Green supply chain finance strategies with market competition and financial constraints.

In the context of sustainable development, market competition is intensifying, and financial constraints have emerged as a significant hindrance to green project investment. Green Supply Chain Finance (GSCF), characterized by long-term collaboration, has emerged as a crucial financial approach to mitigate corporate financial limitations and channel capital flows into environmentally friendly industries. We propose a two-echelon supply chain with one supplier and two competing retailers over a single period and investigate ordering, sales, and financing decisions simultaneously under competition. Retailers constrained by financial considerations may secure GSCF or traditional bank financing (BF) loans. This study investigates the influence of competition on pricing and sales strategies during the selling season. The results demonstrate that retailers select between clearance and responsive selling strategies based on the level of market competition. During the ordering season, retailers share the product market equally when interest rates are uniform, and the supplier formulates a supply chain contract while considering the financing interest rate. In the presence of differential interest rates, retailers may not always opt for the GSCF, even when they offer an interest rate advantage, due to the comprehensive impacts of operational and financial strategies. Remarkably, competitive retailers do not choose the GSCF when their initial green investment capital surpasses a certain threshold.

Association between organic cation transporter genetic polymorphisms and metformin response and intolerance in T2DM individuals: a systematic review and meta-analysis.

Background: Variants in organic cation transporter (OCT) genes play a crucial role in metformin pharmacokinetics and are critical for diabetes treatment. However, studies investigating the effect of OCT genetic polymorphisms on metformin response have reported inconsistent results. This review and meta-analysis aimed to evaluate the associations between OCT genetic polymorphisms and metformin response and intolerance in individuals with type 2 diabetes mellitus (T2DM). Method: A systematic search was conducted on PubMed, EMBASE, CNKI, WANFANG DATA, and VIP database for identifying potential studies up to 10 November 2022. The Q-Genie tool was used to evaluate the quality of included studies. Pooled odds ratios (OR) or standardized mean differences (SMD) and 95% confidence intervals (95% CI) were calculated to determine the associations between OCT genetic polymorphisms and metformin response and intolerance that were reflected by glycemic response indexes, such as glycated hemoglobin level (HbA1c%) or change in glycated hemoglobin level (ΔHbA1c%), fasting plasma level (FPG) or change in fasting plasma glucose level (ΔFPG), the effectiveness rate of metformin treatment, and the rate of metformin intolerance. A qualitative review was performed for the variants identified just in one study and those that could not undergo pooling analysis. Results: A total of 30 related eligible studies about OCT genes (SLC22A1, SLC22A2, and SLC22A3) and metformin pharmacogenetics were identified, and 14, 3, and 6 single nucleotide polymorphisms (SNPs) in SLC22A1, SLC22A2, and SLC22A3, respectively, were investigated. Meta-analysis showed that the SLC22A1 rs622342 polymorphism was associated with a reduction in HbA1c level (AA vs. AC: SMD [95% CI] = -0.45 [-0.73--0.18]; p = 0.001). The GG genotype of the SLC22A1 rs628031 polymorphism was associated with a reduction in FPG level (GG vs. AA: SMD [95 %CI] = -0.60 [-1.04-0.16], p = 0.007; GG vs. AG: -0.45 [-0.67-0.20], p < 0.001). No statistical association was found between the remaining variants and metformin response and intolerance. Conclusion: SLC22A1 rs622342 and rs628031 polymorphisms were potentially associated with glycemic response to metformin. This evidence may provide novel insight into gene-oriented personalized medicine for diabetes.

A deep learning-based recognition for dangerous objects imaged in X-ray security inspection device.

Several limitations in algorithms and datasets in the field of X-ray security inspection result in the low accuracy of X-ray image inspection. In the literature, there have been rare studies proposed and datasets prepared for the topic of dangerous objects segmentation. In this work, we contribute a purely manual segmentation for labeling the existing X-ray security inspection dataset namely, SIXRay, with the pixel-level semantic information of dangerous objects. We also propose a composition method for X-ray security inspection images to effectively augment the positive samples. This composition method can quickly obtain the positive sample images using affine transformation and HSV features of X-ray images. Furthermore, to improve the recognition accuracy, especially for adjacent and overlapping dangerous objects, we propose to combine the target detection algorithm (i.e., the softer-non maximum suppression, Softer-NMS) with Mask RCNN, which is named as the Softer-Mask RCNN. Compared with the original model (i.e., Mask RCNN), the Softer-Mask RCNN improves by 3.4% in accuracy (mAP), and 6.2% with adding synthetic data. The study result indicates that our proposed method in this work can effectively improve the recognition performance of dangerous objects depicting in the X-ray security inspection images.

