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     <title><![CDATA[NUST Institutions Library Catalogue Search for 'kw,wrdl: (su-br:&quot;Degeneration&quot;)']]></title>
     <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?idx=kw&amp;q=%28su-br%3A%22Degeneration%22%29&amp;format=rss</link>
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     <description><![CDATA[ Search results for 'kw,wrdl: (su-br:&quot;Degeneration&quot;)' at NUST Institutions Library Catalogue]]></description>
     <opensearch:totalResults>5</opensearch:totalResults>
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     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
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     <item>
       <title>
    Five faces of modernity :


    modernism, avant-garde, decadence, kitsch, postmodernism /





</title>
       <dc:identifier>ISBN:0822307677 (paperback) | 9780822307679 (paperback)</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=14737</link>
        
       <description><![CDATA[









	   <p>By Calinescu, Matei.. 
	   [S.l.] : Duke University Press Books, 1987
                        . 422 p. ;
                        
                         21 cm.. 
                         0822307677 (paperback) | 9780822307679 (paperback)
       </p>

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						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=14737</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Persia in crisis :


    safavid decline and the fall of isfahan /





</title>
       <dc:identifier>ISBN:184511745X (hardcover) | 9781845117450 (hardcover)</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=15843</link>
        
       <description><![CDATA[









	   <p>By Matthee, Rudi.. 
	   [S.l.] : I. B. Tauris, 2011
                        . 336 p. ;
                        
                         25 cm.. 
                         184511745X (hardcover) | 9781845117450 (hardcover)
       </p>

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						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=15843</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
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     <item>
       <title>
    Effectivity of Rutin-bound Carbon dots in preventing the aggregation of Amyloid beta /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608744</link>
        
       <description><![CDATA[









	   <p>By Noor Afza. 
	   
                        . 78p.
                        , According to the World Health Organization up to 55 million people have dementia
resulting in concerning socio-economic implications. About 60-80% cases of dementia are
associated with Alzheimer's disease. With all the advances in medicine, there still is no cure.
Blood-brain barrier monitors the entry and exit of nutrients and molecules which makes it
difficult for various drugs and therapeutic molecules to cross it. Carbon dots are made from
glucose to overcome the BBB. Rutin is a naturally existing flavonoid extracted from plants
and has therapeutic effects in neuroprotection. This study aims to improve the effectiveness
of rutin combined with targeted delivery of carbon dots. Carbon dots were loaded with Rutin
to make CD-Rutin, a nano-sized combination with a targeted drug. FTIR, UV-IR, and SEM
analysis have produced positive results regarding the doping of CDs with Rutin.
Administration of CD-Rutin was done in AD-like rat models at eight to twelve months of age.
Alzheimer's was induced in rats with Aluminum Chloride and D-galactose through IP
administration for two weeks. Behavioral tests were performed to check the progression of
the disease. In silico analysis was also done to check ligand-protein interaction to check
variation in the binding of Aβ isoforms with Rutin. Afterward, a single injection of CD-Rutin
(10 mg/kg) was given intraperitoneally as well. Behavioral testing was done after the
administration of the drug. Characterization techniques revealed the successful formation of
CDs and subsequent loading of Rutin onto the CDs resulting in a CD-Rutin combination. In
silico analysis provided strong binding affinities of Rutin with Aβ isoforms affirming Rutin
as a favorable treatment to target amyloid aggregates. 3D configuration showed binding of
Rutin with hydrophobic domains of protein oligomers Behavioral testing provided significant
difference in the treated group with better memory retention and performance in activities
involved in behavioral testing. After behavioral testing, rats were dissected for molecular
analysis including H&amp;E to assess cell degeneration and Thioflavin T staining to assess
amyloid aggregates in the brain tissues. Results provided positive data in terms of cell count
in the cortex. Overall results suggest that memory impairment and cognitive abilities were
significantly improved after injections. The results demonstrate the positive therapeutic
potential of CD-Rutin in Alzheimer's treatment.
                         30cm. 
                        
       </p>

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						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608744</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
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       <title>
    Investigating Chrysoeriol-Mediated Protection in MPTP-Induced Mouse Model of Parkinson's Disease /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=611348</link>
        
       <description><![CDATA[









	   <p>By Ali ,Mehak. 
	   
