An internal hernia may be either congenital or acquired. The reported incidence of such hernias is 1–2%. In rare cases, internal hernias are the cause of small bowel obstruction, with a reported incidence of 0.2–0.9%. Transmesocolic hernia of the ascending colon is especially rare. We report a case of transmesocolic hernia of the ascending colon with intestinal obstruction diagnosed preoperatively. A 91-year-old Japanese female was admitted to our hospital with abdominal distention and vomiting of 3 days duration. She had no past history of any abdominal surgery. Abdominal examination revealed distention and tenderness in the right iliac fossa. Abdominal computed tomography revealed ileus in the sac at the left side of the ascending colon and dilatation of the oral side of the intestine. We diagnosed a transmesocolic hernia of the ascending colon with intestinal obstruction and performed emergency surgery. At the time of operation, there was internal herniation of ileal loops through a defect in the ascending mesocolon, without any strangulation of the small bowel. The contents were reduced and the tear in the ascending mesocolon was closed. The postoperative course was uneventful and the patient was discharged 14 days after surgery. In conclusion, preoperative diagnosis of bowel obstruction caused by a congenital mesocolic hernia remains difficult despite the techniques currently available, so it is important to consider the possibility of a transmesocolic hernia when diagnosing a patient with ileus with no past history of abdominal surgery.

Objectives

To clarify the difference in health-promoting lifestyles between agricultural and non-agricultural workers in Japan, a cross-sectional study was conducted on 627 residents living in a town with a mixed rural–urban population.

Methods

The subjects were divided into 8 groups by job (agricultural and non-agricultural), age (young and old), and gender (male and female). To evaluate the subjects’ lifestyles, the Health Promoting Lifestyle Profile II (HPLP-II) was applied. The Bartlett test and the Kendall rank test were performed for statistical analysis.

Results

There was no significant difference in the overall score of the HPLP-II between the two job groups. However, for the HPLP-II subscales, a significantly higher score for “spiritual growth” and a significantly lower score for “physical activity” were seen in the agricultural group than in the non-agricultural group. In general, the old and female groups showed higher scores than the corresponding groups, regardless of job type.

Conclusions

It was determined that the major countermeasures to maintain a healthy lifestyle in agricultural workers should be associated with how to introduce daily activities that maintain and enhance “spiritual growth” and improve “physical activity”.

Summary

Although a decrease in cerebrovascular reserves (CVR) is known to enhance the risk of stroke, changes in this parameter after carotid artery stenting (CAS) have rarely been investigated. The present study is the first to compare CVR recoveries after applying CAS to patients with symptomatic carotid artery disease.

CAS was performed for 31 consecutive patients with symptomatic carotid artery disease. They underwent acetazolamide-challenged single photon emission computed tomography (SPECT) before and after CAS to obtain data on resting stage cerebral blood flow (CBFrest values) in various regions of interest (ROIs) defined by a three-dimensional stereotactic ROI template. CVR values on ipsilateral and contralateral hemispheric sides were then calculated based on the CBFrest data.

The 31 patients were dichotomized into unilateral (n=22) and bilateral (n=9) lesion groups, and no significant between-group differences were observed in CBFrest before and after CAS. In the unilateral group, there were no differences in CVR values before and after CAS. In the bilateral group, however, the CVR values significantly increased in nearly all the investigated ROIs on the contralateral side. Also, the hemispheric CVR values on both sides significantly increased after CAS in the bilateral group, while no such increase was observed in the unilateral group.

CAS in patients with symptomatic bilateral carotid artery disease has the potential utility for their haemodynamic improvement even on the contralateral hemispheric side.

