Effects of age and flight experience on prefrontal cortex activity in airline pilots: An fNIRS study.

It is essential for airlines to have a deep understanding of the cognitive impact of aging among pilots. The current literature on executive function indicates that compensatory mechanisms in the brain may counteract age-related cognitive decline, at least up to certain task load levels. However, few studies have been administered to evaluate changes in aircrew competence as they age. The present study focuses on dorsolateral prefrontal cortex (DLPFC) activity as it is implicated in cognitive performance and working memory, which are associated with skill proficiency. We measured the DLPFC activity for airline pilots, including trainees, during maneuvering using a flight simulator. Our preliminary results indicated that only expert (aged) pilots demonstrated higher activity of the left DLPFC than the right one. However, for youth trainees, not only was the error rate high while using the flight simulator, but the activity of the DLFPC was also lower than that of the expert pilots, and there was no statistically significant difference between the left and right DLPFC. Although these findings partially differ from those reported in previous studies on age-related changes, it is evident that training as an airline pilot for over 20 years may affect such results. We believe that this noninvasive approach to objective quantification of skill will facilitate the development of effective assessment competence in aging.

Essential Role of COPII Proteins in Maintaining the Contractile Ring Anchoring to the Plasma Membrane during Cytokinesis in Drosophila Male Meiosis.

Coatomer Protein Complex-II (COPII) mediates anterograde vesicle transport from the endoplasmic reticulum (ER) to the Golgi apparatus. Here, we report that the COPII coatomer complex is constructed dependent on a small GTPase, Sar1, in spermatocytes before and during Drosophila male meiosis. COPII-containing foci co-localized with transitional endoplasmic reticulum (tER)-Golgi units. They showed dynamic distribution along astral microtubules and accumulated around the spindle pole, but they were not localized on the cleavage furrow (CF) sites. The depletion of the four COPII coatomer subunits, Sec16, or Sar1 that regulate COPII assembly resulted in multinucleated cell production after meiosis, suggesting that cytokinesis failed in both or either of the meiotic divisions. Although contractile actomyosin and anilloseptin rings were formed once plasma membrane ingression was initiated, they were frequently removed from the plasma membrane during furrowing. We explored the factors conveyed toward the CF sites in the membrane via COPII-mediated vesicles. DE-cadherin-containing vesicles were formed depending on Sar1 and were accumulated in the cleavage sites. Furthermore, COPII depletion inhibited de novo plasma membrane insertion. These findings suggest that COPII vesicles supply the factors essential for the anchoring and/or constriction of the contractile rings at cleavage sites during male meiosis in Drosophila.

Cyclin B Export to the Cytoplasm via the Nup62 Subcomplex and Subsequent Rapid Nuclear Import Are Required for the Initiation of Drosophila Male Meiosis.

The cyclin-dependent kinase 1 (Cdk1)-cyclin B (CycB) complex plays critical roles in cell-cycle regulation. Before Drosophila male meiosis, CycB is exported from the nucleus to the cytoplasm via the nuclear porin 62kD (Nup62) subcomplex of the nuclear pore complex. When this export is inhibited, Cdk1 is not activated, and meiosis does not initiate. We investigated the mechanism that controls the cellular localization and activation of Cdk1. Cdk1-CycB continuously shuttled into and out of the nucleus before meiosis. Overexpression of CycB, but not that of CycB with nuclear localization signal sequences, rescued reduced cytoplasmic CycB and inhibition of meiosis in Nup62-silenced cells. Full-scale Cdk1 activation occurred in the nucleus shortly after its rapid nuclear entry. Cdk1-dependent centrosome separation did not occur in Nup62-silenced cells, whereas Cdk1 interacted with Cdk-activating kinase and Twine/Cdc25C in the nuclei of Nup62-silenced cells, suggesting the involvement of another suppression mechanism. Silencing of roughex rescued Cdk1 inhibition and initiated meiosis. Nuclear export of Cdk1 ensured its escape from inhibition by a cyclin-dependent kinase inhibitor. The complex re-entered the nucleus via importin ß at the onset of meiosis. We propose a model regarding the dynamics and activation mechanism of Cdk1-CycB to initiate male meiosis.

Anti-Tumor Effect of Turandot Proteins Induced via the JAK/STAT Pathway in the mxc Hematopoietic Tumor Mutant in Drosophila.

