Sump syndrome is a rare complication of side-to-side choledochoduodenostomy (CDD) and occasionally occurs after spontaneous gallbladder-bile duct-digestive tract fistula or end-to-side choledochojejunostomy.Before the development of minimally invasive surgery,conventional surgical operation used to be the most important treatment method.This article reviews the research advances in sump syndrome in recent years and points out that endoscopic retrograde cholangiopancreatography is the major diagnostic method for this disease,and endoscopic sphincterotomy combined with bile duct debridement is the most simple and effective measure for the treatment of sump syndrome.Meanwhile,this article briefly reviews sump syndrome with reference to related literature and clinical practice,in order to raise the awareness for sump syndrome.

A novel electrochemical method based on dehydroabietylamine schiff base( DBS) and multi-walled carbon nano-tubes( MWCNTs) composite modified glassy carbon electrode was presented for determination of Pb2+. The electrochemical behaviors of Pb2+on the modifled electrode were investigated by cyclic voltammetry ( CV) and differential pulse anodic stripping voltammetry ( DPASV ) . The results showed that under the optimized conditions including 0 . 2 mol/L NaAc-HAc used as supporting buffer ( pH 5 . 5 ) , -1 . 1 V of accumulating potential, 250 s of accumulating time, the oxidation peak current was proportional to Pb2+concentration in the range between 1 × 10-8 mol/L and 1 × 10-6 mol/L with the linear regression equation as I(μA)= 6. 6173c(μmol/L)+0. 2597(R=0. 9971) and the detection limit as 5. 0×10-9 mol/L (S/N=3). The proposed sensor was successfully employed to determine Pb2+ in real samples with satisfactory results. In addition, this method showed the advantages of simple operation, short assay time, good accuracy, satisfactory efficiency and good selectivity for determination of low concentration lead in water samples.

OBJECTIVE:To strengthen the management of dismounting drugs in hospital and improve pharmacist working effi-ciency by designing and mading an oral dispending desk. METHODS:In order to solve the small number of placing dismounting drugs induced by small capacity of the desk and disorder placement of placing medicines in inpatient pharmacy,our pharmacists de-signed a new kind of oral dispensing desk that can solve the above problems,produced it and put it in the daily clinical work. The application effects were evaluated by comparing the number of placing drugs and deployment time of medical orders before and af-ter applying it. RESULTS:The designed oral dispensing desk included square slots in the bench,round slots on the side,operating table,multi-panel drawer and ordinary drawer,in which,the first two parts could be used for placing drugs with different shapes and different sizes,multi-panel drawer could place oral liquid,granules,etc. The total number of placing drugs was increased from 237 to 290,and the average deployment time of each medical order was shortened from(4.55±0.38)s to(3.52±0.16)s. CON-CLUSIONS:Application of new dispensing desk has not only solved the limited capacity of the desk,disorderly placing dismount-ing drugs,being difficult to locate and manage and other problems,but also improved the deployment speed of pharmacists and promoted standardized management of dismounting drugs.

Objective To observe the effects of Toxoplasma lysate antigen(TLA)on growth inhibition and tumor angiogenesis in mice B16 melanoma.Methods Twenty mice bearing B16 melanoma were established by subcutaneous inoculating with B16 cells and were randomly divided into the treatment group and the control group 0.1 ml TLA was administered once every two days for the treatment group starting on the seventh day after inoculation.and an equivalent volume of sterile saline was administered similarly in the control group.The mice were sacrificed on 21 th day after the tumor cells was injected.The anti-tumor effects of TLA were observed by measuring the size and weight of tumor.The microvessel density(MVD)and expression of vascdar endotheilial growth factor(VEGF)were observed by immunohistochemical method.Results TLA Can markedly inhibit the B16 melamoa growth in mice.The volume and weight of the tumors in the experimental group were significantly decreased compared with the control group(P＜0.05),and the turnout inhibitory rate was 49.6%.The MVD of experimental group and control was(44.4000±4.7888)and(31.9000±2.6012)respectively,and with a significant difference between two groups(P＜0.05).The VEGF in the treatment group were significantly lower than those in the control group(P＜0.05).Conclusion TLA can inhibit the growth of the B16 melanoma in mice.suggesting that the anti-tumor effect induced by TLA via a possible antianigionesis mechanism.