Lysophosphatidic acid receptor (LPA1) signaling initiates neuropathic pain through demyelination of the dorsal root (DR). Although LPA is found to cause down-regulation of myelin proteins underlying demyelination, the detailed mechanism remains to be determined. In the present study, we found that a single intrathecal (i.t.) injection of LPA evoked a dose- and time-dependent down-regulation of myelin-associated glycoprotein (MAG) in the DR through LPA1 receptor. A similar event was also observed in ex vivo DR cultures. Interestingly, LPA-induced down-regulation of MAG was significantly inhibited by calpain inhibitors (calpain inhibitor X, E-64 and E-64d) and LPA markedly induced calpain activation in the DR. The pre-treatment with calpain inhibitors attenuated LPA-induced neuropathic pain behaviors such as hyperalgesia and allodynia. Moreover, we found that sciatic nerve injury activates calpain activity in the DR in a LPA1 receptor-dependent manner. The E-64d treatments significantly blocked nerve injury-induced MAG down-regulation and neuropathic pain. However, there was no significant calpain activation in the DR by complete Freund’s adjuvant treatment, and E-64d failed to show anti-hyperalgesic effects in this inflammation model. The present study provides strong evidence that LPA-induced calpain activation plays a crucial role in the manifestation of neuropathic pain through MAG down-regulation in the DR.

Objectives

The present study aimed to define the framework of an environment conducive to the well-being of children with intellectually disability (CID).

Methods

A questionnaire composed of 31 items was developed through literature review. Then a 2-round Delphi survey was conducted with 3 different panels: health professionals (HPs), parents of CID, and teachers. The participants were asked to rate each item, select and rank the 10 most important items, and suggest additional ones.

Results

A total of 71 participants responded to the first round: 24 HPs, 22 parents, and 25 teachers. In the second round the overall response rate was 83%. At the end of the exercise, 12 items reached global consensus, i.e., in all groups. Only 5 items were ranked as most important by all groups: attitudes of family members at home; attitudes of HPs and teachers; support from family members at home; support at school (classmates and teachers); and government policies. Nevertheless, the panelists’ views diverged on the remaining items. Several additional elements were suggested.

Conclusions

The views of HPs, teachers, and parents are complementary for the improvement of quality of life (QOL) of CID. The present findings will be used as a basis for the development of an instrument to assess the living environment of CID.

Background

Although neuropathic pain is frequently observed in demyelinating diseases such as Guillain-Barré syndrome and multiple sclerosis, the molecular basis for the relationship between demyelination and neuropathic pain behaviors is poorly understood. Previously, we found that lysophosphatidic acid receptor (LPA1) signaling initiates sciatic nerve injury-induced neuropathic pain and demyelination.

Results

In the present study, we have demonstrated that sciatic nerve injury induces marked demyelination accompanied by myelin-associated glycoprotein (MAG) down-regulation and damage of Schwann cell partitioning of C-fiber-containing Remak bundles in the sciatic nerve and dorsal root, but not in the spinal nerve. Demyelination, MAG down-regulation and Remak bundle damage in the dorsal root were abolished in LPA1 receptor-deficient (Lpar1-/-) mice, but these alterations were not observed in sciatic nerve. However, LPA-induced demyelination in ex vivo experiments was observed in the sciatic nerve, spinal nerve and dorsal root, all which express LPA1 transcript and protein. Nerve injury-induced dorsal root demyelination was markedly attenuated in mice heterozygous for autotaxin (atx+/-), which converts lysophosphatidylcholine (LPC) to LPA. Although the addition of LPC to ex vivo cultures of dorsal root fibers in the presence of recombinant ATX caused potent demyelination, it had no significant effect in the absence of ATX. On the other hand, intrathecal injection of LPC caused potent dorsal root demyelination, which was markedly attenuated or abolished in atx+/- or Lpar1-/- mice.

Conclusions

These results suggest that LPA, which is converted from LPC by ATX, activates LPA1 receptors and induces dorsal root demyelination following nerve injury, which causes neuropathic pain.

The DIX domain of rat axin has been purified and crystallized. Crystals diffracted to 2.9 Å resolution using synchrotron radiation.

