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简介：AbstractBackground:Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Genome-wide association studies in non-Asian population revealed a link between COPD and mutations in the PTCH1 gene encoding Patched1, a receptor in the Hedgehog signaling pathway important for lung morphogenesis and pulmonary function. The aim of this study was to investigate the association between PTCH1 polymorphisms and the COPD risk in the Chinese Han population.Methods:We performed a case-control study including 296 patients with COPD and 300 healthy individuals. Single-nucleotide polymorphisms in the PTCH1 gene were identified and genotyped based on the linkage disequilibrium analysis in all participants. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression analysis after adjustment for age, gender, and smoking.Results:In total, 28 single-nucleotide polymorphisms were identified in patients with COPD. Among them, "A" allele of rs28491365 (OR: 1.388, 95% CI: 1.055-1.827, P = 0.018), and "G" alleles of rs10512248 (OR: 1.299, 95% CI: 1.021-1.653, P = 0.033) and rs28705285 (OR: 1.359, 95% CI: 1.024-1.803, P = 0.033; respectively) were significantly associated with an increased COPD risk. Genetic model analysis revealed that the "T/T" genotype of rs34695652 was associated with a decreased COPD risk under the recessive model (OR: 0.490, 95% CI: 0.270-0.880, P = 0.010), whereas rs28504650/rs10512248 haplotype CG was significantly associated with an increased COPD risk after adjustment for age, gender, and smoking status (OR: 6.364, 95% CI: 1.220-33.292, P = 0.028).Conclusions:The study provides a new insight into the role of PTCH1 polymorphisms in the susceptibility to COPD in the Chinese Han population.

简介：AbstractBackground:Air pollution and poor ambient air quality are significantly related to multiple health risks. One associated disease is chronic obstructive pulmonary disease (COPD), a preventable disease with several contributing factors and one of the leading causes of morbidity/mortality locally and globally. A potentially high-risk population are traffic enforcers who are constantly exposed to air pollution. In the Philippines, the MMDA has the widest coverage in traffic management. The study determined the risk of COPD among Metro Manila Development Authority (MMDA) traffic enforcers in relation to ambient air quality level, as well as identified other factors that increase the risk of developing COPD.Methods:Fifty-two MMDA traffic enforcers deployed in PM2.5 air quality sensor areas in Metro Manila from 2016 to 2018 were recruited through stratified sampling. The International Primary Airways Guidelines (IPAG) questionnaire was utilized to measure risk of COPD. Respiratory health and working history were obtained through questionnaires. Department of environment and natural resources provided PM2.5 ambient air quality data which aided in the construction of the Exposure-Month Index. Ordinal logistic regression was used to examine the association of PM2.5 together with the relevant factors and the risk of COPD.Results:We found statistically significant associations between PM2.5 and COPD among high risk category [odds risk (OR): 1.24, 95% confidence interval (CI): 1.07-1.44]. Age (Moderate, OR: 1.16, 95% CI: 0.98-1.38 and High, OR: 10.06, 95% CI: 4.02-25.17) and chest pain (Moderate, OR: 68.65, 95% CI: 1.71-2.75 × 103) were potential risk factors, whereas body mass index (BMI) (OR: 0.05, 95% CI: 0.01-0.53) exhibited protective effect.Conclusions:Exposure to PM2.5 was associated with an increased risk of COPD among high-risk category MMDA traffic enforcers. Age and chest pain were potential risk factors to risk of COPD, whereas BMI exhibited a potential protective effect. Results of this study can be used for clinical management of high-risk populations, such that of MMDA traffic enforcers.

