Objective To study pharmacokinetics of domestic sufentanil as a single intravenous injection in Chinese patients undergoing abdominal surgery. Methods Ten patients undergoing abdominal surgery, ASA Ⅰ-Ⅱ grade,age from 51 to 65 years old,weighing from 58～68 kg were studied. Intravenous and intra-arterial cannulae were placed in advance. After general anesthesia, sufentanil 2 μg/kg was administered as a rapid bolus intravenously. Blood samples were obtained at 1,3,5,10,20,30,60,120,180,240 and 360 min after sufentanil injection. Plasma was separated from blood samples immediately and stored at -80 ℃ until assayed. Plasma concentration of sufentanil were determined by liquid chromatography mass spectrometry, pharmacokinetic parameters were calculated by 3P97 pharmacology program:central volume of distribution(Vc), apparent volume of distribution (Vd), rapid distribution half-life(t1/2 π), slow distribution half-life(t1/2 α), terminal elimination half-life(t1/2 β),speed constant(P, A, B, π, α, β, k10, k12, k21, k13, k31), clearance(CL)and area under curve(AUC)and so on. Results Pharmacokinetics of sufentanil in patients ndergoing gastrectomy was best fitted to three-compartment open model,the tri-exponential equation :Cp(t)= 2. 86e-0.8241t + 0.75e-0.0604t + 0.14e-0.0050t. Main pharmacokinetic parameter t1/2π =(1.29 ± 0.81)min, t1/2α =(12.20 ± 2.84)min, t1/2β =(150.50 ±48.71)min,Vc =(0.552 ±0.104)L/kg,Vd =(9.008 ±0. 754)L/kg,CL =(0.044 ±0. 011)L/(kg · min)and AUC =(47.58 ±11.88)ng/(ml · min). Conclusions Pharmacokinetics of domestic sufentanil in patients undergoing abdominal surgery was best fitted to three-compartment open model, and the pharmacokinetic characteristics of sufentanil were consistent with its clinical pharmacology.

Objective To assess the effect of different ages on sufentanil pharmacokinetics in patients undergoing cardiac valve replacement.Methods Sixteen NYHA Ⅱ or Ⅲ patients undergoing selective cardiac valve replacement were randomly divided into two groups:elderly group (aged 65-69 years,group Ⅰ,n =8) and young adult group (aged 36-45 years,group Ⅱ,n =8).Intravenous and intra-arterial cannulae were placed.Sufentanil 5 μg/kg injected intravenously during anesthesia induction.Blood samples from the radial artery were obtained at 1,3,5,10,20,30,60,120,180,240 and 360 min after sufentanil injection (3 ml each).Then 1 ml plasma was immediately separated from the 3 ml blood sample and stored at - 80 ℃ until being assayed.Plasma sufentanil concentration was determined with liquid chromatography mass spectrometry and pharmacokinetic parameters were calculated with 3P97 pharmacologicl program.Results Plasma sufentanil concentration versus the time decay curve in patients undergoing cardiac valve replacement before cardiopulmonary bypass (CPB) was fitted to a twocompartment model and could be expressed by bi-exponential equations:Cp (t) =27.4 e-0.41t + 3.2 e-0.029t in group Ⅰ and Cp (t) =14.4 e-0.51t +3.4 e-0.032t in group Ⅱ,respectively.There were significant differences in t 1/2 α,t1/2 β and CL between the two groups ( P ＜ 0.05 or 0.0l ).During CPB,plasma sufentanil concentration versus the time decay curve in patients undergoing cardiac valve replacement was fitted to a three-compartment model and could be expressed by tri-exponential equations:Cp(t) =22 e-0.51t + 3.5 e-0.045t + 0.21 e-0.0029 t in group Ⅰand Cp(t) =15 e-0.52t + 3.9 e-0.048t + 0.32 e-0.004t in group Ⅱ,respectively.There were no significant differences in pharmacokinetic parameters between the two groups ( P ＞ 0.05).Conclusion There are significant differences in sufentanil phannacokinetic characteristics before CPB but different ages have no obvious influence on sufentanil pharmaco-kinetics during CPB.

