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Retinoblastoma(RB)is the most common intraocular malignant tumor of children. Chemotherapy is a preferred method in RB treatment, which includes intravenous chemotherapy, intra-arterial chemotherapy and intravitreal chemotherapy. However, the occurrence of chemotherapy resistance often leads to the failure of eye-preserving treatment in RB patients. Therefore, exploring the mechanism of the occurrence of chemotherapy resistance and searching for new strategies and combined medicines for RB treatment are of great clinical significance. This article reviews that RB cells obtain chemotherapy resistance through ATP binding cassette protein(ABC transporter), non-coding RNA, epigenetics modification, autophagy, epithelial mesenchymal transformation, extracellular matrix changes and other ways, and the potential therapeutic targets for chemotherapy resistance are also summarized, in the hope of providing some references for further research on chemotherapy resistance of RB.

Purpose: To investigate the pharmacokinetics and tissue distribution of VGB racemate and its single enantiomers, and explore the potential of clinic development for single enantiomer S-VGB. Methods: In the pharmacokinetics study, male Sprague-Dawley rats were gavaged with VGB racemate or its single enantiomers dosing 50, 100 or 200 mg/kg, and the blood samples were collected during 12 h at regular intervals. In the experiment of tissue distribution, VGB and its single enantiomers were administered intravenously dosing 200 mg/kg, and the tissues including heart, liver, spleen, lung and kidney, eyes, hippocampus, and prefrontal cortex were separated at different times. The concentrations of R-VGB and S-VGB in the plasma and tissues were measured using HPLC. Results: Both S-VGB and R-VGB could be detected in the plasma of rats administered with VGB racemate, reaching Cmax at approximately 0.5 h with t1/2 2–3 h. There was no significant pharmacokinetic difference between the two enantiomers when VGB racemate was given 200 mg/kg and 100 mg/kg. However, when given at the dose of 50 mg/kg, S-VGB presented a shorter t1/2 and a higher Cl/F than R-VGB, indicating a faster metabolism of S-VGB. Furthermore, when single enantiomer was administered respectively, S-VGB presented a slower metabolism than R-VGB, as indicated by a longer t1/2 and MRT but a lower Cmax. Moreover, compared with the VGB racemate, the single enantiomers S-VGB and R-VGB had shorter t1/2 and MRT, higher Cmax and AUC/D, and lower Vz/F and Cl/F, indicating the stronger oral absorption and faster metabolism of single enantiomer. In addition, regardless of VGB racemate administration or single enantiomer administration, S-VGB and R-VGB had similar characteristics in tissue distribution, and the content of S-VGB in hippocampus, prefrontal cortex and liver was much higher than that of R-VGB. Conclusions: Although there is no transformation between S-VGB and R-VGB in vivo, those two enantiomers display certain disparities in the pharmacokinetics and tissue distribution, and interact with each other. These findings might be a possible interpretation for the pharmacological and toxic effects of VGB and a potential direction for the development and optimization of the single enantiomer S-VGB.

Conclusion: MLT levels decreased in patients with T2DM and were associated with neuropsychiatric impairments and inflammatory status, and MLT might be developed as a therapeutic agent and predictive indicator for T2DM-associated executive impairment and depression status.

ObjectivesTo estimate the association of previous pregnancy loss with subsequent cardiovascular health during gestation and to examine the role of high-sensitivity C reactive protein (hs-CRP) in the association.MethodsA total of 2,778 nulliparous pregnant women were recruited between March 2015 and November 2020 in Hefei city, China. Their cardiovascular health (CVH) including prepregnancy body mass index (BMI), blood pressure, total cholesterol, fasting plasma glucose, and smoke status were recorded at 24–28 weeks’ gestation, as well as their reproductive history. Multivariate linear and logistic regression were performed to examine the association of pregnancy loss with cardiovascular health. And the role of hs-CRP between pregnancy loss and CVH was assessed by the mediation analysis.ResultsCompared with women who have no pregnancy loss, women with a history of spontaneous or induced abortions had higher BMI (β, 0.72, 95% CI, 0.50 to 0.94) and fasting plasma glucose (β, 0.04, 95% CI, 0.01 to 0.07), and had lower total CVH scores after adjusting for confounders (β, −0.09, 95% CI, −0.18 to −0.01). CVH scores were most significantly decreased among women with 3 or more induced abortions (β, −0.26, 95% CI, −0.49, −0.02). The contribution of pregnancy loss to poorer gestational CVH mediated by increased hs-CRP levels was 23.17%.ConclusionPrevious pregnancy loss was associated with poorer cardiovascular health during gestation, which may be mediated by their gestational inflammatory status. Exposure to miscarriage alone was not a significant predictor of poorer CVH.

