Готові списки джерел за темами / Study the Pathogenesis of a Disease

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Добірка наукової літератури з теми "Study the Pathogenesis of a Disease"

Автор: Grafiati
Опубліковано: 26 жовтня 2023

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Статті в журналах з теми "Study the Pathogenesis of a Disease"

1

Yang, Kan, Yuqing Yan, Anni Yu, Ru Zhang, Yuefang Zhang, Zilong Qiu, Zhengyi Li, Qianlong Zhang, Shihao Wu, and Fei Li. "Mitophagy in neurodegenerative disease pathogenesis." Neural Regeneration Research 19, no. 5 (September 22, 2023): 998–1005. http://dx.doi.org/10.4103/1673-5374.385281.

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Abstract Mitochondria are critical cellular energy resources and are central to the life of the neuron. Mitophagy selectively clears damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis. Mature neurons are postmitotic and consume substantial energy, thus require highly efficient mitophagy pathways to turn over damaged or dysfunctional mitochondria. Recent evidence indicates that mitophagy is pivotal to the pathogenesis of neurological diseases. However, more work is needed to study mitophagy pathway components as potential therapeutic targets. In this review, we briefly discuss the characteristics of nonselective autophagy and selective autophagy, including ERphagy, aggrephagy, and mitophagy. We then introduce the mechanisms of Parkin-dependent and Parkin-independent mitophagy pathways under physiological conditions. Next, we summarize the diverse repertoire of mitochondrial membrane receptors and phospholipids that mediate mitophagy. Importantly, we review the critical role of mitophagy in the pathogenesis of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Last, we discuss recent studies considering mitophagy as a potential therapeutic target for treating neurodegenerative diseases. Together, our review may provide novel views to better understand the roles of mitophagy in neurodegenerative disease pathogenesis.
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2

Ashu and Rakesh Sharma. "Nidanapanchakatmak study of Aamvata." Journal of Ayurveda and Integrated Medical Sciences 8, no. 4 (May 25, 2023): 46–48. http://dx.doi.org/10.21760/jaims.8.4.7.

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In Ayurveda there are various approaches to diagnose a disease; the concept of Nidan Panchak is one such modality of Ayurveda. Nidan Panchak helps to diagnose diseases at various stages. Knowing the definite Nidana (etiological factors), Dosha vitiation, Samprapti (pathogenesis or progress of disease) and to check it at early stage is given prime importance. Nidan Panchaka plays vital role to identify types of disease. It consists of five subtypes which are Nidan (causes), Purvarupa (Prodromal Features), Rupa (Clinical features), Upashaya (Therapeutic methods), and Samprapti (Pathogenesis). These five elements collectively or selectively help in making an accurate diagnosis. Aamvata is a diseased caused by Dushti of Rasavaha Strotas in which there is formation of Ama due to Jatharagni Mandya. The Aamvata condition closely resembles with Rheumatoid arthritis, an autoimmune inflammatory condition characterised by symmetrical polyarthritis. Aamvata disease was first described in Laghutrayee by Acharya Madhava. Before the Acharya Madhava the concept of Aamvata was vague. Aamvata develops due to Dushti or Prakopa of Ama as well as Vata Dosha. As the disease Aamvata is very prevalent in society, it’s important to know the exact diagnosis along with treatment. In our current review we had tried to elaborate about the Nidanapanchaka of Aamvata.
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3

ARAI, Satoshi. "Study on Pathogenesis of Periodontal Disease in Gnotobiotic Mice." Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology) 36, no. 4 (1994): 776–93. http://dx.doi.org/10.2329/perio.36.776.

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4

Tsyganova, Tatiana Vasilyevna, and Anna Nikolaevna Melisheva. "ALZHEIMER’S DISEASE: MODERN VIEWS ON THE PATHOGENESIS OF THE DISEASE." Chronos 7, no. 11(73) (December 13, 2022): 39–41. http://dx.doi.org/10.52013/2658-7556-73-11-11.

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Alzheimer’s disease (AD) in the modern definition of the disease is a progressive neurodegenerative disease. Extracellular aggregates of amyloid plaques β (Aß) and intracellular neurofibrillary tangles, which consist of hyperphosphorylated tau protein, play a major role in the pathogenesis of this disease. BA is manifested by progressive dementia, which affects elderly people. Initially, clinical symptoms are manifested by memory loss, and in the later stages by neuropsychiatric disorders and, subsequently, by a change in a person’s personality. Based on new statistics, the prevalence of the disease is growing worldwide. There are about 50 million patients with AD, and the incidence tends to double every 5 years after the age of 65. As BA was studied, many pathogenetic mechanisms of the disease were formulated. Currently, the theory of the amyloid cascade and hyperphosphorylation of tau has received the main recognition, but all the processes of disease development are still unclear. Many other theories of the occurrence of the disease are also considered, therefore, the study of the pathogenesis of AD is quite an urgent problem.
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Santos-Ocaña, Carlos, María V. Cascajo, María Alcázar-Fabra, Carmine Staiano, Guillermo López-Lluch, Gloria Brea-Calvo, and Plácido Navas. "Cellular Models for Primary CoQ Deficiency Pathogenesis Study." International Journal of Molecular Sciences 22, no. 19 (September 22, 2021): 10211. http://dx.doi.org/10.3390/ijms221910211.

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Primary coenzyme Q10 (CoQ) deficiency includes a heterogeneous group of mitochondrial diseases characterized by low mitochondrial levels of CoQ due to decreased endogenous biosynthesis rate. These diseases respond to CoQ treatment mainly at the early stages of the disease. The advances in the next generation sequencing (NGS) as whole-exome sequencing (WES) and whole-genome sequencing (WGS) have increased the discoveries of mutations in either gene already described to participate in CoQ biosynthesis or new genes also involved in this pathway. However, these technologies usually provide many mutations in genes whose pathogenic effect must be validated. To functionally validate the impact of gene variations in the disease’s onset and progression, different cell models are commonly used. We review here the use of yeast strains for functional complementation of human genes, dermal skin fibroblasts from patients as an excellent tool to demonstrate the biochemical and genetic mechanisms of these diseases and the development of human-induced pluripotent stem cells (hiPSCs) and iPSC-derived organoids for the study of the pathogenesis and treatment approaches.
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6

Parfenova, M. A., I. E. Belousova, and A. V. Samtsov. "Ulceronecrotic Mucha Habermann’s disease: case study." Vestnik dermatologii i venerologii 89, no. 4 (August 15, 2013): 73–78. http://dx.doi.org/10.25208/vdv619.

