菌紫质膜对315nm辐照的光反应

利用仪器本身的测量光束３１５ｎｍ光照对紫膜薄膜中菌紫质的光反应的影响的ＣＤ谱研究说明：３１５ｎｍ的近紫外光可以激发薄膜中菌紫质的光反应,３１５ｎｍ与４０８ｎｍ、３３５ｎｍ光激发的光反应变化类型一致,但与５６８ｎｍ光激发的反应变化类型不一致;３１５ｎｍ光激发的光反应与菌紫质的初始样品状态有关,与菌紫质所处的分子状态的分布有关,而不是直接与初始样品状态存在的表现条件有关。结果认为利用包括近ＵＶ光在内的不同光照条件来调控ＢＲ的光反应是有可能的。     

三种因素对紫膜（PM）薄膜中菌紫质（BR）光反应类型的影响

由中性和碱性ｐＨ成膜液形成的ＰＭ薄膜在不同ＲＨ时ＣＤ语及其不同波长预光照产生的ＤＣＤ谱的研究发现,不同波长预光照产生的ＤＣＤ谱,按照在７００－４６０ｎｍ间的特征可分为全正型、长正短负型和短正长负型三大类。无论成膜液的ｐＨ是中性还是碱性,也不管ＰＭ薄膜的ＲＨ如何,≤４２８ｎｍ的近紫外光照都产生全正型ＤＣＤ谱,而≥６０ｎｍ的光照都产生短正长负型ＤＣＤ谱,但是５０６ｎｍ－５９０ｎｍ间的光照产生的ＤＣＤ谱却不仅与成膜液的ｐＨ有关,而且也与ＰＭ薄膜的ＲＨ有关,成膜液ｐＨ为１０．０的ＰＭ薄膜在ＲＨ７５％时未见有长正短负型ＤＣＤ谱。在近紫外的Ｍ峰区第一、三类ＤＣＤ谱无正峰,而在第二类中为正峰。这些特征都是ＰＭ薄膜中不同结构状态的ＢＲ分子配分浓度分布变化的反映。结果认为,成膜液的ｐＨ、膜所处的ＲＨ和预光照的波长均对ＢＲ的光循环反应有调控作用。这些信息可用于ＢＲ的调控研究,对ＢＲ分子器件的研制开发有重要的参考价值。     

菌紫质膜对315nm辐照的光反应

利用仪器本身的测量光束３１５ｎｍ光照对紫膜薄膜中菌紫质的光反应的影响的ＣＤ谱研究说明：３１５ｎｍ的近紫外光可以激发薄膜中菌紫质的光反应,３１５ｎｍ与４０８ｎｍ、３３５ｎｍ光激发的光反应变化类型一致,但与５６８ｎｍ光激发的反应变化类型不一致;３１５ｎｍ光激发的光反应与菌紫质的初始样品状态有关,与菌紫质所处的分子状态的分布有关,而不是直接与初始样品状态存在的表现条件有关。结果认为利用包括近ＵＶ光在内的不同光照条件来调控ＢＲ的光反应是有可能的。     

冷冻干燥对紫膜菌紫质圆二色性的影响

无论是先冷冻后干燥,还是先干燥后冷冻,或只冷冻处理,或只干燥处理的干湿紫膜样品,也无论是在处理后将其悬浮在水中,或在十六烷中,或在大豆磷脂正己烷液中,紫膜中的菌紫质分子均丧失了天然紫膜水悬浮液中的圆二色谱的双相性。然而,对于先冷冻后干燥,只干燥处理的紫膜水悬浮液,这种双相性可以缓慢地恢复。该现象提示,冷冻和/或干燥处理对紫膜菌紫质的圆二色性的影响,可能主要通过影响脂区间接实现的;用环三体激子理论难以圆满解释该现象。     

紫膜菌紫质分子的光生物物理学研究

本文介绍了紫膜细菌视紫红质的微观结构,质子泵功能和光循环过程,及其菌紫质分子中发色团和蛋白质相互作用(结合位点)的几种光谱研究,最后讨论了菌紫质分子原初事件量子产率的双重性和相应的分子动力学模型。     

