A novel diagnostic method for human immunodeficiency virus type-1 in plasma by near-infrared spectroscopy

Presently, the diagnosis of virus infections is based mainly on serological assays. Although polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) have been increasingly used for the diagnosis of such viral infections, the risk of transfusion-transmitted blood-borne viruses remains. Furthermore, PCR and ELISA are expensive and time-consuming, and sometimes cause falsepositive or false-negative results. Therefore, a rapid, accurate and cost-effective diagnostic procedure is needed. We subjected plasma from individuals infected with human immunodeficiency virus type-1 (HIV-1), the causative agent of acquired immune deficiency syndrome (AIDS), as well as plasma from uninfected individuals as a control to near-infrared (NIR) spectroscopy, which may provide a rapid diagnostic method for HIV-1 infection without using any reagent. NIR spectra in the 600-1,000 nm region for plasma from pre-serologically HIV-1-infected individuals and healthy donors were subjected to partial least squares (PLS) regression analysis and leave-out cross-validation to develop a multivariate model to estimate the concentration of HIV-1. Simultaneously, the same plasma samples were examined for HIV-1 p24 by ELISA. The results obtained by the NIR spectroscopy model for HIV-1 yielded a good correlation with those obtained by the reference method (HIV-1 p24 ELISA). These results suggest that NIR spectroscopy using plasma could provide a rapid, accurate, cost-effective tool for large-scale diagnosis of HIV-1 infection.     

Overexpression of CIN85 suppresses the growth of herpes simplex virus in HeLa cells

The adaptor protein CIN85 is widely distributed in different tissues and has three Src homology 3 (SH3) domains, a proline-rich region (PRR), and a coiled-coil domain. During studies on the function of CIN85, it was reported to form a complex with herpes simplex virus 1 (HSV-1) infected cell protein 0 (ICP0), which plays a key role in enabling viral replication. Here, we demonstrate that plaque formation by HSV-1 is reduced on HeLa cells expressing CIN85 ectopically. The PRR of CIN85 was found to be essential for the inhibition of virus growth, whereas the three SH3 domains were not required. CIN85 also suppressed HSV-1 growth in Chinese hamster ovary (CHO) cells expressing the receptor for herpes simplex virus entry (herpes virus entry mediator A; HVEM). However, immunoprecipitation experiments showed that CIN85 did not interact with HVEM directly, indicating that CIN85 is not involved in the HSV-1 cell-entry pathway, but rather in another downstream pathway. Collectively, our data indicate that CIN85 might play an important role in HSV-1 infection.     

Prepro-tachykinin gene expression in the brain of the honeybee<Emphasis Type="Italic"> Apis mellifera</Emphasis>

We have recently identified a tachykinin-related peptide (AmTRP) from the mushroom bodies (MBs) of the brain of the honeybee Apis mellifera L. by using direct matrix-assisted laser desorption/ionization with time-of-flight mass spectometry and have isolated its cDNA. Here, we have examined prepro-AmTRP gene expression in the honeybee brain by using in situ hybridization. The prepro-AmTRP gene is expressed predominantly in the MBs and in some neurons located in the optic and antennal lobes. cDNA microarray studies have revealed that AmTRP expression is enriched in the MBs compared with other brain regions. There is no difference in AmTRP-expressing cells among worker, queen, and drone brains, suggesting that the cell types that express the prepro-AmTRP gene do not change according to division of labor, sex, or caste. The unique expression pattern of the prepro-AmTRP gene suggests that AmTRPs function as neuromodulators in the MBs of the honeybee brain.This work was supported by a Grant-in-Aid from the Bio-oriented Technology Research Advancement Institution (BRAIN)     

Identification of autotaxin as a neurite retraction-inducing factor of PC12 cells in cerebrospinal fluid and its possible sources