简介：嗜中性的渗入是含酒精的steatohepatitis的一个特点；然而，内在的机制仍然保持不清楚。我们以前报导synergistically喂的chronic-plus-binge乙醇导致neutrophils的肝的招募，它贡献肝损害。在这份报纸，我们在chronic-plus-binge乙醇喂导致调查了不变的自然漂亮T(iNKT)房间的角色肝的嗜中性的渗入和肝损害。野类型并且iNKT的二紧张房间缺乏的老鼠(CD1d缺乏并且Jα；18-deficient老鼠)受到喂的chronic-plus-binge乙醇。肝损害和发炎被检验。synergistically喂的Chronic-plus-binge乙醇增加了肝的iNKT房间的数字并且导致了他们的激活，与独自的长期的喂或饮酒作乐相比。iNKT房间缺乏的老鼠被保护免受chronic-plus-binge的伤害导致乙醇的肝的嗜中性的渗入和肝损害。而且，显著地喂几基因的肝的表示在野类型的老鼠与发炎和嗜中性的招募联系了的upregulated的chronic-plus-binge乙醇，而是这些基因的正式就职在iNKT被废除房间缺乏的老鼠。重要地，几cytokines和chemokines(例如，MIP-2，MIP-1，IL-4，IL-6和osteopontin)在嗜中性的渗入包含了在肝的NKT房间的upregulated从chronic-plus-binge被孤立与喂对的老鼠相比的喂乙醇的老鼠。最后，有堵住抗体的CD1d的处理，堵住iNKT房间激活，部分阻止了chronic-plus-binge导致乙醇的肝损害和发炎。喂的Chronic-plus-binge乙醇激活肝的iNKT房间，它在早含酒精的肝损害的发展起一个关键作用，部分地由释放招募的调停人neutrophils到肝，并且这样，iNKT房间为含酒精的肝的治疗代表一个潜在的治疗学的目标疾病。

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简介：AbstractIntroduction:While majority of infants with bronchopulmonary dysplasia (BPD) can be discharged home without low flow oxygen or on supplemental low flow oxygen, some require long term home mechanical ventilation.Case presentation:We present a case of an extremely premature infant with severe bronchopulmonary dysplasia who was successfully managed at home on a new feature of non-invasive ventilation called average volume assured pressure support (AVAPS) without the need for tracheostomy. The AVAPS feature enables the machine to deliver a consistent tidal volume by automatically adjusting the inspiratory pressure within a set range.Conclusion:The use of AVAPS feature in our case improved ventilation as indicated by a more stable gas exchange profile, making home non-invasive ventilation a more practicable method of managing severe BPD in this infant.

简介：AbstractBackground:The COVID-19 novel coronavirus is contagious, and the mortality is higher in the elderly population. Lockdown in different parts of the world has been imposed since January 2020. Chronic subdural haematoma (cSDH) has a unique natural history in which symptoms can be non-specific, and the onset is insidious. This study aims to evaluate the impact of the COVID-19 pandemic on the presentation of cSDH.Methods:Consecutive adult cSDH patients admitted from 1 March 2020 to 30 April 2020 were reviewed. Exclusion criteria including those who had no definite history of head injury or the diagnosis of cSDH were made from a scheduled follow-up scan. Corresponding data during the same period in 2019 were reviewed for comparison. The primary outcome was the interval between the initial head injury and the final radiological diagnosis of cSDH. Secondary outcomes include Markwalder chronic subdural haematoma grade upon admission, length of stay in the acute hospital, and the modified Rankin scale (mRS) upon discharge.Results:For the primary outcome, the average interval between head injury and the diagnosis of cSDH was significantly longer at 56.6 days (49 to 74 days, SD 9.83 days) during the period from March to April 2020, versus 29.4 days (17 to 42 days, SD 8.59 days) in 2019 for the corresponding period (p = 0.00703). There was no significant difference in the functional outcome upon discharge.Conclusions:cSDH patients can present late during the COVID-19 lockdown period. The functional outcome was comparable when operations for drainage were timely performed.

简介：AbstractA significant number of SARS-CoV-2 (COVID-19) pandemic patients have developed chronic symptoms lasting weeks or months which are very similar to those described for myalgic encephalomyelitis/chronic fatigue syndrome. This study reviews the current literature and understanding of the role that mitochondria, oxidative stress and antioxidants may play in the understanding of the pathophysiology and treatment of chronic fatigue. It describes what is known about the dysfunctional pathways which can develop in mitochondria and their relationship to chronic fatigue. It also reviews what is known about oxidative stress and how this can be related to the pathophysiology of fatigue, as well as examining the potential for specific therapy directed at mitochondria for the treatment of chronic fatigue in the form of antioxidants. This study identifies areas which require urgent, further research in order to fully elucidate the clinical and therapeutic potential of these approaches.