Abstract Background Alzheimer's disease (AD) is a neurodegenerative disease characterized by a progressive decline in cognitive ability. Exosomes derived from bone-marrow mesenchymal stem cells (BMSC-exos) are extracellular vesicles that can execute the function of bone-marrow mesenchymal stem cells (BMSCs). Given the versatile therapeutic potential of BMSC and BMSC-exos, especially their neuroprotective effect, the aim of this study was to investigate the potential effect of BMSC-exos on AD-like behavioral dysfunction in mice and explore the possible molecular mechanism. Methods BMSC-exos were extracted from the supernatant of cultured mouse BMSCs, which were isolated from the femur and tibia of adult C57BL/6 mice, purified and sorted via flow cytometry, and cultured in vitro. BMSC-exos were identified via transmission electron microscopy, and typical marker proteins of exosomes were also detected via Western blot. A sporadic AD mouse model was established by intracerebroventricular injection of streptozotocin (STZ). Six weeks later, BMSC-exos were administered via lateral ventricle injection or caudal vein injection lasting five consecutive days, and the control mice were intracerebroventricularly administered an equal volume of solvent. Behavioral performance was observed via the open field test (OFT), elevated plus maze test (EPM), novel object recognition test (NOR), Y maze test (Y-maze), and tail suspension test (TST). The mRNA and protein expression levels of IL-1β, IL-6, and TNF-α in the hippocampus were measured via quantitative polymerase chain reaction (qPCR) and Western blot, respectively. Moreover, the protein expression of Aβ1-42, BACE, IL-1β, IL-6, TNF-α, GFAP, p-Tau (Ser396), Tau5, synaptotagmin-1 (Syt-1), synapsin-1, and brain-derived neurotrophic factor (BDNF) in the hippocampus was detected using Western blot, and the expression of GFAP, IBA1, Aβ1−42 and DCX in the hippocampus was measured via immunofluorescence staining. Results Lateral ventricle administration, but not caudal vein injection of BMSC-exos improved AD-like behaviors in the STZ-injected mouse model, as indicated by the increased number of rearing, increased frequency to the central area, and increased duration and distance traveled in the central area in the OFT, and improved preference index of the novel object in the NOR. Moreover, the hyperactivation of microglia and astrocytes in the hippocampus of the model mice was inhibited after treatment with BMSC-exos via lateral ventricle administration, accompanied by the reduced expression of IL-1β, IL-6, TNF-α, Aβ1-42, and p-Tau and upregulated protein expression of synapse-related proteins and BDNF. Furthermore, the results of the Pearson test showed that the preference index of the novel object in the NOR was positively correlated with the hippocampal expression of BDNF, but negatively correlated with the expression of GFAP, IBA1, and IL-1β. Apart from a positive correlation between the hippocampal expression of BDNF and Syt-1, BDNF abundance was found to be negatively correlated with markers of glial activation and the expression of the inflammatory cytokines, Aβ1-42, and p-Tau, which are characteristic neuropathological features of AD. Conclusions Lateral ventricle administration, but not caudal vein injection of BMSC-exos, can improve AD-like behavioral performance in STZ-injected mice, the mechanism of which might be involved in the regulation of glial activation and its associated neuroinflammation and BDNF-related neuropathological changes in the hippocampus.

