耳穴静态电测量中的瞬变响应

耳穴电参数时变关系实验表明，在测量起始ｔ＜２τ时，因瞬变作用，电位Ｅ（ｔ）和压降Ｕ（ｔ）为瞬态响应，响应函数呈指数关系，特征参数为弛豫时间τ，τ≈ＲＣ；ｔ＞２τ时，为时变间期。电路分析给出数学描述，并与耳穴和模拟实验结果较相符。提示，时变特征应以ｔ＞２τ后提取，静态电测量时，采样应避开瞬变期，可提高准确性。该工作对正确鉴别时变性和特征提取，全面认识耳穴电特性具有重要意义。     

Class II defective avian sarcoma viruses: Comparative analysis of genome structure

The genomes of class II avian sarcoma viruses PRCII, PRCII-p, PRCIV, and Fujinami sarcoma virus (FSV), were studied by oligonucleotide fingerprinting, heteroduplex mapping, and nucleic acid hybridization. All of these viruses are genetically defective and have a small RNA genome between 4.5 and 6.1 kilobases (kb) in length. They contain helper-related sequences at both the 5′- and 3′-ends, but most of the retroviral sequences in the middle of the genome are deleted. In place of this deleted information, a contiguous stretch of transformation-specific sequences, termed fps, is found. These putative oncogenic sequences are about 1.2 kb in PRCII, and those in PRCII-p and PRCIV are roughly 2.9 kb. From the analysis of oligonucleotides, it appears that the fps sequences of PRCII represent a subset of those of PRCII-p. Most of the additional sequences present in PRCII-p but absent from PRCII are at the 5′-half of fps. The helper-related sequences in PRCII and PRCII-p are almost indistinguishable, except that PRCII-p contains slightly more retroviral information at the 3′-end of the genome. Therefore, it is possible that PRCII has been derived by deletion from PRCII-p. By contrast, PRCII-p and PRCIV were found to contain identical fps sequences, but their helper-related sequences have diverged substantially. These two sarcoma viruses either represent two independent isolates or, if derived from a single isolate, they have undergone extensive mutation and recombination with diverse avian retroviruses. FSV was found to differ to a greater extent from other class II sarcoma viruses in both helper-related and fps sequences. The difference in fps sequences is localized in the 5′-half of that region. Considering the variation in fps among all members of class II avian sarcoma viruses, it appears that the 3′-half of that genetic region is more conserved than the 5′-half.     

Effects of temporomandibular joint stimulation on nociceptive and nonnociceptive neurons of the cat's trigeminal subnucleus caudalis (medullary dorsal horn)

1. The extracellular activity of 196 single neurons in subnucleus caudalis (medullary dorsal horn) of the trigeminal (V) spinal tract nucleus was examined in chloralose-anesthesized, paralyzed cats. Electrical, mechanical, and algesic chemical stimuli were applied to the exposed temporomandibular joint (TMJ) in order to activate TMJ afferents. Seventy-eight neurons were studied that responded to electrical stimulation of the TMJ at a mean latency of 9.9 +/- 4.8 (SD) ms. 2. All neurons with TMJ input received additional afferent input, predominantly from facial skin or intraoral sites. Caudalis neurons were classified on the basis of their cutaneous mechanoreceptive field properties as low-threshold mechanoreceptive (LTM), wide dynamic range (WDR), or nociceptive specific (NS); a few neurons unresponsive to cutaneous stimuli were responsive to manipulation of deep subcutaneous structures. A sample of caudalis neurons was tested for responsiveness to electrical TMJ stimulation after the mechanoreceptive field properties of the neurons were determined. In this sample, 24% of the LTM neurons, 29% of the WDR neurons, 36% of the NS neurons, and 57% of the neurons with input from deep structures were responsive to TMJ stimulation. The WDR and NS neurons with TMJ inputs had mechanoreceptive field properties and laminar locations in caudalis that were comparable to those previously described for cutaneous nociceptive neurons in caudalis; also in accordance with recent studies, 74% of the neurons tested showed convergence of tooth pulp and/or hypoglossal (XII) nerve afferent inputs. 3. In contrast to the LTM neurons, the WDR and NS neurons were especially responsive to intense mechanical and algesic chemical stimulation of the TMJ as well as to electrical stimulation of TMJ afferents. For example, 71% of the WDR and NS neurons excited by electrical stimulation of the TMJ afferents and tested for their responsiveness to injections of algesic chemicals (7% NaCl, KCl, bradykinin, histamine) into the TMJ responded to at least one of these chemicals. The temporal characteristics of these responses were quantified. 4. The TMJ afferent inputs to the WDR and NS neurons were considered to be predominantly of a nociceptive character because of (1) the long latency and high threshold of most TMJ-evoked responses, which are consistent with previous demonstrations that small-diameter afferents predominantly supply the TMJ and, (2) the preferential responsiveness to noxious mechanical and chemical stimulation of TMJ afferents of neurons which were functionally identified as cutaneous nociceptive neurons.(ABSTRACT TRUNCATED AT 400 WORDS)     

