Pseudomonas azotogensis—an associate symbiont of Bajra (Pennisatum americanum)

Summary Bajra (Pennisatum americanum) — a millet crop grown in the semi-arid, subtropical region of India, was surveyed for associative nitrogen-fixing bacteria in roots. Out of 20 root samples collected from 10 locations, 15 showed a high population ofPseudomonas azotogensis. The bacterium produced mucoid colonies with a greenish tinge on nitrogen-free malate medium and showed appreciable nitrogenase activity in pure culture.     

Effect of Sclerospora graminicola infection on total nitrogen content and free aminoacid composition of bajra plants

Summary Studies on the total nitrogen content and free aminoacid composition of healthy Bajra (Pennisetum typhoides Stapf &Hubb.) plants and those infected withSclerospora graminicola (Sacc.)Schroet. were made. Total nitrogen content of the diseased tissues increased as a result of infection. Considerable difference existed in free aminoacid composition of healthy and diseased tissues. Tryptophane was one of the aminoacids which was constantly isolated from the extracts of diseased tissues only.     

根据“肠-肾轴”理论治疗慢性肾脏病的研究进展

有研究报道在慢性肾脏病的发生发展过程中可发现一系列肠道变化,并有学者用"肠-肾轴"理论阐述肾脏病中肠道的变化以及疾病过程中肾脏与肠道之间的联系,提示调节肠道菌群或可成为治疗慢性肾脏病的新方法。本文根据"肠-肾轴"理论,综述了在慢性肾脏病发展过程中肠道出现的变化,如肠内代谢物异常、肠道损伤以及肠道菌群失调等。以慢性肾脏病发生发展过程中肠道的异常变化为治疗切入点,总结了以大黄为主的中药在调节肠道功能、修复肠道屏障、纠正肠道代谢物异常等方面具有的显著疗效,为治疗慢性肾脏病及减少并发症等提供新的治疗思路和新方法。     

Nitration in neurodegeneration: deciphering the "Hows" "nYs"

Recent literature has ushered in a new awareness of the diverse post-translational events that can influence protein folding and function. Among these modifications, protein nitration is thought to play a critical role in the onset and progression of several neurodegenerative diseases. While previously considered a late-stage epiphenomenon, nitration of protein tyrosine residues appears to be an early event in the lesions of amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease. The advent of highly specific biochemical and immunological detection methods reveals that nitration occurs in vivo with biological selectively and site specificity. In fact, nitration of only a single Tyr residue is often sufficient to induce profound changes in the activity of catalytic proteins and the three-dimensional conformation of structural proteins. Presumably, nitration modifies protein function by altering the hydrophobicity, hydrogen bonding, and electrostatic properties within the targeted protein. Most importantly, however, nitrative injury may represent a unifying mechanism that explains how genetic and environmental causes of neurological disease manifest a singular phenotype. In this review and synthesis, we first examine the pathways of protein nitration in biological systems and the factors that influence site-directed nitration. Subsequently, we turn our attention to the structural implications of site-specific nitration and how it affects the function of several neurodegeneration-related proteins. These proteins include Mn superoxide dismutase and neurofilament light subunit in amyotrophic lateral sclerosis, alpha-synuclein and tyrosine hydroxylase in Parkinson's disease, and tau in Alzheimer's disease.     

The nature of and the interrelations between the concepts of "life","disease" and "aging"

An attempt is made to consider disease and aging following from the concepts of the essence of life. The proposed definition of life represents a modified Engels' (1878) definition. Proceeding from the analysis of possible mechanisms of different disturbances in the life process leading to a decreased probability of the organism existence it is concluded that disease develops either as a result of hereditary changes in the genome or due-to disorders in its realization under certain unfavorable conditions. Aging is determined by the properties of the genome itself and develops in connection with age increase.     

Some Aspects of Floral Histogenesis in Bajra (Pennisetum typhoides S. & H.)