Genetic regulation of THBS1 methylation in diabetic retinopathy.

Background: Diabetic retinopathy (DR) is a common and serious microvascular complication of diabetes mellitus (DM), but its pathological mechanism, especially the formation mechanism of new blood vessels remains unclear. Thrombospondin-1 (THBS1) is a potent endogenous inhibitor of angiogenesis and it was found over expressed in DR in our previous study. Our study aimed to determine whether overexpression of THBS1 is associated with its promoter methylation level, and whether methylation of THBS1 is regulated by genetic variants in DR. Methods: Patients diagnosed with DR and DM patients without retinal problems were included in the case-control study. DNA methylation detection of THBS1 by bisulfite sequencing and genotyping of specific SNPs by MassARRAY analysis were performed in the patients recruited from 2019-2020. Real time quantitative PCR was performed to obtain mRNA expression of THBS1 in the patients recruited from August to October 2022. The differentially methylated CpG loci of THBS1 were identified by logistic regression, and associations between 13 SNPs and methylation levels of CpG loci were tested by methylation quantitative trait loci (meQTLs) analysis. Mediation analysis was applied to determine whether CpG loci were intermediate factors between meQTLs and DR. Results: 150 patients diagnosed with DR and 150 DM patients without retinal complications were enrolled in the first recruitment, seven DR patients and seven DM patients were enrolled in the second recruitment. The patients with DR showed promoter hypomethylation of THBS1 (P value = 0.002), and six out of thirty-nine CpG sites within two CpG islands (CGIs) showed hypomethylation(P value < 0.05). THBS1 mRNA expression in peripheral blood was significantly higher in DR patients than in DM patients. Five out of thirteen cis-meQTLs were identified to be associated with CpG sites: rs13329154, rs34973764 and rs5812091 were associated with cis-meQTLs of CpG-4 (P value=0.0145, 0.0095, 0.0158), rs11070177 and rs1847663 were associated with cis-meQTLs of CpG-2 and CpG-3 respectively (P value=0.0201, 0.0275). CpG-4 methylation significantly mediated the effect of the polymorphism rs34973764 on DR (B=0.0535, Boot 95%CI: 0.004~0.1336). Conclusion: THBS1 overexpression is related to THBS1 hypomethylation in patients with DR. DNA methylation may be genetically controlled in DR.

Non-convex optimization based optimal bone correction for various beam-hardening artifacts in CT imaging.

Tube of X-ray computed tomography (CT) system emitting a polychromatic spectrum of photons leads to beam hardening artifacts such as cupping and streaks, while the metal implants in the imaged object results in metal artifacts in the reconstructed images. The simultaneous emergence of various beam-hardening artifacts degrades the diagnostic accuracy of CT images in clinics. Thus, it should be deeply investigated for suppressing such artifacts. In this study, data consistency condition is exploited to construct an objective function. Non-convex optimization algorithm is employed to solve the optimal scaling factors. Finally, an optimal bone correction is acquired to simultaneously correct for cupping, streaks and metal artifacts. Experimental result acquired by a realistic computer simulation demonstrates that the proposed method can adaptively determine the optimal scaling factors, and then correct for various beam-hardening artifacts in the reconstructed CT images. Especially, as compared to the nonlinear least squares before variable substitution, the running time of the new CT image reconstruction algorithm decreases 82.36% and residual error reduces 55.95%. As compared to the nonlinear least squares after variable substitution, the running time of the new algorithm decreases 67.54% with the same residual error.

PARP-1 overexpression does not protect HaCaT cells from DNA damage induced by SiO2 nanoparticles.

