1,354,501 research outputs found
Life and Works of Šemʿōn d-Taibūtēh (7th century): A Tentative Reconstruction
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198845.pdf (Publisher’s version ) (Open Access)Radboud University, 11 december 2018Promotores : Teule, H.G.B., Tamcke, H.C
A Comparison of Radiographic and Scintigraphic Techniques to Assess Aseptic Loosening of a Total Hip Prosthesis
Teule, G.J.J. [Promotor]Heyligers, I.C. [Copromotor]Raijmakers, P.G.H.M. [Copromotor
Uchunguzi wa Sababu za Mwitiko wa Hadhira Unaojitokeza katika Filamu Teule za Kitanzania za Mtandaoni
Makala hii imechunguza sababu za mwitiko wa hadhira unaojitokeza katika filamu teule za Kitanzania ambazo zinapatikana katika mtandao wa Netflix za Bahasha (2018) na Binti (2021). Makala hii imeongozwa na Nadharia ya Upokezi. Uchambuzi wa Makala hii umetumia mkabala wa kitaamuli. Uchambuzi wa data na uwasilishaji wa matokeo katika makala hii umefanywa kwa maelezo. Vilevile, data za uwandani na za mtandaoni zimechambuliwa kwa njia ya kimaelezo. Data za Makala hii zilipatikana uwandani kutoka katika kata tatu za Mkoa wa Dar es Salaam za Kariakoo, Ilala na Mwenge. Aidha, data za makala hii zilipatikana mtandaoni kutoka katika mtandao wa Netflix na You-Tube. Data za makala hii ni sehemu ya data zilizokusanywa kwa ajili ya shahada ya uzamivu ya mwandishi wa makala hii. Mbinu ya usaili ilitumika kukusanya data kutoka kwa hadhira ya filamu teule. Sampuli ilihusisha jumla ya filamu teule mbili na watoataarifa 15. Matokeo ya makala hii yameonesha sababu mbalimbali za mwitiko wa hadhira unaojitokeza katika filamu teule za Kitanzania. Sababu hizi zinatokana na hadhira au filamu yenyewe. Miongoni mwa sababu hizi ni pamoja na: maudhui, mandhari, ufundi wa kuwachora wahusika, maleba, muktadha wa kiutamaduni na uhusiano wa kihisia. Makala hii imependekeza kwamba watayarishaji wa filamu wanatakiwa kuzingatia sababu hizi zinazoathiri na kusababisha mwitiko wa hadhira ili kuboresha uzoefu wa filamu na kuelewa umuhimu wa filamu kama chombo cha mawasiliano pamoja na kupata hadhira pana zaidi. Makala hii imegawanyika katika sehemu nne: utangulizi na mapitio ya maandishi, Nadharia ya Upokezi, sababu za mwitiko wa hadhira unaojitokeza katika filamu teule na hitimish
Abnormal medial prefrontal cortex connectivity and defective fear extinction in the presymptomatic G93A SOD1 mouse model of ALS
Amyotrophic lateral sclerosis (ALS) is a fatal progressive neuropathy associated with the degeneration of spinal and brainstem motor neurons. Although ALS is essentially considered as a lower motor neuron disease, prefrontal cortex atrophy underlying executive function deficits have been extensively reported in ALS patients. Here, we examine whether prefrontal cortex neuronal abnormalities and related cognitive impairments are present in presymptomatic G93A Cu/Zn superoxide dismutase mice, a mouse model for familial ALS. Structural characteristics of prelimbic/infralimbic (PL/IL) medial prefrontal cortex (mPFC) neurons were studied in 3-month-old G93A and wild-type mice with the Golgi-Cox method, while mPFC-related cognitive operations were assessed using the conditioned fear extinction paradigm. Sholl analysis performed on the dendritic material showed a reduction in dendrite length and branch nodes on basal dendrites of PL/IL neurons in G93A mice. Spine density was also decreased on basal dendrite segments of branch order five. Consistent with the altered morphology of PL/IL cortical regions, G93A mice showed impaired extinction of conditioned fear. Our findings indicate that abnormal prefrontal cortex connectivity and function are appreciable before the onset of motor disturbances in this model
Environmental modulation of dendritic spine dynamics in mouse hippocampus
Ephrins and their tyrosine kinase receptors are involved in patterning of axonal connections during development in the nervous system of vertebrates [1]. They also play a role in neuronal plasticity in the adult brain, with particular reference to the hippocampus [2], in which they also modulate LTP induction [3]. We have raised C57/BL6 mice in an enriched environment, which increases adult hippocampal activity and alters hippocampal-dependent behaviors in rodents [4], to examine whether experience-dependent stimulation induces behavioral ameliorations, modifications in neuronal morphology and variations in the expression of ephrins, such as ephrin-B2 and eph-B2 receptor, in such structure. After an eight-week enrichment training, mice were challenged by the context-dependent fear conditioning test and Morris Water Maze, which are behavioral paradigms sensitive to hippocampal modifications [5], and by the cue-dependent fear conditioning test, which mainly relies on amygdala functions. Enriched mice (EM) performed better than non-enriched ones (CM) in the context-dependent fear conditioning and Morris Water Maze tests, but not in the cue-dependent fear conditioning test.
