The standard liver volume (LV) of a recipient is estimated in liver transplantation to determine the minimum LV necessary for the recipient. Simple linear formulas of LV estimation were developed for the Japanese and Caucasian populations. The present study examined the applicability of the reported formulas to the Korean population. Liver density ( L iver transplantation is a gold standard of therapy for a patient with end-stage liver disease. Living donor liver transplantation and split liver transplantation were originally developed to overcome the shortage of pediatric donors. 1 Since living donor liver transplantation was successfully applied to an adult patient, 2 the practice of adult-to-adult living donor liver transplantation has steadily increased in countries where living donors are practically the only source of organs due to the scarcity of cadaver donors. 3 -6 A major concern in liver transplantation is to determine the minimum graft volume required for a recipient to meet his or her metabolic demand. 7 -9 The transplantation of a large-for-size graft to a small recipient can pose an increased risk of immunological impairments and graft and vascular compromises due to compression. 10 On the other hand, the transplantation of a small-for-size graft to a large recipient may cause impaired metabolic functions of the liver, such as hyperbilirubinemia and coagulopathy, and reduce the probability of graft survival after implantation. 7,11 It is generally accepted that a ratio of graft volume to standard liver volume (LV) needs to be at least 30% to 40% to fit the hepatic metabolic demand of the recipient. 3,6,7 Accurate estimation of standard LV is vital at the preoperative stage to determine the minimum LV necessary for the recipient and to evaluate qualification of the donor.Urata et al. 12 and Heinemann et al. 13 established simple linear equations that estimate standard LV from body surface area (BSA) in the Japanese and Caucasian populations, respectively. However, these formulas produced LV estimates quite different from each other. 13 The aims of the present study were to examine the applicability of the reported formulas to the Korean population and to develop a better model of LV estimation as necessary. Materials and Methods Liver Density DeterminationThe data of liver weight (LW) and LV were collected by measuring 24 healthy livers. The livers were weighed and their volumes were measured by the principle of Archimedes. Liver density (LD) was calculated by LW / LV.

Glutamine (Gln) supplementation is known to play a beneficial role in a number of settings of critical illness as well as laboratory models of endotoxin shock. We have investigated a molecular mechanism of the protective role of Gln in lipopolysaccharide (LPS)-induced shock using a mouse model. To examine the effectiveness of Gln, Gln was administered before or after LPS injection. Treatment of Gln before, but not after, LPS injection resulted in inhibition of nuclear factor kappaB activation and tumor necrosis factor alpha synthesis. In contrast, protection of animal from LPS-mediated death by Gln was observed when the Gln treatment was performed after LPS injection, suggesting that nuclear factor kappaB/tumor necrosis factor alpha signaling does not play an important role in this process. LPS injection induced phosphorylation of cytoplasmic phospholipase A2 (cPLA2), which was blocked by Gln treatment after LPS injection. Similarly, the LPS-stimulated cPLA2 activity was also inhibited by Gln treatment after LPS injection. Moreover, a cPLA2 inhibitor not only inhibited LPS-induced activation of cPLA2, but also significantly prevented LPS-mediated death. These observations indicate that Gln has a capability to inhibit cPLA2 phosphorylation and activation and suggest that Gln might be of a great therapeutic value for controlling inflammatory diseases in which cPLA2 plays an important role in the pathogenesis of the diseases.