PurposeTo investigate the changes of plasma 25(OH)D levels in type 2 diabetes mellitus (T2DM) patients and explore its role in the dysfunction of glucose and lipid metabolism and cognition.MethodsOne hundred and thirty-two T2DM patients were enrolled and the demographic and clinical data were collected. The plasma concentration of 25(OH)D was detected and the patients were divided into two groups including a Vitamin D insufficient (VDI) group and a normal VD group according to the clinical diagnostic criterial of VDI with the plasma 25(OH)D level less than 29 ng/mL. The glycolipid metabolic and routine blood biochemical indices were detected, the plasma concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), soluble myeloid soluble trigger receptor 1 (sTREM1) were measured. The cognitive function was assessed using the Behavior Rating Inventory of Executive Function-Adult Version (BRIEF-A). The depressive symptomatology was assessed using the Center for Epidemiological Survey Depression Scale (CES-D). Sleep quality was assessed using the Pittsburgh sleep quality index (PSQI).ResultsThere were 70 T2DM patients with VDI (70/132, 53.03%) in this study. The plasma concentrations of glycated hemoglobin (HbA1c), fasting plasma glucose (FPG), postprandial blood glucose (PBG), IL-6, and sTREM1 were remarkably increased in T2DM patients with VDI as compared with that with the normal VD, accompanied with an elevated BRIEF-A scores. There was no significant difference between groups with regard to the indices of blood lipid, liver function, and scores in CES-D and PSQI. Moreover, results of Pearson correlation test showed that the plasma 25(OH)D levels were negatively correlated with HbA1c, FPG, PBG, CRP, IL-6, sTREM1, CES-D sum scores, and PSQI sum scores, but positively correlated with the plasma levels of Serum creatinine (Scr). Furthermore, result of Receiver Operating Characteristic (ROC) curve analysis showed a predictive role of VDI levels in discriminating T2DM patients with higher cognitive impairments, with the sensitivity and specificity being 62.12% and 62.12%, respectively.ConclusionVDI is harmful for T2DM patients with a significant relation with the hyperglycosemia and cognitive dysfunction.

Abstract Background Quercetin (QUE) is a flavonol reported with anti-inflammatory and antioxidant activities, and previous results from the group of this study have demonstrated its neuroprotective effect against lipopolysaccharide-induced neuropsychiatric injuries. However, little is known about its potential effect on neuropsychiatric injuries induced or accompanied by metabolic dysfunction of glucose and lipids. Methods A nonalcoholic fatty liver disease (NAFLD) rat model was induced via a high-fat diet (HFD), and glucolipid parameters and liver function were measured. Behavioral performance was observed via the open field test (OFT) and the Morris water maze (MWM). The plasma levels of triggering receptor expressed on myeloid cells-1 (TREM1) and TREM2 were measured via enzyme-linked immunosorbent assay (ELISA). The protein expression levels of Synapsin-1 (Syn-1), Synaptatogmin-1 (Syt-1), TREM1 and TREM2 in the hippocampus were detected using western blotting. Morphological changes in the liver and hippocampus were detected by HE and Oil red or silver staining. Results Compared with the control rats, HFD-induced NAFLD model rats presented significant metabolic dysfunction, hepatocyte steatosis, and impaired learning and memory ability, as indicated by the increased plasma concentrations of total cholesterol (TC) and triglyceride (TG), the impaired glucose tolerance, the accumulated fat droplets and balloon-like changes in the liver, and the increased escaping latency but decreased duration in the target quadrant in the Morris water maze. All these changes were reversed in QUE-treated rats. Moreover, apart from improving the morphological injuries in the hippocampus, treatment with QUE could increase the decreased plasma concentration and hippocampal protein expression of TREM1 in NAFLD rats and increase the decreased expression of Syn-1 and Syt-1 in the hippocampus. Conclusions These results suggested the therapeutic potential of QUE against NAFLD-associated impairment of learning and memory, and the mechanism might involve regulating the metabolic dysfunction of glucose and lipids and balancing the protein expression of synaptic plasticity markers and TREM1/2 in the hippocampus.

Epilepsy is a common and disastrous neurological disorder characterized by abnormal firing of neurons in the brain, affecting about 70 million people worldwide. Long non-coding RNAs (LncRNAs) are a class of RNAs longer than 200 nucleotides without the capacity of protein coding, but they participate in a wide variety of pathophysiological processes. Alternated abundance and diversity of LncRNAs have been found in epilepsy patients and animal or cell models, suggesting a potential role of LncRNAs in epileptogenesis. This review will introduce the structure and function of LncRNAs, summarize the role of LncRNAs in the pathogenesis of epilepsy, especially its linkage with neuroinflammation, apoptosis, and transmitter balance, which will throw light on the molecular mechanism of epileptogenesis, and accelerate the clinical implementation of LncRNAs as a potential therapeutic target for treatment of epilepsy.

