This article retrospectively analyzed the involvement of clinical pharmacists in the treatment process and implementation of pharmacological supervision in a patient with septic arthritis secondary to tophi ulceration.The patient was admitted to the hospital and the emergency debridement and tophi removal were performed.Piperacillin-tazobactam,imipenem cilastatin,levofloxacin,linezolid,and vancomycin were given successively,and multiple debridement and drainage were performed,but the patient remained febrile and had recurrent infection indicators.According to the relevant guidelines and evidence-based evidence,combined with the patient's infection indicators,pathogen results and creatinine clearance rate,the clinical pharmacists recommended stopping vancomycin and changing to cefazolin,and the clinicians adopted it.After that,the patient's inflammatory indicators gradually decreased,and the body temperature stabilized.After 28 days of piperacillin-tazobactam administration,the patient developed a reduction in white blood cell count(2.34×109·L-1)and potassium(2.98 mmol·L-1).The pharmacist recommended prompt discontinuation of the drug,and the patient's white blood cell count and potassium gradually recovered.Eventually,after anti-infective treatment and surgical intervention,the patient was discharged with closure of the infected foci,conversion of multiple blood cultures to negative,and stabilisation of body temperature and renal function.This case reflects the role of clinical pharmacists in the management of drug treatment of critically ill patients,and may provide practical experience and reference for clinical treatment of such cases.

Objective:To investigate effect of cordycepin on lung injury in rats with acute respiratory distress syndrome(ARDS)and its mechanism.Methods:Sixty Wistar rats were randomly divided into control group,lipopolysaccharide group(LPS),cordyce-pin low-dose group(5 mg/kg),cordycepin medium-dose group(15 mg/kg),cordycepin high-dose group(30 mg/kg),Compound C group(high-dose cordycepin 30 mg/kg+AMPK inhibitor 15 mg/kg),with 10 rats in each group.ARDS model of LPS rats was estab-lished,pathological changes of lung tissues were observed by HE staining and lung tissue pathological injury score was performed;wet/dry weight ratio(W/D)of rat lungs was measured;activity of myeloperoxidase(MPO)was detected;IL-6,IL-1β and TNF-α were measured by ELISA;malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione peroxidase(GSH)were detected by kit;Western blot was used to detect expressions of AMP-activated protein kinase(AMPK),p-AMPK,mammalian target of rapamy-cin(mTOR),p-mTOR,P70 ribosomal protein S6 kinase(p70S6K)and p-p70S6K.Results:Compared with control group,rats in LPS group had obvious lung tissue damage,and a large number of inflammatory cells infiltration,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were increased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expres-sions were increased(P<0.05),SOD,GSH levels were decreased,p-AMPK/AMPK protein expression was decreased(P<0.05);after treatment with cordycepin,lung tissue damage was reduced,a small amount of inflammatory cells were infiltrated,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were decreased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expressions were decreased(P<0.05),SOD,GSH levels were increased,p-AMPK/AMPK protein expressions were increased(P<0.05);AMPK inhibitor Compound C reversed improvement of cordycepin on lung injury in ARDS rats.Conclusion:Cordycepin can improve LPS induced lung injury of rats,reduce inflammatory and oxidative stress,whose mechanism may be related to regulation of AMPK/mTOR/p70S6K pathway.

This article retrospectively analyzed the involvement of clinical pharmacists in the treatment process and implementation of pharmacological supervision in a patient with septic arthritis secondary to tophi ulceration.The patient was admitted to the hospital and the emergency debridement and tophi removal were performed.Piperacillin-tazobactam,imipenem cilastatin,levofloxacin,linezolid,and vancomycin were given successively,and multiple debridement and drainage were performed,but the patient remained febrile and had recurrent infection indicators.According to the relevant guidelines and evidence-based evidence,combined with the patient's infection indicators,pathogen results and creatinine clearance rate,the clinical pharmacists recommended stopping vancomycin and changing to cefazolin,and the clinicians adopted it.After that,the patient's inflammatory indicators gradually decreased,and the body temperature stabilized.After 28 days of piperacillin-tazobactam administration,the patient developed a reduction in white blood cell count(2.34×109·L-1)and potassium(2.98 mmol·L-1).The pharmacist recommended prompt discontinuation of the drug,and the patient's white blood cell count and potassium gradually recovered.Eventually,after anti-infective treatment and surgical intervention,the patient was discharged with closure of the infected foci,conversion of multiple blood cultures to negative,and stabilisation of body temperature and renal function.This case reflects the role of clinical pharmacists in the management of drug treatment of critically ill patients,and may provide practical experience and reference for clinical treatment of such cases.