Nano-SiO2 is increasingly used in diagnostic and biomedical research because of its ease of production and relatively low cost and which is generally regarded as safe and has been approved for use as a food or animal feed ingredient. Although recent literature reveals that nano-SiO2 may present toxicity and DNA damage, however, the underlying mechanism remains poorly understood. Since in previous studies, we found that nano-SiO2 treatment down-regulated the expression of the poly(ADP-ribose) polymerases-1 (PARP-1), a pivotal DNA repair gene, in human HaCaT cells and PAPR-1 knockdown can aggravate DNA damage induced by nano-SiO2. Therefore, we speculate whether PARP-1 overexpression can protect DNA from damage induced by nano-SiO2. However, our data demonstrated that overexpression of PARP-1 in HaCaT cells slightly enhanced the cellular proliferation of undamaged cells, when compared with both empty vector control cells and parental cells, but had drastic consequences for cells treated with nano-SiO2. The PARP-1 overtransfected cells were sensitized to the cytotoxic effects and DNA damage of nano-SiO2 compared with control parental cells. Meanwhile, flow cytometric analysis of nano-SiO2 stimulated poly(ADP-ribose) synthesis revealed consistently larger fractions of cells positive for this polymer in the PARP-1 overexpression cells than in control clones. Combining our previous research on PARP-1 knockdown HaCaT cells, we hypothesize that an optimal level of cellular poly(ADP-ribose) accumulation exists for the cellular recovery from DNA damage.

Genetic polymorphisms of superoxide dismutase 1 are associated with the serum lipid profiles of Han Chinese adults in a sexually dimorphic manner.

Inspired by the mechanistic correlations between superoxide dismutase 1 (SOD1) and lipid metabolism, the associations of SOD1 single nucleotide polymorphisms (SNPs) with circulating lipid levels were explored. In 2621 Chinese Han adults, randomly recruited from a health examination center without organic diseases, cancers, and pregnancy, three tag SNPs, rs4998557, rs1041740, and rs17880487 selected by Haploview software were genotyped with a probe-based real-time quantitative PCR method. In both genders, most parameters of the dyslipidemia adults were inferior (P < 0.001) to those of the non-dyslipidemia adults, and genotype frequencies of rs4998557 and rs17880487 were significantly different (P < 0.05) between the normal and abnormal subgroups of total cholesterol (TC) or high-density lipoprotein cholesterol (HDLC). Adjusted for confounding factors, logistic regression analyses revealed that in males rs4998557A, rs1041740T, and rs17880487T reduced the risk of high TC and/or LDLC (P < 0.05), and rs4998557A and rs17880487T increased the risk of low HDLC (P < 0.05); but in females, none of the SNPs had associations with any of the lipid parameters (P > 0.05). Conclusively, characterized by a sexual dimorphism, the SOD1 polymorphisms were associated with the lipid disorders in the adult males but not females of the Chinese Han population.

High serum concentration of selenium, but not calcium, cobalt, copper, iron, and magnesium, increased the risk of both hyperglycemia and dyslipidemia in adults: A health examination center based cross-sectional study.

BACKGROUND: Metabolic disorders of glucose and lipid were associated with some mineral elements, and data were warranted from various contexts to make the association more explicit. OBJECTIVE: To investigate the relationships between the serum concentrations of six mineral elements (calcium, cobalt, copper, iron, magnesium, and selenium) and the risk of hyperglycemia and dyslipidemia in adults. METHODS: The basic information and the over-night fasting serum samples of adults were randomly collected at a health examination center. The serum concentrations of glucose and lipids were measured with an automatic biochemical analyzer, and the mineral elements were measured with an inductively coupled plasma mass spectrometer. Data were analyzed between the hyperglycemia group (HGg) and the normal glucose group (NGg) as well as between the dyslipidemia group (DLg) and the normal lipid group (NLg). RESULTS: A total of 1466 adults aged 22-81 years (male/female = 1.8) were included, 110 in the HGg and 1356 in the NGg, or 873 in the DLg and 593 in the NLg. The serum element concentration medians [P50 (P25-P75)] significantly different between the HGg and the NGg were 0.83 (0.75-0.94) vs. 0.76 (0.68-0.87) mg/L for copper and 100 (90-110) vs. 94 (87-103) µg/L for selenium (P < 0.001), while those between the DLg and the NLg were 99 (92-110) vs. 97 (90-106) mg/L for calcium, 0.78 (0.69-0.88) vs. 0.75 (0.66-0.85) mg/L for copper, 1.7 (1.4-2.0) vs. 1.6 (1.3-2.0) mg/L for iron, 24 (22-28) vs. 23 (22-27) mg/L for magnesium, and 97 (89-106) vs. 92 (84-100) µg/L for selenium (P < 0.05). When the copper and selenium between the HGg and the NGg were analyzed by logistic regression with age, gender, body mass index, and mineral elements adjusted, only the highest quartile of selenium concentration had association with the increased risk of hyperglycemia [quartile (Q) 4 against Q1: OR = 2.9, 95 % CI = 1.5-5.5, P < 0.001). When the five differed mineral elements between the DLg and the NLg were similarly analyzed, only iron and selenium had associations with the increased risk of dyslipidemia (e.g., Q4 against Q1: OR = 1.4, 95 % CI = 1.1-2.0 for iron and OR = 2.9, 95 % CI = 2.1-4.0 for selenium, P < 0.05). CONCLUSION: In contrast to those of calcium, cobalt, copper, iron, and magnesium, the higher serum concentration of selenium increased the risk of both hyperglycemia and dyslipidemia in the study population of adult Chinese.