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The rare dermatosis febrile ulceronecrotic Mucha Gabermann’s disease is described. Etiology, pathogenesis, clinical and pathomorphological criteria of diagnosis, treatment of the disease are discussed. Based on the literature review describes the historical and current data classification of the disease and patient management tactics.
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7

Tsimmerman, Y. S. "Wilson’s disease — hepatocerebral dystrophy." Bulletin of the Club of Pancreatologists 40, no. 2 (June 6, 2018): 54–60. http://dx.doi.org/10.33149/vkp.2018.02.08.

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The article presents a detailed review of modern ideas on Wilson’s disease – hepatocerebral dystrophy. The definition, terminology, history of the study of the disease are stated. Special attention is paid to the analysis of the pathogenesis of hepatocerebral dystrophy, including the genetic basis of its development, the disturbance of copper metabolism. The clinical picture is thoroughly described, taking into account the characteristics of liver lesion and extrahepatic manifestations, diagnostics, classification. Particular attention is paid to the means of pathogenetic and symptomatic treatment.
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8

Virata, M. J., and R. W. Zeller. "Ascidians: an invertebrate chordate model to study Alzheimer's disease pathogenesis." Disease Models & Mechanisms 3, no. 5-6 (March 2, 2010): 377–85. http://dx.doi.org/10.1242/dmm.003434.

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9

Yao, Q., J. Myles, B. Shen, and C. McDonald. "NOD2-associated autoinflammatory disease: an exploratory study of its pathogenesis." Rheumatology 53, no. 5 (November 19, 2013): 958–60. http://dx.doi.org/10.1093/rheumatology/ket384.

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10

Shafik, Ahmed, Ismail Ahmed, Ali A. Shafik, and Olfat El Sibai. "Diverticular Disease: Electrophysiologic Study and a New Concept of Pathogenesis." World Journal of Surgery 28, no. 4 (March 4, 2004): 411–15. http://dx.doi.org/10.1007/s00268-003-7268-1.

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Дисертації з теми "Study the Pathogenesis of a Disease"

1

Cheung, Nga-yin Annie, and 張雅賢. "Pathobiological study of gestational trophoblastic disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31981690.

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Alexopoulou, Zoi. "The study of the deubiquitinase USP8 in Parkinson's disease pathogenesis." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:47c2941b-5232-4bd0-92fa-e59aac16af7c.

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Parkinson's disease is the second commonest neurodegenerative disease currently treated symptomatically. It is a multifactorial disease involving mechanisms ranging from protein aggregation to mitochondrial dysfunction, oxidative stress and dopamine dysregulation. The levels of α-synuclein have been causatively linked to the development and progression of Parkinson's disease. Therefore α-synuclein lowering strategies are valid approaches in Parkinson's disease. Neuropathologically, Lewy Bodies in the vulnerable substantia nigra of Parkinson's disease patients are less ubiquitinated and specifically less K-63 ubiquitinated than Lewy bodies in the cortex, suggesting differential activation or regulation of ubiquitin interactors. A targeted screen for such interactors revealed that the Deubiquitinating enzyme Usp8 is upregulated in the substantia nigra of Parkinson's disease brains and is inversely correlated with the degree of total and K-63 ubiquitination. Using genetic knockdown and overexpression techniques, Usp8 was found to colocalize and directly interact with α-synuclein. It was found to de-ubiquitinate α-synuclein and increase its half-life. Its knockdown increased the total and K-63 α-synuclein ubiquitination and decreased its levels by 35% at least partly by increasing its degradation via the lysosome. In vivo in the Drosophila melanogaster, Usp8 knockdown demonstrated protection against α-synuclein toxicity. It rescued in a specific manner the rough eye phenotype, the age-dependent locomotive defect and the loss of dopaminergic neurons caused by the expression of α-synuclein. Specific and effective pharmacological Usp8 inhibition also has the potential to lower α-synuclein levels. Collectively, the evidence produced in my thesis suggests that Usp8 could be a potential target for the future disease-modifying therapies in Parkinson's disease.
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3

Hofner, Maureen Catherine. "A study of foot-and-mouth disease virus pathogenesis in cattle." Thesis, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338844.

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4

Goldman, Jonathan Howard. "A study of immune mechanisms in the pathogenesis of idiopathic dilated cardiomyopathy." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339209.

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5

Higgins, Damien. "Chlamydial Disease of the Koala: A Study of Pathogenesis and Host Response." Thesis, The University of Sydney, 2004. https://hdl.handle.net/2123/25063.

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Chlamydial infection occurs commonly in koalas (Phascolarctos cinereus) and, as in humans, can cause proliferative conjunctivitis and disease of the urinary and reproductive tracts. Past studies suggest that increased expression of chlamydial disease in koalas is associated with habitats disturbed by humans, but the mechanisms and specific factors influencing susceptibility of koalas to disease have not been studied in detail. This thesis aims to further the goal of describing pathogenic mechanisms and the host-pathogen-environment interaction for chlamydial disease in koalas by developing techniques to begin exploring in koalas some of the concepts that are central to our understanding of this condition in humans. These concepts include the role of T helper 1 (Thl)/ T helper 2 (Th2) lymphocyte balance and interferon gamma, and the association of reproductive tract fibrosis and infertility with serological responses to chlamydial heat shock proteins.
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Thunberg, Therese. "Study of pathogenesis and immune response in human Puumala virus infection." Doctoral thesis, Umeå universitet, Institutionen för klinisk mikrobiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-76706.

