Anxiety and Depression Survey and Analysis of Hospital Staff in a Designated Hospital in Shannan City During the COVID-19 Pandemic.

BACKGROUND The aim of this study was to evaluate the psychological status of anxiety and depression of hospital staff in the designated hospital in the city of Shannan during the COVID-19 pandemic in order to provide a theoretical basis for effective psychological intervention. MATERIAL AND METHODS A cross-sectional survey was performed from September 10 to 16, 2022, by administering an online questionnaire to the hospital staff on duty in the hospital. We collected participants' demographic and general information. The Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS) were used to investigate the anxiety and depression of hospital staff. RESULTS Among 267 hospital staff, anxiety was found in 98 individuals, with a prevalence of 36.70%. Depression was found in 170 individuals, with a prevalence of 63.67%. Anxiety combined with depression was found in 84 individuals, with a prevalence of 31.46%. The prevalence of depression was higher in women, Tibetan personnel, hospital staff with primary or lower titles, staff without career establishment, and non-aid Tibetan personnel, and the differences were all statistically significant (P.

Interferometric Imaging, and Beam-Formed Study of a Moving Type-IV Radio Burst with LOFAR.

Type-IV radio bursts have been studied for over 50 years. However, the specifics of the radio emission mechanisms is still an open question. In order to provide more information about the emission mechanisms, we studied a moving Type-IV radio burst with fine structures (spike group) by using the high-resolution capability of the Low-Frequency Array (LOFAR) on August 25, 2014. We present a comparison of Nançay Radioheliograph (NRH) and the first LOFAR imaging data of the Type-IV radio burst. The degree of circular polarization (DCP) is calculated at frequencies in the range 20 - 180 MHz using LOFAR data, and it was found that the value of DCP gradually increased during the event, with values of 20 - 30%. LOFAR interferometric data were combined with white-light observations in order to track the propagation of this Type-IV burst. The kinematics shows a westward motion of the radio sources, slower than the CME leading edge. The dynamic spectrum of LOFAR shows a large number of fine structures with durations of less than 1 s and high brightness temperatures ( T B ), i.e., 10 12 - 10 13 K. The gradual increase of DCP supports gyrosynchrotron emission as the most plausible mechanism for the Type IV. However, coherent emissions such as Electron Cyclotron Maser (ECM) instability may be responsible for small-scale fine structures. Countless fine structures altogether were responsible for such high T B . Supplementary Information: The online version contains supplementary material available at 10.1007/s11207-022-02042-0.

Blood vessel assessment using computed tomography : Effects of ephedrine on uterine artery.

BACKGROUND: Ephedrine increased blood pressure due to the contractile properties of resistance vessels. Excessive contraction of the uterine arteries might cause fetal distress. This study was to determine the diameter of the uterine artery of female New Zealand rabbits after the administration of different doses of ephedrine using CT. METHODS: Thirty-two rabbits were randomly divided into a control group (Group C), low dosage group (Group L), medium dosage group (Group M) and high dosage group (Group H). Normal saline and doses corresponding to the human dose of 7.5, 15 and 30 mg of ephedrine were injected respectively. The marginal ear and uterine artery diameters were measured 5, 10, 15, 30, and 45 min after injection using CT, and the hemodynamic changes were recorded. RESULTS: The increase in mean arterial pressure in group M (p = 0.009), and H (p = 0.013) was higher than that in group C. Compared with group C, substantial contraction of the marginal ear artery was observed at the three doses of ephedrine. There were no differences in the uterine artery diameter among groups L, M and C, However, in Group H, a significant contraction of the uterine artery compared with the other groups (p < 0.001) was observed. DISCUSSION: CT can be used to evaluate the effects of drugs on organs and blood vessels. Ephedrine can not only constrict the peripheral blood vessels but also do not affect the uterine artery at a dose of 15 mg or less. However, the dose should not exceed 30 mg, which may cause severe uterine artery depression.

An autophagy-associated lncRNAs model for predicting the survival in non-small cell lung cancer patients.