简介：Theacquisitionofsecondarychromosomalaberrationsinchronicmyeloidleukemia(CML)patientswithPhiladelphiachromosome-positive(Ph+)karyotypesignifiesclonalevolutionassociatedwiththeprogressionofthediseasetoitsacceleratedorblasticphase.Therefore,theseaberrationshaveclinicalandbiologicalsignificance.T(3;12)(q26;p13),whichisarecurrentchromosomalaberrationobservedinmyeloidmalignancies,istypicallyassociatedwithdysplasiaofmegakaryocytes,multilineageinvolvement,shortdurationofanyblasticphase,andextremelypoorprognosis.Wehaveidentifiedarecurrentreciprocaltranslocationbetweenchromosomes3and12withdifferentbreakpointatbands3q21inthemalignantcellsfroma28-year-oldman.ThepatientwasinitiallydiagnosedashavingPh+CMLinthechronicphase.Thet(3;12)(q21;p13)translocationoccurred4yearsafterthepatientwasfirstdiagnosedwithCMLwhileundergoingtyrosinekinaseinhibitortherapy.Weconfirmedthet(3;12)(q21;p13)translocationviafluorescenceinsituhybridizationassaybyusingwhole-chromosomepaintprobesforchromosomes3and12.Ourfindingsdemonstratethat,similartootherrecurrenttranslocationsinvolving3q26suchast(3;3)andt(3;21),thet(3;12)(q21;p13)translocationisimplicatednotonlyinmyelodysplasticsyndromeandacutemyeloidleukemiabutalsointheprogressionofCML.Thesefindingsextendthediseasespectrumofthiscytogeneticaberration.

简介：Objectiveandbackground:Althoughp21rashasbeenreportedtobeupregulatedinhepatocellularcarcinomacomplicatingchronichepatitisCtypeI,p21rashasadifferentroleinadvancedstages,asithasbeenfoundtobedownregulated.Thegoalofthisstudywastoinvestigatethestatusofp21rasinearly-stage/low-gradeandlate-stage/high-gradehepatocellularcarcinomaanditspossiblelinktoapoptosis.Materialandmethods:Thirty-fivecaseseachofchronicHCVhepatitistype4(groupI)andcirrhosiswithhepatocellularcarcinoma(HCC)complicatingchronicHCVhepatitis(groupsIIandIII)wereimmunohistochemicallyevaluatedusingap21raspolyclonalantibody.Theapoptoticindexwasdeterminedinhistologicsectionsusingtheterminaldeoxynucleotidyltransferase-mediatedd-UTPbiotinnickendlabeling(TUNEL)assay.Results:Significantdifferences(P=0.001)weredetectedinp21rasproteinexpressionbetweenthethreegroups.Anear2-foldincreaseinp21rasstainingwasobservedinthecirrhoticcasescomparedtothehepatitiscases,andp21rasexpressionwasdecreasedintheHCCgroup.p21rasexpressioncorrelatedwithstage(r=0.64,P=0.001)andgrade(r=-0.65,P=0.001)intheHCCgroupandgradeintheHCVgroup(r=0.44,P=0.008).Bothp21rasexpressionandTUNEL-LIweresignificantlylowerinlargeHCCscomparedtosmallHCCs(P=0.01each).TheTUNELvalueswerenegativelycorrelatedwithstageintheHCCgroup(r=-0.85,P=0.001).TheTUNELvalueswerealsonegativelycorrelatedwithgradeinboththeHCVandHCCgroups(r=0.89,P=0.001andr=-0.53,P=0.001,respectively).Thep21rasscoresweresignificantlycorrelatedwiththeTUNEL-LIvaluesintheHCCgroup(r=0.63,P=0.001)andHCVgroup(r=0.88,P=0.001).Conclusions:p21rasactsasaninitiatorinHCCcomplicatingtype4chronicHCVandisdownregulatedwithHCCprogression,whichmostlikelypromotestumorcellsurvivalbecauseitfacilitatesthedownregulationofapoptosiswithtumorprogression.

简介：AbstractBackground:The development of carotid-cavernous fistulas (CCFs) during surgical recanalization of chronic internal carotid artery occlusion (ICAO) may be secondary to severe ICA dissection rather than a focal tear of the cavernous ICA seen in typical traumatic CCFs. The purpose of this study is to investigate the causal relationship between the CCFs and severe ICA dissections and to characterize technical outcomes after treatment with stenting.Methods:Five patients underwent treatment with self-expanding stents due to intraprocedural CCF and ICA dissection following surgical removal of ICAO plaque. The stents were telescopically placed via true channel of the dissection. Safety of the procedure was evaluated with 30-day stroke and death rate. Procedural success was determined by the efficacy of CCF obliteration and ICAO recanalization with angiography.Results:All CCFs were associated with spiral and long segmental dissection from the cervical to cavernous ICA. After stenting, successful dissection reconstruction with TICI 3 was achieved in all patients, with complete (n = 4) or partial CCF (n = 1) obliteration. No patient had CCF syndrome, stroke, or death during follow-up of 6 to 37 months; but one patient had pulsatile tinnitus, which resolved 1 year later. Angiography at 6 to 24 months demonstrated CCF obliteration in all 5 patients and durable ICA patency in 4 patients.Conclusions:Intraprocedural CCFs with spiral and cervical-to-cavernous ICA dissection during ICAO surgery are dissection-related because of successful obliteration after stenting for dissection reconstruction. Self-expanding stenting through true channel of the dissection, serving as implanting stent-autograft, may be an optimal therapy for the atypical CCF complication from ICAO surgery.