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Hantaviruses can cause two severe human diseases: hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS). Hantaviruses are spread to humans mainly through inhalation of infectious virions, secreted from infected rodents. The human diseases are characterized by an increased capillary leakage syndrome. Hantaviruses are known to infect endothelial cells, but they are non-cytopathogenic. The mechanism behind human disease is not well understood, but an overactive immune response is implicated in the pathogenesis. The aim of my thesis has been to investigate parts of innate and adaptive immune responses in Puumala virus-infected patients. In paper I we found a sex difference in the cytokine profile during acute infection. Females had significantly higher plasma levels of IL-9, FGF-2, GM-CSF and lower levels of IL-8 and IP-10 compared to males. These differences may affect the activation and function of the immune response. In paper II we studied the phenotype and kinetics of NK cells. We observed that CD56dim NK cells were elevated during acute infection and that these, predominantly NKG2C+ NK cells, remained elevated for at least two months after symptom debut. Our novel finding of a prolonged NK cell response, implicates that NK cells may possess adaptive immunity features.  In paper III we observed a vigorous cytotoxic T cell (CTL) response during acute infection, which contracted in parallel with decrease in viral load. The CTL response was not balanced by an increase in regulatory T cells. The T cells expressed inhibitory immunoregulatory receptors, known to dampen intrinsic T cell activity.  In paper IV, we found that a low IgG response in patients was significantly associated with more severe disease, while the viral load did not affect the outcome. Our findings support the use of passive immunization as a treatment alternative for hantavirus-infected patients. In conclusion, my thesis contributes to an increased knowledge about the immune response in hantavirus-infected patients. The findings, combined with future studies, will hopefully lead to a better understanding of the pathogenesis and possible treatment alternatives.
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Chen, Liqiong. "The development of a novel in vitro model of human liver for the study of disease pathogenesis." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11020/.

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The development of systems for the long term in vitro culture of functional liver tissue is a major research goal. The central limitation of experimental systems to date has been the early de-differentiation of primary hepatocytes in cultures. Several factors including cell-cell interaction, cell-matrix interaction, soluble factors and 3D structures have been identified as the keys to overcome this limitation. The first aim of this project is to compare the established 3D model, co-culture of hepatocytes and hepatic stellate cells (HSCs) on PDLLA coated surfaces, to other best available systems using collagen and Matrigel. The hypothesis is that hepatocytes functionalities, established by cell-cell interaction, 3D structures and soluble factors, can be further enhanced by introduction of cell-matrix interaction. In order to test the hypothesis, rat hepatocytes were cultured in five different systems, including monoculture of hepatocytes on collagen gel, in collagen-Matrigel sandwich, co-culture of hepatocytes and HSCs on collagen gel, in collagen-Matrigel sandwich and on PDLLA coated surface. Hepatocyte specific function assays, namely albumin secretion, urea secretion, testosterone metabolism by HPLC and CYP activities by LC-MS-MS, were used to analyze cell functionalities. Homo-spheroids were only formed in monoculture on collagen gel, but hetero-spheroids were developed in all the co-culture systems. The results of function assays showed hepatocytes in collagen-Matrigel sandwich configuration had the best secretion of albumin and urea and best CYP activities during the culture period. These data demonstrated the hypothesis that hepatocyte functions of the established model can be further improved by introduction of cell-matrix interaction. In addition to establishment of rat hepatocyte culture systems, hetero-spheroids of primary human hepatocytes and primary human HSCs on PDLLA coated plates were developed successfully, due to the great improvements of isolation and culture of primary human HSCs. However, hepatocyte function assays have not been applied yet. Hepatic cell lines have several advantages that are not applicable to primary cultured human hepatocytes, namely unlimited lifespan and stable phenotype. The immortalized Fa2N-4 cell lines have recently been assessed as replacements of primary human hepatocytes in CYP induction studies. The second aim of this study was to simultaneously characterize CYP1A2, CYP2C9, CYP3A4 and CYP2B6 induction in Fa2N-4 cells through assessment of mRNA, protein and activity endpoints for a range of prototypical compounds (previously assessed in human hepatocytes) with known positive and negative induction potential. LC-MS-MS and RT-PCR were used for assessment of activity and mRNA endpoints respectively. As a result, it is considered that Fa2N-4 cells offer a substitute for primary human hepatocytes for CYP1A2 and CYP3A4 induction but not for CYP2B6 due to lack of cytosolic CAR expression.
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8

Jacob, Ashok J. "A study of the prevalence, pathogenesis and natural history of heart muscle disease associated with HIV infection." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20587.

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Heart muscle disease was found in 14.2% of HIV patients and took three principal forms - dilated cardiomyopathy, borderline left ventricular dysfunction and isolated right ventricular dilation. Dilated cardiomyopathy was associated significantly with a very low CD4 count indicative of late stage HIV disease. It was invariably irreversible. In contrast, some patients with borderline left ventricular dysfunction and isolated right ventricular dilation subsequently reverted to normal. The latter was usually related to pressure or volume overload of the right ventricle rather than to a primary myopathic process. Survival curves were calculated and these showed that HIV patients with dilated cardiomyopathy met a significantly earlier death from an AIDS related condition than those from all the other groups, even after accounting for their low CD4 count. This remained true when patients with dilated cardiomyopathy were matched individually with a group of patients identical in every respect except for the presence of cardiac disease. Heart muscle disease in HIV infection is common and takes a number of forms. Dilated cardiomyopathy occurs in late stage disease, is invariably irreversible and is associated with a particularly poor prognosis. This is in contrast to borderline left ventricular dysfunction and isolated right ventricular dilation which occur at an earlier stage of HIV infection, are potentially reversible and do not carry adverse prognostic implications. Neither infection with Toxoplasma gondii and cytomegalovirus nor treatment with zidovudine appear to have a primary role in the development of heart muscle disease. Although HIV is often found within the myocardium, it does not appear to replicate within this tissue. Low serum selenium concentrations are widespread in HIV patients but do not correlate with cardiac dysfunction.
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9

Brown, Graham Alfred. "A study of bovine herpesvirus 1 pathogenesis using laboratory models." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304239.

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10

Sun, Jun. "Study of neuronal networks and mechanisms implicated in locomotor reactivity and Parkinson's disease pathogenesis in the Drosophila model." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS434.