The young reproductive apex in Bajra (Pennisetum typhoides S.& H.) possesses a biseriate tunica and a massive corpus.The cells of three or four peripheral layers and six to eightlayers at the summit of the apex are eumeristematic. The centralregion consists of elongated, highly vacuolated, and lightlystained cells arranged in files. The initiation of the spikeletbud is by periclinal divisions first in the corpus and laterin T₂ cells. Similarly the longer bristle or the extension ofthe fascicular axis develops from the corpus and T₂ cells. Theother bristles develop from the tunica layers. The chaff membersare initiated and develop like a leaf. The development of thestamen resembles that of a spikelet or an axillary bud. Thedevelopment of the carpel is similar to that of the leaf primordium.The origin and development of the male flower is like that ofan axillary bud.     

Role of L-alanine: 4,5-dioxovalerate transaminase in chlorophyll synthesis in Bajra (Pennisetum typhoideum) seedlings

L-alanine:4,5-dioxovalerate transaminase activity and chlorophyll levels were estimated in lead and mercury treated Bajra seedlings. The enzyme activity increased with age upto 2nd day of germination and decreased on consequent days, where as the chlorophyll content increased with age upto 4th day and remained constant on day 5. Both the metals have no effect on L-alanine: 4,5-dioxovalerate transaminase activity but reduced chlorophyll levels. In vitro incubation of the enzyme with metal solutions showed that the enzyme activity was inhibited by mercury, while lead had no effect. Studies on sub-cellular localization of the L-alanine:4,5-dioxovalerate transaminase showed that it is present in all fractions. The non-correlation between L-alanine: 4,5-dioxovalerate transaminase activity and chlorophyll synthesis is evident from different activity profiles with age and response to heavy metal treatment in the seedlings. Hence, our results suggest the non-involvement of L-alanine:4,5-dioxovalerate transaminase in chlorophyll synthesis in bajra seedlings.     

一体化病证结合帕金森病大鼠模型中医证候属性研究

目的探讨6-OHDA帕金森病（PD）大鼠模型的中医证候属性。方法 采用经典的6-羟基多巴胺损毁注射法制作PD模型,随机分为模型组和药物治疗组,并分别采用天麻钩藤饮、桃红四物汤和涤痰汤进行反证治疗,同时设立正常对照组、假手术组。分别观察各组动物的神经行为学、舌象、氧化应激、环核苷酸、血管活性物质等的变化,从症状（行为学和舌象）、药物治疗反证、客观检测指标等方面对6-羟基多巴胺制作的PD模型进行综合分析,评价该模型的中医证候属性。结果（1）舌象：PD模型大鼠显微舌象分析结果为红舌。（2）行为学方面：PD模型大鼠的旋转圈数明显升高,与各药物组比较,差异均有显著性（P〈0.01）;天麻钩藤饮与桃红四物汤组、涤痰汤组比较,差异亦均有显著性（P〈0.05）,而桃红四物汤组与涤痰汤组差异无显著性（P〉0.05）。（3）客观指标：与正常对照组、假手术组比较,PD模型组MDA、cAMP、ET、TXB2含量明显升高,SOD、GSH、GSH-Px、cGMP、6-keto-PGF1α含量下降（P〈0.01）;天麻钩藤饮可明显降低MDA、cAMP、ET、TXB2（P〈0.05或P〈0.01）,升高SOD、GSH、GSH-Px、cGMP、6-keto-PGF1α（P〈0.01）,桃红四物汤组、涤痰汤可升高SOD、GSH、GSH-Px（P〈0.05,或P〈0.01）,降低cAMP（P〈0.05）、ET（P〈0.01）。天麻钩藤饮与涤痰汤组在SOD、GSH、cGMP,与桃红四物汤组在SOD、GSH、GSH-Px、cGMP、6-keto-pgf1α、TXB2,差异有显著性（P〈0.05,或P〈0.01）。涤痰汤组与桃红四物汤组TXB2（P〈0.05）,余各指标间差异无显著性（P〉0.05）。结论 6-羟基多巴胺制作的PD大鼠模型的中医证候属性属于阴虚动风证。     

