BACKGROUND & AIMS: :A mouse perfusion model using fluorescently labeled dextran has been developed to investigate the functionality of blood vessels during cutaneous wound healing. By immunostaining cryostat sections of perfused wounds with antibodies that identify vessels, we were able to assess their functionality. There was an increase in the proportion of CD31(+)-perfused vessels in all wound regions with time, although the vessels of the wound margins and superficial granulation tissue (GT) took the longest to become perfused. More than 50% of the latter vessels were not perfused at 10 days postwounding. This is consistent with the growth of functional vessels from the wound base proceeding to the more superficial GT. The CD34 marker was expressed by a subpopulation of CD31(+) vessels. However, in contrast to CD31(+) vessels, the functionality of CD34(+) vessels did not change significantly with time and 50-75% of CD34(+) vessels in the GT and wound margins were nonfunctional. This might be explained either by apoptosis of the CD34(+) vessels or the loss of the marker with time. This study has important implications for assays of wound-healing angiogenesis based on histology and immunohistochemical markers for vessels, because vessel functionality differs both spatially and temporally during wound healing.

背景与目标： : 已经开发了使用荧光标记的葡聚糖的小鼠灌注模型，以研究皮肤伤口愈合过程中血管的功能。通过用识别血管的抗体对灌注伤口的低温恒温器切片进行免疫染色，我们能够评估其功能。尽管伤口边缘和浅表肉芽组织 (GT) 的血管灌注时间最长，但所有伤口区域中CD31 () 灌注血管的比例随时间增加。超过50% 的后一种血管在伤后10天没有灌注。这与从伤口基部到更浅表的GT的功能性血管的生长是一致的。CD34标记由CD31 () 血管的亚群表达。然而，与CD31(+) 血管相反，CD34(+) 血管的功能没有随时间显着变化，并且GT和伤口边缘中的50-75% CD34(+) 血管无功能。这可以通过CD34 () 血管的凋亡或标记物随时间的丢失来解释。这项研究对基于血管的组织学和免疫组织化学标记的伤口愈合血管生成测定具有重要意义，因为在伤口愈合过程中，血管功能在空间和时间上均不同。

BACKGROUND & AIMS: Compactness has been used to locate discontinuous structural units containing one or more polypeptide chains in proteins of known structure. Rather than exhaustively calculating the compactness of all possible units, our procedure uses a screening algorithm to find discontinuous regions that are potentially compact. Precise calculations of compactness are restricted only to units in these regions. With our procedure, compactness can be used to discover discontinuous domains with virtually any number of disjoint peptides. Small, single-domain proteins may contain several compact regionsthus, compact regions do not always correspond to folding domains.

Because a domain is an independent folding unit and should contain a hydrophobic core, compact units were further examined for the presence of hydrophobic clusters (Zehfus MH, 1995, Protein Sci 41188-1202). This added constraint limits the number of acceptable units and helps greatly in the location of the true structural domains. The larger hydrophobically stabilized compact units correspond to domains, while the smaller units may correspond to folding intermediates.

背景与目标： 致密性已用于在已知结构的蛋白质中定位包含一个或多个多肽链的不连续结构单元。我们的程序不是详尽地计算所有可能单元的紧密性，而是使用筛选算法来查找可能紧凑的不连续区域。紧凑度的精确计算仅限于这些区域中的单位。通过我们的程序，紧致性可用于发现具有几乎任何数量的不相交肽的不连续结构域。小的单结构域蛋白质可能包含几个紧凑区域。因此，紧凑区域并不总是对应于折叠结构域。
因为结构域是一个独立的折叠单元，应该包含疏水核心，所以进一步检查了紧凑单元是否存在疏水簇 (Zehfus MH，1995，蛋白质Sci 41188-1202)。此添加的约束限制了可接受单元的数量，并极大地帮助了真正的结构域的位置。较大的疏水稳定的致密单元对应于域，而较小的单元可能对应于折叠中间体。