[Performance verification of direct chemiluminescence immunoassay to detect the serum 25-hydroxyvitamin D concentration].

OBJECTIVE: To test the performance of direct chemiluminescence immunoassay(CLIA) in the determination of serum 25-hydroxyvitamin D [25(OH)D] concentration. METHODS: The CLIA analyzer of Italy DiaSorin was used to measure the 25(OH)D concentrations in the Standard Reference Material 972 a of National Institute of Standards and Technology, DiaSorin control materials, blind samples of Vitamin D External Quality Assessment Scheme(DEAQS), and outpatient serum samples. The functional sensitivity, precision, accuracy, recovery, and linearity were evaluated, and the samples of mild hemolysis, 5 days' storage at 4 ₿ and >1 year's storage at-80 ₿were tested for 25(OH)D. RESULTS: The functional sensitivity was<4 ng/mL. The coefficient of variations of intra-and inter batch were<8. 1%. The relative deviation was-3. 1%-5. 7%. The recovery rates were 82. 8%-112. 9% and it had good linearity in the range of 7. 6-128. 1 ng/mL. Compared with fresh serum, the serum 25(OH)D concentration was not affected by mild hemolysis or being stored at 4 ₿for 5 days, but averagely decreased at 7. 6% by being stored at-80 ₿for more than 1 year. Compared with others, the deviation was-2. 9%-3. 6%. The differences in precision, accuracy and recovery of this method among the three different hospitals is slightly. CONCLUSION: The performance of direct CLIA for 25(OH)D assay meet the basic technical requirements for laboratory medicine, and is laborsaving and timesaving.

[Screening for reference genes in various tissues of rats fed at different dietary selenium concentrations].

OBJECTIVE: To screen for the most stable reference genes(RGs) in various tissues of rats fed at different dietary concentrations of selenium(Se). METHODS: Twenty-four weaning male SD rats were fed Se deficient diet for 5 weeks, and then randomly divided into 4 groups for<0. 01, 0. 25, 3 and 5 mg Se/kg diet feeding, respectively. After 4 weeks, animals were sacrificed for sample collection of liver, testis, muscle and fat tissue. Twelve candidate RGs of Actb, Atp5f1, B2m, Gapdh, Gusb, Hprt, Pgk1, Ppia, Rplp2, Rps18, Tbp and Ywhaz were tested for their quantitative cycle numbers of mRNA abundances with the quantitative PCR method. The stabilities of the candidate RGs were evaluated by the arithmetic packages of geNorm, NormFinder, BestKeeper, Delta CT and RefFinder. RESULTS: The top 4 most stable RGs were Ppia >Atp5f1 > Rplp2 >Hprt in liver; Ywhaz > Atp5f1 >Rplp2> Ppia in testis; Tbp > Ppia > B2m > Rps18 in muscle; Hprt>Tbp >Atp5f1>Pgk1 in fat tissue; and Rps18>Hprt> Rplp2>Atp5f1 when all the 4 tissues combined for analysis. CONCLUSION: To analyze the expressions of the target genes in rats fed different concentrations of dietary Se, the best RGs should be selected depending on the tissue types.

The GC2 haplotype of the vitamin D binding protein is a risk factor for a low plasma 25-hydroxyvitamin D concentration in a Han Chinese population.