Several antimicrobial peptides suppress the growth of lymph gland (LG) tumors in Drosophila multi sex comb (mxc) mutant larvae. The activity of another family of polypeptides, called Turandots, is also induced via the JAK/STAT pathway after bacterial infection; however, their influence on Drosophila tumors remains unclear. The JAK/STAT pathway was activated in LG tumors, fat body, and circulating hemocytes of mutant larvae. The mRNA levels of Turandot (Tot) genes increased markedly in the mutant fat body and declined upon silencing Stat92E in the fat body, indicating the involvement of the JAK/STAT pathway. Furthermore, significantly enhanced tumor growth upon a fat-body-specific silencing of the mRNAs demonstrated the antitumor effects of these proteins. The proteins were found to be incorporated into small vesicles in mutant circulating hemocytes (as previously reported for several antimicrobial peptides) but not normal cells. In addition, more hemocytes containing these proteins were found to be associated with tumors. The mutant LGs contained activated effector caspases, and a fat-body-specific silencing of Tots inhibited apoptosis and increased the number of mitotic cells in the LG, thereby suggesting that the proteins inhibited tumor cell proliferation. Thus, Tot proteins possibly exhibit antitumor effects via the induction of apoptosis and inhibition of cell proliferation.

Ectopic expression of matrix metalloproteinases and filopodia extension via JNK activation are involved in the invasion of blood tumor cells in Drosophila mxc mutant.

Drosophila mxcmbn1 mutant exhibits severe hyperplasia in larval hematopoietic tissue called the lymph glands (LGs). However, the malignant nature of these cells remains unknown. We aimed to identify if mxcmbn1 LG cells behave as malignant tumor cells and uncover the mechanism(s) underlying the malignancy of the mutant hemocytes. When mutant LG cells were allografted into normal adult abdomens, they continued to proliferate; however, normal LG cells did not proliferate. Mutant circulating hemocytes also attached to the larval central nervous system (CNS), where the basement membrane was disrupted. The mutant hemocytes displayed higher expression of matrix metalloproteinase (MMP) 1 and MMP2 and higher activation of the c-Jun N-terminal kinase (JNK) pathway than normal hemocytes. Depletion of MMPs or JNK mRNAs in LGs resulted in reduced numbers of hemocytes attached to the CNS, suggesting that the invasive phenotype involved elevated expression of MMPs via hyperactivation of the JNK pathway. Moreover, hemocytes with elongated filopodia and extra lamellipodia were frequently observed in the mutant hemolymph, which also depended on JNK signaling. Thus, the MMP upregulation and overextension of actin-based cell protrusions were also involved in hemocyte invasion in mxcmbn1 larvae. These findings contribute to the understanding of molecular mechanisms underlying mammalian leukemic invasion.

Loss of PWT7, Located on a Supernumerary Chromosome, Is Associated with Parasitic Specialization of Pyricularia oryzae on Wheat.

Pyricularia oryzae, a blast fungus of gramineous plants, is composed of various host genus-specific pathotypes. The avirulence of an Avena isolate on wheat is conditioned by PWT3 and PWT4. We isolated the third avirulence gene from the Avena isolate and designated it as PWT7. PWT7 was effective as an avirulence gene only at the seedling stage or on leaves. PWT7 homologs were widely distributed in a subpopulation of the Eleusine pathotype and the Lolium pathotype but completely absent in the Triticum pathotype (the wheat blast fungus). The PWT7 homolog found in the Eleusine pathotype was one of the five genes involved in its avirulence on wheat. A comparative analysis of distribution of PWT7 and the other two genes previously identified in the Eleusine pathotype suggested that, in the course of parasitic specialization toward the wheat blast fungus, a common ancestor of the Eleusine, Lolium, Avena, and Triticum pathotypes first lost PWT6, secondly PWT7, and, finally, the function of PWT3. PWT7 or its homologs were located on core chromosomes in Setaria and Eleusine isolates but on supernumerary chromosomes in Lolium and Avena isolates. This is an example of interchromosomal translocations of effector genes between core and supernumerary chromosomes. [Formula: see text] Copyright © 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Major proliferation of transposable elements shaped the genome of the soybean rust pathogen Phakopsora pachyrhizi.

