reported that serum PG I and II level, but not PG I/II ratio, were significantly higher in serum CagA antibody positive compared with negative children.[26] Serum PG was reported to be correlated with gastric inflammatory score.[27] In addition, the cagA status was reported to be associated with various kinds of cytokines including interleukin-8 (IL-8) and may cause severe inflammation

in the stomach.[28] It is also possible that gastritis increases Epigenetics inhibitor permeability of the gastric epithelial surface, enabling back diffusion of PGs after secretion.[27] These findings suggest that serum CagA antibody titer was associated with gastric inflammation, but not atrophy. Shimoyama et al. reported that inflammation in the antrum and the corpus was more significant in serum CagA antibody positive when they examined the presence of serum CagA antibody by

immunoblot.[29] In the present study, although there were no significant differences of each histological score between serum CagA antibody positive and negative this website group, the mucosal inflammation in the corpus was significantly correlated with serum CagA antibody titer. This finding also supported that different level of antibody production from lymphocytes induced by H. pylori infection can contribute to the various serum CagA antibody level. Interestingly, positive correlation between the inflammatory score and serum CagA antibody titer was found only in the corpus but not in the antrum. Corpus dominant gastritis rather than antrum dominant gastritis was a risk factor to develop gastric ulcer and gastric cancer.[3, 30] In addition, even when only serum CagA antibody positive group was selected, serum CagA antibody titer was significantly correlated with inflammation and activity in the corpus. Therefore, antibody titer rather than the presence of antibody can be a useful marker for advanced inflammation in the stomach in Japan. This suggests that serum CagA antibody titer might be an available marker to predict click here a gastric cancer in Japan. It has also been reported that measurement of serum levels of C-reactive protein (CRP) using a high-sensitivity assay (hs-CRP) can reveal

subclinical inflammatory states that may reflect vascular inflammation.[31] Recent report showed that the mean serum level of hs-CRP was significantly higher in H. pylori-positive group than H. pylori-negative group, although the level of hs-CRP was not different between CagA antibody positive and negative group in Iran.[32] It is better to examine the association between serum CagA antibody and hs-CRP in Japan in the further study. In our study, in spite of cagA positive by PCR, the prevalence of serum CagA antibody was 75.0%, which was consistent with previous studies from Japan.[17, 33] The cagA gene is located at one end of the cag pathogenicity island (PAI), an approximately 40-kbp region that is thought to have been incorporated into the H. pylori genome by horizontal transfer from an unknown source.

Sixteen percent of CH patients state that oxygen is unaffordable while 12% are getting

welder grade oxygen because of costs of medical grade oxygen, and this form of oxygen could be potentially dangerous to the individual user. Conclusions.— Oxygen is underutilized Hormones antagonist by CH patients living in the United States. Current recommended oxygen treatment regime is not meeting the needs of many CH patients. Prescribed oxygen flow rates are too low for efficacy. Oxygen can be expensive and very difficult to obtain. Physicians need to be better educated on the use of inhaled oxygen for CH. “
“Background.— The brain of migraineurs is hyperexcitable, particularly the occipital cortex, which is probably hypersensitive to light. Photophobia or hypersensitivity to light may be accounted for by an increased excitability of trigeminal, the visual pathways, and the occipital cortex. Objective.— To study light sensitivity and photophobia by assessing the response to light stimuli with functional magnetic Dorsomorphin purchase resonance imaging–blood oxygenation level dependent (fMRI-BOLD) of the occipital cortex in migraineurs and in controls. Also, to try to decipher the contribution of the occipital cortex to photophobia and whether the cortical reactivity of migraineurs may be part of a constitutional (defensive) mechanism or represents an acquired (sensitization) phenomenon. Methods.— Nineteen patients with migraine

(7 with aura and 12 without aura) and 19 controls were studied with fMRI-BOLD during 4 increasing