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La maladie de Parkinson (MP) est un trouble moteur neurodégénératif progressif, caractérisé par la perte des neurones dopaminergiques (DA) de la substance noire et la présence d'inclusions cytoplasmiques composées principalement de synucléine α (syn α), appelées corps de Lewy. Les objectifs de mon travail de thèse étaient de caractériser un modèle de la MP développé chez la drosophile afin de comprendre comment l'accumulation de syn α dans les neurones DA peut perturber progressivement la locomotion et de rechercher de nouvelles protéines neuroprotectrices. Nous avons d'abord identifié des réseaux cérébraux impliqués dans la modulation de la réactivité locomotrice chez la drosophile, qui incluent des sous-ensembles de neurones DA associés aux corps pédonculés. Nous avons ensuite obtenu des évidences que l'expression de la syn α dans les neurones DA perturbe la dynamique mitochondriale à la fois dans ces neurones eux-mêmes et, par un processus non-autonome cellulaire, dans les neurones-cibles cholinergiques des corps pédonculés. Enfin, nous montrons que la protéine Argonaute Piwi est induite par le stress oxydatif et a un effet neuroprotecteur dans un modèle de MP sporadique chez la drosophile. Dans l’ensemble, ces travaux mettent en lumière des mécanismes pathologiques et neuroprotecteurs qui pourraient constituer de nouvelles cibles pour le traitement thérapeutique de la MP
Parkinson's disease (PD) is a progressive neurodegenerative motor disorder, characterized by the loss of dopaminergic neurons from the substantia nigra and the presence of cytoplasmic inclusions composed mainly of α-synuclein (α-syn), called Lewy bodies. The objectives of my thesis work were to characterize a PD model developed in Drosophila in order to understand how the accumulation of α-syn in DA neurons can progressively disturb locomotion and to search for new neuroprotective proteins. We first identified brain networks involved in modulating locomotor reactivity in Drosophila, which include subsets of DA neurons associated with the mushroom bodies. We then obtained evidence that the expression of α-syn in DA neurons disrupts mitochondrial dynamics both in these neurons themselves and, through a non-cell-autonomous process, in their cholinergic target neurons of the mushroom bodies. Finally, we show that the Argonaute Piwi protein is induced by oxidative stress and has a neuroprotective effect in a sporadic PD model in Drosophila. Our evidence suggests that Piwi could delay neuronal aging and PD progression by reducing deleterious transcription of transposable elements. Overall, these studies highlight pathological and neuroprotective mechanisms that may constitute novel targets for the therapeutic treatment of PD
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Книги з теми "Study the Pathogenesis of a Disease"

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Anorexia and its impact upon cachexia in cancer disease: A study with emphasis on the multifactorial pathogenesis and consequences of impaired feeding behavior. Amsterdam: Rodopi, 1985.

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2

Kim, Ŭng-gwŏn. Abellino kangmak iyŏngyangchŭng ŭi pyŏngin palgyŏn mit chʻiryopŏp kaebal =: A study for the identification of pathogenesis and treatment of Avellino corneal dystrophy. [Seoul]: Pogŏn Pokchibu, 2007.

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3

H, Thiers Bruce, and Dobson Richard L, eds. Pathogenesis of skin disease. New York: Churchill Livingstone, 1986.

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4

Hanneke, Schuitemaker, and Miedema F, eds. AIDS pathogenesis. Dordrecht: Kluwer Academic, 2000.

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5

Snape, William J., ed. Pathogenesis of Functional Bowel Disease. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5694-3.

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6

Murray, Dawson Ted, ed. Parkinson's disease: Genetics and pathogenesis. New York: Informa Healthcare, 2007.

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7

J, Snape William, ed. Pathogenesis of functional bowel disease. New York: Plenum Medical Book Co., 1989.

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8

Plant pathogenesis and disease control. Boca Raton, FL: Lewis Publishers, 1994.

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9

Crohn's disease: Treatment and pathogenesis. Boca Raton, Fla: CRC Press, 1987.

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10

N, Cadwallader Jack, ed. Crohn's disease: Etiology, pathogenesis & interventions. New York: Nova Science Publishers, 2008.

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Частини книг з теми "Study the Pathogenesis of a Disease"

1

Sahai, Seema, Richa Goel, Mashiur Rahman, and Sachi Nandan Mohanty. "Technology Acceptance Using COVID-19 Pandemic: Case Study of Health Sector in India." In Medical Virology: From Pathogenesis to Disease Control, 421–41. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-7317-0_21.

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2

Hatami, Asa, and Marie-Francoise Chesselet. "Transgenic Rodent Models to Study Alpha-Synuclein Pathogenesis, with a Focus on Cognitive Deficits." In Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease, 303–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/7854_2014_355.

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3

Goel, Richa, and Seema Sahai. "Can Technology Fight the Loneliness Lockdown: A Study of Factors Affecting Loneliness in NCR During COVID-19." In Medical Virology: From Pathogenesis to Disease Control, 477–98. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-7317-0_25.

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4

Swain, Sukanta Chandra. "Psycho-economic Impact of Obligatory Job Switching During Covid-19 Pandemic: A Study of Hawkers in Bhubaneswar (India)." In Medical Virology: From Pathogenesis to Disease Control, 499–510. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-7317-0_26.

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5

Jeffries, Matlock A. "The Development of Epigenetics in the Study of Disease Pathogenesis." In Advances in Experimental Medicine and Biology, 57–94. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-3449-2_2.

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Sahoo, Sanjaya Kumar, and Sukanta Chandra Swain. "Impact of Repatriated Migrants on the Production Possibility of Agricultural Sector Owing to Covid: A Study on the Basis of Inferential Statistics." In Medical Virology: From Pathogenesis to Disease Control, 553–67. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-7317-0_29.

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Inui, K., J. Nishimoto, M. Taniike, M. Midorikawa, H. Tsukamoto, S. Okada, and H. Yabuuchi. "Study of Pathogenesis in Twitcher Mouse, an Enzymatically Authentic Model of Human Krabbe’s Disease." In Studies in Inherited Metabolic Disease, 383–85. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1069-0_58.

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Gutierrez-Barbosa, Hernando, Sandra Medina-Moreno, Harry Davis, Joseph Bryant, Joel V. Chua, and Juan C. Zapata. "Humanized Mice for the Study of Dengue Disease Pathogenesis: Biological Assays." In Methods in Molecular Biology, 271–89. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1879-0_19.

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Epstein, C. J. "Trisomic and Transgenic Mice in the Study of the Pathogenesis of Alzheimer’s Disease and Down’s Syndrome." In Genetics and Alzheimer’s Disease, 95–108. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73647-6_9.