Using semiserial sections from 19 human fetuses of 8-30 weeks gestation, we examined the topohistology of the upper abdominal lymphatics and compared it with that of the lower abdominal and pelvic lymphatics. The upper abdominal lymphatics were characterized by an intimate relationship with the peritoneal lining, a common mesentery for the celiac trunk and superior mesenteric artery (SMA). Lymphatic connections from the upper abdominal viscera to the paraaortic and paracaval areas followed two routes: (1) from the intestinal mesentery, along the peritoneum on the left aspect of the proximal SMA, via the chain of lymph follicles (LFs) lying along the retropancreatic fusion fascia, to drain into the LFs around the left renal vein; (2) from sites along the peritoneum on the posterior wall of the omental bursa, via the root of the hepatoduodenal ligament, to drain into LFs around the vena cava. The development of these two posterior drainage routes seemed to be promoted by the peritoneum or a peritoneal remnant (i.e., fusion fascia) attaching to the great vessels, and inhibited or impeded by the developing nerves and diaphragm. No paraaortic, paracaval, or pelvic LFs lay along the peritoneum. The pelvic Abbreviations used: AO ¼ aorta; CHA ¼ common hepatic artery; crus ¼ crus of the diaphragm; CT ¼ celiac trunk; D1, D2, D3, and D4 ¼ the first, second, third, or fourth portion of the duodenum, respectively; GL ¼ autonomic ganglion; IVC ¼ inferior vena cava; JA ¼ upper jejunal artery; LGA ¼ left gastric artery; LF ¼ lymph follicle; LRV ¼ left renal vein; panc ¼ pancreas; PC ¼ peritoneal cavity; PV ¼ portal vein; RGEA ¼ right gastroepiploic artery; SMA ¼ superior mesenteric artery; SMV ¼ superior mesenteric vein; SPA ¼ splenic artery; t.colon ¼ transverse colon; TD ¼ thoracic duct; VP ¼ Vater's papilla.

SummaryNon-essential amino acid L-glutamine (Gln) possesses anti-inflammatory activity via deactivating cytosolic phospholipase A 2 (cPLA 2 ). We showed previously that Gln deactivated cPLA 2 indirectly via dephosphorylating p38 mitogen-activated protein kinase (MAPK), the major kinase for cPLA 2 phosphorylation, through inducing MAPK phosphatase-1 (MKP-1). In this study, we investigated the precise mechanism underlying Gln deactivation of cPLA 2 . In lipopolysaccharide (LPS)-treated mice, Gln injection resulted in dephosphorylation of phosphorylated cPLA 2 (p-cPLA 2 ), which coincided with rapid Gln induction of MKP-1. MKP-1 small interfering RNA (siRNA) abrogated the ability of Gln to induce MKP-1 as well as the dephosphorylation of cPLA 2 . Co-immunoprecipitation and in-situ proximity ligation assay revealed a physical interaction between MKP-1 and p-cPLA 2 . In a murine model of allergic asthma, we also demonstrated the physical interaction between MKP-1 and p-cPLA 2 . Furthermore, Gln suppressed various allergic asthma phenotypes, such as neutrophil and eosinophil recruitments into the airway, airway levels of T helper type 2 (Th2) cytokines [interleukin (IL)-4, IL-5 and IL-13], airway hyperresponsiveness, mucin production and metabolites (leukotriene B 4 and platelet-activating factor) through inhibiting cPLA 2 in a MKP-1-dependent manner. These data suggest that MKP-1 uses cPLA 2 , in addition to p38, as a substrate, which further potentiates the anti-inflammatory action of Gln.

The aim of the present study is to determine the role of sesamin, the most abundant lignan in sesame seed oil, on the regulation of allergic airway inflammation in a murine asthma model. A BALB/c mouse model with allergic asthma was used to evaluate the effects of sesamin on nuclear factor-kappa B (NF-κB) activation. An enzyme-linked immunosorbent assay was used to determine protein expression in bronchoalveolar lavage (BAL) fluids. Hematoxylin and eosin staining was performed to examine histological changes. Moreover, western blot analysis was used to detect the expression of proteins in tissues. Prior to administering sesamin, the mice developed the following pathophysiological features of asthma: An increase in the number of inflammatory cells, increased levels of interleukin (IL)-4, IL-5 and IL-13, decreased levels of interferon-γ in BAL fluids and lung tissues, increased immunoglobulin E (IgE) levels in the serum and an increased activation of NF-κB in lung tissues. Following treatment with sesamin, the mice had evidently reduced peribronchiolar inflammation and airway inflammatory cell recruitment, inhibited production of several cytokines in BAL fluids and lung tissues, and decreased IgE levels. Following inhalation of ovalbumin, the administration of sesamin also inhibited the activation of NF-κB. In addition, sesamin administration reduced the phosphorylation of p38 mitogen-activated protein kinases (MAPKs). The present study demonstrates that sesamin decreases the activation of NF-κB in order to attenuate allergic airway inflammation in a murine model of asthma, possibly via the regulation of phosphorylation of p38 MAPK. These observations provide an important molecular mechanism for the potential use of sesamin in preventing and/or treating asthma, as well as other airway inflammatory disorders.