light intensities. Eight axial image sections of 0.5 cm that covered the occipital cortex were acquired for each intensity. We measured the extension and the intensity of activation for every light stimuli. Photophobia was estimated according to a 0 to 3 semiquantitative scale of light discomfort. Results.— Migraineurs had a significantly higher number of fMRI-activated voxels at low (320.4 for migraineurs [SD = 253.9] and 164.3 for controls [SD = 102.7], P = .027) and medium-low luminance levels (501.2 for migraineurs [SD = 279.5] and 331.1 for controls [SD = 194.3], P = .034) but not at medium-high (579.5 for migraineurs [SD = 201.4] and 510.2 for controls [SD = 239.5], P = .410) and high light stimuli (496.2 for migraineurs [SD = 216.2] and 394.7 for controls [SD = 240], P = .210). No differences were found with respect selleckchem to the voxel activation intensity (amplitude of the BOLD wave) between migraineurs and controls (8.98 [SD = 2.58] vs 7.99 [SD = 2.57], P = .25; 10.82 [SD = 3.27] vs 9.81 [SD = 3.19], P = .31; 11.90 [SD = 3.18] vs 11.06 [SD = 2.56], P = .62; 11.45 [SD = 2.65] vs 10.25 [SD = 2.22], P = .16). Light discomfort was higher in the group of migraineurs at all the intensities tested, but there was no correlation with the number of activated voxels in the occipital cortex and photophobia. Repetitive light stimuli failed to demonstrate a lack of habituation in migraineurs. Conclusions.

Sixteen percent of CH patients state that oxygen is unaffordable while 12% are getting

welder grade oxygen because of costs of medical grade oxygen, and this form of oxygen could be potentially dangerous to the individual user. Conclusions.— Oxygen is underutilized BTK inhibition by CH patients living in the United States. Current recommended oxygen treatment regime is not meeting the needs of many CH patients. Prescribed oxygen flow rates are too low for efficacy. Oxygen can be expensive and very difficult to obtain. Physicians need to be better educated on the use of inhaled oxygen for CH. “
“Background.— The brain of migraineurs is hyperexcitable, particularly the occipital cortex, which is probably hypersensitive to light. Photophobia or hypersensitivity to light may be accounted for by an increased excitability of trigeminal, the visual pathways, and the occipital cortex. Objective.— To study light sensitivity and photophobia by assessing the response to light stimuli with functional magnetic this website resonance imaging–blood oxygenation level dependent (fMRI-BOLD) of the occipital cortex in migraineurs and in controls. Also, to try to decipher the contribution of the occipital cortex to photophobia and whether the cortical reactivity of migraineurs may be part of a constitutional (defensive) mechanism or represents an acquired (sensitization) phenomenon. Methods.— Nineteen patients with migraine

(7 with aura and 12 without aura) and 19 controls were studied with fMRI-BOLD during 4 increasing

light intensities. Eight axial image sections of 0.5 cm that covered the occipital cortex were acquired for each intensity. We measured the extension and the intensity of activation for every light stimuli. Photophobia was estimated according to a 0 to 3 semiquantitative scale of light discomfort. Results.— Migraineurs had a significantly higher number of fMRI-activated voxels at low (320.4 for migraineurs [SD = 253.9] and 164.3 for controls [SD = 102.7], P = .027) and medium-low luminance levels (501.2 for migraineurs [SD = 279.5] and 331.1 for controls [SD = 194.3], P = .034) but not at medium-high (579.5 for migraineurs [SD = 201.4] and 510.2 for controls [SD = 239.5], P = .410) and high light stimuli (496.2 for migraineurs [SD = 216.2] and 394.7 for controls [SD = 240], P = .210). No differences were found with respect selleck kinase inhibitor to the voxel activation intensity (amplitude of the BOLD wave) between migraineurs and controls (8.98 [SD = 2.58] vs 7.99 [SD = 2.57], P = .25; 10.82 [SD = 3.27] vs 9.81 [SD = 3.19], P = .31; 11.90 [SD = 3.18] vs 11.06 [SD = 2.56], P = .62; 11.45 [SD = 2.65] vs 10.25 [SD = 2.22], P = .16). Light discomfort was higher in the group of migraineurs at all the intensities tested, but there was no correlation with the number of activated voxels in the occipital cortex and photophobia. Repetitive light stimuli failed to demonstrate a lack of habituation in migraineurs. Conclusions.

29 However, based on our current observation, it is plausible that OATP1B1 functions as a key pathway in the network for modulation of hepatic bile acid concentration through its ability to mediate the sodium-independent hepatic uptake of bile acids and thereby enhance bile acid sensing through FXR and modulation of target gene expression. It seems noteworthy that another hepatic OATP capable of bile acid uptake, OATP1B3,29 has been shown to also be positively regulated by FXR.17, 18 Indeed, in human hepatocytes,