"Emerging" parasitic infections in arctic ungulates

Important drivers for emergence of infectious disease in wildlifeinclude changes in the environment, shrinking habitats or concentrationof wildlife, and movement of people, animals, pathogens, orvectors. In this paper we present three case-studies of emergingparasitic infections and diseases in ungulates in the Canadiannorth. First we discuss climate warming as an important driverfor the emergence of disease associated with Umingmakstrongyluspallikuukensis, a nematode lungworm of muskoxen. Then we examinehow Protostrongylus stilesi, the sheep lungworm, emerged (orre-emerged) in muskoxen after re-introduction of this host intoits historical range made it sympatric with Dall's sheep. Finally,we consider Teladorsagia boreoarcticus, a newly described andcommon abomasal nematode of muskoxen that is emerging as a disease-causingparasite and may be an important regulator for muskox populationson Banks Island, Northwest Territories. These and other arctichost-parasite systems are exquisitely tuned and constrainedby a harsh and highly seasonal environment. The dynamics ofthese systems will be impacted by climate change and other ecologicaldisruptions. Baseline knowledge of parasite biodiversity andparasite and host ecology, together with predictive models andlong-term monitoring programs, are essential for anticipatingand detecting altered patterns of host range, geographic distribution,and the emergence of parasitic infections and diseases.     

An evaluation of straw-extract agar media for the growth and sporulation of Madurella mycetomatis

Four new media, namely Wheat straw extract agar, Bajra straw extract agar, Jowar straw extract agar and Paddy straw extract agar, were evaluated for their potential to stimulate the growth and sporulation of Madurella mycetomatis in comparison with the conventional Sabouraud dextrose agar and Soil extract agar. Vegetative growth of M. mycetomatis on the four types of Straw extract agars was superior to that obtained on Sabouraud dextrose agar. Isolates of M. mycetomatis sporulated better and faster on the Straw extract agars than on the Sabouraud dextrose agar and Soil extract agar. Straw extract agar is recommended as a sporulation medium for M. mycetomatis. It may prove useful especially for studies of the conidium ontogeny of the fungus for elucidating its taxonomic status.     

Acute unilateral ischemic renal injury induces progressive renal inflammation, lipid accumulation, histone modification, and "end-stage" kidney disease

There is an emerging concept in clinical nephrology that acute kidney injury (AKI) can initiate chronic kidney disease (CKD). However, potential mechanisms by which this may occur remain elusive. Hence, this study tested the hypotheses that 1) AKI triggers progressive activation of selected proinflammatory genes, 2) there is a relative failure of compensatory anti-inflammatory gene expression, 3) proinflammatory lipid accumulation occurs, 4) these changes correspond with "gene-activating" histone acetylation, and 5) in concert, progressive renal disease results. CD-1 mice were subjected to 30 min of unilateral renal ischemia. Assessments were made 1 day, 1 wk, or 3 wk later. Results were contrasted to those observed in uninjured contralateral kidneys or in kidneys from normal mice. Progressive renal injury occurred throughout the 3-wk postischemic period, as denoted by stepwise increases in neutrophil gelatinase-associated lipocalin gene induction and ongoing histologic damage. By 3 wk postischemia, progressive renal disease was observed (massive tubular dropout; 2/3rds reduction in renal weight). These changes corresponded with progressive increases in proinflammatory cytokine/chemokine gene expression (MCP-1, TNF-α, TGF-β1), a relative failure of anti-inflammatory enzyme/cytokine (heme oxygenase-1; IL-10) upregulation, and progressive renal lipid (cholesterol/triglyceride) loading. Stepwise increases in collagen III mRNA and collagen deposition (Sirius red staining) indicated a progressive profibrotic response. Postischemic dexamethasone treatment significantly preserved renal mass, indicating functional significance of the observed proinflammatory state. Progressive gene-activating H3 acetylation was observed by ELISA, rising from 5% at baseline to 75% at 3 wk. This was confirmed by chromatin immunoprecipitation assay of target genes. In sum, these results provide experimental support for the clinical concept that AKI can trigger CKD, this is partially mediated by progressive postischemic inflammation, ongoing lipid accumulation results (potentially evoking "lipotoxicity"), and increasing histone acetylation at proinflammatory/profibrotic genes may contribute to this self-sustaining injury-promoting state.     