Axin is a negative regulator of the canonical Wnt signalling pathway that mediates the phosphorylation of β-catenin by glycogen synthase kinase 3β. The DIX domain of rat axin, which is important for its homooligomerization and interactions with other regulators in the Wnt pathway, was purified and crystallized by the sitting-drop vapour-diffusion technique using polyethylene glycol 6000 and lithium sulfate as crystallization agents. Crystals belong to space group P61 or P65, with unit-cell parameters a = b = 91.49, c = 84.92 Å. An X-ray diffraction data set has been collected to a nominal resolution of 2.9 Å.

We initially identified a nuclear protein, prothymosin-α1 (ProTα), as a key protein inhibiting necrosis by subjecting conditioned media from serum-free cultures of cortical neurons to a few chromatography steps. ProTα inhibited necrosis of cultured neurons by preventing rapid loss of cellular adenosine triphosphate levels by reversing the decreased membrane localization of glucose transporters but caused apoptosis through up-regulation of proapoptotic Bcl2-family proteins. The apoptosis caused by ProTα was further inhibited by growth factors, including brain-derived neurotrophic factor. The ProTα-induced cell death mode switch from necrosis to apoptosis was also reproduced in experimental ischemia-reperfusion culture experiments, although the apoptosis level was markedly reduced, possibly because of the presence of growth factors in the reperfused serum. Knock down of PKCβII expression prevented this cell death mode switch. Collectively, these results suggest that ProTα is an extracellular signal protein that acts as a cell death mode switch and could be a promising candidate for preventing brain strokes with the help of known apoptosis inhibitors.

This study aimed to investigate the preventive effects of green tea fractions (GTFs) on rat model of oxygen-induced retinopathy (OIR). Neonatal Sprague-Dawley rats were exposed to daily cycles of 80% oxygen (20.5 h), ambient air (0.5 h), and progressive return to 80% oxygen (3 h) until postnatal day 12 (P12), then the rats were placed in ambient air until P18. The green tea was fractionated by DM-A50, DM-W, M-B, and M-W. The rats were treated once daily from P6 to P17 by gastric gavage of GTFs (0.05 or 0.01 g/ml) or distilled water (DW) at 50 µl/10 g body weight. On P18, the rats were sacrificed and the retinal samples were collected. The retinal neovascularization (NV) was scored and avascular areas (AVAs) were measured as a % of total retinal area (%AVAs) in ADPase stained retinas. The NV scores in 0.01 g/ml M-W were significantly lower than those in DW. The %AVAs in 0.05 g/ml DM-A50 and in 0.05 g/ml and 0.01 g/ml M-W were significantly lower than those in DW. There were less catechins, and less caffeine in M-W fraction compared with other GTFs, suggesting components of green tea except for catechins and caffeine might suppress the neovascularization in rat model of OIR.

This study was conducted to determine whether the regional factors were related to the increase in the percentage of low birthweight (LBW: <2,500g) infants in Kumamoto Pref., and to establish a tentative structure model for predicting low birthweight infants. Analyses for frequency of LBW infants between 1974 and 1997, and a multiple regression model and covariance structure model were conducted using data from the vital statistics between 1992 and 1997 and regional indicators concerned with LBW infants from official registered statistical data between 1992 and 1997. The 72 regional factors were clustered into four groups linked with agricultural areas such as Urban, Flat, Hilly and Mountainous areas. The recent increase in the incidence of LBW infants resulted from the increase in moderate-LBW (MLBW: 2,000-2,500 g) infants of full term-LBW infants. There was a steady annual increase in the Urban agricultural area LBW infants since 1992. The two structure analyses revealed that the Urban area had a marked effect on the increase in LBW infants, whereas, farm villages in Hilly or Moutainous areas had less effect on the increase in LBW infants. These findings suggest that the regional factors relating to the mothers’ life-style or regional environments play a key role in the etiology and prevention of LBW, and will be a useful in the analyses using official registered material.