we were able to confirm that treatment with CDCA results in OATP1B3 induction (Fig. 7). However, unlike OATP1B1, OATP1B3 Selleckchem Tigecycline does not appear to be regulated by LXRα (Fig. 7). We hypothesize that regulation of the bile acid transporters is multifactorial and includes several components (Fig. 8). Protein kinase A exhibits cyclic adenosine monophosphate (cAMP)-dependent catalytic activity and is involved in the regulation RXDX-106 molecular weight of several intracellular processes, including

the activity of transcription factors such as HNF4α as well as OATP1B1.30 HNF4α not only regulates OATP1B1, but also the expression of NTCP (SLC10A1), the sodium-dependent transporter for bile acids.31, 32 Introducing an additional factor to this network of OATP1B1 expression is the G protein–coupled receptor TGR5, which induces intracellular cAMP levels upon binding of bile acids.33 Thus, increased bile acid levels would reduce the expression of both bile acid transporters through suppression of HNF4α activity and expression of the transporters

that facilitate the uptake of bile acid FXR ligands. This notion is supported by findings showing that cAMP protects against hepatocellular apoptosis induced by hydrophilic bile acids such as GCDCA,34 although expression find more and function of TGR5 in human hepatocytes is controversial.35, 36 There are reports suggesting moderate but functional expression of TGR5 in hepatocytes.29 In terms of LXRα, there has been significant progress using LXRα as a therapeutic target to treat metabolic disorders and atherosclerosis.37 Indeed, our observed effects of an LXRα agonist in human hepatocytes suggest that such a strategy might result in the induction of hepatic drug transporters such as OATP1B1 (Fig. 6), which for drugs such as the statin class of HMG-Co-A reductase inhibitors would result in a higher liver concentration of the drug while lowering systemic exposure. This may be viewed as a therapeutically beneficial effect of LXRα. Given the importance of regulated conversion of cholesterol to bile acids by LXRα target genes, regulation of OATP1B1 by LXRα is consistent with an important physiological role of OATP1B1 to hepatic cholesterol and bile acid homeostasis In conclusion, we show for the first time that OATP1B1 is dual nuclear receptor–regulated through the actions of the bile acid sensor FXR and the cholesterol sensor LXRα, but not by the typical xenobiotic receptors such as PXR and CAR.

In the present study, owing to the metabolism of the trace elements is altered in either infection or inflammation, we explored the treatment of H. pylori infection and its association with the changes of some serum essential trace elements for the first time. Methods: Subjects

were collected according to the treatment and non-treatment for H.pylori. Patients Doxorubicin treated with amoxicillin and clarithromycin were classified as first line treatment, while the patients treated with bismuth, tetracycline and metronidazole were classified as second line treatment. The final treatment used bismuth, amoxicillin and levofloxacin were classified as third line treatment. Every group consisted of twenty subjects. Essential trace elements including iron, copper, zinc, and selenium were analyzed using high sensitive Inductively coupled plasma mass spectrometry. Results: Our major findings indicated that a significant difference (p < 0.05) in serum iron concentration was observed in second line treatment when compared with those of first line treatment. Also, our results showed that the third line treatment would have higher serum iron concentration than those of the control group with significant difference (p < 0.05). In addition, a significant difference (p < 0.05) in serum www.selleckchem.com/products/Nolvadex.html zinc concentration was observed in second line treatment when compared with those of first line treatment. Conclusion: Some

serum essential trace elements such as iron and zinc might play certain

roles in the evaluation of the treatment efficiency of H.pylori. Further study could devote to explore the existence of H.pylori and its relationship with iron and /or zinc. Key Word(s): 1. Helicobacter pylori; 2. Iron; 3. Zinc; Presenting Author: YANYAN SHI Additional Authors: LINNA LIU, YUEXIA ZHANG, selleck screening library XIANGMEI CHEN, TING ZHANG, JING ZHANG, YE WANG, SHIGANG DING Corresponding Author: SHIGANG DING Affiliations: Peking University Third Hospital; Peking University Health Science Center Objective: Helicobacter pylori (H. pylori) infection has been proved to be related to the development of gastric diseases, but the pathogenic mechanism has not been clear. We want to identify the pathogenic properties of H. pylori, and to investigate the identified protein. Methods: H. pylori strains were isolated from endoscopic biopsy specimens of gastric mucosa from patients with gastric cancer, peptic ulcer, and gastritis. The proteins were analyzed by two-dimensional gel electrophoresis and mass spectrometry. Then the expressions of Trx1 were analyzed by real-time PCR. H. pylori expressing high or low Trx1 levels was co-cultured with gastric cancer cell line BGC-823 and gastric epithelial cell line GES-1 respectively. MTT, cell cycle and cell apoptosis were used to estimate cell growth. Western blot was used to measure the related proteins. The two strains were used to make chronic animal models by infecting Mongolian gerbils for 91 weeks. Results: Trx1 expression of H.