Long non-coding RNAs (lncRNAs) can influence the proliferation, autophagy, and apoptosis of non-small cell lung cancer (NSCLC). LncRNAs also emerge as valuable prognostic factors for NSCLC patients. Consequently, we set out to discover more autophagy-associated lncRNAs. We acquired autophagy-associated genes and information on lncRNAs from The Cancer Genome Atlas database (TCGA), and the Human Autophagy Database (HADb). Then, the prognostic prediction signature was constructed through using co-expression and Cox regression analysis. The signature was constructed including 7 autophagy-associated lncRNAs (ABALON, NKILA, LINC00941, AL161431.1, AL691432.2, AC020765.2, MMP2-AS1). After that, we used univariate and multivariate Cox regression analysis to calculate the risk score. The survival analysis and ROC curve analysis confirmed good performances of the signature. GSEA indicated that the high-risk group was principally enriched in the adherens junction pathway. In addition, biological experiments showed that ABALON promoted the proliferation, metastasis and autophagy levels of NSCLC cells. These findings demonstrate that the risk signature consisting of 7 autophagy-associated lncRNAs accurately predicts the prognosis of NSCLC patients and should be investigated for potential therapeutic targets in clinic.

CLCA2 suppresses the proliferation, migration and invasion of cervical cancer.

Ca2+-activated Cl- channel A2 (CLCA2), a tumor suppressor, is associated with the development of several cancers. However, little is known about CLCA2 in human cervical cancer. Therefore, the aim of the present study was to investigate the effects of CLCA2 on cervical cancer. Reverse transcription-quantitative (RT-q)PCR was used to examine the mRNA expression levels of CLCA2 in eight pairs of cervical cancer tissues. Immunohistochemistry was used to investigate CLCA2 protein expression in 144 archived cervical cancer specimens. The association of the CLCA2 with clinicopathological parameters was statistically evaluated. Cell proliferation and invasion capability were examined by MTT and Transwell assays, respectively. RT-qPCR analysis revealed that CLCA2 expression was decreased in cervical cancer compared with that in adjacent normal tissues. The expression levels of CLCA2 in patients were correlated with tumor stage (P=0.028), tumor size (P=0.009), and human papillomavirus (HPV) infection status (P=0.041). In addition, CLCA2 upregulation was associated with longer overall and recurrence-free survival time after surgery (P=0.016 and P=0.009, respectively). Multivariate Cox regression analysis demonstrated that CLCA2 expression had a predictive value for overall survival of patients with cervical cancer (P=0.017 and P=0.025, respectively). Knockdown of CLCA2 by small interfering RNA suppressed tumor cell proliferation and migration. Mechanistically, CLCA2 was involved in Wnt/ß-catenin signaling. In conclusion, the results of the present study demonstrated that CLCA2 suppressed the proliferation, migration and invasion of cervical cancer cells, and that CLCA2 may be a potential therapeutic target of cervical cancer.

Absorption, Metabolism, and Excretion, In Vitro Pharmacology, and Clinical Pharmacokinetics of Ozanimod, a Novel Sphingosine 1-Phosphate Receptor Modulator.

Ozanimod is approved for the treatment of relapsing forms of multiple sclerosis. Absorption, metabolism, and excretion of ozanimod were investigated after a single oral dose of 1.0 mg [14C]ozanimod hydrochloride to six healthy subjects. In vitro experiments were conducted to understand the metabolic pathways and enzymes involved in the metabolism of ozanimod and its active metabolites. The total mean recovery of the administered radioactivity was ∼63%, with ∼26% and ∼37% recovered from urine and feces, respectively. Based on exposure, the major circulating components were active metabolite CC112273 and inactive metabolite RP101124, which together accounted for 50% of the circulating total radioactivity exposure, whereas ozanimod accounted for 6.7% of the total radioactive exposure. Ozanimod was extensively metabolized, with 14 metabolites identified, including two major active metabolites (CC112273 and CC1084037) and one major inactive metabolite (RP101124) in circulation. Ozanimod is metabolized by three primary pathways, including aldehyde dehydrogenase and alcohol dehydrogenase, cytochrome P450 isoforms 3A4 and 1A1, and reductive metabolism by gut microflora. The primary metabolite RP101075 is further metabolized to form major active metabolite CC112273 by monoamine oxidase B, which further undergoes reduction by carbonyl reductases to form CC1084037 or CYP2C8-mediated oxidation to form RP101509. CC1084037 is oxidized rapidly to form CC112273 by aldo-keto reductase 1C1/1C2 and/or 3ß- and 11ß-hydroxysteroid dehydrogenase, and this reversible oxidoreduction between two active metabolites favors CC112273. The ozanimod example illustrates the need for conducting timely radiolabeled human absorption, distribution, metabolism, and excretion studies for characterization of disproportionate metabolites and assessment of exposure coverage during drug development. SIGNIFICANCE STATEMENT: Absorption, metabolism, and excretion of ozanimod were characterized in humans, and the enzymes involved in complex metabolism were elucidated. Disproportionate metabolites were identified, and the activity of these metabolites was determined.

