BackgroundThe prevalence of nonalcoholic fatty liver disease (NAFLD) and alcohol-associated/related liver disease (ALD) with metabolic syndrome is globally increasing. Metabolic syndrome and excessive alcohol consumption synergically exacerbate liver pathologies; therefore, drinking-speci c serum markers unaffected by liver injury or metabolic syndrome are essential to assess alcohol consumption. We evaluated the ratio of carbohydrate-de cient transferrin to total transferrin (%CDT) in patients with fatty liver disease, particularly focusing on its correlation with metabolic factors (UMIN000033550). MethodsA total of 120 patients with fatty liver disease, including ALD and NAFLD, were screened for alcohol misuse using the Alcohol Use Disorders Identi cation Test. Associations of metabolic syndrome-related factors and hepatic steatosis/liver stiffness with drinking markers such as %CDT, gamma-glutamyl transferase (GGT), and mean corpuscular volume (MCV) were assessed using multiple linear regression analyses. Results%CDT signi cantly increased with 3-4 drinks/day. The optimal cut-off value for identifying non-to light drinkers was 1.78% (sensitivity, 71.8%; speci city, 83.7%; area under the receiver operating characteristic curve [AUROC], 0.851), which was signi cantly higher than that for GGT. The cut-off value for identifying heavy drinkers was 2.08% (sensitivity, 65.5%; speci city, 86.8%; AUROC, 0.815). Multiple regression analysis revealed that this proportion was negatively correlated with body mass index, whereas GGT and MCV were in uenced by multiple factors involved in liver injury and dyslipidemia. Conclusions%CDT showed a strong correlation with alcohol consumption, independent of liver damage, steatosis/stiffness, or metabolic syndrome-related factors, indicating that it is a useful drinking marker for the accurate diagnosis of NAFLD and ALD.

SummaryObesity was induced in neonatal mice by subcutaneous injections of monosodium glutamate (MSG) at an early neonatal stage. The process of adipocyte formation was studied comparatively in the developing epididymal adipose tissue of the MSG-treated mice and in normal mice during the period from the 6th to the 100th postnatal day. Tritiated thymidine autoradiographic studies showed that cell prolife ration activity was the highest on the 6th postnatal day both in the MSG -treated and the control mice. In normal mice, however, cell proliferation took place less frequently aftef 6 days and had almost ceased after 49 days. In the obese mice, as evidenced by relatively high labeling indices, cell proliferation continued to occur even after 49 days. Ultimately there was no difference in the number of adipocytes counted by Hirsch's method in the MSG-treated and the control mice at the 100th postnatal day. The storage of fat droplets became more noticeable in obese mice than in normal mice after 35 days. The mean size of fat droplets of the obese mice was twice as large as that in normal mice on the 49th postnatal day. These results indicate that the MSG-induced obesity is of the hypertrophic type.

The prognosis of the liver transplant patients was frequently deteriorated by ischemia and reperfusion injury (IRI) in the liver. Infiltration of inflammatory cells is reported to play critical roles in the pathogenesis of hepatic IRI. Although T lymphocytes, neutrophils and monocytes infiltrated into the liver underwent IRI, we found that neutrophil depletion significantly attenuated the injury and serum liver enzyme levels in a murine model. Interestingly, the expression of CD321/JAM-A/F11R, one of essential molecules for transmigration of circulating leukocytes into inflammatory tissues, was significantly augmented on hepatic sinusoid endothelium at 1 h after ischemia and maintained until 45 min after reperfusion. The intraportal administration of anti-CD321 monoclonal antibody (90G4) significantly inhibited the leukocytes infiltration after reperfusion and diminished the damage responses by hepatic IRI (serum liver enzymes, inflammatory cytokines and hepatocyte cell death). Taken together, presented results demonstrated that blockade of CD321 by 90G4 antibody significantly attenuated hepatic IRI accompanied with substantial inhibition of leukocytes infiltration, particularly inhibition of neutrophil infiltration in the early phase of reperfusion. Thus, our work offers a potent therapeutic target, CD321, for preventing liver IRI.

SummaryA female infant with distal 18q trisomy, confirmed by G-and Q-banding was reported. Her karyotype was 46,XX,-6,+der(6), t(6;18) (18qter---~18q21 :: 6p24 or 25--*6pter)pat. She had the following clinical stigmata: hypertelorism, coloboma, bulbous nose with shallow nasal bridge, high arched palate, small chin, folds of redundant nuchal skin, hemangioma and limited abduction of the hip joints.

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