Objective: To establish an Alzheimer's disease (AD) mouse model, investigate the behavioral performance changes and intracerebral molecular changes induced by bilateral intracerebroventricular injection of streptozotocin (STZ/I.C.V), and explore the potential pathogenesis of AD. Methods: An AD mouse model was established by STZ/I.C.V. The behavioral performance was observed via the open field test (OFT), novel object recognition test (NOR), and tail suspension test (TST). The mRNA and protein expressions of interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) in the hippocampus were measured via qPCR and Western blot. The expression of β-amyloid 1–42 (Aβ1–42), phosphorylated Tau protein (p-Tau (Ser396)), Tau5, β-site amyloid precursor protein (APP) cleaving enzyme (BACE), insulin receptor substrate 1 (IRS1), brain-derived neurotrophic factor (BDNF), Copine6, synaptotagmin-1 (Syt-1), synapsin-1, phosphoinositol 3 kinase (PI3K), serine/threonine kinase (Akt), phosphorylated serine/threonine kinase (p-Akt (Ser473)), triggering receptor expressed on myeloid cells-1/2 (TREM1/2) were detected using Western blot, and the expression of glial fibrillary acidic protein (GFAP), ionized calcium binding adapter molecule 1 (IBA1), Aβ1–42, p-Tau(Ser396), Syt-1, BDNF were measured via immunofluorescence staining. Results: STZ/I.C.V induced AD-like neuropsychiatric behaviors in mice, as indicated by the impairment of learning and memory, together with the reduced spontaneous movement and exploratory behavior. The expression of BACE, Aβ1–42, p-Tau(Ser396), and TREM2 were significantly increased in the hippocampus of model mice, while the expression of IRS1, BDNF, Copine6, Syt-1, synapsin-1, PI3K, p-Akt(Ser473), and TREM1 were decreased as compared with that of the controls. Furthermore, the model mice presented a hyperactivation of astrocytes and microglia in the hippocampus, accompanied by the increased mRNA and protein expressions of IL-1β, IL-6 and TNF-α. Conclusion: STZ/I.C.V is an effective way to induce AD mice model, with not only AD-like neuropsychiatric behaviors, but also typic AD-like neuropathological features including neurofibrillary tangles, deposit of β-amyloid (Aβ), neuroinflammation, and imbalanced synaptic plasticity.

Attachment and separation of sulfate-reducing bacteria (SRB) biofilm on stainless steel (SS) in simulated cooling water with and without different sterilization treatments was investigated by calculation of surface energy, theoretical work of adhesion and analysis of Scanning Electron Microscope/Energy Dispersive Spectrometer. Two types of biocides, glutaraldehyde and Polyhexamethylene guanidine (PHMG), and electromagnetic treatment were used in this paper. The results show that PHMG had the best bactericidal performance, followed by glutaraldehyde, and electromagnetic treatment was the lowest one. The theoretical work of adhesion was used to quantitatively evaluate the adhesion of biofilm on the surface of the metal. Theoretical work of adhesion between biofilm and SS in simulated cooling water increased with time. The theoretical adhesion work and adhesive capacity of biofilm to SS surface increased after treating with glutaraldehyde while decreasing after treating with PHMG and electromagnetic field. As the theoretical adhesion work decreased, the biofilm was gradually removed from the stainless steel surface. On the contrary, the biofilm adhered more firmly. The results of SEM were also consistent with the calculation results of theoretical adhesion work. The results obtained indicated that electromagnetic treatment had the lowest effect in sterilization but the best in biofilm separation.

Transmembrane proteins have critical biological functions and play a role in a multitude of cellular processes including cell signaling, transport of molecules and ions across membranes. Approximately 60% of transmembrane proteins are considered as drug targets. Missense mutations in such proteins can lead to many diverse diseases and disorders, such as neurodegenerative diseases and cystic fibrosis. However, there are limited studies on mutations in transmembrane proteins. In this work, we first design a new feature encoding method, termed weight attenuation position-specific scoring matrix (WAPSSM), which builds upon the protein evolutionary information. Then, we propose a new mutation prediction algorithm (cascade XGBoost) by leveraging the idea learned from consensus predictors and gcForest. Multi-level experiments illustrate the effectiveness of WAPSSM and cascade XGBoost algorithms. Finally, based on WAPSSM and other three types of features, in combination with the cascade XGBoost algorithm, we develop a new transmembrane protein mutation predictor, named MutTMPredictor. We benchmark the performance of MutTMPredictor against several existing predictors on seven datasets. On the 546 mutations dataset, MutTMPredictor achieves the accuracy (ACC) of 0.9661 and the Matthew’s Correlation Coefficient (MCC) of 0.8950. While on the 67,584 dataset, MutTMPredictor achieves an MCC of 0.7523 and area under curve (AUC) of 0.8746, which are 0.1625 and 0.0801 respectively higher than those of the existing best predictor (fathmm). Besides, MutTMPredictor also outperforms two specific predictors on the Pred-MutHTP datasets. The results suggest that MutTMPredictor can be used as an effective method for predicting and prioritizing missense mutations in transmembrane proteins. The MutTMPredictor webserver and datasets are freely accessible at http://csbio.njust.edu.cn/bioinf/muttmpredictor/ for academic use.