Concentration-QTc Modeling of Ozanimod's Major Active Metabolites in Adult Healthy Subjects.

Ozanimod, approved by regulatory agencies in multiple countries for the treatment of adults with relapsing multiple sclerosis, is a sphingosine 1-phosphate (S1P) receptor modulator, which binds with high affinity selectively to S1P receptor subtypes 1 and 5. The relationships between plasma concentrations of ozanimod and its major active metabolites, CC112273 and CC1084037, and the QTc interval (C-QTc) from a phase I multiple-dose study in healthy subjects were analyzed using nonlinear mixed effects modeling. QTc was modeled linearly as the sum of a sex-related fixed effect, baseline, and concentration-related random effects that incorporated interindividual and residual variability. Common linear, power, and maximum effect (Emax ) functions were assessed for characterizing the relationship of QTc with concentrations. Model goodness-of-fit and performance were evaluated by standard diagnostic tools, including a visual predictive check. The placebo-corrected change from baseline in QTc (ΔΔQTc) was estimated based on the developed C-QTc model using a nonparametric bootstrapping approach. QTc was better derived using a study-specific population formula (QTcP). Among the investigated functions, an Emax function most adequately described the relationship of QTcP with concentrations. Separate models for individual analytes characterized the C-QTcP relationship better than combined analytes models. Attributing QT prolongation independently to CC1084037 or CC112273, the upper bound of the 95% confidence interval of the predicted ΔΔQTcP was ~ 4 msec at the plateau of the Emax curves. Therefore, ΔΔQTcP is predicted to remain below 10 msec at the supratherapeutic concentrations of the major active metabolites.

Multiple-Dose Pharmacokinetics of Ozanimod and its Major Active Metabolites and the Pharmacodynamic and Pharmacokinetic Interactions with Pseudoephedrine, a Sympathomimetic Agent, in Healthy Subjects.

INTRODUCTION: The aims of this study were to characterize the multiple-dose pharmacokinetics (PK) of ozanimod's major active metabolites (CC112273 and CC1084037) and to evaluate the pharmacodynamic and PK interactions with pseudoephedrine (PSE). METHODS: In this phase 1, single-center, randomized, double-blind, placebo-controlled study, 56 healthy adult subjects were randomized to receive either placebo or ozanimod once daily for 30 days (0.23 mg on days 1-4, 0.46 mg on days 5-7, 0.92 mg on days 8-10, and 1.84 mg on days 11-30). On day 30, a single oral dose of PSE 60 mg was co-administered with placebo or ozanimod. Maximum time-matched change in systolic blood pressure (SBP) from baseline (day 29) following PSE administration on day 30 was calculated. Plasma PK parameters for ozanimod, CC112273, CC1084037, and PSE were estimated using noncompartmental methods. RESULTS: Fifty-two subjects (92.9%) completed the study. Following multiple dosing, approximately 94% of circulating total active drug exposure was represented by ozanimod (6%), CC112273 (73%), and CC1084037 (15%). Exposures of CC112273 and CC1084037 were highly correlated. Mean maximum time-matched change from baseline for SBP was not significantly different between ozanimod + PSE and placebo + PSE. Ozanimod also had no effect on the PK of PSE. Co-administration of ozanimod with a single dose of PSE in healthy subjects was generally well tolerated. While CC112273 and CC1084037 selectively inhibited monoamine oxidase (MAO)-B in vitro, both active metabolites do not inhibit platelet MAO-B activity in vivo. CONCLUSION: Concomitant administration of ozanimod with PSE, a sympathomimetic agent, did not potentiate the effects on blood pressure. TRIAL REGISTRATION: NCT03644576.

Single-Dose Pharmacokinetics of Ozanimod and its Major Active Metabolites Alone and in Combination with Gemfibrozil, Itraconazole, or Rifampin in Healthy Subjects: A Randomized, Parallel-Group, Open-Label Study.

