Our preliminary data suggest that TDF use in the third trimester is safe, and effectively prevents VT of HBV from high viremic HBeAg-positive mothers.

The ability of high-density lipoprotein (HDL) to promote cholesterol efflux is an important component of its ability to protect against cardiovascular disease. In addition, the anti-inflammatory properties of HDL are important as well. As part of the innate immune system, HDL appears to have evolved to increase inflammation in the presence of an acute phase response but to inhibit inflammation in the absence of an acute phase response. In a study of humans with coronary heart disease, it was found that the patients who had proinflammatory HDL prior to statin therapy (and half of them despite a profound decrease in plasma lipids following statin therapy) continued to have proinflammatory HDL. Anti-inflammatory HDL was effective in promoting cholesterol efflux whereas proinflammatory HDL was relatively weak in its ability to promote cholesterol efflux. Oxidative alterations of the main protein of HDL, apolipoprotein A-I, impaired its capacity to promote cholesterol efflux from monocyte macrophages. Therefore, HDL composition, structure, and function appear to be more crucial than HDL cholesterol concentrations in determining risk for cardiovascular disorders.

We sought to determine if the bile acid ratio of cholic acid to chenodeoxycholic acid (CA:CDCA) is an important component for diagnosis of intrahepatic cholestasis of pregnancy (ICP). We assessed the addition of bile acid CA:CDCA ratio information in diagnosing ICP in a database of patients evaluated for ICP by serum bile acids and hepatic transaminases. Patients were considered to test positive for ICP if there was elevation in total bile acid, CA:CDCA ratio, or transaminase. Of 231 specimens evaluated for ICP with bile acid and transaminases, 17.1% had elevated total bile acids, 29.4% had elevated transaminase, and 8.2% had an elevated bile acid ratio. Most specimens with elevated bile acid ratio also had elevated total bile acid; 35.5% of specimens tested positive by total bile acid and/or transaminases, increasing minimally to 35.9% with bile acid ratio information. Similar results were found using lower total bile acid and bile acid ratio thresholds. The bile acid CA:CDCA ratio contributed little to the diagnosis of ICP. The use of total bile acid and hepatic transaminases without bile acid ratios decreased positive tests by less than 2%.

Brain injury in the premature infant is associated with a high risk of neurodevelopmental disability. Previous small-animal models of brain injury attributable to extreme prematurity typically fail to generate a spectrum of pathology and behavior that closely resembles that observed in humans, although they provide initial answers to numerous cellular, molecular, and therapeutic questions. We tested the hypothesis that exposure of rats to repeated hypoxia from postnatal day 1 (P1) to P3 models the characteristic white matter neuropathological injury, gray matter volume loss, and memory deficits seen in children born extremely prematurely. Male Sprague Dawley rats were exposed to repeated hypoxia or repeated normoxia from P1 to P3. The absolute number of pre-oligodendrocytes and mature oligodendrocytes, the surface area and g-ratio of myelin, the absolute volume of cerebral white and gray matter, and the absolute number of cerebral neurons were quantified stereologically. Spatial memory was investigated on a radial arm maze. Rats exposed to repeated hypoxia had a significant loss of (1) pre-oligodendrocytes at P4, (2) cerebral white matter volume and myelin at P14, (3) cerebral cortical and striatal gray matter volume without neuronal loss at P14, and (4) cerebral myelin and memory deficits in adulthood. Decreased myelin was correlated with increased attention deficit hyperactivity disorder-like hyperactivity. This new small-animal model of extreme prematurity generates a spectrum of short-and long-term pathology and behavior that closely resembles that observed in humans. This new rat model provides a clinically relevant tool to investigate numerous cellular, molecular, and therapeutic questions on brain injury attributable to extreme prematurity.

The purpose of this study was to determine the influence of the D1-selective partial agonist SKF 38393 on the odor detection performance of rats using high precision olfactometry and a go/no-go operant task. Previous studies have found that the D2 receptor partial agonist quinpirole decreases such performance, but the influences of D1 receptor activation are unknown. In experiment 1, such detection performance to the odorant ethyl acetate was enhanced by SKF 38393, relative to saline, in male rats at 7.5 and 10.0 mg/kg i.p. dose levels, but not at the lower doses of 1.0, 2.5, and 5.0 mg/kg. In experiment 2, this enhancement was replicated at the 7.5 and 10.0 mg/kg doses and was shown to occur at the 12.5 mg/kg dose as well. In experiment 3, similar enhancement was shown for the odorant eugenol in female rats at the 7.5, 10.0 and 12.5 mg/kg doses, suggesting this effect is neither sex-specific nor confined to the odorant ethyl acetate. In experiment 4, a 0.025 mg/kg dose of the D1 receptor antagonist SCH 23390 depressed the enhancement produced to ethyl acetate by 7.5 mg/kg SKF 38393 to control levels. Overall, these data demonstrate that, in contrast to quinpirole, SKF 38393 improves odor detection performance in the rat and that this phenomenon can be attenuated by the D1 receptor blocker SCH 23390.