Mast cell "disappearance" in chronic murine graft-vs-host disease (GVHD)-ultrastructural demonstration of "phantom mast cells"

Mast cells were studied during the induction of chronic graft-vs-host disease (GVHD) induced in mice across minor histocompatibility barriers. B10.D2 spleen cells (or control BALB/c cells) were injected into irradiated (600 rad) BALB/c recipients. Serial skin biopsies were taken over 26 days, during which time changes occurred resembling scleroderma, namely, dermal fibrosis, a mononuclear cell infiltrate, and loss of fat and appendages. Mast cells, when stained with toluidine blue, "disappeared" from GVHD, but not from control skin. Ultrastructural analysis showed that mast cells in GVHD skin were indeed present but underwent degranulation. Some mast cells showed only pale expanded sacs, indicating granule depletion. Because these cells could not be seen by toluidine blue staining but were plainly present, we have called them "phantom mast cells." Cellular activation occurred in many GVHD mast cells as shown by increased cytoplasmic activity, with numerous Golgi complexes, ribosomes, granular endoplasmic reticulum, and small vesicles. No identifiable mast cells were seen after day 19. No significant changes were seen in the mast cells of syngeneic control mice. We believe that immunologic processes in chronic GVHD cause a slow release of mast cell granule contents, which is different from anaphylactic degranulation. The depleted mast cells (invisible by toluidine blue staining) are also activated, perhaps in an attempt to replete their stores of granule contents. We discuss the relation of mast cell changes to fibrosis.     

The "suspicious" gynecologic smear

"Suspicious" gynecologic smears from 842 patients over a seven-year period were analyzed for their causes and outcomes. The frequency of the cytologic diagnosis of "suspicious" ranged between 0.5% in 1979 and 1.44% in 1975 of all smears examined. Review of the smears showed that this classification was used to report a variety of conditions, including equivocal possible precancerous changes as well as the presence of severe inflammation, degenerative or atrophic changes, abnormal glandular cells and metaplasia. The cytologic follow-up, following anti-inflammatory or hormonal therapy, showed a conversion to negative findings in 65.1% of all cases, usually within 12 months. In 294 cases, histologic analysis became necessary, revealing precancerous changes or cancer in 147 patients (17.5% of the study group). Smears of postmenopausal women with suspicious glandular or endometrial cells received special analysis. Significant numbers of such cases had histologic findings positive for malignancy (20% of smears with glandular cells and 21.3% with endometrial cells), as did also smears showing post-irradiative changes (34.6%) or atrophic and degenerative changes (17.1%). Therefore, "suspicious" smears in these groups were considered to indicate an increased risk of malignancy. A regimen for the proper management of cases with "suspicious" smears has been established.     

Adoption of an "open" envelope conformation facilitating CD4 binding and structural remodeling precedes coreceptor switch in R5 SHIV-infected macaques

A change in coreceptor preference from CCR5 to CXCR4 towards the end stage disease in some HIV-1 infected individuals has been well documented, but the reasons and mechanisms for this tropism switch remain elusive. It has been suggested that envelope structural constraints in accommodating amino acid changes required for CXCR4 usage is an obstacle to tropism switch, limiting the rate and pathways available for HIV-1 coreceptor switching. The present study was initiated in two R5 SHIV(SF162P3N)-infected rapid progressor macaques with coreceptor switch to test the hypothesis that an early step in the evolution of tropism switch is the adoption of a less constrained and more "open" envelope conformation for better CD4 usage, allowing greater structural flexibility to accommodate further mutational changes that confer CXCR4 utilization. We show that, prior to the time of coreceptor switch, R5 viruses in both macaques evolved to become increasingly sCD4-sensitive, suggestive of enhanced exposure of the CD4 binding site and an "open" envelope conformation, and this correlated with better gp120 binding to CD4 and with more efficient infection of CD4(low) cells such as primary macrophages. Moreover, significant changes in neutralization sensitivity to agents and antibodies directed against functional domains of gp120 and gp41 were seen for R5 viruses close to the time of X4 emergence, consistent with global changes in envelope configuration and structural plasticity. These observations in a simian model of R5-to-X4 evolution provide a mechanistic basis for the HIV-1 coreceptor switch.     