With >7000 species the order of rust fungi has a disproportionately large impact on agriculture, horticulture, forestry and foreign ecosystems. The infectious spores are typically dikaryotic, a feature unique to fungi in which two haploid nuclei reside in the same cell. A key example is Phakopsora pachyrhizi, the causal agent of Asian soybean rust disease, one of the world's most economically damaging agricultural diseases. Despite P. pachyrhizi's impact, the exceptional size and complexity of its genome prevented generation of an accurate genome assembly. Here, we sequence three independent P. pachyrhizi genomes and uncover a genome up to 1.25 Gb comprising two haplotypes with a transposable element (TE) content of ~93%. We study the incursion and dominant impact of these TEs on the genome and show how they have a key impact on various processes such as host range adaptation, stress responses and genetic plasticity.

A basic charge cluster near the C-terminus of the cytoplasmic tail contributes to the molecular stability of human herpesvirus 8 E3 ubiquitin ligases.

Human herpesvirus 8 (HHV8; also known as Kaposi's sarcoma-associated herpesvirus [KSHV]) utilizes the viral E3 ubiquitin ligase family members K3 and K5 for immune evasion. Both K3 and K5 mediate the ubiquitination of host MHC class I (MHC-I) molecules, which play a key role in antigen presentation to cytotoxic T lymphocytes (CTLs). Because ubiquitinated MHC-I is immediately down-regulated from the cell surface, HHV8-infected cells can escape surveillance by CTLs. K3 and K5 have similar domain structures and topologies. They contain an N-terminal RINGv ubiquitin ligase domain, two transmembrane helices, and an intrinsically disordered cytoplasmic tail at the C-terminus. The cytoplasmic tail contains a membrane-proximal "conserved region" involved in ligase activity. On the other hand, the role of the membrane-distal region of the cytoplasmic tail, termed the "C-tail" in this study, remains unclear. Here, we demonstrate that the C-tail contributes to the protein expression of both K3 and K5. The C-tail-truncated K3 and K5 mutants were rapidly reduced in cells. The recombinant C-tail proteins bind to acidic lipids via a basic charge cluster located near the C-terminus of the C-tails. Similar to the C-tail-truncated mutants, the basic charge cluster-substituting mutants showed decreased protein expression of K3 and K5. These findings suggest that the basic charge cluster near the C-terminus of the cytoplasmic tail contributes to the molecular stability of K3 and K5.

Selective deployment of virulence effectors correlates with host specificity in a fungal plant pathogen.

The hemibiotrophic fungal plant pathogen Colletotrichum orbiculare is predicted to secrete hundreds of effector proteins when the pathogen infects cucurbit crops, such as cucumber and melon, and tobacco (Nicotiana benthamiana), a distantly related Solanaceae species. Here, we report the identification of sets of C. orbiculare effector genes that are differentially required for fungal virulence to two phylogenetically distant host species. Through targeted gene knockout screening of C. orbiculare 'core' effector candidates defined based on in planta gene expression, we identified: four host-specific virulence effectors (named effector proteins for cucurbit infection, or EPCs) that are required for full virulence of C. orbiculare to cucurbit hosts, but not to the Solanaceae host N. benthamiana; and five host-nonspecific virulence effectors, which collectively contribute to fungal virulence to both hosts. During host infection, only a small subset of genes, including the host-specific EPC effector genes, showed preferential expression on one of the hosts, while gene expression profiles of the majority of other genes, including the five host-nonspecific effector genes, were common to both hosts. This work suggests that C. orbiculare adopts a host-specific effector deployment strategy, in addition to general host-blind virulence mechanisms, for adaptation to cucurbit hosts.

Mitotic progression and dual spindle formation caused by spindle association of de novo-formed microtubule-organizing centers in parthenogenetic embryos of Drosophila ananassae.

Facultative parthenogenesis occurs in many animal species that typically undergo sexual reproduction. In Drosophila, such development from unfertilized eggs involves diploidization after completion of meiosis, but the exact mechanism remains unclear. Here we used a laboratory stock of Drosophila ananassae that has been maintained parthenogenetically to cytologically examine the initial events of parthenogenesis. Specifically, we determined whether the requirements for centrosomes and diploidization that are essential for developmental success can be overcome. As a primal deviation from sexually reproducing (i.e. sexual) strains of the same species, free asters emerged from the de novo formation of centrosome-like structures in the cytosol of unfertilized eggs. Those microtubule-organizing centers had distinct roles in the earliest cycles of parthenogenetic embryos with respect to mitotic progression and arrangement of mitotic spindles. In the first cycle, an anastral bipolar spindle self-assembled around a haploid set of replicated chromosomes. Participation of at least one microtubule-organizing center in the spindle was necessary for mitotic progression into anaphase. In particular, the first mitosis involving a monastral bipolar spindle resulted in haploid daughter nuclei, one of which was associated with a microtubule-organizing center whereas the other was not. Remarkably, in the following cycle, biastral and anastral bipolar spindles formed that were frequently arranged in tandem by sharing an aster with bidirectional connections at their central poles. We propose that, for diploidization of haploid nuclei, unfertilized parthenogenetic embryos utilize dual spindles during the second mitosis, as occurs for the first mitosis in normal fertilized eggs.