Age-associated alterations in CXCL1 chemokine expression by murine B cells

Background  

The CXCL1 chemokines, macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (KC), have been shown to play a role in a number of pathophysiological disease states including endotoxin-induced inflammation and bacterial meningitis. While the expression of these chemokines has been identified in a variety of cell types in the mouse, little is known about their expression with murine B-lymphocytes.     

5一羟色胺能神经对横断损伤脊髓的再支配-脊髓内移植研究

用成年SD大鼠20只在脊髓的低位胸髓完全横断损伤,分别在1周和1月后,用富含5一羟色胺(5—HT)神经元的胚鼠脑干中缝组织悬液植人损伤尾侧的脊髓内,动物存活2个月,脊髓作5—HT免疫组化观察.结果:(1)胚5-HT能神经元能在成年大鼠脊髓内存活,5-HT纤维大多在灰质中延伸并向靶区分布,(2)损伤后1周移植组的5-HT能神经元存活量,5-HT纤维在宿主脊髓内延伸距离,以及5-HT末梢再分布的密度都优于损伤后1月移植组.     

Evaluation of United States-licensed human immunodeficiency virus immunoassays for detection of group M viral variants

Six Food and Drug Administration (FDA)-licensed human immunodeficiency virus type 1 (HIV-1) and HIV-1/2 immunoassays, including five enzyme immunoassays and one rapid test, were challenged with up to 250 serum samples collected from various global sites. The serum samples were from individuals known to be infected with variants of HIV-1 including group M subtypes A, B, B', C, D, E, F, and G and group O. All immunoassays detected the vast majority of samples tested. Three samples produced low signal over cutoff values in one or more tests: a clade B sample, an untypeable sample with a low antibody titer, and a group O sample. It is concluded that HIV-1 immunoassays used in the United States are capable of detecting most HIV-1 group M variants.     

Identification and characterization of a structural protein of hepatitis B virus: a polymerase and surface fusion protein encoded by a spliced RNA

The hepatitis B virus (HBV) genome is known to contain four conserved and overlapped open reading frames (ORFs) encoding the viral core, polymerase (P), surface (S), and X proteins. Whether HBV encodes other proteins has long been a major interest in the field. Using (32)P-labeling of an introduced protein kinase A site attached to the N- or C-terminus of the HBV polymerase gene, a 43-kDa P-S fusion protein was detected in cell lysate, secreted virions, and 22-nm subviral particles. Immunobiochemical studies showed that the 43-kDa protein contains the epitopes of the N-terminus of polymerase and most parts of the surface proteins. This 43-kDa protein was shown to be a glycoprotein, similar to the surface protein. RT-PCR and sequence analyses identified a spliced mRNA which was derived from pregenomic RNA with a deletion of 454 nucleotides (nt) from nt 2447 to 2902. This splice event creates a P-S fusion ORF. This finding is consistent with the result obtained from an immunobiochemical study. Mutations at the splice donor or acceptor site on the HBV genome abrogated the production of the 43-kDa protein. These mutants had no effect on viral replication in transfected HuH-7 cells. However, this P-S fusion protein is able to substitute for the LS protein in virion maturation. On the basis of these results, we conclude that the 43-kDa protein is a polymerase-surface fusion protein encoded by a spliced RNA. Similar to the LS protein, the 43-kDa P-S fusion protein is a structural protein of HBV and might play a role in the HBV life cycle.