Abstract Background Perioperative immune function plays an important role in the prognosis of patients. Several studies have indicated that low-dose opioid receptor blockers can improve immune function. Methods Sixty-nine patients undergoing video-assisted thoracoscopic resection of the lung cancer were randomly assigned to either the naloxone group (n = 35) or the non-naloxone group (n = 34) for postoperative analgesia during the first 48 h after the operation. Both groups received sufentanil and palonosetron via postoperative analgesia pump, while 0.05 μg·kg− 1·h− 1 naloxone was added in naloxone group. The primary outcomes were the level of opioid growth factor (OGF) and immune function assessed by natural killer cells and CD4+/CD8+ T-cell ratio. Second outcomes were assessed by the intensity of postoperative pain, postoperative rescue analgesia dose, postoperative nausea and vomiting (PONV). Results The level of OGF in the naloxone group increased significantly at 24 h (p

Abstract Background The important property of the quantitative traits of model organisms is time-dependent. However, the methodology for investigating the genetic interaction network over time is still lacking. Our study aims to provide insights into the mechanistic basis of epistatic interactions affecting the phenotypes of model organisms. Results We performed an exhaustive genome-wide search for significant SNP-SNP interactions associated with male birds’ body weight (BW) (n = 475) at multiple time points (day of hatch (BW0) and 1, 3, 5, and 7 weeks (BW1, BW3, BW5, and BW7)). Statistical analysis detected 67, four, and two significant SNP pairs associated with BW0, BW1, and BW3, respectively, with a significance threshold at 8.67 × 10− 12 (Bonferroni-adjusted: 1%). Meanwhile, no significant SNP pairs associated with BW5 and BW7 were found. The SNP-SNP interaction networks of BW0, BW1, and BW3 were built and annotated. Conclusions With strong annotated information and a strict significant threshold, SNP-SNP interactions underpinned the gene-gene interactions that might occur between chromosomes or within the same chromosome. Comparing and combing the networks, the results indicated that the genetic network for chicken body weight was dynamic and time-dependent.

Background: Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, psychiatric symptoms and behavioral disorders, resulting in disability, and loss of self-sufficiency.Objective: To establish an AD-like mice model, investigate the behavioral performance, and explore the potential mechanism.Methods: Streptozotocin (STZ, 3 mg/kg) was microinjected bilaterally into the dorsal hippocampus of C57BL/6 mice, and the behavioral performance was observed. The serum concentrations of insulin and nesfatin-1 were measured by ELISA, and the activation of hippocampal microglia and astrocytes was assessed by immunohistochemistry. The protein expression of several molecular associated with the regulation of synaptic plasticity in the hippocampus and the pre-frontal cortex (PFC) was detected via western blotting.Results: The STZ-microinjected model mice showed a slower bodyweight gain and higher serum concentration of insulin and nesfatin-1. Although there was no significant difference between groups with regard to the ability of balance and motor coordination, the model mice presented a decline of spontaneous movement and exploratory behavior, together with an impairment of learning and memory ability. Increased activated microglia was aggregated in the hippocampal dentate gyrus of model mice, together with an increase abundance of Aβ1−42 and Tau in the hippocampus and PFC. Moreover, the protein expression of NMDAR2A, NMDAR2B, SynGAP, PSD95, BDNF, and p-β-catenin/β-catenin were remarkably decreased in the hippocampus and the PFC of model mice, and the expression of p-GSK-3β (ser9)/GSK-3β were reduced in the hippocampus.Conclusion: A bilateral hippocampal microinjection of STZ could induce not only AD-like behavioral performance in mice, but also adaptive changes of synaptic plasticity against neuroinflammatory and endocrinal injuries. The underlying mechanisms might be associated with the imbalanced expression of the key proteins of Wnt signaling pathway in the hippocampus and the PFC.