Drosophila hemocytes recognize lymph gland tumors of mxc mutants and activate the innate immune pathway in a reactive oxygen species-dependent manner.

Mechanisms of cancer cell recognition and elimination by the innate immune system remains unclear. The immune signaling pathways are activated in the fat body to suppress the tumor growth in mxcmbn1 hematopoietic tumor mutants in Drosophila by inducing antimicrobial peptides (AMP). Here, we investigated the regulatory mechanism underlying the activation in the mutant. Firstly, we found that reactive oxygen species (ROS) accumulated in the hemocytes due to induction of dual oxidase and one of its activators. This was required for the AMP induction and the tumor growth suppression. Next, more hemocytes transplanted from normal larvae were associated with the mutant tumor than normal lymph glands (LGs). Matrix metalloproteinase 1 and 2 (MMP2) were highly expressed in the tumors. The basement membrane components in the tumors were reduced and ultimately lost inside. Depletion of the MMP2 rather than MMP1 resulted in a significantly reduced AMP expression in the mutant larvae. The hemocytes may recognize the disassembly of basement membrane in the tumors and activate the ROS production. Our findings highlight the mechanism via which macrophage-like hemocytes recognize tumor cells and subsequently convey the information to induce AMPs in the fat body. They contribute to uncover the role of innate immune system against cancer.

Downregulating Mitochondrial DNA Polymerase γ in the Muscle Stimulated Autophagy, Apoptosis, and Muscle Aging-Related Phenotypes in Drosophila Adults.

Reactive oxygen species, generated as by-products of mitochondrial electron transport, can induce damage to mitochondrial DNA (mtDNA) and proteins. Here, we investigated whether the moderate accumulation of mtDNA damage in adult muscles resulted in accelerated aging-related phenotypes in Drosophila. DNA polymerase γ (Polγ) is the sole mitochondrial DNA polymerase. The muscle-specific silencing of the genes encoding the polymerase subunits resulted in the partial accumulation of mtDNA with oxidative damage and a reduction in the mtDNA copy number. This subsequently resulted in the production of abnormal mitochondria with reduced membrane potential and, consequently, a partially reduced ATP quantity in the adult muscle. Immunostaining indicated a moderate increase in autophagy and mitophagy in adults with RNA interference of Polγ (PolγRNAi) muscle cells with abnormal mitochondria. In adult muscles showing continuous silencing of Polγ, malformation of both myofibrils and mitochondria was frequently observed. This was associated with the partially enhanced activation of pro-apoptotic caspases in the muscle. Adults with muscle-specific PolγRNAi exhibited a shortened lifespan, accelerated age-dependent impairment of locomotor activity, and disturbed circadian rhythms. Our findings in this Drosophila model contribute to understanding how the accumulation of mtDNA damage results in impaired mitochondrial activity and how this contributes to muscle aging.

Does repeat laparoscopic hepatectomy without extracorporeal Pringle manoeuvre worsen treatment outcomes?