BACKGROUND & AIMS: :A 58 year old man underwent 6 surgical interventions for various complications of massive biventricular myocardial infarction over a period of 2 years following acute occlusion of a possibly "hyperdominant" left anterior descending coronary artery. These included concomitant repair of apicoanterior post-infarction VSD and right ventricular free wall rupture, repeat repair of recurrent VSD following inferoposterior extension of VSD in the infarcted septum 5 weeks later, repair of delayed right ventricular free wall rupture 4 weeks subsequently, repair of a bleeding left ventricular aneurysm eroding through left chest wall 16 months thereafter, repair of right upper lobe lung tear causing massive anterior mediastinal haemorrhage, mimicking yet another cardiac rupture, 2 months later, followed, at the same admission, 2 weeks later, by sternal reconstruction for dehisced and infected sternum using pedicled myocutaneous latissimus dorsi flap. 5 years after the latissimus myoplasty, the patient remains in NYHA class 1 and is leading a normal life.

背景与目标： : 一名58岁的男子在急性闭塞可能是 “显性” 左前降支冠状动脉后，在2年内接受了6次手术治疗，以治疗大规模双心室心肌梗死的各种并发症。其中包括合并修复梗死后前路VSD和右心室游离壁破裂，5周后梗死间隔中VSD的后后反复修复复发性VSD，4周后修复延迟的右心室游离壁破裂，16个月后修复左胸壁侵蚀的出血左心室动脉瘤，修复右上叶肺撕裂，导致前纵隔大出血，模仿另一次心脏破裂，2个月后，随后在同一次入院时，2周后，通过使用带蒂的肌皮背阔肌皮瓣进行胸骨缺损和感染的胸骨重建。背阔肌成形术5年后，患者仍处于NYHA 1级，并过着正常的生活。

BACKGROUND & AIMS: UNLABELLED:In this study, we assessed the accuracy and reliability of MRI-guided SPECT measurements of medial temporal lobe blood flow in Alzheimer's disease (AD).

METHODS:Interactively aligned three-dimensional MP-RAGE MRI and 99mTc-HMPAO SPECT images were used for MRI-guided measurement of medial temporal lobe CBF in eight control subjects and eight patients with probable AD. Intraoperator reliability was assessed by repeated alignment and measurement by one experienced operator. Accuracy was assessed by examining two subjects with fiducial markers.

RESULTS:The alignment error was less than 1 SPECT pixel size (3.5 mm) and the coefficient of variation in repeated measures of medial temporal-to-cerebellar CBF ratios was 3.2%. The difference in mean medial temporal-to-cerebellar CBF ratios between eight control subjects and eight AD patients was 12%. Also by using three-dimensional seed-grow defined healthy brain reference regions, there were significant differences between control subjects and AD patients in medial temporal blood flow. Furthermore, the volumes of the MRI-defined medial temporal ROIs were smaller in the AD patients. The best separation between AD patients and control subjects was achieved by combining MRI measurements of atrophy and SPECT measurements of CBF.

CONCLUSION:These data show that the accuracy and reliability of MRI-guided SPECT measurements of medial temporal CBF clearly allow the detection of changes in AD. Also, a direct comparison of structural and functional changes is possible by this methodology, which might improve the early diagnosis of AD.

背景与目标： 未标记 : 在这项研究中，我们评估了MRI引导的SPECT测量阿尔茨海默氏病 (AD) 内侧颞叶血流的准确性和可靠性。
方法 : 交互式对齐的三维MP-RAGE MRI和99mTc-HMPAO SPECT图像用于MRI引导的8名对照受试者和8名可能患有AD的患者的内侧颞叶CBF测量。一位经验丰富的操作员通过重复对准和测量来评估操作员内部的可靠性。通过检查两个具有基准标记的受试者来评估准确性。
结果 : 对齐误差小于1 SPECT像素大小 (3.5毫米)，并且重复测量的变异系数内侧颞-小脑CBF比3.2%。12% 了八名对照受试者和八名AD患者之间平均内侧颞与小脑CBF比率的差异。同样，通过使用三维种子生长定义的健康大脑参考区域，对照组和AD患者在内侧颞血流方面存在显着差异。此外，在AD患者中，MRI定义的内侧颞roi的体积较小。通过结合萎缩的MRI测量和CBF的SPECT测量，可以实现AD患者与对照组之间的最佳分离。
结论 : 这些数据表明，MRI引导的内侧颞CBF SPECT测量的准确性和可靠性显然可以检测AD的变化。此外，通过这种方法可以直接比较结构和功能变化，这可能会改善AD的早期诊断。