The only workers presently exposed to bagasse dust in Japan are the employees of sugar refineries and lacquerware factories. A follow up study of six former cases of bagassosis from among the retired employees of a paper board factory, closed since 1973, showed that none of the subjects still had bagassosis. Examinations of 70 employees of a sugar refinery for allergic reactions also showed no case of bagassosis. Seven cases with suspicious shadows of bagassosis on chest radiographs and four cases with positive serum precipitin to stored bagasse were, however, found among those 70 subjects. The results show the disappearance of a past episode of bagassosis and the possibility of a new occurrence of bagassosis among the employees of sugar refineries and lacquerware factories in the near future in Japan.

Images

A large cross sectional survey was carried out using a self administered questionnaire to examine the prevalence of laboratory animal allergy (LAA) and the factors associated with its development. Out of 5641 workers who were exposed to animals at 137 laboratory animal facilities in Japan, 23.1% had one or more allergic symptoms related to laboratory animals. The commonest symptom as rhinitis. About 70% of LAA subjects developed symptoms during their first three years of exposure. Atopy (past and family history), the number of animal species handled, and the time spent in handling correlated significantly with the development of LAA as did some types of job. A close relation between nasal symptoms and exposure to rabbits and between skin symptoms and exposure to rats were found. LAA subjects developed symptoms most quickly to rabbits.

We studied biochemical genetics of low density lipoprotein (LDL) receptor mutations in fibroblasts from six homozygous and five heterozygous patients with familial hypercholesterolemia (FH). Three of six homozygotes are receptor-negative type and the other three homozygotes are receptor-defective type. In the cells from three receptor-negative homozygotes, the receptor binding, internalization, and degradation of 125I-LDL were 0.5±0.3 ng/mg protein (mean±SEM), 14±8 and 8±6 ng/mg protein per 6 h (four normal cells; 44±3, 386±32, and 1,335±214 ng/mg protein per 6 h), respectively. In the cells from three receptor-defective homozygotes, the receptor binding, internalization, and degradation of 125I-LDL were 6±2, 29±8, and 90±32 ng/mg protein per 6 h, respectively. In these six homozygotes, two pairs of siblings are included. Two siblings in the same family were classified as receptor-negative and two siblings in another family were classified as receptor-defective. The receptor-negative phenotypes and the receptor-defective phenotypes bred true in individual families. The cells from five heterozygotes showed ∼46% of the normal activities of receptor.

ML-236B, competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), completely inhibited the incorporation of [14C]acetate into digitonin-precipitable sterols in fibroblasts from normal subjects and heterozygous and homozygous patients with FH with the concentration of 0.5 μg/ml. However, at 0.05 μg/ml of ML-236B sterol synthesis in fibroblasts from homozygotes was not completely suppressed in contrast to normal and heterozygous cells. Moreover, after preincubation with 0.05 μg/ml of ML-236B for 24 h in medium containing lipoproteins, sterol synthesis in the cells from receptor-negative homozygote showed 75% of the initial activity compared with that of 25% without preincubation. In the cells from a normal subject and a heterozygote, sterol synthesis was inhibited even after preincubation. These results suggest that (a) the inhibitory effect of ML-236B is overcome in homozygote cells by their high intracellular levels of HMG-CoA reductase and (b) that a higher dose of ML-236B may be required to lower serum cholesterol levels in FH homozygotes than in heterozygotes.

Haemoglobin concentrations in about 1000 women agricultural workers in Japan were measured every year, except in 1972, during the period 1967-77. Improvements were noted in the course of this investigation, and these were predominantly associated with the fact that those in the study community began to pay attention to the problem of low haemoglobin levels and to improve their diet, with an increase in daily food intake, particularly of animal protein and iron. In addition, a marked decrease in anaemia caused by hookworm also played an important role. In this paper, the change in haemoglobin concentration during the period of study are described and the aetiology is discussed.