Introduction: The Pringle manoeuvre is used in most hospitals to counteract intraoperative haemorrhage in laparoscopic hepatectomy by occluding the flow of blood to the liver. However, in laparoscopic repeat hepatectomy (LRH), outcomes of previous surgery and the influence of other factors frequently make it difficult to occlude the inflow of blood. Aim: To discuss the value of inflow occlusion during LRH and provide tips for its performance. Material and methods: Sixty-three patients who underwent LRH with or without the Pringle manoeuvre were analysed retrospectively. We investigated the efficacy and safety of the Pringle manoeuvre in LRH. Student's t and χ2 tests, Mann-Whitney's U test, Wilcoxon's signed-rank test, and Fisher's exact test were used in the statistical analysis. Results: Nineteen patients underwent LRH with the Pringle manoeuvre, and 44 patients underwent LHR without the Pringle manoeuvre. After propensity score matching, there were no significant differences in terms of operative time, estimated blood loss, and postoperative complication rate (p = 0.973, 0.120, and not applicable, respectively). However, the rate of conversion to open repeat hepatectomy (ORH) was significantly lower in the Pringle manoeuvre group (p = 0.034). In many cases, the cause of conversion to ORH was the non-use of inflow occlusion and the resulting inability to control intraoperative haemorrhage. Laboratory data collected after surgery showed no significant difference between the 2 groups regardless of whether blood flow was occluded or not. Conclusions: LRH with the Pringle manoeuvre can be performed safely using various surgical devices. However, it is often challenging to perform the Pringle manoeuvre in patients with a history of cholecystectomy or segment 5 resection of the liver, and caution is required.

Successful Laparoscopic Treatment of Pancreatic Metastasis From Sigmoid Colon Cancer: A Case Report.

Progressive colorectal cancer frequently presents with various manifestations, including hepatic, pulmonary, and peritoneal metastases, as well as local and anastomotic site recurrences. However, pancreatic metastasis is extremely rare. Complete surgical resection is currently considered the most effective and only potentially curative treatment for colorectal cancer with distant metastases. We report the successful laparoscopic treatment of a patient with pancreatic metastasis after initial surgery for Stage IV sigmoid colon cancer with pulmonary metastasis. An 84-year-old man was initially diagnosed with sigmoid colon cancer and pulmonary metastasis. Laparoscopic sigmoidectomy and thoracoscopic partial resection of the right lung were performed in 2017. After 8 months, an approximately 20-mm tumor was detected in the pancreatic tail during imaging investigations. We performed laparoscopic distal pancreatectomy without lymph node dissection at 1 year after the initial operation. The histopathological findings suggested metachronous pancreatic metastasis from the sigmoid colon cancer. The patient has had an uneventful postoperative course with no signs of recurrent disease during 29 months of follow-up after the pancreatic surgery. After prior surgery for Stage IV sigmoid colon cancer with pulmonary metastasis, curative resection was performed for pancreatic metastasis. We believe that curative resection may be useful for pancreatic tumors that involve hematogenous metastasis.

Treating an Intractable Jejunocutaneous Fistula by Endoscopic Metallic Stent Placement: A Case Report of Successful Palliative Endoscopic Treatment in a Case Demonstrating Peritoneal Dissemination with Terminal Stage Gastric Cancer.

A 74-year-old woman with recurrent gastric cancer underwent laparotomy for peritoneal dissemination, and the damaged jejunum formed a jejunocutaneous fistula. Because conservative treatment alone could not cure the fistula, we performed an endoscopic placement of a partially covered self-expandable metallic stent (SEMS) to cover the fistula. After the procedure, the contrast medium no longer leaked from the intestinal lumen. One month after stent placement, the cutaneous opening had closed. This case report demonstrates the potential for using partially covered SEMS to treat intractable jejunocutaneous fistula in patients with terminal-stage malignant tumors.

Difference between delayed anastomosis and early anastomosis in damage control laparotomy affecting the infusion volume and NPWT output volume: is infusion restriction necessary in delayed anastomosis? A single-center retrospective analysis.

Objectives: During temporary abdominal closure (TAC) with damage control laparotomy (DCL), infusion volume and negative-pressure wound therapy (NPWT) output volume are associated with the success and prognosis of primary fascial closure. The same may also hold true for anastomosis. The aim of this research is to evaluate whether the difference between early anastomosis and delayed anastomosis in DCL is related to infusion volume and NPWT output volume. Methods: This single-center retrospective analysis targeted patients managed with TAC during emergency surgery for trauma or intra-abdominal sepsis between January 2011 and December 2019. It included patients who underwent repair/anastomosis/colostomy in the first surgery and patients who underwent intestinal resection in the first surgery followed by delayed anastomosis with no intestinal continuity. Results: Seventy-three patients were managed with TAC using NPWT, including 19 cases of repair, 17 of colostomy, and 37 of anastomosis. In 16 patients (trauma 5, sepsis 11) with early anastomosis and 21 patients (trauma 16, sepsis 5) with delayed anastomosis, there was no difference in the infusion volume (p=0.2318) or NPWT output volume (p=0.7128) 48 hours after surgery. Additionally, there was no difference in the occurrence of suture failure (p=0.8428). During the second-look surgery after 48 hours, the anastomosis was further postponed for 48% of the patients who underwent delayed anastomosis. There was no difference in the infusion volume (p=0.0783) up to the second-look surgery between the patients whose delayed anastomosis was postponed and those who underwent delayed anastomosis, but there was a tendency toward a large NPWT output volume (p=0.024) in the postponed delayed anastomosis group. Conclusion: Delayed anastomosis may be managed with the same infusion volume as that used for early anastomosis. There is also the option of postponing anastomosis if the planned delayed anastomosis is complicated. Level of evidence: Therapeutic/Care Management, Level IV.