BACKGROUND: The GC haplotype of the vitamin D binding protein (encoded by the GC gene) might be a risk factor to the vitamin D (VD) nutritional status for many populations, while evidences from the Chinese Han population are sparse. We test the association between vitamin D binding protein genotypes and VD status as well as the metabolic parameters of glucose and lipids in a Han Chinese population. METHODS: In a cross-sectional study conducted at a health examination centre (registered in ClinicalTrials.gov as QLS2013), 2641 adults were included and grouped according to their plasma 25-hydroxyvitamin D (25OHD) concentrations as VD deficient (VDD), insufficient (VDI), or sufficient (VDS). The rs7041 and rs4588 genotypes were analysed with a molecular beacon-based qPCR method using blood samples. RESULTS: Plasma 25OHD concentrations were lower in the GC2/2, rs7041T/T, and rs4588A/A genotypes than the GC1f/1s, rs7041G/T, and rs4588C/C genotypes (P <  0.05). After adjusting for confounders, the GC2 haplotype increased the risk of low VD status (P <  0.05) in both genders. More genotypic models revealed the negative contributions of rs4588A than rs7041T to low VD status (P <  0.05). The combined rates of VDD and VDI were 80.2% in males and 86.1% in females. Compared with VDI, VDS, or both, VDD showed higher plasma concentrations of fasting blood glucose, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides in males (P <  0.05); however, no significant differences were found with regard to these parameters between the subgroups defined by the GC genotypes (P > 0.05). CONCLUSIONS: In a Han Chinese population, the GC2 haplotype or more exactly rs4588A is a risk factor for low VD status but is not associated with glucose and lipid metabolic disorders, which are inversely correlated with the circulating 25OHD concentration in males. TRIAL REGISTRATION: The study was retrospectively registered in January 2018 as NCT03406234 in the ClinicalTrials.gov online system.

Dietary Selenium Deficiency or Excess Reduces Sperm Quality and Testicular mRNA Abundance of Nuclear Glutathione Peroxidase 4 in Rats.

Background: Glutathione peroxidase (GPX) 4 and selenoprotein P (SELENOP) are abundant, and several variants are expressed in the testis.Objective: We determined the effects of dietary selenium deficiency or excess on sperm quality and expressions of GPX4 and SELENOP variants in rat testis and liver.Methods: After weaning, male Sprague-Dawley rats were fed a Se-deficient basal diet (BD) for 5 wk until they were 9 wk old [mean ± SEM body weight (BW) = 256 ± 5 g]. They were then fed the BD diet alone (deficient) or with 0.25 (adequate), 3 (excess), or 5 (excess) mg Se/kg for 4 wk. Testis, liver, blood, and semen were collected to assay for selenoprotein mRNA and protein abundances, selenium concentration, GPX activity, 8-hydroxy-deoxyguanosine concentration, and sperm quality.Results: Dietary selenium supplementations elevated (P < 0.05) tissue selenium concentrations and GPX activities. Compared with those fed BD + 0.25 mg Se/kg, rats fed BD showed lower (P < 0.05) BW gain (86%) and sperm density (57%) but higher (P < 0.05) plasma 8-hydroxy-deoxyguanosine concentrations (189%), and nonprogressive sperm motility (4.4-fold). Likewise, rats fed BD + 5 mg Se/kg had (P = 0.06) lower BW gain and higher (1.9-fold) sperm deformity rates than those in the selenium-adequate group. Compared with the selenium-adequate group, dietary selenium deficiency (BD) or excess (BD + 3 or 5 mg Se/kg) resulted in 45-77% lower (P < 0.05) nuclear Gpx4 (nGpx4) mRNA abundance in the testis. Rats fed BD had lower (P < 0.05) mRNA levels of 2 Selenop variants in both testis and liver than those in the other groups. Testicular SELENOP was 155-170% higher (P < 0.05) in rats fed BD + 5 mg Se/kg and hepatic c/mGPX4 was 13-15% lower (P < 0.05) in rats fed BD than in the other groups.Conclusions: The mRNA abundance of rat testicular nGPX4 responded to dietary selenium concentrations in similar ways to sperm parameters and may be used as a sensitive marker to assess appropriate Se status for male function.

General monogamy relation for the entanglement of formation in multiqubit systems.

We prove exactly that the squared entanglement of formation, which quantifies the bipartite entanglement, obeys a general monogamy inequality in an arbitrary multiqubit mixed state. Based on this kind of exotic monogamy relation, we are able to construct two sets of useful entanglement indicators: the first one can detect all genuine multiqubit entangled states even in the case of the two-qubit concurrence and n-tangles being zero, while the second one can be calculated via quantum discord and applied to multipartite entanglement dynamics. Moreover, we give a computable and nontrivial lower bound for multiqubit entanglement of formation.

miR-483-5p promotes invasion and metastasis of lung adenocarcinoma by targeting RhoGDI1 and ALCAM.