Images

Background

Given the limited efficacy and high adverse event rate associated with treatment of recurrent hepatitis C after liver transplantation, an individualized treatment strategy should be considered. The aim of this study was to identify predictors of response to antiviral therapy for hepatitis C after living donor liver transplantation (LDLT) and to study the associated adverse events.

Methods

A retrospective chart review was performed on 125 hepatitis C virus (HCV)-positive LDLT recipients who received interferon plus ribavirin and/or peginterferon plus ribavirin therapy at Kyoto University between January 2001 and June 2011.

Results

Serum HCV RNA reached undetectable levels within 48 weeks in 77 (62%) of 125 patients, and these patients were defined as showing virological response (VR). Of 117 patients, 50 (43%) achieved sustained VR (SVR). Predictive factors associated with both VR and SVR by univariate analysis included low pretransplant serum HCV RNA levels, a non-1 HCV genotype, and low pretreatment serum HCV RNA levels. In addition, LDLT from ABO-mismatched donors was significantly associated with VR, and white cell and neutrophil counts before interferon therapy were associated with SVR. Multivariate analysis showed that 2 variables–pretransplant serum HCV RNA level less than 500 kIU/mL and a non-1 HCV genotype–remained in models of both VR and SVR and that an ABO mismatch was associated with VR. No variables with a significant effect on treatment withdrawal were found.

Conclusions

Virological response to antiviral therapy in patients with hepatitis C recurring after LDLT can be predicted prior to transplant, based on pretransplant serum HCV-RNA levels and HCV genotype. LDLT from ABO-mismatched donors may contribute to more efficacious interferon therapy.

Trial Registration

UMIN-CTR UMIN000003286

The purpose of this study was to investigate the effects of 12 weeks of exercise training on gut hormone levels after a single bout of exercise in middle-aged Japanese women. Twenty healthy middle-aged women were recruited for this study. Several measurements were performed pre and post exercise training, including: body weight and composition, peak oxygen consumption (peak VO2), energy intake after the single bout of exercise, and the release of gut hormones with fasting and after the single bout of exercise. Exercise training resulted in significant increases in acylated ghrelin fasting levels (from 126.6 ± 5.6 to 135.9 ± 5.4 pmol/l, P < 0.01), with no significant changes in GLP-1 (from 0.54 ± 0.04 to 0.55 ± 0.03 pmol/ml) and PYY (from 1.20 ± 0.07 to 1.23 ± 0.06 pmol/ml) fasting levels. GLP-1 levels post exercise training after the single bout of exercise were significantly higher than those pre exercise training (areas under the curve (AUC); from 238.4 ± 65.2 to 286.5 ± 51.2 pmol/ml x 120 min, P < 0.001). There was a tendency for higher AUC for the time courses of PYY post exercise training than for those pre exercise training (AUC; from 519.5 ± 135.5 to 551.4 ± 128.7 pmol/ml x 120 min, P = 0.06). Changes in (delta) GLP-1 AUC were significantly correlated with decreases in body weight (r = −0.743, P < 0.001), body mass index (r = −0.732, P < 0.001), percent body fat (r = −0.731, P < 0.001), and energy intake after a single bout exercise (r = −0.649, P < 0.01) and increases in peak VO2 (r = 0.558, P < 0.05). These results suggest that the ability of exercise training to create a negative energy balance relies not only directly on its impact on energy expenditure, but also indirectly on its potential to modulate energy intake.

A new biaryl phosphine ligand, Me3(OMe)tBuXPhos (L3), was designed as a surrogate for Me4tBuXPhos (L1). The Me3(OMe)tBuXPhos could be prepared in a chromatography-free manner from inexpensive and readily available 2,3,6-trimethylphenol. Comparative studies demonstrated that a catalyst based on Me3(OMe)tBuXPhos displayed the same reactivity as a catalyst based on Me4tBuXPhos for Pd-catalyzed C–N and C–O bond-forming processes.