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Ahanger, Ishfaq Ahmad, Anurag Sharma, and Asimul Islam. "The Pathogenesis and Complications Associated with Autism Spectrum Disorder and Alzheimer’s Disease: A Comparative Study." In Autism Spectrum Disorder and Alzheimer's Disease, 43–61. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4558-7_3.

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Тези доповідей конференцій з теми "Study the Pathogenesis of a Disease"

1

Li, Xiaolu, Rong Cao, Fangfei Xiao, Lin Ye, Xufei Wang, and Yizhong Wang. "IDDF2023-ABS-0233 The study of molecular pathogenesis of pediatric clostridiodes difficile infection." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 10–11 June 2023. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2023. http://dx.doi.org/10.1136/gutjnl-2023-iddf.209.

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Wolff, Martin, Natalia El-Merhie, Sebastian Reuter, Torsten Goldmann, Ali Önder Yildirim, Heinz Fehrenbach, and Susanne Krauss-Etschmann. "Relevant murine model to study the development of COPD pathogenesis in smokers with viral infections." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp109.

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Bakhshaliyeva, Afet, and Arif Mekhtiev. "STUDY OF THE ROLE OF DIHYDROPYRIMIDINASE-RELATED PROTEIN 2 IN THE PATHOGENESIS OF ALZHEIMER'S DISEASE." In XIX INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2023. http://dx.doi.org/10.29003/m3173.sudak.ns2023-19/53.

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Bély, M., T. Szentjóbi Szabó, P. Kapp, Á. Apáthy, M. Stancikova, and R. Istok. "AB0108 Complications and formal pathogenesis of progressive systemic sclerosis. a retrospective study." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.256.

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5

Sun, Ling, and Philippe Sucosky. "Contribution of Hemodynamic Shear Stress Magnitude and Frequency Abnormalities to Calcific Aortic Valve Disease Pathogenesis." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14377.

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Calcific aortic valve disease (CAVD) is an active process presumably triggered by interplays between atherogenic risk factors, molecular signaling networks and hemodynamic cues. While our earlier work demonstrated that progressive alterations in fluid shear stress (FSS) on the fibrosa could trigger valvular inflammation [1], the mechanisms of CAVD pathogenesis secondary to side-specific FSS abnormalities are poorly understood. Supported by our previous studies, we hypothesize that valve leaflets are sensitive to both WSS magnitude and pulsatility and that abnormalities in either promote CAVD development. This study aims at elucidating ex vivo the contribution of isolated and combined alterations in FSS magnitude and pulsatility to valvular calcification.
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Sun, Ling, Santanu Chandra, and Philippe Sucosky. "Role of Hemodynamic Shear Stress Abnormalities in the Early Pathogenesis of Bicuspid Aortic Valve Calcification." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14079.

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With a prevalence of 1.3 million cases in the United States, the bicuspid aortic valve (BAV) is the most common congenital cardiac anomaly and is frequently associated with calcific aortic valve disease (CAVD) [1]. The most prevalent type-I morphology, which results from left-/right-coronary cusp fusion, generates different hemodynamics than a tricuspid aortic valve (TAV). While valvular calcification has been linked to genetic and atherogenic predispositions, hemodynamic abnormalities are increasingly pointed as potential pathogenic contributors [2–3]. In particular, the wall shear stress (WSS) produced by blood flow on the leaflets regulates homeostasis in the TAV. In contrast, WSS alterations cause valve dysfunction and disease [4]. While such observations support the existence of synergies between valvular hemodynamics and biology, the role played by BAV WSS in valvular calcification remains unknown. The objective of this study was to isolate the acute effects of native BAV WSS abnormalities on CAVD pathogenesis.
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Lezhniova, Vera Runarovna, Ekaterina Vladimirovna Martynova, Timur Il'dusovich Khaibullin, Ilnur Il'dusovich Salafutdinov, Mariia Ivanovna Markelova, Aleksandr Vladimirovich Laikov, Leonid Valentinovich Lopukhov, and Svetlana Frantsevna Khaibullina. "Seasonal changes in serum metabolite and cytokine levels in Multiple Sclerosis." In All-Russian scientific conference with International Participation. Publishing house Sreda, 2022. http://dx.doi.org/10.31483/r-102302.

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Multiple sclerosis (MS) is a chronic debilitating disease of unknown etiology. The disease has a seasonal exacerbation of clinical symptoms, which are frequently described in spring and summer. However, the mechanisms of such seasonal exacerbations remain unknown. In this study, we used targeted metabolomics analysis of serum samples using LC-MC/MC to determine seasonal changes in metabolites. We have found changes in multiple metabolites which differed depending on season. The ceramides, belonging to the sphingolipid pathway, were found activated in spring-summer (SS) and fall-winter (FW) MS, suggesting their central role in disease pathogenesis. Our identification of ceramide activation suggests a mechanism of neuron damage in MS which could be further investigated as therapeutic targets.
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Grigoli, Marina, Danielle de Oliveira, Paloma Zanarelli, Patrícia Manzine, and Márcia Cominetti. "INSULIN PATHWAY PROTEINS ARE ALTERED IN PATIENTS WITH CONCOMITANT ALZHEIMER’S DISEASE AND DIABETES MELLITUS." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda001.

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Background: Alterations in the insulin pathway proteins have been associated with brain disorders, including Alzheimer’s disease (AD). Objectives: To investigate the peripheral levels of the insulin pathway proteins between cognitively and metabolically preserved participants, patients with DM2, AD and those with the concomitant presence of AD and DM2. Methods: The study was approved by the UFSCar’s ethics committee (CAAE: 31634720.9.0000.5504). Patients were diagnosed with AD using the criteria of the National Institute on Aging/Alzheimer’s Association (NIA/AA). DM2 was defined as self-report of taking oral antidiabetic medication. Plasma was collected by venipuncture from 36 participants. The levels of the of following proteins were analyzed by ELISA (Enzyme Enzyme-Linked Immunosorbent Assay): ISNR, IGF1R, IGF, IRS1, Akt1/PKB, PI3KCD/PI3Kdelta, MAPK1/ERK2, MAPK8/JNK1, PTP1B and IDE (Life-Span Biosciences). Results: Several proteins of the insulin pathway were altered in patients with AD, DM2 and AD+DM2, compared to healthy controls, reinforcing the strong correlation between DM2 and AD. Conclusions: This study shows peripheral alterations in the insulin signaling pathway proteins, confirming the relation between DM2 and AD and pointing out the importance of characterizing in detail the insulin signaling pathways, as they may play a key role in the pathogenesis of AD.
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Maher, Eoghan, Arthur Creane, Sherif Sultan, Niamh Hynes, Caitríona Lally, and Daniel J. Kelly. "Mechanical Characterization of Fresh Human Carotid Atherosclerotic Plaque." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206271.