简介：SpinaldorsalhornN-Methyl-D-asparticacidreceptor2B(NR2B)overexpressionplaysanimportantroleintheproductionandmaintenanceofneuropathicpain.BecausesmallinterferingRNA(siRNA)caninhibitNR2Bexpression,siRNAmayprovideanovelapproachtotreatneuropathicpainandpossiblynerveinjury.However,anefficientandsafevectorforNR2BsiRNAhasnotbeendiscov-ered.Thisstudyshowsthatawatersolublelipopolymer(WSLP)comprisedoflowmolecularweightpolyethyleneimine(PEI)andcholesterolcandeliversiRNAtargetingNR2Bforthetreatmentofneuropathicpain.ResultsshowthatintrathecalinjectionofWSLP/siRNAcomplexesfor3daysin-hibitNR2BgeneexpressionwithreductionsinmRNAandproteinlevelsby59%and54%,respec-tively,comparedwithcontrolrats(P<0.01).InjectionofWSLPcomplexedwithscrambledsiRNA,orPEIwithsiRNAdidnotshowthisinhibitoryeffect.Moreover,injectionofWSLP/siRNAcomplexessignificantlyrelievedneuropathicpainat3,7,12,and21days,whileinjectionofWSLPwithscrambledsiRNAorPEIwithsiRNAdidnot.TheseresultsdemonstratethatWSLPcanefficientlydeliversiRNAtargetingNR2Binvivoandrelieveneuropathicpain.

简介：AbstractBackground:NOTCH1 mutation is an essential molecular biologic aberration in chronic lymphocytic leukemia (CLL). CLL patients with NOTCH1 mutation have shown an unfavorable survival and a poor response to chemoimmunotherapy. This study aims to present the mechanisms of adverse prognosis caused by NOTCH1 mutation from the perspective of the splicing factor heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1).Methods:The microarray data in Gene Expression Omnibus datasets were analyzed by bioinformatics and the function of hnRNPA1 was checked by testing the proliferation and apoptosis of CLL-like cell lines. Afterward, quantitative reverse transcription-polymerase chain reaction and Western blotting were applied to explore the relationship among NOTCH1, c-Myc, and hnRNPA1.Results:RNA splicing was found to play a vital part in NOTCH1-mutated CLL cells; hence, hnRNPA1 was selected as the focus of this study. Higher expression of hnRNPA1 validated in primary NOTCH1-mutated CLL samples could promote proliferation and inhibit apoptosis in CLL. The expression of hnRNPA1 increased when NOTCH1 signaling was activated by transfection with NOTCH1 intracellular domain (NICD)-overexpressed adenovirus vector and declined after NOTCH1 signaling was inhibited by NOTCH1-shRNA. Higher expression of c-Myc was observed in NICD-overexpressed cells and hnRNPA1 expression was downregulated after applying c-Myc inhibitor 10058-F4. Moreover, in NICD-overexpressed cells, hnRNPA1 expression decreased through c-Myc inhibition.Conclusion:Overexpression of c-Myc-dependent hnRNPA1 could promote proliferation and inhibit apoptosis in NOTCH1- mutated CLL cells, which might partly account for the poor prognosis of patients with NOTCH1 mutation.