脂质泡中的菌紫质旋转运动的介质依赖性

用闪光诱导瞬间二向色性方法测量了蔗糖和甘油对菌紫质（ＢＲ）分子在脂质泡中的旋转扩散运动的影响。结果表明脂质囊泡本身在悬浮液中的运动并不会影响ＢＲ分子在膜中的旋转运动的测量。蔗糖和甘油对ＢＲ旋转运动的影响在相变温度以上和相变温度以下是不同的,相变温度以下的主要作用是相分离,使运动减慢,相变温度以上的作用可能是脂的分散,使运动加快。     

菌紫质研究的新进展

菌紫质(BR)是嗜盐菌紫膜中的唯一蛋白质,野生型的BR分子含有248个氨基酸残基,其中一个视黄醛通过希夫碱基连结在第216位赖氨酸上,它具有质子泵的功能．光照下,BR进行光循环,光循环又与质子泵过程相关联．菌紫质的结构和功能方面的研究已有很大进展,但其光循环途径和质子泵的机理还不太清楚．文章概述了近年来对菌紫质结构,光循环和质子泵机理研究的进展,尤其对争论较大的菌紫质光循环途径的四类模型作了较详细的介绍．     

铜／封口膜／酰化紫膜LB膜／氧化铟锡型菌紫质光电池的光电特性

ＲＨ５７％的ＡＰＭＬＢＦ构制的Ｃｕ／Ｐａｒａｆｉｌｍ／ＡＰＭＬＢＦ／ＩＴＯ型ＢＲ光电池具有的光电响应能力随ＡＰＭＬＢＦ暗适应程度增加而增大,光适应后趋于稳定。光电响应信号的大小随被光照的截面减小而变小;不同引线输出的信号极性与质子泵运相一致。结果认为这种光电池可用于进一步构制光电池组以模拟视网膜的某些功能。     

膜脂环境对紫膜蛋白的影响

紫膜蛋白菌紫质（bacteriorhodopsin,BR）处于不同的膜脂环境中,通过吸收光谱、荧光光谱和闪光动力学光谱的测定,比较了3种不同膜脂环境对菌紫质分子结构和功能的影响。实验结果表明：天然膜脂是BR最稳定的膜脂环境,可以形成以三聚体为单位的二维六角形品格结构。二豆蔻酰脂酰胆碱（dimyristoyl phosphatidylcholine,DMPC）也是BR分子的稳定脂环境,但以单体形式存在于膜脂环境中,功能受到一定影响。经TritonX-100增溶处理的紫膜膜脂环境中BR为单体,不稳定,容易发生结构和功能的变化。     

山莨菪碱对紫膜中菌紫质结构的影响及其与膜脂的关系

本文用吸收光谱和可见圆二色谱研究了不同浓度的山莨菪碱对紫膜中菌紫质结构的影响,并设计了用不同浓度的去垢剂Triton X-100作为脂环境的扰动剂,研究山莨菪碱对菌紫质的影响与膜脂关系的实验.结果表明山莨菪碱不仅影响菌紫质分子本身的构象变化而且扰动了菌紫质分子之间的激子偶联作用.通过吸收差光谱技术表明山莨菪碱对菌紫质结构的影响与膜脂密切相关并指出紫膜中菌紫质的三体结构对膜功能的贡献是不容忽视的.     

Treatment of the painful shoulder syndrome with amitriptyline and lithium carbonate

Thirty-four patients with painful shoulder syndrome (PSS) were psychologically assessed and the results compared with those from a control group presenting other musculoskeletal disorders. A significantly greater prevalence of depression was found in the former group. Fifty-six patients with PSS were treated with only lithium and amitriptyline for four months; 44 patients showed marked clinical improvement and radiologic clearing of dystrophic calcification. Lithiumamitriptyline therapy, when compared with physiotherapy in another series of 11 patients, was found to be far superior. Some possible biochemical links between depression and PSS are outlined, and the theory that PSS may be a clinical entity of psychogenic origin is discussed.     