INTRODUCTION: The aims of this study were to characterize the single-dose pharmacokinetics (PK) of the major active metabolites of ozanimod, CC112273 and CC1084037, and to evaluate the effect of gemfibrozil (a strong inhibitor of cytochrome P450 [CYP] 2C8), itraconazole (a strong inhibitor of CYP3A and P-glycoprotein [P-gp]), and rifampin (a strong inducer of CYP3A/P-gp and moderate inducer of CYP2C8) on the single-dose PK of ozanimod and its major active metabolites in healthy subjects. METHODS: This was a phase 1, randomized, parallel-group, open-label study with two parts. In part 1, 40 subjects were randomized to receive a single oral dose of ozanimod 0.46 mg (group A, n = 20) or oral doses of gemfibrozil 600 mg twice daily for 17 days with a single oral dose of ozanimod 0.46 mg on day 4 (group B, n = 20). In part 2, 60 subjects were randomized to receive a single oral dose of ozanimod 0.92 mg (group C, n = 20), oral doses of itraconazole 200 mg once daily for 17 days with a single oral dose of ozanimod 0.92 mg on day 4 (group D, n = 20), or oral doses of rifampin 600 mg once daily for 21 days with a single oral dose of ozanimod 0.92 mg on day 8 (group E, n = 20). Plasma PK parameters for ozanimod, CC112273, and CC1084037 were estimated using noncompartmental methods. RESULTS: Dose-proportional increases in maximum observed concentration (Cmax) and area under the concentration-time curve (AUC) were observed for ozanimod, CC112273, and CC1084037. The mean terminal elimination half-life (t1/2) for ozanimod was approximately 20-22 h while the mean t1/2 for CC112273 and CC1084037 were approximately 10 days. CC112273 and CC1084037 exposures were highly correlated with or without interacting drugs. Itraconazole increased ozanimod AUC by approximately 13% while rifampin reduced ozanimod AUC by approximately 24%, suggesting a minor role of CYP3A and P-gp in the overall disposition of ozanimod. Gemfibrozil increased the AUC for CC112273 and CC1084037 by approximately 47% and 69%, respectively. Rifampin reduced the AUC for CC112273 and CC1084037, primarily via CYP2C8 induction, by approximately 60% and 55%, respectively. CONCLUSIONS: Ozanimod's major active metabolites, CC112273 and CC1084037, exhibited similar single-dose PK properties and their exposures were highly correlated. CYP2C8 is one of the important enzymes in the overall disposition of CC112273 and subsequently its direct metabolite CC1084037. TRIAL REGISTRATION: Clinical trial: NCT03624959.

miR106a Promotes the Growth of Transplanted Breast Cancer and Decreases the Sensitivity of Transplanted Tumors to Cisplatin.

OBJECTIVE: To explore the effect of miR106a on the growth of breast cancer xenografts and the sensitivity of chemotherapeutic agents. METHODS: Breast cancer cell lines (MDA-MB231 and MCF7) were transfected with an miR106 mimic and miR106a inhibitor. BALB/c female nude mice were selected to construct a transplanted-tumor model. Cisplatin treatment was performed 2 weeks after inoculation. After 5 weeks, tumor tissue was weighed. Apoptosis of tumor cells was detected by TUNEL staining. The expression of these proteins (Ki67, ß-catenin, cyclin D1 and cMyc) was detected by immunohistochemistry. The contents of P53, RUNX3, ABCG2, ß-catenin, BAX, and BCL2 mRNA were detected by qRT-PCR. RESULTS: The miR106a mimic (MM) group's tumor volume and weight were significantly bigger than those of the model group. miR106a mRNA content was higher than the blank control group, and ß-catenin and Ki67 protein were strongly positive. ß-catenin, BCL2, and ABCG2 mRNA content was were increased. P53, BAX, and RUNX3 mRNA content was decreased. The number of positive cells on TUNEL staining was significantly lower in the miR106a inhibitor (MI) group. After cisplatin treatment, inhibition of tumor growth was most obvious in the MI+DDP (cisplatin) group. Compared with the MM group, tumor growth in the MM+FH535 (Wnt-pathway inhibitor) group was significantly lower, and Wnt-pathway activity was decreased. CONCLUSION: Overexpression of miR106a can promote the growth of transplanted breast cancer and decrease the sensitivity of transplanted tumors to cisplatin. The mechanism may be related to abnormal activation of the Wnt-signaling pathway.

Coagulation Factor Plasma Levels Following Administration of a 4-Factor Prothrombin Complex Concentrate for Rapid Vitamin K Antagonist Reversal in Japanese Patients.