BACKGROUND & AIMS: :The nature of the temporal relationship between antibacterial consumption and Streptococcus pneumoniae penicillin resistance is investigated using population level data across time. IMS Health Global Services provided national outpatient antibiotic prescription data for the years 1996-2003 from France, Spain, Italy, Germany, the United Kingdom, and the United States. Surveillance data consist of S. pneumoniae isolates obtained from a surveillance database in the same geographic regions from 1996 to 2003. A linear mixed model for repeated measures was used to analyze the association between resistance and several antibacterial classes through time. Changes in penicillin resistance through time in any country are better explained by the weighted cumulative antibacterial consumption with a 2-year lag. Narrow-spectrum penicillins are associated with lower resistance rates. Large reductions in consumption at the population level are needed to affect resistance. There is a peak level of penicillin resistance associated with cumulative exposure to a combination of antibiotic classes that is unique for every country.

背景与目标： : 使用跨时间的人群水平数据研究了抗菌药物消耗与肺炎链球菌青霉素耐药性之间的时间关系的性质。IMS Health Global Services提供了来自法国，西班牙，意大利，德国，英国和美国的1996-2003年全国门诊抗生素处方数据。监视数据由从2003年1996年相同地理区域的监视数据库中获得的肺炎链球菌分离株组成。使用用于重复测量的线性混合模型来分析耐药性与几种抗菌剂之间的关系。在任何国家，青霉素耐药性随时间的变化都可以通过滞后2年的加权累积抗菌药物消耗量来更好地解释。窄谱青霉素与较低的耐药率相关。为了影响抵抗力，需要大量减少人口消费。青霉素耐药性的峰值水平与累积暴露于抗生素类别的组合有关，这在每个国家都是独一无二的。

BACKGROUND & AIMS: :Event-related potentials (ERP) were recorded during auditory oddball tasks for a patient prior to and soon after left anterior temporal lobectomy. The N100 amplitude decreased bilaterally although the latency did not change after the lobectomy. The P300 amplitude decreased in the left hemisphere at 1 and 2 weeks after surgery, then recovered to the pre-operative level at 4 weeks. These findings suggest that the medial temporal structure participates in the generating system of P300.

背景与目标： : 在左前颞叶切除术之前和之后，在患者的听觉怪异任务中记录了事件相关电位 (ERP)。尽管肺叶切除术后潜伏期没有改变，但N100振幅双侧降低。术后1周和2周，左半球P300振幅降低，4周后恢复至术前水平。这些发现表明，内侧颞结构参与了p300的生成系统。

BACKGROUND & AIMS: :Heat shock protein 90 (HSP90) is required for structural folding and maintenance of conformational integrity of various proteins, including several associated with cellular signaling. Recent studies utilizing 17-allylamino-17-demethoxygeldanamycin (17-AAG), an inhibitor of HSP90, demonstrated an antitumor effect in solid tumors. To test whether HSP90 could be targeted in multiple myeloma (MM) patients, we first investigated expression of HSP90 by immunofluorescence and flow cytometric analysis in a myeloma cell line (U266) and primary myeloma cells. Following demonstration of HSP90 expression in myeloma cells, archival samples of 32 MM patients were analysed by immunoperoxidase staining. Myeloma cells in all patients showed strong cytoplasmic expression of HSP90 in all samples and 55% also demonstrated concurrent nuclear immunopositivity. Treatment of U266 and primary MM cells with 17AAG resulted in significantly increased apoptosis compared to untreated control cells. Analysis of anti-apoptotic BCL2 family proteins and akt in MM cells incubated with 17-AAG revealed down-regulation of BCL-2, BCL-XL, MCL-1 and akt. Furthermore, although a low concentration of bortezomib resulted in no cell death, a combination of 17AAG and bortezomib treatment revealed a synergistic apoptotic effect on the U266 cell line. These data suggest that targeted inhibition of HSP90 may prove to be a valid and innovative strategy for the development of future therapeutic options for MM patients.