In the present study, owing to the metabolism of the trace elements is altered in either infection or inflammation, we explored the treatment of H. pylori infection and its association with the changes of some serum essential trace elements for the first time. Methods: Subjects

were collected according to the treatment and non-treatment for H.pylori. Patients Saracatinib treated with amoxicillin and clarithromycin were classified as first line treatment, while the patients treated with bismuth, tetracycline and metronidazole were classified as second line treatment. The final treatment used bismuth, amoxicillin and levofloxacin were classified as third line treatment. Every group consisted of twenty subjects. Essential trace elements including iron, copper, zinc, and selenium were analyzed using high sensitive Inductively coupled plasma mass spectrometry. Results: Our major findings indicated that a significant difference (p < 0.05) in serum iron concentration was observed in second line treatment when compared with those of first line treatment. Also, our results showed that the third line treatment would have higher serum iron concentration than those of the control group with significant difference (p < 0.05). In addition, a significant difference (p < 0.05) in serum LBH589 zinc concentration was observed in second line treatment when compared with those of first line treatment. Conclusion: Some

serum essential trace elements such as iron and zinc might play certain

roles in the evaluation of the treatment efficiency of H.pylori. Further study could devote to explore the existence of H.pylori and its relationship with iron and /or zinc. Key Word(s): 1. Helicobacter pylori; 2. Iron; 3. Zinc; Presenting Author: YANYAN SHI Additional Authors: LINNA LIU, YUEXIA ZHANG, selleck products XIANGMEI CHEN, TING ZHANG, JING ZHANG, YE WANG, SHIGANG DING Corresponding Author: SHIGANG DING Affiliations: Peking University Third Hospital; Peking University Health Science Center Objective: Helicobacter pylori (H. pylori) infection has been proved to be related to the development of gastric diseases, but the pathogenic mechanism has not been clear. We want to identify the pathogenic properties of H. pylori, and to investigate the identified protein. Methods: H. pylori strains were isolated from endoscopic biopsy specimens of gastric mucosa from patients with gastric cancer, peptic ulcer, and gastritis. The proteins were analyzed by two-dimensional gel electrophoresis and mass spectrometry. Then the expressions of Trx1 were analyzed by real-time PCR. H. pylori expressing high or low Trx1 levels was co-cultured with gastric cancer cell line BGC-823 and gastric epithelial cell line GES-1 respectively. MTT, cell cycle and cell apoptosis were used to estimate cell growth. Western blot was used to measure the related proteins. The two strains were used to make chronic animal models by infecting Mongolian gerbils for 91 weeks. Results: Trx1 expression of H.

McCuskey, Narci Teoh, Geoffrey C. Farrell Background: Non-alcoholic steatohepatitis (NASH) is characterized

by hepatic steatosis, elevated levels of circulating free fatty acids (FFA) and hepatocyte lipoapotosis. This lipoapoptosis requires activation of the pro-apoptotic BH3-only proteins Bim and PUMA. Keap1 is a BTB-kelch protein that can regulate the expression of Bcl-2 protein and control apoptotic cell death. Yet, a role for Keap1 in mediating hepatocyte lipotoxicity is unknown. In vivo, keap1 deletion worsened insulin resistance and increased hepatocyte injury in diet-induced and genetic obesity, suggesting a protective role of Keap1 regarding these parameters. Thus, our aim was to determine if Keap1 was dysregulated during lipotoxicity by FFA. Methods: Hepatocarcinoma cell lines BTK inhibitor Hep3B and Huh-7, or mouse primary hepatocytes were treated with www.selleckchem.com/products/jq1.html saturated FFA palmitate (PA) (400-600 microM). Keap1, PUMA, Bim expression and JNK activation were examined by real-time PCR and/or immunoblot analysis. Keap1 expression was selectively knocked-down using shRNA. Cell death was assessed by trypan blue exclusion assay, DAPI staining and caspase 3/7 activation using a fluorogenic assay. Results: PA is toxic to liver cells and induces significant cell death by 8h and 16h after

treatment. Interestingly, Keap1 protein underwent rapid selleck chemicals cellular elimination within 2 to 4 hours after treatment with PA. PA-induced decrease in Keap1 protein was associated with JNK activation and upregulation of Bim and PUMA protein levels. In contrast, no alteration in Keap1 expression was noted following incubation with oleic acid, a non-toxic FFA. PA did not alter Keap1 mRNA expression, excluding a transcriptional regulation of Keap1 during this process. Keap1 degradation was not affected by either proteasome inhibition with