BACKGROUND: Four-factor prothrombin complex concentrates (4F-PCCs) have been approved for urgent vitamin K antagonist reversal in Western countries for many years. Ethnicity and genetic variations between populations may influence the pharmacokinetic profile of 4F-PCC treatments. OBJECTIVE: To report plasma levels of vitamin K-dependent coagulation factors and proteins C and S in Japanese patients following administration of a 4F-PCC approved recently in Japan. METHODS: This was a subanalysis of a prospective, open-label, Phase IIIb study in Japanese patients requiring rapid vitamin K antagonist reversal owing to major bleeding (n = 6) or need for urgent surgery (n = 5). International normalized ratio and plasma levels of factors II, VII, IX, and X, and proteins C and S were measured before PCC infusion and at specific time points for the next 24 hours. Adverse events and serious adverse events were recorded up to Day 14 and 45, respectively. RESULTS: Rapid increases in plasma concentrations 30 minutes following 4F-PCC infusion were seen for all factors and proteins C and S, with median concentrations compared with baseline increasing by ≥100% and 70% in the bleeding and surgical groups, respectively. A concurrent decrease in international normalized ratio was observed. Plasma levels for each factor and protein remained within physiologic levels throughout the assessment period. No relationship between thromboembolic events and elevated plasma levels was identified. CONCLUSIONS: Administration of 4F-PCC in Japanese patients receiving vitamin K antagonist anticoagulation therapy resulted in rapid and sustained increases in plasma levels and was well tolerated, indicating that this treatment is effective for the urgent reversal of vitamin K antagonist therapy in this population.

The correlation analysis of tumor necrosis factor-alpha-308G/A polymorphism and venous thromboembolism risk: A meta-analysis.

OBJECTIVE: Venous thromboembolism is a common complex disorder, being the resultant of gene-gene and gene-environment interactions. Tumor necrosis factor-alpha is a proinflammatory cytokine which has been implicated in venous thromboembolism risk. A promoter 308G/A polymorphism in the tumor necrosis factor-alpha gene has been suggested to modulate the risk for venous thromboembolism. However, the published findings remain inconsistent. METHODS: In this study, we conducted a meta-analysis of all available data regarding this issue. Eligible studies were identified through search of Pubmed, EBSCO Medline, Web of Science, and China National Knowledge Infrastructure (CNKI, Chinese) databases up to June 2014. Pooled Odd ratios (ORs) with 95% confidence intervals were applied to estimating the strength of the genetic association in the random-effects model or fixed-effects model. RESULTS: A total of 10 studies involving 1999 venous thromboembolism cases and 2166 controls were included in this meta-analysis to evaluate the association between tumor necrosis factor-alpha-308G/A polymorphism and venous thromboembolism risk. Overall, no significantly increased risk venous thromboembolism was observed in all comparison models when all studies were pooled into the meta-analysis. However, in stratified analyses by ethnicity, there was a pronounced association with venous thromboembolism risk among West Asians in three genetic models (A vs. G: OR = 1.82, 95%CI = 1.13-2.94; GA vs. GG: OR = 1.82, 95%CI = 1.08-3.06; AA/GA vs. GG: OR = 1.88, 95%CI = 1.12-3.16). When stratifying by source of controls, no significant result was detected in all genetic models. CONCLUSION: This meta-analysis demonstrates that tumor necrosis factor-alpha 308G/A polymorphism may contribute to susceptibility to venous thromboembolism among West Asians. Studies are needed to ascertain these findings in larger samples and different racial groups.

Classification of hospital acquired complications using temporal clinical information from a large electronic health record.

Hospital acquired complications (HACs) are serious problems affecting modern day healthcare institutions. It is estimated that HACs result in an approximately 10% increase in total inpatient hospital costs across US hospitals. With US hospital spending totaling nearly $900 billion per annum, the damages caused by HACs are no small matter. Early detection and prevention of HACs could greatly reduce strains on the US healthcare system and improve patient morbidity & mortality rates. Here, we describe a machine-learning model for predicting the occurrence of HACs within five distinct categories using temporal clinical data. Using our approach, we find that at least $10 billion of excessive hospital costs could be saved in the US alone, with the institution of effective preventive measures. In addition, we also identify several keystone features that demonstrate high predictive power for HACs over different time periods following patient admission. The classifiers and features analyzed in this study show high promise of being able to be used for accurate prediction of HACs in clinical settings, and furthermore provide novel insights into the contribution of various clinical factors to the risk of developing HACs as a function of healthcare system exposure.

