Background Preoperative portal vein embolization is increasingly employed for those with hepatocellular carcinoma and cirrhosis to gain a volume-shifting effect. However, the alterations of ...histologic architecture and hepatocyte function of future liver remnant (FLR) remain unexplored. Methods Portal vein ligation (PVL) was performed in cirrhotic and noncirrhotic rats. Regeneration indices that include the DNA synthesis index, restituted liver mass, and the redistributed volume ratio were measured. The indocyanine green 15′ retention test (ICG-R15), histologic changes, total Knodell score, and activated hepatic stellate cells (HSCs) were measured before and after PVL. Tc-99m sulfur-colloid liver single photon emission computed tomography (SPECT) and diisopropyl iminoacetic acid (DISIDA) SPECT were conducted. Results The redistributed volume ratio of cirrhotic rats was less than noncirrhotic rats (63% vs 80%, P < .01). The ICG-R15 of cirrhotic rats at day 7 after PVL was improved compared with baseline (6.0 ± 4.1% vs 15.8 ± 4.6%, P < .01). The total Knodell score and activated HSCs of FLR in cirrhotic rats both were decreased compared with those of baseline. The redistributed volume ratio of noncirrhotic and cirrhotic rats based on 99mTc sulfur-colloid SPECT were 79% and 64%, respectively. The clearance T1/2 of FLR in cirrhotic rats based on DISIDA SPECT was decreased compared with baseline (5.2 ± 1.9 min vs 8.6 ± 3.1 min). Conclusion The regenerated functional liver mass of cirrhotic rats after PVL is less than noncirrhotic rats, whereas the hepatocyte function of FLR in cirrhotic rats is improved relevant to tissue remodeling.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Background:
Metabolic reprogramming is closely linked to the tumorigenesis and drug resistance of gastrointestinal stromal tumors (GISTs). Mapping the metabolic orbit of GISTs is a prerequisite if ...intervention against the metabolic vulnerability of refractory GISTs is desirable.
Methods:
A total of 43 patients with treatment-naïve GISTs who had undergone surgical resections were enrolled, on whom a metabolomics profile detected from surgical specimens was constructed based on the
1
H-nuclear magnetic resonance (NMR) platform. The mRNA and protein levels of GLUT1, HK2, ACSS2, and FASN were assayed. Dual-tracer
18
F-FDG/11C-acetate PET imaging was introduced before surgery in 15 patients.
Results:
1
H-NMR-based metabolomics revealed that GISTs were characterized by upregulation of glutamate, ascorbate, aspartate and glycine and downregulation of choline, creatine, glucose and glycerol. Bioinformatics analysis showed that the TCA cycle and alanine, aspartate, and glutamate metabolism were the two leading pathways. High- and nonhigh-risk (including intermediate-, low-, and very low-risk) GISTs preferentially displayed upregulation of HK2 and ACSS2, respectively, echoed by in vivo imaging that high- and nonhigh-risk GISTs preferentially exhibited higher uptake of
18
F-FDG and
11
C-acetate, respectively, while
18
F-FDG and
11
C-acetate were complementary to each other. Nuclear ACSS2 was exclusively identified in high-risk GISTs.
Conclusion:
We describe a metabolic landscape of GISTs that read aspartate as a de facto “oncometabolite,” which was replenished via the TCA cycle and alanine, aspartate, and glutamate metabolism. Glycolysis and ACSS2-mediated acetate metabolism competed and complemented fatty acid synthesis, although glycolysis remained an aggressive phenotype.