Differential selectivity of hyaluronidase inhibitors toward acidic and basic hyaluronidases

Hyaluronidase (HAase), a class of enzymes which degrade hyaluronic acid (HA), are involved in the spread of infections/toxins, ovum fertilization, and cancer progression. Thus, HAase inhibitors may have use in disease treatments. We evaluated 21 HAase inhibitors against HYAL-1, testicular, honeybee, and Streptomyces HAases. Among these inhibitors, polymers of poly (styrene-4-sulfonate) (PSS) (i.e., molecular weight 1400-990,000 or PSS 1400-PSS 990,000) and O-sulfated HA (sHA) derivatives (sHA2.0, 2.5, and 2.75) were the most effective. HYAL-1 and bee HAases were the most sensitive, followed by testicular HAase; Streptomyces HAase was resistant to all inhibitors, except PSS 990,000 and VERSA-TL 502 (i.e., PSS 10(6) dalton). The length of the PSS polymer determined their potency (e.g., IC50 for HYAL-1, PSS 990,000: 0.0096 microM; PSS 210 no inhibition; IC50 for testicular HAase, PSS 990,000: 0.042 microM; PSS 210 no inhibition). The presence, but not the number, of sulfate groups on the sHA molecule determined its potency (e.g., IC50 for HYAL-1: sHA2.0, 0.019 microM; sHA2.75, 0.0083 microM). Other known HAase inhibitors, such as gossypol, sodium-aurothiomalate, 1-tetradecane sulfonic acid, and glycerrhizic acid, were not effective. Both PSS and sHA inhibited HAases by a mixed inhibition mechanism (i.e., competitive + uncompetitive) and were 5- to 17-fold better as uncompetitive inhibitors than as competitive inhibitors. These results demonstrate that HAase inhibitors show selectivity toward the different types of HAases, which could be exploited to inhibit specific HAases involved in a variety of pathophysiologic conditions.     

The main challenges for social life cycle assessment (SLCA) to support the social impacts analysis of product-service systems

Purpose

This paper aims to investigate the applicability of social life cycle assessment (SLCA) to the social impacts analysis of product-service systems (PSS). The purpose is to discuss the main challenges for this approach to comparing PSS business model alternatives and analyzing the social consequences of PSS introduction into the market.

Methods

Two PSS solutions were considered to investigate the applicability and the challenges for SLCA when applied to PSS assessment. A comparative analysis was discussed based on UNEP/SETAC guidelines. The subcategories and social indicators suggested in the guidelines were analyzed, and the indicators considered suitable for the comparison of PSS alternatives, considering the use phase, were identified. Other indicators from the PSS literature were also added to those from the guidelines. To analyze the consequences of PSS implementation, the applicability of consequential SLCA was discussed.

Results and discussion

The main results pointed out that only a few indicators in the SLCA guidelines could be used for comparative PSS analysis. This occurred because only some of the guidelines could be linked to the processes of each PSS. Other indicators identified in the PSS literature are suggested to complement the comparative analysis of PSS alternatives. Concerning the effects of PSS introduction, it can cause social impacts with regard to the company and stakeholders directly involved in the changes in addition to the effects that may occur in other products and services systems as a result of consumers’ behavior and PSS interaction in the market. The consequential modeling is suggested as appropriate for this analysis.

Conclusions

The SLCA approach can be considered suitable for PSS social issues analysis, although there are limitations for a full analysis in this study. Some major challenges for its applicability were identified. First, PSS functional unit modeling should be investigated considering all PSS elements (products and services) and the functions provided by the system. Second, only few indicators in the guidelines were considered appropriate for PSS comparative analysis before its introduction. Finally, concerning consequential SLCA, this could be explored in the context of PSS, but there is still scarce research on this subject. In short, to establish SLCA as a useful and applicable methodology to assess the social impacts of a PSS, further research is required, especially regarding the consequential SLCA.