"Scleroderma linearis: hemiatrophia faciei progressiva (Parry-Romberg syndrom) without any changes in CNS and linear scleroderma "en coup de sabre" with CNS tumor

Background

Hemifacial atrophy (Parry-Romberg syndrome) is a relatively rare disease. The etiology of the disease is not clear. Some authors postulate its relation with limited scleroderma linearis. Linear scleroderma "en coup de sabre" is characterized by clinical presence of most commonly one-sided linear syndrome. In a number of patients, neurological affection is the medium of the disease. The treatment of both scleroderma varieties is similar to the treatment of limited systemic sclerosis.

Case presentation

We present two cases of a disease: a case of a 49-year-old woman with a typical image of hemifacial atrophy, without any changes of the nervous system and a case of a 33-year-old patient with an "en coup de sabre" scleroderma and with CNS tumor.

Conclusion

We described typical cases of a rare diseases, hemifacial atrophy and "en coup de sabre" scleroderma. In the patient diagnosed with Parry-Romberg syndrome, with Borrelia burgdoferi infection and with minor neurological symptoms, despite a four-year case history, there was a lack of proper diagnosis and treatment. In the second patient only skin changes without any neurological symptoms could be observed and only a precise neurological diagnosis revealed the presence of CNS tumor.     

Linkage analysis of "necessary" disease loci versus "susceptibility" loci.

The association of some diseases with specific alleles of certain genetic markers has been difficult to explain. Several explanations have been proposed for the phenomenon of association, e.g. the existence of multiple, interacting genes (epistasis) or a disease locus in linkage disequilibrium with the marker locus. One might suppose that when marker data from families with associated diseases are analyzed for linkage, the existence of the association would assure that linkage will be found, and found at a tight recombination fraction. In fact, however, linkage analyses of some diseases associated with HLA, as well as diseases associated with alleles at other loci located throughout the genome, show significant evidence against linkage, and others show loose linkage, to the puzzlement of many researchers. In part, the puzzlement arises because linkage analysis is ideal for looking for loci that are necessary, even if not sufficient, for disease expression but may be much less useful for finding loci that are neither necessary nor sufficient for disease expression (so-called susceptibility loci). This work explores what happens when one looks for linkage to susceptibility loci. A susceptibility locus in this case means that the allele increases risk but is neither necessary nor sufficient for disease expression. It might be either an allele at the marker locus itself that is increasing susceptibility or an allele at a locus in linkage disequilibrium with the marker. This work uses computer simulation to examine how linkage analyses behave when confronted with data from such a model.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rheumatoid arthritis "in the buff": erosive arthritis in defleshed bones

Examination of isolated bones from patients with unequivocal rheumatoid arthritis provides only a glimpse of the disease but has been the only "gold standard" for recognition of osseous lesions as compatible with the diagnosis of rheumatoid arthritis. Documentation of skeletal pathologic changes in confidently diagnosed individuals has been a major missing link in the transition from clinical to skeletal analysis. Availability of appropriate skeletal material from two patients with long-standing, well-documented rheumatoid arthritis provided the opportunity for acquiring such information. The osseous appearance, skeletal distribution, and distinguishing features of rheumatoid arthritis "in the buff" were delineated in two contemporary patients and in a skeletal population of 2,906 individuals. The preconceived notion of anticipated severity of disease has hereby been tested and found wanting. Severe lesions are not recognizable or distinguishable from artifact in relatively fragile rheumatoid arthritis-affected bones, whether freshly prepared or remotely sampled. Characterization of the nature and epidemiology of osseous alterations in two contemporary skeletal populations permitted the development of a standard for recognition of the disease in skeletal populations.     