Objective:To investigate effect of cordycepin on lung injury in rats with acute respiratory distress syndrome(ARDS)and its mechanism.Methods:Sixty Wistar rats were randomly divided into control group,lipopolysaccharide group(LPS),cordyce-pin low-dose group(5 mg/kg),cordycepin medium-dose group(15 mg/kg),cordycepin high-dose group(30 mg/kg),Compound C group(high-dose cordycepin 30 mg/kg+AMPK inhibitor 15 mg/kg),with 10 rats in each group.ARDS model of LPS rats was estab-lished,pathological changes of lung tissues were observed by HE staining and lung tissue pathological injury score was performed;wet/dry weight ratio(W/D)of rat lungs was measured;activity of myeloperoxidase(MPO)was detected;IL-6,IL-1β and TNF-α were measured by ELISA;malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione peroxidase(GSH)were detected by kit;Western blot was used to detect expressions of AMP-activated protein kinase(AMPK),p-AMPK,mammalian target of rapamy-cin(mTOR),p-mTOR,P70 ribosomal protein S6 kinase(p70S6K)and p-p70S6K.Results:Compared with control group,rats in LPS group had obvious lung tissue damage,and a large number of inflammatory cells infiltration,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were increased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expres-sions were increased(P<0.05),SOD,GSH levels were decreased,p-AMPK/AMPK protein expression was decreased(P<0.05);after treatment with cordycepin,lung tissue damage was reduced,a small amount of inflammatory cells were infiltrated,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were decreased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expressions were decreased(P<0.05),SOD,GSH levels were increased,p-AMPK/AMPK protein expressions were increased(P<0.05);AMPK inhibitor Compound C reversed improvement of cordycepin on lung injury in ARDS rats.Conclusion:Cordycepin can improve LPS induced lung injury of rats,reduce inflammatory and oxidative stress,whose mechanism may be related to regulation of AMPK/mTOR/p70S6K pathway.

AIM:To investigate the role of proviral integration site for Moloney murine leukemia virus 1(PIM1)in the phenotypic switching of vascular smooth muscle cells(VSMCs)induced by oxidized low-density lipoprotein(oxLDL),and to explore the underlying mechanisms.METHODS:Eighteen male ApoE-/-mice(8 weeks old)were ran-domly divided into general diet group and high-fat diet group,with 9 mice per group.After 16 weeks,aortic samples were analyzed using HE staining to observe plaque formation.In vitro,VSMCs were exposed to oxLDL to induce phenotypic transformation.Western blot and immunofluorescence were used to measure the protein expression levels of PIM1 and phe-notypic markers including α-smooth muscle actin(α-SMA),smooth muscle protein 22α(SM22α),osteopontin(OPN),and CD68.Glycolysis levels were assessed by detecting the expression of glycolytic enzymes 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase(PFKFB3)and hexokinase 2(HK2)by Western blot,and lactate secretion was measured using a lactate test kit.The effects of SMI-4a(a specific inhibitor of PIM1)and PIM1 small interfering RNA on oxLDL-in-duced phenotypic markers in VSMCs were evaluated.Moreover,the impact of 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one(3PO;a glycolysis inhibitor)on oxLDL-induced phenotypic switching and glycolysis in VSMCs was investigated.RESULTS:HE staining revealed atherosclerotic plaque formation in the aortas of ApoE-/-mice fed with high-fat diet.Im-munofluorescence showed high accumulation of PIM1 and OPN in the tunica intima of atherosclerotic plaques.Compared with control group,aortic plaques exhibited significantly elevated levels of PIM1,OPN and CD68 proteins(P<0.01),ac-companied by reduced expression of contractile phenotype markers α-SMA and SM22α(P<0.01).In vitro,oxLDL treat-ment led to gradual decrease in α-SMA and SM22α expression(P<0.05 or P<0.01),while OPN and CD68 expression in-creased(P<0.05 or P<0.01).Moreover,oxLDL significantly up-regulated the protein expression of PIM1,PFKFB3 and HK2,and increased lactate secretion in VSMCs(P<0.05 or P<0.01).Knockdown of PIM1 or treatment with SMI-4a markedly attenuated these oxLDL-induced effects on VSMCs(P<0.05 or P<0.01).Treatment with 3PO also abolished ox-LDL-induced phenotypic transformation and glycolysis in VSMCs(P<0.05 or P<0.01).CONCLUSION:PIM1 highly accumulates in the atherosclerotic plaques of ApoE-/-mice.The phenotypic transformation of VSMCs was correlated with the expression of PIM1.PIM1 can regulate the phenotypic transformation of oxLDL-treated VSMCs by inducing glycolysis.