                        . 105p. ;
                        , Parkinson's disease (PD) is a neurodegenerative condition characterized by the progressive loss of dopamine-producing neurons in the substantia nigra pars compacta, which results in severe motor impairments. While the precise cause of PD remains unknown, research indicates that factors such as oxidative stress, mitochondrial dysfunction, and the triggering of apoptotic pathways play key roles in the degeneration of these neurons. Current treatments focus on stabilizing dopamine levels but do not halt disease progression. Therefore, exploring compounds that can mitigate apoptotic neuronal loss is promising for therapy. Chrysoeriol, a 3’-O-methoxy flavone and luteolin derivative, is known for its anti-cancer, anti-diabetic, antioxidant, anti-inflammatory, and neuroprotective properties. Despite extensive research, its effect on PD mouse models is still unclear. This study examines the neuroprotective effects of 5 mg/kg of Chrysoeriol administered intraperitoneally for 14 days in an in vivo sub-acute PD model, established using 20 mg/kg MPTP administered via intraperitoneal injections at two-hour intervals for a total of four doses in one day. Behavioral tests, including the Pole test, Y-maze test, forced swim test, and tail suspension test, showed significant recovery from PD-induced neurological deficits in Chrysoeriol-treated mice. Hematoxylin and Eosin staining confirmed reduced neuronal damage in Chrysoeriol-treated mice in different areas of the brain, including the midbrain, cerebellum, cortex, and hippocampus. qPCR analysis was used to detect the relative expression of α-Synuclein, Bcl-2 (anti-apoptotic) and Bax (pro-apoptotic) proteins. The levels of α-synuclein, a major protein implicated in PD pathology, were significantly downregulated in the treatment group compared to the diseased group, indicating that Chrysoeriol plays a role in the downregulation of α-synuclein. Moreover, in the diseased group, Bax levels were up-regulated, and Bcl-2 levels were downregulated, reducing the Bcl-2/Bax ratio. Chrysoeriol treatment significantly reversed this downregulation. Our results demonstrated that Chrysoeriol treatment significantly reduced MPP+- induced toxicity, downregulated α-synuclein expression levels, and improved Bcl-2/Bax ratio expression levels in in vivo mouse models. Our research indicates that Chrysoeriol offers protection against MPP+-induced apoptosis in mice by activating the PI3K/Akt signaling pathway. This finding suggests that Chrysoeriol could be a promising therapeutic option for PD.
                         30cm.. 
                        
       </p>

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						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=611348</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
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       <title>
    Investigating the Neuroprotective Effects of Chenodeoxycholic Acid in MPTP-induced Parkinson’s disease in BALB/c mice /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=611349</link>
        
       <description><![CDATA[









	   <p>By Mehreen ,Mehwish. 
	   
                        . 77p. ;
                        , Parkinson's disease (PD) remains a major challenge in the field of neurodegenerative diseases and requires innovative therapeutic approaches. In this study, we investigated the therapeutic potential of chenodeoxycholic acid (CDCA) in PD using a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model. CDCA, a naturally occurring bile acid, has previously shown promise in various neurological disorders by reducing neuronal degeneration and promoting neuronal health, however its utility in PD has not been studied. Mice were divided into a control group, an MPTP-induced PD model (20 mg/kg, intraperitoneally) and a treatment group injected intraperitoneally with CDCA (90 mg/kg). CDCA reduced motor impairment and ameliorated anxiety-like behavior as assessed by the pole test and open field test, demonstrated antidepressant effects in the forced swim test and tail suspension test, and results of the Y-maze test showed improved cognitive performance. Furthermore, the effective defense against MPTP-induced dopaminergic degeneration was provided by CDCA through improving the morphological and histological features of neurons in the midbrain, hippocampus, cortex and cerebellum. Additionally, the biomarkers used in this study are brain-derived neurotrophic factor (BDNF) and α-synuclein. Hence, treatment with CDCA significantly mitigated MPTP-induced elevations in α- synuclein levels, indicating that it may have potential to preserve and recover neuronal function. Moreover, the neurotrophic role of CDCA was demonstrated by improving the low levels of BDNF in the presence of MPTP. The results of this study promise valuable insights into the potential therapeutic properties of CDCA in reducing the effects of PD and provide a basis for further research into bile acid-based treatments in neurodegenerative diseases.
                         30cm.. 
                        
       </p>

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						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=611349</guid>
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