Dynamics of motile-sperm subpopulation structure in boar ejaculates subjected to "in vitro" capacitation and further "in vitro" acrosome reaction

Incubation of diluted boar sperm from fresh ejaculates in a previously established "in vitro" capacitation medium induced a significant, time-dependent increase in several mean parameters of sperm motility, such as curvilinear velocity (VCL), linear velocity (VSL), mean velocity (VAP), linearity coefficient (LIN), straightness coefficient (STR) and wobble coefficient (WOB). Furthermore, motile boar-sperm semen samples were structured in four definite subpopulations. Subpopulation 1 showed the lowest values of VCL, VSL and VAP and also low values of linearity. Subpopulation 2 showed the second lowest values of VCL and VAP and higher values of LIN and STR. Subpopulation 3 was characterized by high values of velocity and low values of linearity. Finally, Subpopulation 4 was characterized by high values of velocity and linearity. "In vitro" capacitation and further acrosome reaction induced changes in the motility characteristics of each subpopulation as well as in their percentage distribution, Subpopulations 3 and 4 being those that showed the most significant changes. However, despite these changes, the observed, overall four-subpopulation structure was firmly maintained during the entire "in vitro" capacitation and acrosome-reaction process. Our results suggest that capacitation-induced motility changes are related to specific changes in the percentage of each motile-sperm subpopulation in the ejaculate without losing the overall, specific four-subpopulation structure. In this way, the maintenance of a four-subpopulation structure seems to be important in the control of the whole ejaculate physiology.     

纸坊病病毒病因的研究

1985年4～10月与1986年6～8月,在贵州省沿河县的纸坊村和崔家坨村先后发生了病因不明的传染病。纸坊村约有1/5的村民发病,病死率为12％,崔家坨村有1/10的村民发病,病死率高达30％。发病波及各年龄组,以青壮年为多,有家庭集聚现象。 本病起病急,轻症者只有头晕、乏力、肌痛、多汗、心悸伴以低热,有的初期有短暂的腹泻。重症者有高热(40℃以上)、大汗、心悸、游走性肌肉痉挛伴有明显疼痛和触痛,以腰骶部及四肢肌肉为好发部位。病人烦燥不安,2～5天内死亡。经实验室检查,排除了食物中毒、农药中毒、钩端螺旋体病和弓形体感染。从病人和接触者的粪便中分离到9株病毒,性状一致,为RNA型25nm的球形颗粒,耐酸,耐乙醚,能凝集人“O”型血球。经血清学鉴定为ECHO3型病毒。16份病人双份血清的检测结果表明,恢复期血清对该病毒中和抗体有4倍以上升高者共8例(纸坊村和崔家坨各4例)。病人单份血清也都有较高的抗体。有理由认为两年中先后在两个村庄发生的传染病与ECHO3型病毒有密切关系。查阅文献,尚未见有关ECHO3型病毒引起以肌痛、游走性肌痉挛为特征的疾病的报道。     

Studies on "stiffness of extremities disease" in the yak (Bos mutus)

Wild yak (Bos mutus) are affected by a disorder known colloquially as "stiffness of extremities disease," characterized by emaciation, lameness, stiffness in the gait, enlargement of the costochondral junctions, and abnormal curvature in the long bones. Results from preliminary epidemiologic and clinical observations suggested that this was a local, nutritional and metabolic disease associated with some mineral deficiency. Our objective was to determine the possible relationship between this disease and phosphorus (P) deficiency. We found that P concentrations in forage samples from affected areas were significantly lower than were those from unaffected areas, and the mean calcium:P ratio in the affected forage was 14:1. Phosphorus concentrations of blood, bone, teeth, and hair from affected yak were also significantly lower than were those from reference yak. Serum P levels of affected animals were much lower than were those of reference yak, whereas serum alkaline phosphatase levels were significantly higher than were those from reference yak. The P deficiency disease could be cured with supplement of disodium hydrogen phosphate (Na(2)HPO(4)). We conclude that the disease is mainly caused by P deficiency in forage.