Search

To analyze the low weight gain (WG) from birth to 4 and 6wk of life to predict the development of retinopathy of prematurity (ROP) among very low birth weight (VLBW) preterm babies. Three hundred and three newborns with VLBW were analyzed. Body weight measurements were recorded weekly. In all patients, the proportion of the WG was defined as the preterm weight measured at the 4th and 6th weeks of life minus the birth weight (BW) divided by the BW. Other risk factors for ROP were also analyzed. Mean gestational age and mean BW of the whole cohort were 29.56±1.44wk and 1270.58±176.18g respectively. WG proportion at 4wk postnatal age (18.89%±13.58%) were significantly lower in infants with ROP (P=0.003). WG proportion at 6wk was not different between ROP and no ROP group (42.48%±20.36% vs 46.43%±15.65% P=0.118). When all the other risk factors significant for ROP were included in the logistic regression poor WG did not arise as an independent risk factor. Area under the ROC curve was 0.591 (95%CI: 0.515-0.666; P=0.016). For ROP, the best discriminative cutoff of 18.06% of the proportional WG at the 4th week over the BW, sensitivity and specificity values were 67.3% and 50.0% respectively. Low WG proportion in the first 4wk of life is maybe an additional predictor of ROP in very low BW infants. Preterm babies with low BW and low WG proportion should be followed closely for ROP.

T cell immunoglobulin- and mucin-domain-containing molecule-4 (Tim-4) receives much attention as a potentially negative regulator of immune responses. However, its modulation on macrophages has not been fully elucidated so far. This study aimed to identify the role of Tim-4 in nitric oxide (NO) modulation.Macrophages were stimulated with 100 ng/ml LPS or 100 U/ml IFN-γ. RT-PCR was performed to detect TIM-4 mRNA expression. Tim-4 blocking antibody and NF-κB inhibitory ligand were involved in the study. NO levels were assayed by Griess reaction. Phosphorylation of NF-κB, Jak2 or Stat1 was verified by western blot.Tim-4 was up-regulated in murine macrophages after interferon-gamma (IFN-γ) stimulation. Tim-4 over-expression decreased NO production and inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS) or IFN-γ-stimulated macrophages. Consistently, Tim-4 blockade promoted LPS or IFN-γ-induced NO secretion and iNOS expression. Tim-4 over-expression decreased LPS-induced nuclear factor kappa B (NF-κB) p65 phosphorylation in macrophages, which was abrogated by NF-κB inhibitory ligand. On the contrary, Tim-4 blocking increased LPS-induced NF-κB signaling, which was also abrogated by NF-κB inhibition. In addition, Tim-4 blockade promoted Jak2 and Stat1 phosphorylation in IFN-γ stimulated macrophages.These results indicate that Tim-4 is involved in negative regulation of NO production in macrophages, suggesting the critical role of Tim-4 in immune related diseases.

We report an improved test of the weak equivalence principle by using a simultaneous 85Rb-87Rb dual-species atom interferometer. We propose and implement a four-wave double-diffraction Raman transition scheme for the interferometer, and demonstrate its ability in suppressing common-mode phase noise of Raman lasers after their frequencies and intensity ratios are optimized. The statistical uncertainty of the experimental data for Eötvös parameter η is 0.8 × 10-8 at 3200 s. With various systematic errors corrected, the final value is η = (2.8 ± 3.0) × 10-8. The major uncertainty is attributed to the Coriolis effect. [ABSTRACT FROM AUTHOR]