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Quantifying the properties of atherosclerotic plaques is critical to improving our understanding of the pathogenesis of the disease. Furthermore realistic tissue properties are vital in order to obtain legitimate results from finite element models of surgical interventions used to treat cardiovascular disease. The aim of this study is to determine the mechanical properties of fresh human carotid plaques immediately following removal during endarterectomy. A number of studies have reported atherosclerotic plaque properties previously [1–3], however all of these tested cadaveric tissue. This study will further investigate in-patient and inter-patient variability, the relationship between plaque properties and their clinical classification (calcified, mixed or echolucent) and the location of the sample (common, internal, external carotid).
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Jorge, Frederico Mennucci de Haidar, Angela Genge, Ammar Al Chalabi, Orla Hardiman, Alice Shen, Jennifer Shoskes, and David Weinstein. "MERIDIAN: A phase 2, randomized, double-blind, placebo-controlled, multicenter study to evaluate the efficacy and safety of pegcetacoplan in patients with amyotrophic lateral sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.744.

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Introduction: Inflammation underlies the pathogenesis of numerous neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). In ALS, the complement system has been implicated in the neuropathology of disease and disease progression. Pegcetacoplan, a subcutaneously administered C3 complement inhibitor, is being investigated in hematology, nephrology, and neurology. The current clinical study (NCT04579666) is investigating whether pegcetacoplan can improve survival and function in people diagnosed with apparent sporadic ALS. Objectives and Methodology: Evaluate the efficacy and safety of pegcetacoplan compared to placebo among people diagnosed with ALS in a global, multicenter, randomized, double-blind, placebo-controlled, phase 2 study. Approximately 228 patients diagnosed with apparent sporadic ALS, ≥18 years of age and with an ALS Functional Rating Scale-Revised (ALSFRS-R) score ≥30, slow vital capacity (SVC) ≥60% of the predicted value at screening, and with symptom onset within 72 weeks before screening, are eligible for enrollment. After screening, patients will be randomized 2:1 to treatment groups receiving either subcutaneous pegcetacoplan (1080 mg) or placebo twice weekly for a duration of 52 weeks. The primary efficacy endpoint is the difference in the Combined Assessment of Function and Survival (CAFS) ranked score at 52 weeks after treatment initiation. Additional, secondary functional efficacy (ALSFRS-R, percent SVC, muscle strength, quality of life, and caregiver burden) and safety endpoints will be analyzed at 52 weeks. After the placebo-controlled period, all patients will have the option to receive pegcetacoplan in an open-label period for an additional 52 weeks. Results: This ongoing study is currently enrolling participants. Conclusions: Results of this study will determine the role of complement and C3 inhibition in patients with ALS.
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Звіти організацій з теми "Study the Pathogenesis of a Disease"

1

Yogev, David, Ricardo Rosenbusch, Sharon Levisohn, and Eitan Rapoport. Molecular Pathogenesis of Mycoplasma bovis and Mycoplasma agalactiae and its Application in Diagnosis and Control. United States Department of Agriculture, April 2000. http://dx.doi.org/10.32747/2000.7573073.bard.

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Mycoplasma bovis and M. agalactiae are two phylogenetically related mycoplasmas which cause economically significant diseases in their respective bovine or small ruminant hosts. These organisms cause persistent asymptomatic infections that can result in severe outbreaks upon introduction of carrier animals into susceptible herds. Little is known about the mechanisms underlying mycoplasma-host interaction, variation in virulence, or of the factors enabling avoidance of the host immune system. In recent years it has become apparent that the ability of pathogenic microorganisms to rapidly alter surface antigenic structures and to fine tune their antigenicity, a phenomena called antigenic variation, is one of the most effective strategies used to escape immune destruction and to establish chronic infections. Our discovery of a novel genetic system, mediating antigenic variation in M. bovis (vsp) as well as in M. agalactiae (avg) served as a starting point for our proposal which included the following objectives: (i) Molecular and functional characterization of the variable surface lipoproteins (Vsp) system of M. bovis and comparison with the Vsp-counterpart in M. agalactiae (ii) Determination of the role of Vsp proteins in the survival of M. bovis when confronted by host defense factors, (iii) Assessment of Vsp-based genetic and antigenic typing of M. bovis and M. agalactiae for epidemiology of infection and (iv) Improvement of diagnostic tests for M. bovis and M. agalactiae based on the vsp-and vsp-analogous systems. We have carried out an extensive molecular characterization of the vsp system and unravelled the precise molecular mechanism responsible for the generation of surface antigenic variation in M. bovis. Our data clearly demonstrated that the two pathogenic mycoplasma species possess large gene families encoding variable lipoprotein antigens that apparently play an important role in immune evasion and in pathogen-host interaction during infection. Phase variable production of these antigens was found to be mediated by a novel molecular mechanism utilizing double site-specific DNA inversions via an intermediate vsp configuration. Studies in model systems indicate that phase variation of VspA is relevant in interaction between M. bovis and macrophages or monocytes, a crucial stage in pathogenesis. Using an ELISA test with captured VspA as an antigen, phase variation was shown to occur in vivo and under field conditions. Genomic rearrangements in the avg gene family of M. agalactiae were shown to occur in vivo and may well have a role in evasion of host defences and establishment of chronic infection. An epidemiological study indicated that patterns of vsp-related antigenic variation diverge rapidly in an M. bovis infected herd. Marked divergence was also found with avg-based genomic typing of M. agalactiae in chronically infected sheep. However, avg-genomic fingerprints were found to be relatively homogeneous in different animals during acute stages of an outbreak of Contagious Agalactiae, and differ between unrelated outbreaks. These data support the concept of vsp-based genomic typing but indicate the necessity for further refinement of the methodology. The molecular knowledge on these surface antigens and their encoding genes provides the basis for generating specific recombinant tools and serological methods for serodiagnosis and epidemiological purposes. Utilization of these methods in the field may allow differentiating acutely infected herds from chronic herds and disease-free herds. In addition the highly immunogenic nature of these lipoproteins may facilitate the design of protective vaccine against mycoplasma infections.
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Sordillo, Lorraine, Don Wojchowski, Gary Perdew, Arthur Saran, and Gabriel Leitner. Identification of Staphylococcus aureaus Virulence Factors Associated with Bovine Mastitis. United States Department of Agriculture, February 2001. http://dx.doi.org/10.32747/2001.7574340.bard.