The retina exhibits an inherent autofluorescence that is imaged ophthalmoscopically as fundus autofluorescence. In clinical settings, fundus autofluorescence examination aids in the diagnosis and follow-up of many retinal disorders. Fundus autofluorescence originates from the complex mixture of bisretinoid fluorophores that are amassed by retinal pigment epithelial (RPE) cells as lipofuscin. Unlike the lipofuscin found in other cell-types, this material does not form as a result of oxidative stress. Rather, the formation is attributable to non-enzymatic reactions of vitamin A aldehyde in photoreceptor cells; transfer to RPE occurs upon phagocytosis of photoreceptor outer segments. These fluorescent pigments accumulate even in healthy photoreceptor cells and are generated as a consequence of the light capturing function of the cells. Nevertheless, the formation of this material is accelerated in some retinal disorders including recessive Stargardt disease and ELOVL-4-related retinal degeneration. As such, these bisretinoid side-products are implicated in the disease processes that threaten vision. In this article, we review our current understanding of the composition of RPE lipofuscin, the structural characteristics of the various bisretinoids, their related spectroscopic features and the biosynthetic pathways by which they form. We will revisit factors known to influence the extent of the accumulation and therapeutic strategies being used to limit bisretinoid formation. Given their origin from vitamin A aldehyde, an isomer of the visual pigment chromophore, it is not surprising that the bisretinoids of retina are light sensitive molecules. Accordingly, we will discuss recent findings that implicate the photodegradation of bisretinoid in the etiology of age-related macular degeneration.

The trans-Golgi network (TGN) contains multiple sorting domains and acts as the compartment for cargo sorting. Recent evidence indicates that the TGN also functions as an early endosome, the first compartment in the endocytic pathway in plants. The SYP4 group, plant Qa-SNAREs localized on the TGN, regulates both secretory and vacuolar transport pathways. Consistent with a secretory role, SYP4 proteins are required for extracellular resistance to fungal pathogens. However, the physiological role of SYP4 in abiotic stress remains unknown. Here, we report the phenotypes of a syp4-mutant in regard to salinity and osmotic response, and describe the physiological roles of the SYP4 group in the abiotic stress response.

Two classic learning mutants in Drosophila, rutabaga (rut) and dunce (dnc), are defective in cAMP synthesis and degradation, respectively, exhibiting a variety of neuronal and behavioral defects. We ask how the opposing effects of these mutations on cAMP levels modify subsets of phenotypes, and whether any specific phenotypes could be ameliorated by biochemical counter balancing effects in dnc rut double mutants. Our study at larval neuromuscular junctions (NMJs) demonstrate that dnc mutations caused severe defects in nerve terminal morphology, characterized by unusually large synaptic boutons and aberrant innervation patterns. Interestingly, a counterbalancing effect led to rescue of the aberrant innervation patterns but the enlarged boutons in dnc rut double mutant remained as extreme as those in dnc. In contrast to dnc, rut mutations strongly affect synaptic transmission. Focal loose-patch recording data accumulated over 4 years suggest that synaptic currents in rut boutons were characterized by unusually large temporal dispersion and a seasonal variation in the amount of transmitter release, with diminished synaptic currents in summer months. Experiments with different rearing temperatures revealed that high temperature (29–30 °C) decreased synaptic transmission in rut, but did not alter dnc and WT. Importantly, the large temporal dispersion and abnormal temperature dependence of synaptic transmission, characteristic of rut, still persisted in dnc rut double mutants. To interpret these results in a proper perspective, we reviewed previously documented differential effects of dnc and rut mutations and their genetic interactions in double mutants on a variety of physiological and behavioral phenotypes. The cases of rescue in double mutants are associated with gradual developmental and maintenance processes whereas many behavioral and physiological manifestations on faster time scales could not be rescued. We discuss factors that could contribute to the effectiveness of counter balancing interactions between dnc and rut mutations for phenotypic rescue.

