?SMA and SM?MHC was positive when PMVECs were incubated with the serum of patients with obstructive jaundice. Compared with the serum of healthy volunteers, the expression of SM?MHC was significantly up?regulated when PMVECs were incubated with the serum of patients with obstructive jaundice (P<0.05). The expression of calponin, α?SMA and SM?MHC was significantly up?regulated at T2,3 compared with that at T1 , and at T3 compared with that at T2 when PMVECs were incubated with the serum of patients with obstructive jaundice ( P<0.05) . Conclusion The serum of patients with obstructive jaundice promotes myogenic differentiation of human PMVECs, which is probably one of the mechanisms underlying intrapulmonary microvascular dilatation.

Objective To explore the correlation between hypokalemia and sudden death in young and middle-aged people. Methods One hundred and twenty-nine young and middle-aged patients with sudden death during treatment were selected as observation group. Then 100 cases of healthy volunteers were randomly selected as control group. The incidence of cardiovascular disease, incidence of hypokalemia and intake of potassium were compared between 2 groups. Results The incidences of hypertension, arrhythmia, myocardial infarction, heart failure and hypokalemia in observation group were significantly higher than those in control group: 17.05% (22/129) vs. 5.00%(5/100), 13.18% (17/129) vs. 2.00% (2/100), 26.36% (34/129) vs. 9.00% (9/100), 9.30% (12/129) vs. 1.00% (1/100) and 55.04% (71/129) vs. 12.00% (12/100), and there were statistical differences (P<0.01). The ratios of higher, common, lower intake of potassium in observation group were 1.55%(2/129), 27.91% (36/129) and 70.54%(91/129), in control group were 15.00% (15/100), 58.00% (58/100) and 27.00% (27/100), and there was statistical difference (P<0.01). Logistic regression analysis result showed that hypertension, arrhythmia, myocardial infarction, heart failure, hypokalemia and lower intake of potassium were the risk factor for sudden death (P<0.01). The incidences of hypertension, arrhythmia, myocardial infarction and heart failure in hypokalemia patients were significantly higher than those in normokalemia patients: 28.92% (24/83) vs. 2.05% (3/146), 19.28% (16/83) vs. 2.05% (3/146), 44.58%(37/83) vs. 4.11% (6/146) and 13.25% (11/83) vs. 1.37% (2/146), and there were statistical differences (P<0.01). The incidence of hypokalemia in people with lower intake of potassium was significantly higher than that in people with higher and common intake of potassium: 56.78% (67/118) vs. 2/17 and 14.89%(14/94), and there was statistical difference (P<0.01). Conclusions There is a significant correlation between hypokalemia and sudden death in young and middle-aged people. Preventive measures of sudden death should be made according to serum potassium level in clinic. People should pay attention to the uptake of potassium in daily life.

Objective To investigate the effects of triptolide on proliferation,apoptosis and the changes of Ski,Smad3,Smad7 and collagen type I(ColI) in cultured rat mesangial cells induced by transforming growth factor (TGF)-β1.Methods Cultured HBZY-1 rat mesangial cells were divided into 5 groups:(1)normal control group; (2)TGF-β1 group (10 μg/L); (3)-(5)triptolide (0.4,2,10 μg/L)+TGF-β1 (10 μg/L) groups.The cell proliferation was detected by MTT.Apoptosis of mesangial cells was detected by TUNEL assay.The expressions of Ski,Smad3,Smad7 mRNA were examined by real-time quantitative PCR.The expressions of Ski,Smad3,Smad7 and ColI protein were detected by Western blotting.The localizations of Ski and Smad3 protein were detected by laser confocal fluorescence microscope.Results Compared with the normal control,TGF-β1 (10 μg/L) significantly stimulated mesangial cells proliferation,while decreased apoptosis.The mRNA and protein expressions of Ski,Smad7,Smad3 and ColI protein expression in TGF-β1 group were increased (P ＞0.05).In comparison with TGF-β1 group,triptolide could significantly inhibit TGF-β1-induced mesangial cells proliferation in dose-dependent manner,and promote the apoptosis of mesangial cells.In TGF-β1 group,mRNA and protein expresscons of Ski and Smad7 were increased (P＜0.05),Smad3 mRNA and protein were decreased (P ＞0.05),and ColI protein was decreased (P＜0.01).In comparison with TGF-β1 group,fluorescence intensity of Ski,Smad3 proteins was significantly increased in cytoplasm,while decreased in nucleus.Conclusions Triptolide can inhibit TGF-β1-induced mesangial cells proliferation through regulating the expressions of Ski,Smad7 mRNA and protein,inhibiting Ski.Smad7 translocation to the nucleus,and down-regulating Smad3 mRNA and protein expression.Triptolide can promote apoptosis of mesangial cells.