     

Genetic mapping of resistance to purple seed stain in PI 80837 soybean

Purple seed stain (PSS) of soybean caused by Cercospora kikuchii is an important disease that reduces market grade and can affect seed germination and vigor. A single dominant gene was shown to confer PSS resistance in PI 80837. The objective of this research was to map the PSS resistance gene in PI 80837 using simple sequence repeat (SSR) markers. A cross was made between the PSS-susceptible cultivar Agripro 350 (AP 350) and PI 80837. The F2 population and parents were grown in the field, and the resistance or susceptibility of individual plants was determined by assaying the seed for infection by C. kikuchii. DNA of parent and F2 plants was extracted for SSR analysis and mapping. Segregation ratios for seed infection and for SSR markers showed that a single dominant gene conditions resistance to PSS in PI 80837. The candidate resistance gene was mapped between Sat_308 (6.6 cM) and Satt594 (11.6 cM) on molecular linkage group G. These markers may be useful in marker-assisted selection for utilizing PSS resistance from PI 80837 in a breeding program.     

Circulating antibodies against neonatal cardiac muscarinic acetylcholine receptor in patients with Sjögren's syndrome

Isolated congenital heart block may be associated with Primary Sjogren's Syndrome. In this work we demonstrated that IgG present in the sera ofpatients with Primary Sjogren's Syndrome (PSS) could bind and activate muscarinic acetylcholine receptors of rat neonatal atria. These antibodies were able to inhibit in a irreversible manner the binding of ³H-QNB to muscarinic cholinergic receptors of purified rat atria membranes. Moreover, IgG from PSS individuals could modify biological effects mediated by muscarinic cholinoceptors activation, i.e. decrease contractility and cAMP and increase phosphoinositide turnover and cGMP. Atropine blocked all of these effects and carbachol mimicked them; confirming muscarinic cholinergic receptors-mediated PSS IgG action. Neither binding nor biological effect were obtained using adult instead of neonatal rat atria. IgG from sera of normal women were not effective in the studied system. The prevalence of cholinergic antibody was 100% in PSS and was independent of Ro/SS-A and La/SS-B antibodies. It could be concluded that antibody against muscarinic cholinergic receptors may be another serum factor to be considered in the pathophysiology of the development of congenital heart block.     

Phosphatidylserine synthase 2: high efficiency for synthesizing phosphatidylserine containing docosahexaenoic acid

Phosphatidylserine (PS), the major anionic phospholipid in eukaryotic cell membranes, is synthesized by the integral membrane enzymes PS synthase 1 (PSS1) and 2 (PSS2). PSS2 is highly expressed in specific tissues, such as brain and testis, where docosahexaenoic acid (DHA, 22:6n-3) is also highly enriched. The purpose of this work was to characterize the hydrocarbon-chain preference of PSS2 to gain insight on the specialized role of PSS2 in PS accumulation in the DHA-abundant tissues. Flag-tagged PSS2 was expressed in HEK cells and immunopurified in a functionally active form. Purified PSS2 utilized both PE plasmalogen and diacyl PE as substrates. Nevertheless, the latter was six times better utilized, indicating the importance of an ester linkage at the sn-1 position. Although no sn-1 fatty acyl preference was noted, PSS2 exhibited significant preference toward DHA compared with 18:1 or 20:4 at the sn-2 position. Preferential production of DHA-containing PS (DHA-PS) was consistently observed with PSS2 purified from a variety of cell lines as well as with microsomes from mutant cells in which PS synthesis relies primarily on PSS2. These findings suggest that PSS2 may play a key role in PS accumulation in brain and testis through high activity toward DHA-containing substrates that are abundant in these tissues.     

Whole-exome sequencing in a single proband reveals a mutation in the CHST8 gene in autosomal recessive peeling skin syndrome

Generalized peeling skin syndrome (PSS) is an autosomal recessive genodermatosis characterized by lifelong, continuous shedding of the upper epidermis. Using whole-genome homozygozity mapping and whole-exome sequencing, we identified a novel homozygous missense mutation (c.229C>T, R77W) within the CHST8 gene, in a large consanguineous family with non-inflammatory PSS type A. CHST8 encodes a Golgi transmembrane N-acetylgalactosamine-4-O-sulfotransferase (GalNAc4-ST1), which we show by immunofluorescence staining to be expressed throughout normal epidermis. A colorimetric assay for total sulfated glycosaminoglycan (GAG) quantification, comparing human keratinocytes (CCD1106 KERTr) expressing wild type and mutant recombinant GalNAc4-ST1, revealed decreased levels of total sulfated GAGs in cells expressing mutant GalNAc4-ST1, suggesting loss of function. Western blotting revealed lower expression levels of mutant recombinant GalNAc4-ST1 compared to wild type, suggesting that accelerated degradation may result in loss of function, leading to PSS type A. This is the first report describing a mutation as the cause of PSS type A.     