背景与目标： : 热休克蛋白90 (HSP90) 是各种蛋白质的结构折叠和构象完整性维持所必需的，包括与细胞信号传导相关的几种。利用HSP90抑制剂17-allylamino-17-demethoxygeldanamycin (17-AAG) 的最新研究表明，在实体瘤中具有抗肿瘤作用。为了测试HSP90是否可以靶向多发性骨髓瘤 (MM) 患者，我们首先通过免疫荧光和流式细胞仪分析研究了HSP90在骨髓瘤细胞系 (U266) 和原发性骨髓瘤细胞中的表达。在证明骨髓瘤细胞中HSP90表达后，通过免疫过氧化物酶染色分析了32 MM患者的档案样本。所有患者的骨髓瘤细胞在所有样品中均显示出HSP90的强细胞质表达，并且55% 还显示出同时的核免疫阳性。与未处理的对照细胞相比，用17AAG处理U266和原代MM细胞可显着增加细胞凋亡。对与17-aag孵育的MM细胞中抗凋亡BCL2家族蛋白和akt的分析表明，BCL-2，BCL-XL，MCL-1和akt下调。此外，尽管低浓度的硼替佐米不会导致细胞死亡，但17AAG和硼替佐米的组合治疗显示出对U266细胞系的协同凋亡作用。这些数据表明，靶向抑制HSP90可能被证明是开发MM患者未来治疗选择的有效且创新的策略。

BACKGROUND & AIMS: :Foxp3 has been shown to be both necessary and sufficient for the development and function of naturally arising CD4+ CD25+ regulatory T cells in mice. Mutation of Foxp3 in Scurfy mice and FOXP3 in humans with IPEX results in fatal, early onset autoimmune disease and demonstrates the critical role of FOXP3 in maintaining immune homeostasis. The FOXP3 protein encodes several functional domains, including a C2H2 zinc finger, a leucine zipper, and a winged-helix/forkhead (FKH) domain. We have shown previously that FOXP3 functions as a transcriptional repressor and inhibits activation-induced IL-2 gene transcription. To characterize the role of each predicted functional domain on the in vivo activity of FOXP3, we have evaluated the location of point mutations identified in a large cohort of patients with the immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) and found them to cluster primarily within the FKH domain and the leucine zipper, but also present within the poorly defined N-terminal portion of the protein. The molecular functions of each of the IPEX-targeted domains were investigated. We show that FOXP3 is constitutively localized to the nucleus and this localization requires sequences at both the amino and C-terminal ends of its FKH domain. Moreover, FOXP3 was found to homodimerize through its leucine zipper. We also identify a novel functional domain within the N-terminal half of FOXP3, which is required for FOXP3-mediated repression of transcription from both a constitutively active and a NF-AT-inducible promoter. Furthermore, we demonstrate that IPEX mutations in these domains correlate with deficiencies in FOXP3 repressor function, corroborating their in vivo relevance.

背景与目标： : Foxp3已被证明对于小鼠中自然产生的CD4 CD25调节性T细胞的发育和功能既必要又充分。在患有pex的Scurfy小鼠中Foxp3和人类中FOXP3的突变会导致致命的，早发性自身免疫性疾病，并证明了FOXP3在维持免疫稳态中的关键作用。FOXP3蛋白编码几个功能结构域，包括C2H2锌指，亮氨酸拉链和有翼螺旋/叉头 (FKH) 结构域。我们先前已经证明FOXP3作为转录阻遏物起作用并抑制激活诱导的IL-2基因转录。为了表征每个预测的功能域对FOXP3体内活性的作用，我们评估了在免疫失调，多内分泌病，肠病，X连锁综合征 (IPEX)，发现它们主要聚集在FKH结构域和亮氨酸拉链内，但也存在于蛋白质定义不明确的N端部分。研究了每个pex靶向域的分子功能。我们证明FOXP3组成性地定位于细胞核，并且这种定位需要在其FKH结构域的氨基和C末端都具有序列。此外，发现FOXP3通过其亮氨酸拉链同向二聚。我们还在FOXP3的N末端一半内鉴定了一个新的功能结构域，这是FOXP3-mediated抑制组成型活性和NF-AT诱导启动子转录所必需的。此外，我们证明了这些域中的IPEX突变与FOXP3阻遏物功能的缺陷相关，从而证实了它们在体内的相关性。