Objective Ultraviolet radiation can induce the expression of matrix metalloproteinases (MMPs) in pterygium epithelial cells. To investigate the effects of curcumin on the expression of MMP 2 and MMP 9 in human pterygium fibroblasts (HPFs) on UVA-irradiation and its possible mechanism.Methods After optimizing the dose of UVA irradiation and the concentration of curcumin, HPFs in the second generation were divided into control group (no exposure to UVA, no medication), UVA group (exposure to UVA), and UVA + curcumin group (exposure to UVA + curcumin). MMP-2 and MMP-9 levels were tested by zymography. The mRNA expression of MMP-2 and MMP-9 was detected by RT-PCR. The NF-κB-DNA binding activity was detected by electrophoretic mobility shift assay (EMSA).Results Compared with the control group, the secretion of MMP-2 and MMP-9 in the UVA group was increased significantly (P<0.05), which could be suppressed by curcumin (P<0.05). The MMP-9 mRNA levels were also significantly increased in UVA group \[(100±0)% vs (247.0±10.8)%, P<0.05\], and could be inhibited by curcumin \[(88.7±5.1)% vs (247.0±10.8)%, P<0.05\]. The NF-κB-DNA binding was remarkably increased in UVA group (P<0.05), and significantly decreased after treatment with curcumin (P<0.05).Conclusion Curcumin can inhibit the expression of MMP-2 and MMP-9 in UVA-irradiated HPFs, and the mechanism involved in this protective effect might be its inhibitory effect on NF-κB activation.

Objective To formulate a scientific and standardized follow-up checklist for postoperative patients with cervical cancer,and provide a scientific tool to support the follow-up work.Methods The first draft of the follow-up checklist was constructed through literature review and semi-structured interviews,and the final draft of the follow-up checklist was formed by conducting 2 rounds of correspondence with experts using the Delphi method from October to December 2022,screening experts'opinions and revising and improving the checklist.The convenience sampling method was adopted to select 8 nurses and 15 patients with cervical cancer after surgery from a tertiary A hospital in Liaoning Province from February to March 2023 as the research subjects.The nurses made telephone follow-up visits to the patients with the postoperative follow-up list and evaluated the follow-up list.Results The positive coefficients of the experts in the 2 rounds of correspondence were 88.89％and 100％,respectively;the authoritative coefficients were 0.88 and 0.89,respectively;the Kendal harmony coefficient of the primary,secondary and tertiary indicators were 0.177,0.245 and 0.179 in the first round and 0.170,0.118 and 0.107 in the second round,respectively(P＜0.05).The final follow-up checklist for postoperative patients with cervical cancer included 4 primary indicators of physical and daily life support,information support,psychological support,and social support,12 secondary indicators,and 45 tertiary indicators.Both nurses and patients believed that the follow-up list was comprehensive with strong professional and clinical practicability.Conclusion The follow-up checklist is reasonable in structure,comprehensive in content,and reliable,specialized and practical,which can provide a scientific and standardized tool to support post-discharge follow-up of patients with cervical cancer.

The transcription factor SOX10, as a major actor in the development of the neural crest, plays a key role in the maintenance of progenitor cell multipotency, lineage specification, and cell differentiation. Abnormalities of neural crest development in humans lead to a number of genetic diseases known as neurocristopathies or neural crest disorders. The mutation of SOX10 can cause Kallmann syndrome (KS), which is a clinically and genetically heterogeneous condition and defined by the association between anosmia and hypogonadotropic hypogonadism due to incomplete migration of neuroendocrine gonadotropin-releasing hormone (GnRH) cells along the olfactory, vomeronasal, and terminal nerves. Since then, there have been a number of related reports that mutation of SOX10 will lead to KS with deafness. This review focuses on the SOX10 gene and the advances in the diagnosis and genetic studies of KS with deafness caused by the mutatuin of SOX10.
Cell Differentiation ; Deafness ; genetics ; Gonadotropin-Releasing Hormone ; Humans ; Hypogonadism ; Kallmann Syndrome ; genetics ; Mutation ; genetics ; SOXE Transcription Factors ; genetics