Association between JAK2 rs4495487 Polymorphism and Risk of Budd-Chiari Syndrome in China.

Myeloproliferative neoplasms (MPNs) are the leading cause of Budd-Chiari syndrome (BCS), and the C allele of JAK2 rs4495487 was reported to be an additional candidate locus that contributed to MPNs. In the present study, we examined the role of JAK2 rs4495487 in the etiology and clinical presentation of Chinese BCS patients. 300 primary BCS patients and 311 healthy controls were enrolled to evaluate the association between JAK2 rs4495487 polymorphism and risk of BCS. All subjects were detected for JAK2 rs4495487 by real-time PCR. Results. The JAK2 rs4495487 polymorphism was associated with JAK2 V617F-positive BCS patients compared with controls (P < 0.01). The CC genotype increased the risk of BCS in patients with JAK2 V617F mutation compared with individuals presenting TT genotype (OR = 13.60, 95% CI = 2.04-90.79) and non-CC genotype (OR = 12.00, 95% CI = 2.07-69.52). We also observed a significantly elevated risk of combined-type BCS associated with CC genotype in the recessive model (OR = 4.44, 95% CI = 1.31-15.12). This study provides statistical evidence that the JAK2 rs4495487 polymorphism is susceptibility factor JAK2 V617F positive BCS and combined BCS in China. Further larger studies are required to confirm these findings.

SMART on FHIR Genomics: facilitating standardized clinico-genomic apps.

BACKGROUND: Supporting clinical decision support for personalized medicine will require linking genome and phenome variants to a patient's electronic health record (EHR), at times on a vast scale. Clinico-genomic data standards will be needed to unify how genomic variant data are accessed from different sequencing systems. METHODS: A specification for the basis of a clinic-genomic standard, building upon the current Health Level Seven International Fast Healthcare Interoperability Resources (FHIR®) standard, was developed. An FHIR application protocol interface (API) layer was attached to proprietary sequencing platforms and EHRs in order to expose gene variant data for presentation to the end-user. Three representative apps based on the SMART platform were built to test end-to-end feasibility, including integration of genomic and clinical data. RESULTS: Successful design, deployment, and use of the API was demonstrated and adopted by HL7 Clinical Genomics Workgroup. Feasibility was shown through development of three apps by various types of users with background levels and locations. CONCLUSION: This prototyping work suggests that an entirely data (and web) standards-based approach could prove both effective and efficient for advancing personalized medicine.

Right Versus Left Laparoscopic Living-Donor Nephrectomy: A Meta-Analysis.

OBJECTIVES: We assessed the safety and efficacy of right versus left laparoscopic living-donor nephrectomy. Few clinical controlled studies have compared the right and left side, and most trials have a small sample number and varied results. A meta-analysis of published trials was performed to determine the effects of the 2 different approaches. MATERIALS AND METHODS: Major databases including Medline (PubMed), Embase, Ovid, and Cochrane were searched to identify studies comparing right and left laparoscopic living-donor nephrectomy (January 2000 to January 2014). Outcomes evaluated included operative time, warm ischemia time, operative blood loss, 1-year graft loss, donor intraoperative and postoperative complications, recipient postoperative complications, donor blood transfusion, conversion to open donor nephrectomy, length of donor hospital stay, and delayed graft function. RESULTS: There were 15 studies included with 3073 patients (left, 2420 patients [78%]; right, 653 patients [22%]). The right group had shorter operative time (weighted mean difference, -13.44 min; 95% confidence interval, -22.73 to -4.15 min; P = .005) and lower operative blood loss (weighted mean difference, -10.53 mL; 95% confidence interval, -17.43 to -3.64 mL; P = .003) than the left group. There was a higher rate of overall donor intraoperative complications in the left group (odds ratio, 0.53; 95% confidence interval, 0.31-0.92; P = .03). There were no differences between groups in hospital stay, delayed graft function, recipient 1-year graft loss, conversion to open donor nephrectomy, donor blood transfusion, and donor or recipient postoperative complications. CONCLUSIONS: Right and left laparoscopic living-donor nephrectomy were similar in the effect of surgery and postoperative graft function. When there are no differences in bilateral renal function, surgeons can transplant the right or left kidney. However, the longer renal vein of the left kidney could decrease operative difficulty, and we recommend using the left kidney in clinical practice.