Objective To evaluate the effect of hydrogen sulfide combined with mild hypothermia on cerebral ischemia-reperfusion (I/R) injury in rats. Methods Eighty male SD rats, aged 3 months, weighing 250-300 g, were randomly divided into 5 groups ( n = 16 each): sham operation group (group S), cerebral I/R group,mild hypothermia group (group M), sodium hydrosulfide group (group NaHS) and NaHS + mild hypothermia group (group NM). In group I/R, M, NaHS and NM, cerebral I/R was induced by occlusion of 4 vessels (cauterization of bilateral vertebral arteries and 15 min occlusion of bilateral common carotid arteries) followed by reperfusion. In group NaHS and NM, intraperitoneal NaHS 14 μmol/kg was injected immediately after reperfusion, while the equal volume of normal saline was injected in the other three groups. At the same time, the rectal temperature was reduced to 32-33 ℃ within 15 min, lasting for 6 h, in group M and NM, while it was maintained at 36-37 ℃by physical method in other groups. Twelve rats of each group were sacrificed after 6 h of reperfusion, and then the hippocampus was removed for determination of the content of H2 S by using spectrophotometer and the expression of p-CREB and BDNF mRNA by using Western blot and RT-PCR respectively. Four rats in each group were sacririced after 72 h of reperfusion and then the hippocampus was removed for microscopic examination. Results The cerebral I/R injury was attenuated in group M, NaHS and NM compared with group I/R, with the slightest injury in group NM. The H2S content was significantly higher in group I/R, M, NaHS and NM than in group S, and in group NaHS and NM than in group I/R and M. The expression of p-CREB and BNDF mRNA was significantly higher in group I/R, M, NaHS and NM than in group S, and in group M, NaHS and NM than in group I/R. The BDNF mRNA expression was significantly higher in group NM than in group M and NaHS. There was no significant difference in the H2S content and the expression of p-CREB and BNDF mRNA between group NaHS and M.Conclusion Hydrogen sulfide combined with mild hypothermia can attenuate cerebral I/R injury by up-regulating the expression of p-CREB and BDNF mRNA in hippocampus in rats.

Objective To investigate the role of A2B adenosine receptor(A2BAR)in 6% HES 130/0.4-induced reduction of pulmonary capillary permeability in a rat model of sepsis.Methods Fifty male SD rats weighing 250-300 g were randomly divided into 5 groups(n = 10 each): group Ⅰ sham operation(group S);group Ⅱ sepsis(group CLP);group Ⅲ ,Ⅳ,Ⅴ low,medium,high dose HES(group H1,2,3).The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg.Left carotid artery and left femoral vein were cannulated for MAP and HR monitoring and fluid and drug administration.Sepsis was induced by cecal ligation and puncture (CLP).6% HES 130/0.4 7.5,15.0 and 30.0 ml/kg were infused iv over 2 h in group H1,2,3 respectively at 4 h after CLP.The animals were sacrificed at 6 h after CLP.The lungs were isolated for determination of pulmonary capillary permeability(by iv Evans blue injection),the expression of A2BAR and the contents of cAMP,protein kinase A(PKA),TNF-α,IL-6 and IL-10 in the lung tissue.Results CLP significantly increased pulmonary capillary permeability,A2BAR expression and cAMP,IL-6 and TNF-α contents in the lung tissue in group Ⅱ as compared with group S.0.6% HES 130/0.4 significantly reduced pulmonary capillary permeability,increased A2BAR expression,cAMP,PKA and IL-10 and decreased IL-6 and TNF-αcontents in the lung tissue in group H1,2,3 as compared with group CLP.6% HES 130/0.4 decreased pulmonary capillary permeability and up-regulated A2BAR expression in a dose-dependent manner.6% HES 130/0.4 15.0 ml/kg was most effective in increasing cAMP and PKA contents in the lung and depressing inflammatory response.Conclusion 6% HES 130/0.4 decreases pulmonary capillary permeability in a rat model of sepsis by up-regulating A2BAR expression in lung tissue.