The nodal regulatory properties of microRNAs (miRNA) in metastatic cancer may offer new targets for therapeutic control. Here, we report that upregulation of miR-483-5p is correlated with the progression of human lung adenocarcinoma. miR-483-5p promotes the epithelial-mesenchymal transition (EMT) accompanied by invasive and metastatic properties of lung adenocarcinoma. Mechanistically, miR-483-5p is activated by the WNT/ß-catenin signaling pathway and exerts its prometastatic function by directly targeting the Rho GDP dissociation inhibitor alpha (RhoGDI1) and activated leukocyte cell adhesion molecule (ALCAM), two putative metastasis suppressors. Furthermore, we found that downregulation of RhoGDI1 enhances expression of Snail, thereby promoting EMT. Importantly, miR-483-5p levels are positively correlated with ß-catenin expression, but are negatively correlated with the levels of RhoGDI1 and ALCAM in human lung adenocarcinoma. Our findings reveal that miR-483-5p is a critical ß-catenin-activated prometastatic miRNA and a negative regulator of the metastasis suppressors RhoGDI1 and ALCAM.

IKK interacts with rictor and regulates mTORC2.

mTORC2, the mammalian target of rapamycin complex 2 is activated by upstream growth factors, and performs two major functions, phosphorylation of AKT at the serine of 473 and cell cycle-dependent organization of actin cytoskeleton. However, the mechanisms through which mTORC2 is triggered by these signals remain unclear. We demonstrated, for the first time, that inhibitor of nuclear factor κ-B kinase (IKK) interacted with rictor and regulated mTORC2 activity. Not only endogenously, but ectopically expressed IKK α and IKK ß physically interacted with rictor. An in vitro binding assay revealed that rictor interacted with IKKα and IKKß from amino acids 999 to 1397. Moreover, chemical inhibition of IKK, knockdown of IKK by small interference RNA (siRNA), or ectopic expression of kinase-dead IKK (IKK KD) repressed phosphorylation of AKT (S473) in a variety of cell lines and decreased the kinase activity of mTORC2. In NIH 3T3 cells, inhibition of IKK also reduced phosphorylation of protein kinase α (PKCα) (S657) and resulted in disorganization of actin cytoskeleton. Interestingly, the interaction between IKKα/ß and rictor was increased, while the mTOR-rictor association was attenuated by inhibition of IKK. We identified a novel signaling mechanism for the regulation of mTORC2 by IKK: IKK interacted with rictor and regulated the function of mTORC2 including phosphorylation of AKT (S473) and organization of actin cytoskeleton. Inactivated IKK interacted with rictor and competed against mTOR, which resulted in a reduced mTORC2 level and a decrease in mTORC2 activity.

Oxidative injury and hepatocyte apoptosis in total parenteral nutrition-associated liver dysfunction.

PURPOSE: The aim of this study was to investigate the impact of oxidative injury and apoptosis on total parenteral nutrition (TPN)-associated hepatic dysfunction. METHODS: Fifty-nine New Zealand rabbits (6-8 days old) were divided into 4 groups: 12 in the control group (maternal fed), 15 in the PN-3 group (TPN for 3 days), 14 in the PN-7 group (TPN for 7 days), and 18 in the PN-10 group (TPN for 10 days). At the end of the experiment, blood biochemistry analysis and histologic examination of the liver were performed; the malondialdehyde content of liver tissues was determined and hepatocyte apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated nick-end labeling assay. RESULTS: We found that the serum level of direct bilirubin became higher as PN duration was extended. The light microscopy features in the PN-3 and PN-7 groups included inflammatory cells infiltrated in portal areas and some degeneration changes, whereas in the PN-10 group, cholestasis (proliferation of bile ducts and bile pigments in hepatocytes) or diffuse steatosis was shown. Electron microscopic manifestation in PN groups included reduced numbers of microvilli and some preapoptosis changes. Both the malondialdehyde content and apoptosis index were the highest in the PN-10 group; there were more apoptotic hepatocytes in the groups with longer PN duration. CONCLUSIONS: The longer the TPN duration, the more severe the liver injury. Both oxidative injury and apoptosis may play important roles in the mechanism of TPN-associated hepatic dysfunction.