简介：AbstractBackground:The risk for chronic kidney disease (CKD) is influenced by genetic predisposition, sex, and lifestyle. Previous research indicates that coffee is a potentially protective factor in CKD. The current study aims to investigate whether sex disparity exists in the coffee–CKD association, and whether genetic risk of CKD or genetic polymorphisms of caffeine metabolism affect this association.Methods:A total of 359,906 participants from the UK Biobank who were enrolled between 2006 and 2010 were included in this prospective cohort study, which aimed to estimate the hazard ratios for coffee intake and incident CKD using a Cox proportional hazard model. Allele scores of CKD and caffeine metabolism were additionally adjusted for in a subsample with qualified genetic data (n = 255,343). Analyses stratified by genetic predisposition, comorbidities, and sex hormones were performed. Tests based on Bayesian model averaging were conducted to ascertain the robustness of the results.Results:Coffee was inversely associated with CKD in a dose-dependent manner. The effects of coffee did not differ across different strata of genetic risk for CKD, but were more evident among slower genetically predicted caffeine metabolizers. Significant sex disparity was observed (P value for interaction = 0.013), in that coffee drinking was only associated with the risk reduction of CKD in females. Subgroup analysis revealed that testosterone and sex hormone-binding globulin (SHBG), but not estradiol, modified the coffee–CKD association.Conclusions:In addition to the overall inverse coffee–CKD association that was observed in the general population, we could also establish that a sex disparity existed, in that females were more likely to experience the benefit of the association. Testosterone and SHBG may partly account for the sex disparity.

简介：cytokine发信号的Suppressor(SOCS)1在有免疫力的反应和力量起一个关键作用贡献与glucocorticoid对待的肝失败的预测。我们招募了接受glucocorticoid治疗和30健康控制在外部血mononuclear房间在SOCS1的transcriptional水平上决定glucocorticoid的潜在的效果的47个acute-on-chronic肝炎B肝失败(ACHBLF)病人。在glucocorticoid治疗的第三和八分之二十天，SOCS1表示否定地为结束阶段肝疾病与模型一起被相关(吞没)分数。Interleukin-6(IL-6)和肿瘤坏死factor-α；(TNF-α；)层次统计上更低，当SOCS1抄写水平在预告的处理和处理以后的ACHBLF病人两个都比非幸存者在幸存者是更高的时。在ACHBLF病人的SOCS1倡导者的methylation率比在由methylation特定的聚合酶链反应决定了的健康控制病人高。在methylated倡导者的SOCS1的mRNA水平是比从与unmethylatedSOCS1倡导者一起的病人显著地低的。干扰素(IFN)-γ-responsive和STAT1依赖的基因表示在幸存者是更高的并且戏剧性地在glucocorticoid治疗以后与SOCS1的升起的表示被减少。没有methylation，死亡率比为那些在methylated病人是显著地更高的。而且，我们在六发现了五熬过病人在治疗以后在八分之二十天显示了demethylatedSOCS1，当那个数字在非幸存者在10是3时。这些调查结果建议没有SOCS1methylation的ACHBLF病人可以有有利回答到corticosteroid治疗。

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简介：BackgroundItiswellknownthattherewasasignificantlinkbetweenpreproceduralbloodglucoselevelsandshort-termandlong-termadverseoutcomesinpatientsundergoingelectivePCI.However,theroleofpre-proceduralbloodglucoselevelsasapredictorofadverseeventsinCKDpatientswhounderwentPCIoutofestablisheddiabeteshasyettobeidentified.MethodsInourstudy,weconductedaprospectivestudyof331acutecoronarysyndrome(ACS)patientswithCKDwhounderwentPCIoutofestablisheddiabetes.Patientsweredividedintotwogroupsbasedonpre-proceduralglucoselevels(hypoglycemia<7.0mmol/L;hyperglycemia≥7.0mmol/L).Allpatientswerefollowedupprospectivelyformajoradversecardiovascularevents(MACEs)andmortalityfor6months.ResultsInourcohort,hyperglycemiapatientsreportedahigherincidenceofin-hospitalmortalitythanhypoglycemiapatients(7.5%vs.0%,P<0.001).Hyperglycemiapatientsreportedasignificantlyhigherrateof6-monthMACEs(10%vs.2.4%,P=0.007),allcausemortality(7.5%vs.1.6%,P=0.015),andcardiovascularmortality(6.2%vs1.6%,P=0.041)comparedwithhypoglycemiapatientswithpre-proceduralglucoselevels<7.0mmol/L.Multivariateanalysisdisclosedthatapre-proceduralglucoselevel≥7.0mmol/LwasasignificantindependentpredictorofMACEs(OR=2.53,95%CI1.68-17.15,P=0.004),allcausemortality(OR=4.6,95%CI1.10-18.84,P=0.036),andcardiovascularmortality(OR=6.2,95%CI1.53-24.94,P=0.011)at6monthsinpatientsafterPCI.ConclusionThestudysuggestedthatpre-proceduralglucoselevelsareassociatedwithshort-termcardiovascularoutcomeCKDpatientswhounderwentPCIwithoutestablisheddiabetesinthesettingofACS.