The Potential of a Stroke Registry Using Diagnosis Procedure Combination Data from All Hospitals in a Japanese Prefecture.

OBJECTIVES: In Japan, many hospitals have joined the diagnosis procedure combination/per-diem payment system (DPC/PDPS), which provides unified information about inpatients. DPC data are digitized, and the number of participating hospitals has increased recently. Herein, we evaluated the potential of a stroke registry constructed using these unified DPC data from all hospitals in the Iwate Prefecture, Japan. METHODS: The proportion of cerebrovascular disease (CVD) cases registered by DPC-participating hospitals was calculated and compared with all registered cases in the Iwate Stroke Registry in 2008-2017. The cases were categorized based on sex, age-groups, stroke subtypes, and first-ever onset or recurrence onset. Based on the registered cases in the stroke registry, the accuracy of the CVD cases extracted by the disease name from DPC data of a typical core hospital and a typical noncore hospital was evaluated. RESULTS: Of the 71 hospitals with 9,992 beds in the Iwate Prefecture in 2018, 50 hospitals with 8,316 beds participated in the DPC system. The proportion of registered cases from participating hospitals was 95.2% (44,779/47,018) for all stroke types (95.6% men and 94.9% women), 94.3% for cerebral infarction, 97.0% for intracerebral hemorrhage, and 98.7% for subarachnoid hemorrhage, whereas it was 95.7% for first-ever onset and 94.1% for recurrent onset. The proportion of registered cases decreased with increasing patient age. Attending doctors and researchers registered 486 and 41 CVD cases from the core and noncore hospitals, respectively, whereas 455 and 46 CVD cases were extracted from the DPC data of these hospitals, respectively. This yielded 86.6% sensitivity, 99.3% specificity, 92.5% positive predictive value, and 98.7% negative predictive value for the core hospital; these values were 92.7%, 98.6%, 82.6%, and 99.5%, respectively, for the noncore hospital. DISCUSSION/CONCLUSIONS: The stroke registry constructed using DPC data from all hospitals of Iwate Prefecture appears to be adequately complete and accurate.

The Management of Recurrence of Hepatocellular Carcinoma Occurring Within 6 Months After Hepatic Resection: A Comparative Study Using a Propensity Score Matching Analysis.

BACKGROUND: Hepatectomy is currently recommended as the most reliable treatment for hepatocellular carcinoma. However, the association between the choice of treatment for recurrence and the timing of recurrence remains controversial. METHODS: Three-hundred thirty-nine patients who underwent hepatectomy were retrospectively analyzed using a propensity score matching analysis for the risk factors and outcomes for early recurrences within 6 months. The remnant liver volumes and laboratory data were measured postoperatively using multidetector computed tomography on days 7 and months 1, 2, and 5 after surgery. The Student's t test and chi-square test, the likelihood-ratio test, Fisher's exact test, Mann-Whitney U test, or Wilcoxon signed-rank test were used in the statistical analyses. RESULTS: Early recurrence developed in 41/312 patients (13.1%). Vascular invasion and non-curative resection were independent risk factors for the occurrence of early recurrence (P < 0.001 and < 0.001, respectively). Patients with early recurrence had a poorer prognosis than patients who developed later recurrences (P < 0.001). Patients who underwent surgery or other local treatments had better outcomes (P < 0.001). The changes in remnant liver volumes and laboratory data after postoperative month 2 were not significantly different between the two groups. CONCLUSION: Patients with early recurrence within 6 months had a poorer prognosis than patients who developed a later recurrence. However, patients who underwent repeat hepatectomy for recurrences had a better prognosis than did those who underwent other treatments, with good prospects for long-term survival.