The purpose of this study was to explore developmental changes, in terms of spectral fluctuations and temporal periodicity with Japanese- and English-learning infants. Three age groups (15, 20, and 24 months) were selected, because infants diversify phonetic inventories with age. Natural speech of the infants was recorded. We utilized a critical-band-filter bank, which simulated the frequency resolution in adults’ auditory periphery. First, the correlations between the power fluctuations of the critical-band outputs represented by factor analysis were observed in order to see how the critical bands should be connected to each other, if a listener is to differentiate sounds in infants’ speech. In the following analysis, we analyzed the temporal fluctuations of factor scores by calculating autocorrelations. The present analysis identified three factors as had been observed in adult speech at 24 months of age in both linguistic environments. These three factors were shifted to a higher frequency range corresponding to the smaller vocal tract size of the infants. The results suggest that the vocal tract structures of the infants had developed to become adult-like configuration by 24 months of age in both language environments. The amount of utterances with periodic nature of shorter time increased with age in both environments. This trend was clearer in the Japanese environment.

Although excessive fructose intake is epidemiologically linked with dyslipidemia, obesity, and diabetes, the mechanisms regulating plasma fructose are not well known. Cells transfected with sodium/glucose cotransporter 5 (SGLT5), which is expressed exclusively in the kidney, transport fructose in vitro; however, the physiological role of this transporter in fructose metabolism remains unclear. To determine whether SGLT5 functions as a fructose transporter in vivo, we established a line of mice lacking the gene encoding SGLT5. Sodium-dependent fructose uptake disappeared in renal brush border membrane vesicles from SGLT5-deficient mice, and the increased urinary fructose in SGLT5-deficient mice indicated that SGLT5 was the major fructose reabsorption transporter in the kidney. From this, we hypothesized that urinary fructose excretion induced by SGLT5 deficiency would ameliorate fructose-induced hepatic steatosis. To test this hypothesis we compared SGLT5-deficient mice with wild-type mice under conditions of long-term fructose consumption. Paradoxically, however, fructose-induced hepatic steatosis was exacerbated in the SGLT5-deficient mice, and the massive urinary fructose excretion was accompanied by reduced levels of plasma triglycerides and epididymal fat but fasting hyperinsulinemia compared with fructose-fed wild-type mice. There was no difference in food consumption, water intake, or plasma fructose between the two types of mice. No compensatory effect by other transporters reportedly involved in fructose uptake in the liver and kidney were indicated at the mRNA level. These surprising findings indicated a previously unrecognized link through SGLT5 between renal fructose reabsorption and hepatic lipid metabolism.

Introduction. Leiomyosarcomas of vascular origin are particularly rare tumors occurring mainly in the inferior vena cava (IVC). They are malignant, slow-growing tumors with a poor prognosis. This paper reports on a rare case of surgical resection of an IVC leiomyosarcoma mimicking a hepatic tumor. Case Presentation. A 65-year-old Japanese male was admitted for evaluation of an abdominal tumor. Enhanced computed tomography of the abdomen revealed a slightly enhanced heterogeneous tumor, 18 mm in diameter, between the Spiegel lobe of the liver and the IVC in early-phase images, with no enhancement or washout in late-phase images. We diagnosed this tumor as either a hepatic tumor in the Spiegel lobe or a retroperitoneal tumor such as leiomyosarcoma or liposarcoma and performed a laparotomy. On the basis of surgical findings, we extirpated the tumor by performing a wedge resection of the wall of the IVC and suturing the primary IVC wall. Pathological findings led to a further diagnosis of the tumor as a leiomyosarcoma originating in the IVC. Thirty-seven months after the operation, multiple liver and lung metastases were detected, and the patient died from multiple organic failures. Conclusion. We experienced a rare case of a leiomyosarcoma of IVC mimicking hepatic tumor.