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Staphylococcus aureus is a major cause of mastitis in dairy cattle. The organism is able to adhere to and penetrate mammary epithelium, forming deep seated abscesses that result in chronic infections. This study was based on the observation that certain genotypes of S. aureus are isolated more frequently from field cases of bovine mastitis than others and the most prevalent genotypes of S. aureus have an increased ability to resist neutrophil phagocytosis and killing compared to the rare variants. It was hypothesized that these predominating genotypes differentially express virulence factors that allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. The overall objective of this study was to determine the mechanisms by which predominating S. aureus genotypes were able to resist mammary gland defense mechanisms. The following specific aims were accomplished to address the overall objectives of this project: 1. Analyze and compare cell surface and secreted protein profiles of common and rare S. aureus genotypes isolated from field cases of bovine mastitis. 2. Purify and sequence selectively synthesized proteins unique to the most prevalent genotypes of S. aureus . 3. Determine the in vitro effects of isolated proteins on essential host defense mechanisms. Results from each specific aim showed that these redominating genotypes differentially express factors that may allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. Using complementary approaches, both the US and Israeli teams identified differentially expressed S. aureus factors that were positively correlated with virulence as determined by the ability to modify host immune cell responses and increase disease pathogenesis. Several candidate virulence factors have ben identified at both the molecular (US team) and protein (Israeli team) levels. Components of the phosphotransferase system were shown to be differentially expressed in prevalent strains of S. aureus and to modify the growth potential of these strains in a milk microenvironment. Evidence provided by both the Israeli and US teams also demonstrated a potential role of Staphylococcal enterotoxins in the pathogenesis of mastitis. Certain enterotoxins were shown to directly affect neutrophil bactericidal activities which can profoundly affect the establishment of new intramammary infections. Other evidence suggests that S. aureus superantigens can suppress mammary defenses by enhancing lymphoid suppressor cell activity. Collectively, these data suggest that unique factors are associated with predominating S. aureus genotypes that can affect in vitro and in vivo virulence as related to the pathogenesis of bovine mastitis. The potential development of a subunit mastitis vaccine which incorporates only relevant antigenic determinants has not been investigated in depth. Experiments outlined in this proposal has identified putative virulence factors which contribute to the pathogenesis of S. aureus mastitis and which may be used to formulate an efficacious subunit mastitis vaccine. Results from these studies may lead to the development of new methods to prevent this costly disease, providing a viable alternative to less effective mastitis control procedures based on chemotherapy.
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Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.
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4

Young, Alan J. Migratory Leukocytes in the Pathogenesis and Diagnosis of Prion Disease. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada426355.

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Glorioso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada397751.

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Gloricso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada407633.

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Glorioso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, December 1999. http://dx.doi.org/10.21236/ada375299.

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Glorioso, Joseph C. Gene Transfer Studies of the Pathogenesis and Treatment of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada383307.

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Shpigel, Nahum, Raul Barletta, Ilan Rosenshine, and Marcelo Chaffer. Identification and characterization of Mycobacterium paratuberculosis virulence genes expressed in vivo by negative selection. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7696510.bard.

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Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of a severe inflammatory bowel disease (IBD) in ruminants, known as Johne’s disease or paratuberculosis. Johne’s disease is considered to be one of the most serious diseases affecting dairy cattle both in Israel and worldwide. Heavy economic losses are incurred by dairy farmers due to the severe effect of subclinical infection on milk production, fertility, lower disease resistance and early culling. Its influence in the United States alone is staggering, causing an estimated loss of $1.5 billion to the agriculture industry every year. Isolation of MAP from intestinal tissue and blood of Crohn's patients has lead to concern that it plays a potential pathogenic role in promoting human IDB including Crohn’s disease. There is great concern following the identification of the organism in animal products and shedding of the organism to the environment by subclinically infected animals. Little is known about the molecular basis for MAP virulence. The goal of the original proposed research was to identify MAP genes that are required for the critical stage of initial infection and colonization of ruminants’ intestine by MAP. We proposed to develop and use signature tag mutagenesis (STM) screen to find MAP genes that are specifically required for survival in ruminants upon experimental infection. This research projected was approved as one-year feasibility study to prove the ability of the research team to establish the animal model for mutant screening and alternative in-vitro cell systems. In Israel, neonatal goat kids were repeatedly inoculated with either one of the following organisms; MAP K-10 strain and three transposon mutants of K-10 which were produced and screened by the US PI. Six months after the commencement of inoculation we have necropsied the goats and taken multiple tissue samples from the jejunum, ileum and mesenteric lymph nodes. Both PCR and histopathology analysis indicated on efficient MAP colonization of all the inoculated animals. We have established several systems in the Israeli PI’s laboratory; these include using IS900 PCR for the identification of MAP and using HSP65-based PCR for the differentiation between MAV and MAP. We used Southern blot analysis for the differentiation among transposon mutants of K-10. In addition the Israeli PI has set up a panel of in-vitro screening systems for MAP mutants. These include assays to test adhesion, phagocytosis and survival of MAP to/within macrophages, assays that determine the rate of MAPinduced apoptosis of macrophages and MAP-induced NO production by macrophages, and assays testing the interference with T cell ã Interferon production and T cell proliferation by MAP infected macrophages (macrophage studies were done in BoMac and RAW cell lines, mouse peritoneal macrophages and bovine peripheral blood monocytes derived macrophages, respectively). All partners involved in this project feel that we are currently on track with this novel, highly challenging and ambitious research project. We have managed to establish the above described research systems that will clearly enable us to achieve the original proposed scientific objectives. We have proven ourselves as excellent collaborative groups with very high levels of complementary expertise. The Israeli groups were very fortunate to work with the US group and in a very short time period to master numerous techniques in the field of Mycobacterium research. The Israeli group has proven its ability to run this complicated animal model. This research, if continued, may elucidate new and basic aspects related to the pathogenesis MAP. In addition the work may identify new targets for vaccine and drug development. Considering the possibility that MAP might be a cause of human Crohn’s disease, better understanding of virulence mechanisms of this organism might also be of public health interest as well.
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Bacharach, Eran, and Sagar Goyal. Generation of Avian Pneumovirus Modified Clones for the Development of Attenuated Vaccines. United States Department of Agriculture, November 2008. http://dx.doi.org/10.32747/2008.7696541.bard.