Abstract Background The prognostic role of the preoperative lymphocyte-to-monocyte ratio (LMR) in patients with gastric cancer (GC) remains unclear. The aim of this study was to explore the ...prognostic potential of the preoperative LMR in patients with resectable GC. Materials and methods The medical records of 926 consecutive patients with resectable GC between 2005 and 2010 were retrospectively reviewed and analyzed. Patients were stratified into two groups based on the preoperative LMR with a cutoff value of 4.8 (group 1: LMR ≤ 4.8; group 2: LMR > 4.8). Clinicopathologic factors potentially affecting patient outcomes were collected prospectively and analyzed. Results Compared to group 2, in group 1, there was a higher percentage of men, patients aged >48 y, total gastrectomy, tumor size > 4.8 cm, T4 lesions, N3 disease, metastatic tumors, advanced stage, ratio of metastatic to examined lymph nodes > 0.18, R1 resection, and occurrence of vascular or lymphatic invasion. Group 1 also had a higher 30-d surgical mortality rate (groups 1 versus 2 at 2.9% versus 0.5%; P = 0.006) and lower 3-y and 5-y overall survival (53.6% versus 71.9% and 46.4% versus 63.3%, respectively; P < 0.0001). Multivariate analysis showed that preoperative low LMR was an unfavorable prognostic factor for resectable GC. Conclusions Patients with lower LMR had more aggressive tumor behavior, higher surgical mortality rates, and worse long-term survival. The preoperative LMR may serve as an independent prognostic factor for prediction of surgical outcomes and for assisting clinicians in determining future treatment plans.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Abstract Background Despite advances in intensive care medicines, hemorrhagic shock leading to multiple organ failure remains the major causes of death in the injured host. Although studies have ...shown that 17β-estradiol (E2) prevents trauma-hemorrhage-induced lung damage, it remains unknown whether protein kinase B (Akt)/heme oxygenase (HO)-1 plays any role in E2-mediated lung protection after trauma-hemorrhage. Materials and methods After a 5-cm midline laparotomy, male rats underwent hemorrhagic shock (mean blood pressure ∼40 mm Hg for 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were treated with vehicle, E2 (1 kg/mg), E2 plus phosphoinositide 3-kinase inhibitor LY294002 (5 mg/kg), or LY294002. At 2 h after trauma-hemorrhage or sham operation, lung tissue myeloperoxidase activity, wet-to-dry-weight ratio, inflammatory mediators, and apoptosis were measured. Lung Akt, HO-1, and cleaved caspase-3 protein levels were also determined. Results E2 attenuated the trauma-hemorrhage-induced increase in lung myeloperoxidase activity, edema formation, inflammatory mediator levels, and apoptosis, which was blocked by co-administration of LY294002. Administration of E2 normalized lung Akt phosphorylation and further increased HO-1 expression and decreased cleaved caspase-3 levels after trauma-hemorrhage. Co-administration of LY294002 prevented the E2-mediated attenuation of shock-induced lung injury. Conclusions Our results collectively suggest that Akt-dependent HO-1 upregulation may play a critical role in E2-meditated lung protection after trauma-hemorrhage.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Background The prognosis for cholangiocarcinoma remains dismal due to a low resection rate and early recurrence. Cancer cachexia is associated with decreased survival and poor quality of life. ...Herein, we present a rat model of cholangiocarcinoma and demonstrate that thalidomide attenuates tumor growth and improves cachexia. Methods A cholangiocarcinoma model was established using Sprague-Dawley rats that were fed thioacetamide for 40 weeks. Cholangiocarcinoma rats were treated using either thalidomide or saline for 8 weeks. Tumor growth and body weight were recorded for all animals. The expression of CD31, VEGF, and eIF4E of cholangiocarcinoma were determined using immunohistochemistry. Level of apoptosis and Fas-mediated apoptosis genes of cholangiocarcinoma were determined using TUNEL assay and ribonuclease protection assay, respectively. The distribution of fast-twitch soleus skeletal muscle fibers was determined as was the expression of TNFα and TGFβ1 within soleus muscle. Results After an 8-week treatment, the mean weight of saline- and thalidomide-treated rats was 24% and 19%, respectively, less than that of control (ANOVA, P < .05). The tumor volume ( x ¯ ± SD ) of thalidomide-treated rats was less than saline-treated rats (1.9 ± 0.4 vs 4.6 ± 1.3 cm3 , P < .01). The expression of CD31, eIF4E, and VEGF of cholangiocarcinoma was less than thalidomide-treated rats than for saline-treated rats, while the level of apoptosis of tumor cells was greater for thalidomide- treated rats than for saline-treated rats. The expression of mRNA for Fas, caspase-3, and Bax of cholangiocarcinoma in the thalidomide-treated rats was greater than for saline-treated rats. The number of fast-twitch skeletal muscle fibers per 500 mm2 of control, saline-, and thalidomide-treated rats was 43 ± 6, 14 ± 3, and 41 ± 8 (ANOVA, P < .001). The expression of TNFα and TGFβ1 of soleus muscles for thalidomide-treated rats was less than for saline-treated rats. Conclusions Using our rat cholangiocarcinoma model, we demonstrated that thalidomide inhibited tumor growth and was associated with a decrease in expression of reduced eIF4E and VEGF expression; in addition, thalidomide preserved fast-twitch skeletal muscle fibers and was associated with decreased expression of TNFα and TGFβ1.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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