BACKGROUND & AIMS: PURPOSE OF REVIEW:Bortezomib-based combinations are being investigated in relapsed or refractory multiple myeloma with the aim of improving outcomes. This review presents recent data from clinical trials of these combinations and discusses their implications. RECENT FINDINGS:Preclinical findings indicating additive or synergistic activity of bortezomib plus conventional and novel agents for multiple myeloma appear to be supported by clinical studies of bortezomib-based combinations. Bortezomib combined with a broad set of active agents results in enhanced response rates, including high complete response rates. Encouraging responses to bortezomib and its combinations are also seen in elderly patients, patients with adverse prognostic factors such as refractory disease and increased beta2-microglobulin, patients with cytogenetic abnormalities such as chromosome 13 deletion, advanced bone disease, extramedullary involvement, and patients with renal impairment, including patients with renal failure requiring dialysis. Toxicities are predictable and manageable and comparable to those seen with bortezomib monotherapy. SUMMARY:Bortezomib-based combinations show promising activity in relapsed or refractory multiple myeloma, including reversal of chemoresistance to previously used agents. As high complete and overall response rates translate into longer survival, bortezomib-based combinations appear likely to have a significant impact on the multiple myeloma treatment algorithm and on the course of the disease itself.

背景与目标：

BACKGROUND & AIMS: OBJECTIVE:Accumulating findings suggest that in acute myeloid leukemia (AML) patients, proinflammatory cytokines and growth factors play important roles in the proliferation and survival of AML cells in an autocrine and paracrine manner, leading to deterioration of AML. JTE-607 is a multiple cytokine inhibitor that potently suppresses production of proinflammatory cytokines. In the present study, we investigated the potency of JTE-607 as an antileukemic agent by exploiting a SCID mouse acute leukemia model. METHODS:SCID mice injected with anti-asialo-GM1 antibody were exposed to sublethal total-body irradiation at a dose of 3 Gy and then inoculated intravenously with AML cells. JTE-607 was administered using osmotic minipumps. The effects of JTE-607 on mouse survival time, human interleukin (IL)-8 levels in mouse plasma, and proportion of human CD45(+) cells in the bone marrow were studied. RESULTS:The survival time of the mice was strictly dependent on the number of U-937 cells proliferating in vivo. Administration of JTE-607 during the initial 7 days significantly prolonged survival of the mice, suggesting killing activity of JTE-607 against AML cells in vivo. Delayed administration of JTE-607 also prolonged the survival of mice bearing established leukemia with an effect comparable to the maximum tolerable dose of cytarabine. Flow cytometer analysis of bone marrow cells revealed decreased number of human CD45(+) cells. Human IL-8 level was also reduced by JTE-607. CONCLUSION:Our results indicate that JTE-607 has potential to be a new class of antileukemic drug that exerts inhibitory activities against both the proliferation and proinflammatory cytokine production of AML cells.

背景与目标：

BACKGROUND & AIMS: OBJECTIVE:In this article we focus on the role that chemokines and chemokine receptors play in the pathogenesis of multiple myeloma and the associated bone destructive process, and consider their utility as novel therapeutic targets for treating this devastating disease. METHODS:Current research on the role that chemokine and chemokine receptors play in the pathogenesis of myeloma is reviewed. RESULTS:The chemokines, MIP-1alpha, MCP-1, IL-8, and SDF-1, and their receptors play important roles in homing of MM cells, tumor growth, and bone destruction in myeloma. They are attractive therapeutic targets for treating myeloma patients. CONCLUSION:Addition of chemokine antagonists to current treatment regimens for myeloma should result in better therapeutic responses because of the loss of both the protective effect of the marrow microenvironment on the MM cells and the induction of osteoclast activity.