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Abstract (one page maximum, single spaced), include: List the original objectives, as defined in the approved proposal, and any revisions made at the beginning or during the course of project: The main goal described in our original proposal has been the development of a molecular infectious clone of the avian metapneumovirus subtype B (aMPV-B) and the modification of this clone to create mutated viruses for the development of attenuated vaccines. The Achievements and Appendix/Part I sections of this report describes the accomplishments in creating such a molecular clone. These sections also contain the results of a longitudinal study that we made in Israel, demonstrating the infiltration of field strains of aMPV into vaccinated flocks and emphasizing the need for the development of better vaccines. We also describe our unexpected findings regarding the ability of aMPV to establish persistent infection in cell cultures. Although this direction of research was not described in the original proposal we feel that it is highly important for the understanding of aMPV pathogenesis. For example, this direction has provided us with evidence showing that aMPV replication can augment influenza replication. Moreover, we observed that viruses that were produced from chronically-infected cells show reduced ciliostasis. Accordingly, we carried vaccination trials using such viruses. In the original grant proposal we also offered that the American lab will clone and express immunomodulators in the context of an aMPV -based replicon that the Israeli lab has generated. However, as we reported in our annual reports, further analysis of this replicon by the Israeli lab has revealed that the level of expression achieved by this vehicle is relatively poor; thus, the American lab has focused on sequencing the genomes of different aMPV-C isolates that differ in their virulence (including vaccine strains). Achievements and Appendix/Part II sections of this report include the summary of this effort. Background to the topic: The aMPVs belong to the paramyxoviridae family and cause mild to severe respiratory tract diseases mainly in turkeys and also in chickens. Four aMPV subgroups, A, B, C and D, have been characterized; in Israel aMPV-A and B are the common subtypes while in the USA type C is the prevalent one. Although vaccine strains do exist for aMPVs, they do not always provide full protection against virulent strains and the vaccines themselves may induce disease to some extent. Improved vaccines against aMPV are needed, to achieve better protection of the poultry industry against this pathogen. Major conclusions, solutions, achievements: We isolated aMPV-B from a diseased flock and accomplished the sequencing and cloning of its full-genome. In addition, we cloned the four genes encoding the viral replicase. These should serve as the platform for generation of modified aMPV-Bs from molecular clones. We also identified aMPVs that are attenuated in respect to their ciliostatic activity and accordingly showed the potential of such viruses as vaccine strains. For aMPV-C, the different mutations scattered along the genome of different isolates with varied virulence have been determined. Implications, both scientific and agricultural: The newly identified pattern of mutations in attenuated strains will allow better understanding of the pathogenicity of aMPV and the generation of aMPV molecular clones, together with isolation of strains with attenuated ciliostatic activity should generate improved vaccine strains Abstract (one page maximum, single spaced), include: List the original objectives, as defined in the approved proposal, and any revisions made at the beginning or during the course of project: The main goal described in our original proposal has been the development of a molecular infectious clone of the avian metapneumovirus subtype B (aMPV-B) and the modification of this clone to create mutated viruses for the development of attenuated vaccines. The Achievements and Appendix/Part I sections of this report describes the accomplishments in creating such a molecular clone. These sections also contain the results of a longitudinal study that we made in Israel, demonstrating the infiltration of field strains of aMPV into vaccinated flocks and emphasizing the need for the development of better vaccines. We also describe our unexpected findings regarding the ability of aMPV to establish persistent infection in cell cultures. Although this direction of research was not described in the original proposal we feel that it is highly important for the understanding of aMPV pathogenesis. For example, this direction has provided us with evidence showing that aMPV replication can augment influenza replication. Moreover, we observed that viruses that were produced from chronically-infected cells show reduced ciliostasis. Accordingly, we carried vaccination trials using such viruses. In the original grant proposal we also offered that the American lab will clone and express immunomodulators in the context of an aMPV -based replicon that the Israeli lab has generated. However, as we reported in our annual reports, further analysis of this replicon by the Israeli lab has revealed that the level of expression achieved by this vehicle is relatively poor; thus, the American lab has focused on sequencing the genomes of different aMPV-C isolates that differ in their virulence (including vaccine strains). Achievements and Appendix/Part II sections of this report include the summary of this effort. Background to the topic: The aMPVs belong to the paramyxoviridae family and cause mild to severe respiratory tract diseases mainly in turkeys and also in chickens. Four aMPV subgroups, A, B, C and D, have been characterized; in Israel aMPV-A and B are the common subtypes while in the USA type C is the prevalent one. Although vaccine strains do exist for aMPVs, they do not always provide full protection against virulent strains and the vaccines themselves may induce disease to some extent. Improved vaccines against aMPV are needed, to achieve better protection of the poultry industry against this pathogen. Major conclusions, solutions, achievements: We isolated aMPV-B from a diseased flock and accomplished the sequencing and cloning of its full-genome. In addition, we cloned the four genes encoding the viral replicase. These should serve as the platform for generation of modified aMPV-Bs from molecular clones. We also identified aMPVs that are attenuated in respect to their ciliostatic activity and accordingly showed the potential of such viruses as vaccine strains. For aMPV-C, the different mutations scattered along the genome of different isolates with varied virulence have been determined. Implications, both scientific and agricultural: The newly identified pattern of mutations in attenuated strains will allow better understanding of the pathogenicity of aMPV and the generation of aMPV molecular clones, together with isolation of strains with attenuated ciliostatic activity should generate improved vaccine strains.
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