Abstract Cerebrospinal fluid (CSF) induced neurite retraction of differentiated PC12 cells; the action was observed in 15 min (a rapid response) and the activity further increased until 6 h (a long-acting response) during exposure of CSF to the cells. The CSF action was sensitive to monoglyceride lipase and diminished by homologous desensitization with lysophosphatidic acid (LPA) and by pretreatment with an LPA receptor antagonist Ki16425. Although fresh CSF contains LPA to some extent, the LPA content in the medium was increased during culture of PC12 cells with CSF. The rapid response was mimicked by exogenous LPA, and a long-acting response was duplicated by a recombinant autotaxin, lysophospholipase D (lyso-PLD). Although the lyso-PLD substrate lysophosphatidylcholine (LPC) was not detected in CSF, lyso-PLD activity and an approximately 120-kDa autotaxin protein were detected in CSF. On the other hand, LPC but not lyso-PLD activity was detected in the conditioned medium of a PC12 cell culture without CSF. Among neural cells examined, leptomeningeal cells expressed the highest lyso-PLD activity and autotaxin protein. These results suggest that leptomeningeal cells may work as one of the sources for autotaxin, which may play a critical role in LPA production and thereby regulate axonal and neurite morphological change.     

Blätteralkohol (X)

Durch Erhitzen von 3-cis-Hexen-l-ol (Blätteralkohol) mit Natrium wurde die aromatische Verbindung (2-Propyl-5-äthyl-benzylalkohol) hergestellt und auch aus 3-trans-, 2-cis-oder 2-trans-Hexen-l-ol, oder aus 2-trans-Hexen-l-al (Blätteraldehyd) wurde die gleiche Verbindung erhalten. Durch eine gleiche Reaktion, wurde aus 3-Penten-l-ol die aromatische Verbindung (2-Äthyl-5-methyl-benzylalkohol) und aus 2-trans -Buten-l-ol wurde 2-Methyl-benzylalkohol erhalten.

Wir möchten besonders diese interessante Reaktion, bei der aus αβ- oder βγ-ungesättigten, n-primären Alkoholen oder Aldehyden Benzylalkohole mit verschiedenen Substitutionen hergestellt werden, als “Blätteralkohol-Reaktion” bezeichnen.     

Incorporation of beta-amyloid protein through the bovine ileal epithelium before and after weaning: model for orally transmitted amyloidoses

To determine the mechanism of bovine intestinal incorporation of the pathogen, and the pathogenesis of prion protein in the early stage, cows suckling and weaning were orally given a fusion protein of Abeta-EGFP. Abeta-EGFP was incorporated through the villous columnar epithelial cells and accumulated in crypt patches in the ileum of suckling cows. The sites of the uptake and accumulation of Abeta-EGFP are very close to the peripheral nervous system; however, such uptake of Abeta-EGFP was not observed in 6-month-old post-weaning cows. The present study, therefore, suggests that the weaning period is very important for the risk of transmission.     

Biosynthesis of trans-2-hexenal in chloroplasts from Thea sinensis

The biosynthetic pathway of trans-2-hexenal, leaf aldehyde, in isolated chloroplasts of Thea sinensis leaves. was examined using a tracer experiment. A high and specific incorporation of radioactivity into cis-3-hexenal and trans-2-hexenal, was observed when linolenic acid-[U-¹⁴C] was incubated with the isolated chloroplasts. Thus, trans-2-hexenal was biosynthesized via cis-3-hexenal from linolenic acid in the chloroplasts.     

Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress

Deletion of cellular isoform of prion protein (PrP^C) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrP^C‐deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus‐mediated overexpression of PrP^C reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrP^C‐deficient mice reportedly have a more aggressive disease onset and less clinical improvement during the chronic phase than wild‐type mice mice. In mice given oral dextran sulfate, PrP^C has a potential protective role against inflammatory bowel disease. PrP^C‐deficient mice demonstrate significantly greater increases in blood glucose concentrations after intraperitoneal injection of glucose than wild‐type mice. Further in vivo challenges to PrP gene‐deficient models and conditional knockout models with siRNA and in vivo administration of PrP‐ligating agents may assist in refining knowledge of the lymphoid function of PrP^C and predicting the effects of anti‐PrP treatment on the immune system. Together, these findings indicate that PrP^C may have multiple neuroprotective and anti‐inflammatory roles, which explains why this protein is so widely expressed.