背景与目标：

BACKGROUND & AIMS: :cAMP signaling pathways play crucial roles in photoreceptor cells and other retinal cell types. Previous studies demonstrated a circadian rhythm of cAMP level in chick photoreceptor cell cultures that drives the rhythm of activity of the melatonin synthesizing enzyme arylalkylamine N-acetyltransferase and the rhythm of affinity of the cyclic nucleotide-gated channel for cGMP. Here, we report that the photoreceptor circadian clock generates a rhythm in Ca(2+)/calmodulin-stimulated adenylyl cyclase activity, which accounts for the temporal changes in the cAMP levels in the photoreceptors. The circadian rhythm of cAMP in photoreceptor cell cultures is abolished by treatment with the l-type Ca(2+) channel antagonist nitrendipine, while the Ca(2+) channel agonist, Bay K 8644, increased cAMP levels with continued circadian rhythmicity in constant darkness. These results indicate that the circadian rhythm of cAMP is dependent, in part, on Ca(2+) influx. Photoreceptor cell cultures exhibit a circadian rhythm in Ca(2+)/calmodulin-stimulated adenylyl cyclase enzyme activity with high levels at night and low levels during the day, correlating with the temporal changes of cAMP in these cells. Transcripts encoding two of the Ca(2+)/calmodulin-stimulated adenylyl cyclases, type 1 and type 8 (Adcy1 and Adcy8), displayed significant daily rhythms of mRNA expression under a light-dark cycle, but only the Adcy1 transcript rhythm persisted in constant darkness. Similar rhythms of Adcy1 mRNA level and Ca(2+)/calmodulin-stimulated adenylyl cyclase activity were observed in retinas of 2-week-old chickens. These results indicate that a circadian clock controls the expression of Adcy1 mRNA and Ca(2+)/calmodulin-stimulated adenylyl cyclase activity; and calcium influx into these cells gates the circadian rhythm of cAMP, a key component in the regulation of photoreceptor function.

背景与目标： : cAMP信号通路在感光细胞和其他视网膜细胞类型中起着至关重要的作用。先前的研究表明，雏鸡感光细胞培养物中cAMP水平的昼夜节律驱动褪黑激素合成酶芳基烷基胺N-乙酰基转移酶的活性节律和环状核苷酸门控通道对cGMP的亲和力节律。在这里，我们报告了感光体昼夜节律时钟在Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性中产生节律，这说明了感光体中cAMP水平的时间变化。通过用l型Ca(2) 通道拮抗剂尼群地平处理，消除了感光细胞培养物中cAMP的昼夜节律，而Ca(2) 通道激动剂Bay K 8644在持续的黑暗中增加了cAMP水平，并持续了昼夜节律。这些结果表明，cAMP的昼夜节律部分取决于Ca(2) 的流入。感光细胞培养物在Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性中表现出昼夜节律，夜间水平高，白天水平低，与这些细胞中cAMP的时间变化相关。编码两个Ca(2)/钙调蛋白刺激的腺苷酸环化酶 (1型和8型) (Adcy1和Adcy8) 的转录本在明暗循环下显示出明显的每日mRNA表达节律，但只有Adcy1转录本节律持续持续黑暗。在2周龄鸡的视网膜中观察到Adcy1 mRNA水平和Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性的相似节律。这些结果表明，生物钟控制Adcy1 mRNA的表达和Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性; 钙流入这些细胞中，激活了cAMP的昼夜节律，cAMP是调节感光细胞功能的关键组成部分。

BACKGROUND & AIMS: Environmental sensing in bacteria often involves the concerted action of sensor kinases and response regulators. Degenerate oligonucleotide primers were designed on the basis of amino acid similarity in the response regulators of these two-component systems. The primers were used in PCR to specifically amplify an internal DNA segment corresponding to the receiver module domain from genes encoding response regulators. Amplification products of the expected size were obtained from 12 different Gram-positive and Gram-negative bacteria. Sequence analysis revealed that 22 DNA fragments, which clearly originated from response regulator genes, were amplified from Escherichia coli, Agrobacterium tumefaciens, Bacillus subtilis and Lactobacillus bulgaricus. In each of these four species the receiver module of putative response regulator genes, which do not seem to be related to any of the already characterized genes, was identified. This simple and powerful method is therefore particularly useful for discovering new signal transduction systems which cannot be revealed by usual genetic studies.