MG132, or by pan-caspase inhibition with QVD-OPh. In contrast, disruption of the autophagy pathway, by silencing of the autophagy-related protein p62, prevented Keap1 decrease by PA, indicating that PA-induced decrease in Keap1 is due to autophagy degradation. Stable knockdown of Keap1 expression in Hep3B or Huh-7 cells resulted in increased JNK phosphorylation and downstream upregulation of Bim and PUMA protein expression with subsequent increased cell death. Keap1 knockdown also significantly enhanced PA-mediated cell death and caspase 3/7 activity. Finally, primary hepatocytes isolated from liver-specific keap/- mice, which express higher Bim and PUMA protein levels, displayed increased sensitivity to PA-induced apoptosis than WT mouse hepatocyte. Conclusion: These results implicate p62dependent autophagic degradation of Keap1 by palmitate as a mechanism promoting hepatocyte lipoapoptosis. Disclosures: Arun J.

12A,B). Concentrations of proliferating cell nuclear antigen, an indicator of cell proliferation, were elevated in liver-specific Stat5-null mice treated with CCl4 (Supporting Fig. 13A,B). To establish GH or TGF-β–dependent apoptosis signaling in vivo, control mice were injected with GH or TGF-β followed by protein and mRNA analyses. Whereas GH treatment of control mice induced caspase-3 activation and expression

of Nox4, Puma, and Bim, no such increase was observed in the absence of GH (Supporting Fig. 14A). TGF-β treatment of control mice, but not experimental mice, induced caspase-3 activation and expression of Nox4, Puma, and Bim mRNA Selleck Gefitinib levels (Supporting Fig. 14B). This finding suggests that caspase-3 activation and expression of Puma and Bim by GH or TGF-β treatment induced apoptosis by STAT5/NOX4. While in many cell types the transcription factor STAT5 provides proliferative and survival cues by activating respective genetic programs, it serves as a bona fide tumor suppressor in liver tissue.3, 25 Loss of STAT5 from liver tissue leads to hepatosteatosis and the development of HCC upon CCl4 treatment.

STAT5′s function as tumor suppressor can be attributed in part to its ability to regulate the cell XL765 datasheet cycle control genes Cdkn2b and Cdkn1a.25 In addition, the presence of STAT5 also suppresses inappropriate cytokine-induced activation of STAT3, an oncoprotein in its own right. We now provide evidence for additional venues used by STAT5 to control cell death and thus suppress the development of HCC. Whereas CCl4 exposure is required to induce HCC in 3-month-old liver-specific see more Stat5-null mice, 17-month-old mice develop HCC in the absence of this chemical insult. Thus, loss of STAT5 by itself is sufficient to fundamentally alter cellular metabolism conducive to disease development. In this study, we have identified and investigated additional STAT5 target genes whose deregulation

likely contribute to the development of HCC in the absence of STAT5. Notably, STAT5 controls ROS production through the activation of the Nox4 gene and it activates the genes encoding the proapoptotic and tumor suppressive proteins PUMA and BIM. We therefore propose that STAT5 protects hepatocytes through several pathways, including the activation of cell death programs executed by NOX4, PUMA, and BIM. Studies on mice from which the genes encoding NOX4, PUMA, and BIM had been deleted, as well as tissue culture cells expressing reduced levels of these proteins, provided sound evidence for these proteins in cell death programs. In hepatocytes, NOX4 is required for TGF-β–induced apoptosis19 and loss of NOX4 from lung epithelium is protective from TGF-β–induced apoptosis.26 In heart tissue, NOX4 protected cells from pressure overload–induced apoptosis.

The consequent definition of non–life-threatening bleeding episodes that are non-responsive to bypassing treatment provides a global picture of the condition of the patient during such an event. Identification of non-responsiveness is based on various criteria: pain, swelling/tension, mobility, patient perception and laboratory parameters. Criteria can be assessed subjectively by the patient/parent and/or objectively by the clinician.