Frequent outbreaks and widespread transmission of rice black-streaked dwarf virus by Sogatella furcifera (Horváth) (Hemiptera: Delphacidae) have aggravated yield losses of rice in eastern China. The use of insecticides for suppression of the vector has been a fundamental approach to prevent epidemics of the virus disease. However, the status of insecticide resistance in S. furcifera has not been examined recently in China. In this study, dose responses of S. furcifera to buprofezin, imidacloprid, thiamethoxam, chlorpyrifos and pymetrozine were evaluated. Most populations in eastern China have developed moderate resistance to buprofezin (up to 25-fold). Approximately 32% of field populations exhibited moderate resistance to imidacloprid, while other field populations showed minor changes (7.6-fold) in their susceptibility to this insecticide. Low variation of susceptibility to thiamethoxam (<6-fold) was observed among field populations, and no obvious resistance to this product was observed. Obvious variation (10.2-fold) of susceptibility to chlorpyrifos existed in field populations of which 8% displayed moderate resistance, and 32% exhibited low level resistance. Most populations (72%) were susceptible to pymetrozine, and relatively low variation of susceptibility to it was detected among the field populations of S. furcifera. Frequent and extensive use of buprofezin had driven the rapid development of resistance, and buprofezin resistance is widespread in the field populations of S. furcifera in China. To prevent further development of the resistance, use of buprofezin should be limited and rotated with alternative insecticides with different modes of action. [ABSTRACT FROM AUTHOR]

The interplay of mechanisms regulating coronary blood flow (CBF) remains incompletely understood. Previous studies in dogs indicated that CBF regulation by K ATP channels, adenosine, and nitric oxide (NO) follows a nonlinear redundancy design and fully accounted for exercise-induced coronary vasodilation. Conversely, in swine, these mechanisms appear to regulate CBF in a linear additive fashion with considerable exercise-induced vasodilation remaining when all three mechanisms are inhibited. A direct comparison between these studies is hampered by the different doses and administration routes (intravenous vs. intracoronary) of drugs inhibiting these mechanisms. Here, we investigated the role of K ATP channels, adenosine, and NO in CBF regulation in swine using identical drug regimen as previously employed in dogs. Instrumented swine were exercised on a motor-driven treadmill, before and after blockade of K ATP channels (glibenclamide, 50 µg/kg/min ic) and combination of inhibition of NO synthase ( N ω -nitro-l-arginine, NLA, 1.5 mg/kg ic) and adenosine receptors (8-phenyltheophylline, 8PT, 5 mg/kg iv) or their combination NLA + 8PT + glibenclamide. Glibenclamide and NLA + 8PT each produced coronary vasoconstriction both at rest and during exercise, whereas the combination of NLA + 8PT + glibenclamide resulted in a small further coronary vasoconstriction compared with NLA + 8PT that was, however, less than the sum of the vasoconstriction produced by NLA + 8PT and glibenclamide, each. Thus, in contrast to previous observations in the dog, 1 ) the coronary vasoconstrictor effect of glibenclamide was not enhanced in the presence of NLA + 8PT and 2 ) the exercise-induced increase in CBF was largely maintained. These findings show profound species differences in the mechanisms controlling CBF at rest and during exercise. NEW & NOTEWORTHY The present study demonstrates important species differences in the regulation of coronary blood flow by adenosine, NO, and K ATP channels at rest and during exercise. In swine, these mechanisms follow a linear additive design, as opposed to dogs which follow a nonlinear redundant design. Simultaneous blockade of all three mechanisms virtually abolished exercise-induced coronary vasodilation in dogs, whereas a substantial vasodilator reserve could still be recruited during exercise in swine.

Hepatitis B virus (HBV) infection has received increasing public attention. HBV is the prototypical member of hepadnaviruses, which naturally infect only humans and great apes and induce the acute and persistent chronic infection of hepatocytes. A large body of evidence has demonstrated that dysfunction of the host anti-viral immune response is responsible for persistent HBV replication, unresolved inflammation and disease progression. Many regulatory factors are involved in immune dysfunction. Among these, T cell immunoglobulin domain and mucin domain-3 (Tim-3), one of the immune checkpoint proteins, has attracted increasing attention due to its critical role in regulating both adaptive and innate immune cells. In chronic HBV infection, Tim-3 expression is elevated in many types of immune cells, such as T helper cells, cytotoxic T lymphocytes, dendritic cells, macrophages and natural killer cells. Tim-3 over-expression is often accompanied by impaired function of the above-mentioned immunocytes, and Tim-3 inhibition can at least partially rescue impaired immune function and thus promote viral clearance. A better understanding of the regulatory role of Tim-3 in host immunity during HBV infection will shed new light on the mechanisms of HBV-related liver disease and suggest new therapeutic methods for intervention.