Objective To investigate the changes in high voltage-activated (HVA) calcium current in dorsal root ganglion (DRG) neurons isolated from rats with neuropathic pain. Methods Pathogen-free male SD rats aged 4-6 weeks weighing 180-220 g were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg. Neuropathic pain was induced by ligation of L5 spinal nerve between DRG and sciatic nerve. The nerve was transected distal to the ligature. The animals which showed positive signs of neuropathic pain were decapitated on the 14th postoperative day. L5 and L4 DRGs were isolated and the neurons in the ganglia were enzymatically dissociated (group L5 and L4). The control group received no surgery (group C). The HVA Ca2+ current was recorded using whole-cell patch clamp technique. Results Peak calcium current density was significantly lower in group L5 and L4 than in group C, and was significantly lower in group L5 than in group L4 . Halfactivation value (Va 1/2) was also significantly lower in group L5 than in group C and L4 (P ＜ 0.05). The relative contribution of N-type to the total HVA Ca2+ current was significantly greater in group L5 than in group C and L4(P ＜ 0.05). There was no significant difference in the steady-state inactivation curves among the 3 groups. Conclusion In rats with neuropathic pain, the HVA Ca2+ current in the injured DRG neurons may play a key role in the induction of neuropathic pain.

This study was aimed to observe the body weight and behavioral changes of heart-spleen deficiency mouseandtoassesstheefficacyofLing-Qi-Jia (LQJ)oralsolutiononqi-supplementingandmind-tranquilizing. The heart-spleen deficiency syndrome mouse model was established by using loading swimming anddrugdaily.Thebodyweight,foodconsumption,intestinepropulsion,tailsuspensiontest (TST),forced swimmingtest (FST),sleepingtimeandtheamountofbrainneurotransmitterweredetected.Theresultsshowed that mouse suffered loading swimming and drug formed heart-spleen deficiency syndrome model, which were indicated by lowering body weight and food consumption, shortened time in FST, prolonged accumulative immobility time in TST, intestine propulsion hyperfunction, shortened sleeping time and lowering brain neurotransmitter amount. LQJ oral solution can obviously improve experiment indexes mentioned above. It was concluded that LQJ oral solution, which can improve insomnia due to heart-spleen deficiency, might had close relation to the efficacy of qi-supplementing and mind-tranquilizing. Meanwhile, changes of brain neurotransmitters might also be the material basis on its efficacy.

Abstract: The rapid advancements in artificial intelligence (AI) and computational sciences, particularly through the introduction of artificial intelligence drug design (AIDD) and computer-aided drug design (CADD) technologies, have revolutionized pathways in drug development. These include techniques such as natural language processing, image recognition, deep learning, and machine learning. By employing advanced algorithms and data processing techniques, these technologies have significantly enhanced the efficiency and success rate of R&D processes. In drug discovery, AI technologies have accelerated the identification of drug targets, screening of candidate drugs, pharmacological assessments, and quality control, effectively reducing R&D risks and costs. This article delves into the application of AIDD and CADD in drug development, analyzing their roles in enhancing the success rates and efficiencies of drug design, exploring their future trends, and addressing the potential challenges.

Objective To investigate the effect of hydrogen-rich saline combined with mild hypothermia on cerebral ischemia-reperfusion (IR) injury in rats. Methods Fifty male SD rats, aged 9-10 weeks, weiging 250-300 g, were randomly divided into 5 groups (n= 10 each): sham operation group (group S), group IR, hygrogen-rich saline group (group H), mild hypothermia group (group M) and hydrogen-rich saline + mild hypothermia group (group HM). In group IR, H, M and HM cerebral IR was induced by 15 min ligation of bilateral carotid artery followed by 6 h reperfusion. In group H and HM intraperitoneal hydrogen-rich saline 5 ml/kg was injected immediately after reperfusion, while the equal volume of normal saline was injected instead of hydrogen-rich saline in the other three groups. At the same time, the rectal temperature was maintained at 37-38 ℃ in group S,IR and M, while it was reduced to 32-34 ℃ by physical method within 15 min, lasting for 6 h, in group M and HM. The animals were sacrificed after 6 h of reperfusion, and then the hippocampus was removed for microscopic examination. The expression of HO-1 and content of MDA and TNF-α were determined by Western blot. Results The cerebral IR injury was attenuated in group H, M and HM compared with group IR, with the slightest injury in group HM. The expression of HO-1 and content of MDA and TNF-α were significantly higher in group IR, H, M and HM than in group S. The expression of HO-1 was significantly higher, while the content of MDA and TNF-α were lower in group H, M and HM than in group IR, and in group HM than in group H and M. There was no significant difference in the expression of HO-1 and content of MDA and TNF-α between group H and M. Conclusion Hydrogen-rich saline combined with mild hypothermia can attenuate cerebral I/R injury in rats via up-regulating the expression of HO-1 and decreasing the content of MDA and TNF-α in hippocampus.