To assess the effect of elevated CO2 on the development, fecundity, and population dynamic parameters of L. erysimi, the age-stage, two-sex life table was used to predict the individual fitness and population parameters of three successive generations of L. erysimi in this study. The results show that a significantly longer total pre-adult stage before oviposition (TPOP) was observed in the third generation compared with the first generation of L. erysimi under the 800 μL/L CO2 treatment. The fecundity is significantly lower in the 800 μL/L CO2 treatment than that in the 400 μL/L CO2 treatment in the third generation of L. erysimi, which indicates that elevated CO2 had a negative effect on the individual fitness parameters of L. erysimi. Additionally, the life expectancy (exj) is significantly lower under the 800 μL/L CO2 treatment than that under the 400 μL/L CO2 treatment in the three successive generations. A significantly higher intrinsic rate of increase (r) and finite rate of increase (λ) were found in the second generation compared with those in the first and third generations of L. erysimi under the 800 μL/L CO2 treatment. Moreover, significantly lower r and λ were observed under the 800 μL/L CO2 treatment compared with those under the 400 μL/L and 600 μL/L CO2 treatments in the first generation of L. erysimi, which indicates that elevated CO2 has a short-term effect on the population parameters (r and λ) of L. erysimi. Our experiment can provide the data for the comprehensive prevention and control of L. erysimi in the future with increasing CO2 levels.

Nutritional and microbiological psychiatry, especially the contribution of the gut microbiota to depression, has become a promising research field over the past several decades. An imbalance in the “microbiota-gut-brain axis”, which reflects the constant bidirectional communication between the central nervous system and the gastrointestinal tract, has been used as a hypothesis to interpret the pathogenesis of depression. Alterations in gut microbiota composition could increase the permeability of the gut barrier, activate systemic inflammation and immune responses, regulate the release and efficacy of monoamine neurotransmitters, alter the activity and function of the hypothalamic-pituitary-adrenal (HPA) axis, and modify the abundance of brain-derived neurotrophic factor (BDNF), eventually leading to depression. In this article, we review changes in gut microbiota in depressive states, the association between these changes and depression-like behavior, the potential mechanism linking gut microbiota disruptions and depression, and preliminary attempts at using gut microbiota intervention for the treatment of depression. In summary, although the link between gut microbiota and depression and the potential mechanism have been discussed, a more detailed mechanistic understanding is needed to fully realize the importance of the microbiota-gut-brain axis in depression. Future efforts should aim to determine the potential causative mechanisms, which will require further animal and clinical research as well as the development of analytical approaches.

The goal of this study was to determine whether the plasma leptin, nesfatin-1, cortisol, brain-derived neurotrophic factor (BDNF), and inflammatory cytokines could be used as potential biomarkers for the degree of craving in the alcohol-dependent patients after 1 month of abstinence. A total of 83 patients with alcohol use disorder (AUD) and 61 healthy subjects were assessed. Patients with AUD were selected from Department of Material Dependence, Anhui Mental Health Center, and subjects in the control group were selected from healthy volunteers. The Alcohol Urge questionnaire Scale (AUQ) was used to evaluate the extent of craving for alcohol, and the Michigan Alcoholism Screening Test (MAST), the Fagerstrom Test for Nicotine Dependence (FTND), the Self-Rating Anxiety Scale (SAS), and the Self-Rating Depression Scale (SDS) were also assessed in patients with AUD. Enzyme-Linked Immunosorbent Assay (ELISA) was used for the measurement of plasma leptin, nesfatin-1, cortisol, BDNF, Interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) levels. Compare with healthy controls, the average leptin, leptin/BMI, IL-6, CRP, and TNF-α levels in patients with AUD were significantly increased, while the BDNF levels were significantly decreased. Moreover, the partial correlational analysis showed that the AUQ scores of the alcohol-dependent patients were positively correlated with the plasma leptin levels (r = 0.613, P < 0.001), rather than nesfatin-1 (r = 0.066, P = 0.569) after controlling for age as covariate. Furthermore, plasma nesfatin-1 levels were found to be correlated with the SDS scores (r = 0.366, P = 0.001) in the AUD group. In addition, plasma leptin levels were positively associated with the plasma IL-6 (r = 0.257, P = 0.033), CRP (r = 0.305, P = 0.011), and TNF-α (r = 0.311, P = 0.009) levels, and negatively associated with the BDNF levels (r = −0.245, P = 0.042) in patients with AUD. These results suggest that plasma leptin, but not nesfatin-1, might be a potential biomarker for the degree of craving in alcohol-dependent patients after 1 month of abstinence, the mechanism of which might be related to the dysfunction of the inflammatory cytokines and BDNF levels.