Minor salivary gland mesenchymal stromal cells derived from patients with Sjӧgren's syndrome deploy intact immune plasticity

Background aimsMesenchymal stromal cells (MSCs) provide minor salivary glands (MSGs) with support and niche cells for epithelial glandular tissue. Little is known about resident MSG-derived MSCs (MSG-MSCs) in primary Sj?gren's syndrome (PSS). The authors’ objective is to define the immunobiology of endogenous PSS MSG-MSCs.MethodsUsing culture-adapted MSG-MSCs isolated from consenting PSS subjects (n = 13), the authors performed in vitro interrogation of PSS MSG-MSC immunobiology and global gene expression compared with controls. To this end, the authors performed phenotypic and immune functional analysis of indoleamine 2,3-dioxygenase (IDO), programmed death ligand 1 (PD-L1) and intercellular adhesion marker 1 (ICAM-1) before and after interferon γ (IFNγ) licensing as well as the effect of MSG-MSCs on T-cell proliferation. Considering the female predominance of PSS, the authors also addressed the influence of 17-β-estradiol on estrogen receptor α-positive-related MSC function.ResultsThe authors found that MSG-MSCs deployed normal immune regulatory functionality after IFNγ stimulation, as demonstrated by increased protein-level expression of IDO, PD-L1 and ICAM-1. The authors also found that MSG-MSCs suppressed T-cell proliferation in a dose-dependent manner independent of 17-β-estradiol exposure. Gene ontology and pathway analysis highlighted extracellular matrix deposition as a possible difference between PSS and control MSG-MSCs. MSG-MSCs demonstrated increased α-smooth muscle actin expression in PSS, indicating a partial myofibroblast-like adaptation.ConclusionsThese findings establish similar immune regulatory function of MSG-MSCs in both PSS and control patients, precluding intrinsic MSC immune regulatory defects in PSS. PSS MSG-MSCs show a partial imprinted myofibroblast-like phenotype that may arise in the setting of chronic inflammation, providing a plausible etiology for PSS-related glandular fibrosis.     

Phosphatidylserine synthase-1 and -2 are localized to mitochondria-associated membranes

We report the subcellular localization of enzymes involved in phosphatidylserine biosynthesis in mammalian cells. Several lines of evidence suggest that phosphatidylserine synthase-1 (PSS1) is highly enriched in mitochondria-associated membranes (MAM) and is largely excluded from the bulk of the endoplasmic reticulum (ER). Taking advantage of the substrate specificity of PSS1, we showed that (i) MAM contain choline exchange activity, whereas this activity is very low in the bulk of the ER, (ii) serine exchange activity is inhibited by choline to a much greater extent in MAM than in ER, and (iii) MAM use phosphatidylcholine and phosphatidylethanolamine as substrates for phosphatidylserine biosynthesis, whereas the ER utilizes only phosphatidylethanolamine. According to immunoblotting of proteins from both CHO-K1 cells and murine liver, PSS1 is localized to MAM, and in hepatoma cells stably expressing PSS1 this protein is highly enriched in MAM. Since the ER contains serine and ethanolamine exchange activities, we had predicted that PSS2 would account for the serine exchange activity in the ER. Unexpectedly, using immunoblotting experiments, we found that (i) PSS2 of CHO-K1 cells is present only in MAM and (ii) PSS2 is restricted to MAM of McArdle cells expressing recombinant PSS2. These data leave open the question of which enzyme imparts PSS activity to the ER and suggest that a third isoform of PSS might be located in the ER.