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简介：AbstractBackground:Anterior thalamic nuclei (ATN) deep brain stimulation (DBS) is an effective method of controlling epilepsy, especially temporal lobe epilepsy. Mossy fiber sprouting (MFS) plays an indispensable role in the pathogenesis and progression of epilepsy, but the effect of ATN-DBS on MFS in the chronic stage of epilepsy and the potential underlying mechanisms are unknown. This study aimed to investigate the effect of ATN-DBS on MFS, as well as potential signaling pathways by a kainic acid (KA)-induced epileptic model.Methods:Twenty-four rhesus monkeys were randomly assigned to control, epilepsy (EP), EP-sham-DBS, and EP-DBS groups. KA was injected to establish the chronic epileptic model. The left ATN was implanted with a DBS lead and stimulated for 8 weeks. Enzyme-linked immunosorbent assay, Western blotting, and immunofluorescence staining were used to evaluate MFS and levels of potential molecular mediators in the hippocampus. One-way analysis of variance, followed by the Tukey post hoc correction, was used to analyze the statistical significance of differences among multiple groups.Results:ATN-DBS is found to significantly reduce seizure frequency in the chronic stage of epilepsy. The number of ectopic granule cells was reduced in monkeys that received ATN stimulation (P < 0.0001). Levels of 3′,5′-cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) in the hippocampus, together with Akt phosphorylation, were noticeably reduced in monkeys that received ATN stimulation (P = 0.0030 and P = 0.0001, respectively). ATN-DBS also significantly reduced MFS scores in the hippocampal dentate gyrus and CA3 sub-regions (all P < 0.0001).Conclusion:ATN-DBS is shown to down-regulate the cAMP/PKA signaling pathway and Akt phosphorylation and to reduce the number of ectopic granule cells, which may be associated with the reduced MFS in chronic epilepsy. The study provides further insights into the mechanism by which ATN-DBS reduces epileptic seizures.

简介：AbstractBackground:The efficacy of entecavir (ETV) add-on peg-interferon therapy compared with ETV monotherapy in treatment-naïve hepatitis B virus (HBV) patients remains controversial. We investigated whether adding peg-interferon to ongoing ETV treatment leads to a better curative effect or not.Methods:All patients have been recruited between August 2013 and January 2015 from the Shanghai Public Health Clinical Center and Zhongshan Hospital (China). Eligible HBV patients (n = 144) were randomly divided (1:1) to receive either ETV monotherapy (n = 70) or peg-interferon add-on therapy from week 26 to 52 (n = 74). Patients were followed-up for at least 2 years. Indexes including hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) seroconversion rate, sustained virologic response, transient elastography value, and histological scores were evaluated every 3 months until the end of the study. The rate of patients with HBsAg loss was defined as the primary endpoint criteria.Results:At week 26, no patient achieved HBsAg seroconversion in either group. At week 52, one patient in the monotherapy group was HBsAg-negative but there was none in the combination therapy group. The monotherapy group showed significantly better liver function recovery results than the combination therapy group. At week 78, one patient in the combination group had HBsAg seroconverted. At week 104, only three patients in the combination therapy group were HBsAg-negative compared with one patient in monotherapy. The mean alanine aminotransferase and aspartate aminotransferase levels and transient elastography values decreased significantly compared with baseline. Both groups showed a favorable decrease in alpha-fetoprotein (monotherapy: 4.5 [2.8, 7.1] vs. 2.2 [1.8, 3.1] ng/mL, P < 0.001; combination therapy: 5.7 [3.0, 18.8] vs. 3.2 [2.0, 4.3] ng/mL, P < 0.001) and an improved result of liver biopsy examination scores. The combination group showed a better improvement in histology compared with the monotherapy group (mean transient elastography value 6.6 [4.9, 9.8] vs. 7.8 [5.4, 11.1] kPa, P = 0.028). But there was no significant difference in HBsAg conversion rate (1.8% [1/56] vs. 4.1% [3/73], P = 0.809) and HBeAg conversion rate (12.5% [7/56] vs. 11.0% [8/73], P = 0.787), as well as HBV-DNA, sustained virologic response (93.2% vs. 98.5%, P = 0.150) between the two groups.Conclusions:Both therapies supported liver function recovery and histology improvement. Combination therapy did not show better anti-viral efficacy in HBsAg or HBeAg seroconversion compared with monotherapy. However, combination therapy played a more positive role in reversing hepatic fibrosis compared with monotherapy.Trial registration:ClinicalTrials.gov: NCT02849132; https://clinicaltrials.gov/ct2/show/NCT02849132