背景与目标： 细菌中的环境传感通常涉及传感器激酶和响应调节剂的协同作用。简并寡核苷酸引物是根据这些两组分系统的响应调节剂中的氨基酸相似性设计的。引物用于PCR，以从编码反应调节剂的基因中特异性扩增与接收器模块结构域相对应的内部DNA片段。从12种不同的革兰氏阳性和革兰氏阴性细菌中获得了预期大小的扩增产物。序列分析表明，从大肠杆菌，根癌农杆菌，枯草芽孢杆菌和保加利亚乳杆菌中扩增出22个明显源自响应调节基因的DNA片段。在这四个物种中的每一个物种中，都鉴定了假定的反应调节基因的接收器模块，该模块似乎与任何已经表征的基因无关。因此，这种简单而强大的方法对于发现通常的遗传研究无法揭示的新信号转导系统特别有用。

BACKGROUND & AIMS: :A new optical method is proposed to investigate the reflectance of structurally coloured objects, such as Morpho butterfly wing scales and cholesteric liquid crystals. Using a reflected-light microscope and a digital single-lens reflex (DSLR) camera, we have successfully measured the two-dimensional reflection pattern of individual wing scales of Morpho butterflies. We demonstrate that this method enables us to measure the bidirectional reflectance distribution function (BRDF). The scattering image observed in the back focal plane of the objective is projected onto the camera sensor by inserting a Bertrand lens in the optical path of the microscope. With monochromatic light illumination, we quantify the angle-dependent reflectance spectra from the wing scales of Morpho rhetenor by retrieving the raw signal from the digital camera sensor. We also demonstrate that the polarization-dependent reflection of individual wing scales is readily observed using this method, using the individual wing scales of Morpho cypris. In an effort to show the generality of the method, we used a chiral nematic fluid to illustrate the angle-dependent reflectance as seen by this method.

背景与目标： : 提出了一种新的光学方法来研究结构上色的物体的反射率，例如Morpho蝴蝶翅鳞和胆甾型液晶。使用反射光显微镜和数字单镜头反射 (DSLR) 相机，我们成功地测量了Morpho蝴蝶单个翅膀鳞片的二维反射模式。我们证明了该方法使我们能够测量双向反射率分布函数 (BRDF)。通过在显微镜的光路中插入Bertrand透镜，将在物镜的后焦平面中观察到的散射图像投影到相机传感器上。使用单色光照明，我们通过从数码相机传感器检索原始信号，从Morpho rhetenor的机翼尺度量化与角度相关的反射光谱。我们还证明，使用这种方法，使用Morpho cypis的单个机翼尺度，很容易观察到单个机翼尺度的偏振相关反射。为了显示该方法的通用性，我们使用了手性向列流体来说明该方法所看到的与角度有关的反射率。

BACKGROUND & AIMS: :Alkenylboronic acids have shown important biological activities that contribute to neuroprotection. We have determined their influence on the β-amyloid (βA) aggregation process, β-secretase and acethylcholinesterase activities on cell-free systems, on the redox and lipid peroxidation status, and on the vulnerability to apoptotic death in an APPswe neuroblastoma cell line, before and after hydrogen peroxide treatment. We have discovered that 2-arylvinylboronic acids and some of their esters possess a set of properties which makes them highly useful as neuroprotective agents affecting multiple biological targets involved in AD. These properties are not paralleled by the related 2-arylboronic acids.

背景与目标： : 烯基硼酸显示出重要的生物活性，有助于神经保护。我们已经确定了它们对 β-淀粉样蛋白 (β a) 聚集过程，β-分泌酶和乙胆碱酯酶在无细胞系统上的活性，对氧化还原和脂质过氧化状态以及对APPswe神经母细胞瘤细胞凋亡死亡的脆弱性的影响过氧化氢治疗之前和之后。我们发现2-芳基乙烯基硼酸及其某些酯具有一系列特性，这使它们作为影响AD中涉及的多个生物靶标的神经保护剂非常有用。这些性质与相关的2-芳基硼酸不平行。