Although the precise timing of each determination should be at the discretion of the physician, bleeds should be considered non-responsive if the clinical situation meets the specified criteria 24 h from Small molecule library the start of treatment. Although it is not intended to replace clinical judgment, this definition can guide the optimal course of treatment for patients with haemophilia

and inhibitors. “
“Summary.  Antibody responses to clotting factor concentrates remain a major treatment limitation. In conjucation with ongoing clinical studies, the pathogenesis and potential treatment of clotting factor immune responses is being evaluated in a variety of animal models. In 2010, the most important treatment-related complication of coagulation factor replacement is the development of neutralizing antibodies to the therapeutic protein. This complication occurs in approximately 25% of haemophilia selleck compound A (HA) patients and 3% of haemophilia B subjects. While significant progress has been made in our understanding of the pathogenic mechanisms involved in this phenomenon, much remains to be learnt. The investigation of the immune selleck products response to coagulation factor exposure in human haemophiliacs is limited by a number of biological and practical considerations. Thus, while it remains critical to continue the evaluation of this treatment complication in human populations, this experimental approach will need to be complemented with

observations made in animal models of haemophilia. This chapter focuses on three specific aspects of the immune response to factors VIII (FVIII) and factor IX (FIX): the development of novel transgenic mouse models to facilitate the characterization of this process, the study of tolerance mechanisms in haemophilic mice and finally, the association of inhibitors with haemophilia gene therapy studies. About 25% of patients with severe HA develop neutralizing antibodies against FVIII, after replacement therapy [1,2]. The antibody response to FVIII is a polyclonal IgG response that is not restricted isotypically. Although IgG4 is frequently the major component of anti-FVIII antibodies, all IgG subclasses have been found [3,4]. While the antibodies against FVIII are well characterized [5–8], limited information is available on the regulation of the antibody response. In particular, the reason why some patients develop antibodies while others do not is far from clear.

The mean Fibroscan values of CLD patients, non alcoholic fatty liver patients and controls were 24.16 ± 2.27 kPa, 6.63 ± 0.27 kPa and 5.29 ± 0.28 kPa respectively. The mean Fibroscan values of CTP A(n = 32), CTP B(n = 44) and CTP C(n = 17) cirrhosis was 10.05 ± 1.78 kPa, 26.78 ± 3.40 and 44.13 ± 4.68 respectively (p < 0.01). The mean Fibroscan values of patients with MELD score <10(n = 43), 10-17(n = 38) and ≥18(n = 12) were 12.77 ± 2.0 kPa,29.61 ± 3.3 and 49.54 ± 6.7 respectively (p < 0.01). However the difference between controls, fatty liver patients and CTP A cirrhosis (or patients with MELD < 10) was not significant (p > 0.05).

Conclusion: Fibroscan correlates well with Child Pugh and MELD scoring

system. However it fails to differentiate CTP A (MELD < 10) JQ1 solubility dmso buy Maraviroc cirrhosis from controls or Fatty liver. Key Word(s): 1. Fibroscan; 2. liver stiffness; 3. MELD score; 4. CTP score; Presenting Author: JIANPING QIN Additional Authors: MINGDE JIANG Corresponding Author: JIANPING QIN Affiliations: Chengdu Military General Hospital Objective: To study the location of the right hepatic vein and portal vein and their spatial relationship through image analysis and provide a basis for performing the portal vein puncture and safety assessment of TIPS. Methods: Images of the right hepatic vein and portal vein were taken from 128 post-TIPS patients. With corresponding vertebra and vertebral interspace as reference points, the location of the right hepatic vein opening, the location of the portal vein selleck bifurcation,

and the layout of the portal vein branches, as well as their relationship with factors including gender, age and Child classification of the patients, were assessed. Results: The relationship between the right hepatic vein and portal vein is upper-rear and lower-front; all right hepatic vein openings are located above the portal vein bifurcation. The right hepatic vein opening is located at the 10th thoracic vertebra (T10) plane in 75 patients (58.6%), and the portal vein bifurcation is located at the T11 plane in 63 patients (49.2%). These results indicate that the right hepatic vein opening is mostly located at plane T10, while the majority of the portal vein bifurcations is on plane T11. In 114 patients (89.1%), the distance between the right hepatic vein opening and the portal vein bifurcation is greater than one vertebra. In 117 patients (91.4%), the portal vein has 2 branches, while in 11 patients (8.6%), the portal vein has 3 branches. Among those patients who had 2 portal vein branches, the rear right branch of the portal vein originates from the main portal vein in 3 patients (2.3%), and the frontal right branch of the portal vein came from the left branch of the portal vein in another 3 patients (2.3%).