After the enrichment period, dendritic arborization and spine density of Golgi-Cox stained CA1 hippocampal neurons were increased with respect to CM. After the fear conditioning testing however, spine density of EM hippocampal neurons decreased below the level of CM.
Immunohistochemical analysis revealed a specific higher abundance of ephrin-B2 and eph-B2 receptor in the pyramidal layer of the CA1 area and in cortical layers, but not the amygdala, of EM.
We suggest that: hippocampal neuron complexity is enhanced by enrichment along with spatial learning, but is rapidly decreased by an aversive experience; ephrin-B2 and eph-B2 receptor are involved in dendritic spine dinamycs during learning
Fmr1-KO mice failure to detect object novelty associates with a post-test decrease of structural and synaptic plasticity upstream of the hippocampus
: Mice with deletion of the FMR1 gene show episodic memory impairments and exhibit dendritic spines and synaptic plasticity defects prevalently identified in non-training conditions. Based on evidence that synaptic changes associated with normal or abnormal memory emerge when mice are cognitively challenged, here we examine whether, and how, fragile entorhinal and hippocampal synapses are remodeled when mice succeed or fail to learn. We trained Fmr1 knockout (KO) and wild-type C57BL/6J (WT) mice in the novel object recognition (NOR) paradigm with 1 h or 24 h training-to-test intervals and then assessed whether varying the time between the presentation of similar and different objects modulates NOR performance and plasticity along the entorhinal cortex-hippocampus axis. At the 1 h-interval, KO mice failed to discriminate the novel object, showed a collapse of spines in the lateral entorhinal cortex (LEC), and of long-term potentiation (LTP) in the lateral perforant path (LPP), but a normal increase in hippocampal spines. At the 24 h, they exhibited intact NOR performance, typical LEC and hippocampal spines, and exaggerated LPP-LTP. Our findings reveal that the inability of mice to detect object novelty primarily stands in their impediment to elaborate, and convey to the hippocampus, sensory/perceptive object representations
Spine growth in the anterior cingulate cortex is necessary for the consolidation of contextual fear memory
Remodeling of cortical connectivity is thought to allow initially hippocampus-dependent memories to be expressed independently of the hippocampus at remote time points. Consistent with this, consolidation of a contextual fear memory is associated with dendritic spine growth in neurons of the anterior cingulate cortex (aCC). To directly test whether such cortical structural remodeling is necessary for memory consolidation, we disrupted spine growth in the aCC at different times following contextual fear conditioning in mice. We took advantage of previous studies showing that the transcription factor myocyte enhancer factor 2 (MEF2) negatively regulates spinogenesis both in vitro and in vivo. We found that increasing MEF2-dependent transcription in the aCC during a critical posttraining window (but not at later time points) blocked both the consolidation-associated dendritic spine growth and subsequent memory expression. Together, these data strengthen the causal link between cortical structural remodeling and memory consolidation and, further, identify MEF2 as a key regulator of these processes.</jats:p
Ukoloni Mamboleo na Utanda Wazi katika Tamthilia Teule
Utafiti huu umechunguza jinsi ukoloni mamboleo unavyodhihirika katika muktadha wa
utandawazi kwa kurejelea tamthilia mbili teule: Posa za Bikisiwa (2008) ya S. A.
Mohamed na K. King'ei na Sudana (2006) ya Alamin Mazrui na K. Njogu. Utafiti huu
uliongozwa na nadharia ya Baada Ukoloni. Utafiti ulifanyiwa maktabani. Mtafiti alisoma
makala mengi yaliyohusiana na mada ya utafiti ili kupata data iliyokusudiwa. Mtafiti pia
alifanya utafiti wa nyanjani kwa kuwahoji watunzi. Vilevile, mtafiti aliwahoji wataalamu
na wanafunzi wenzake. Aidha mtafiti alichanganua tamthilia hizi mbili teule ili kupata
data iliyokusudiwa ili kutimiza matakwa ya utafiti huu. Data iliyokusanywa ilirekodiwa
na kuchanganuliwa kwa kuzingatia malengo ya utafiti na nadharia ya Baada Ukoloni.
Data zilizokusanywa zimewasilishwa kwa njia ya maelezo. Kazi hii imewasilishwa kwa
sura tano. Utafiti huu umeonyesha kwamba utandawazi ni mbinu mpya ya kisasa ya
kuendeleza ukoloni mamboleo dhidi ya mataifa maskini
Mbinu za Kukabiliana na Utamaushi katika Fasihi ya Kiswahili: Ulinganisho wa Wimbo Teule wa Jux na Diamond Platnumz na Kazi Teule za Kezilahabi
Makala hii inakusudia kuonesha namna utamaushi unavyojitokeza katika wimbo wa “Enjoy” na kazi teule za Kezilahabi. Kutokana na maisha kuonekana kama kitu cha kukatisha tamaa (kutamausha) kwa kadri yalivyogubikwa na madhila mbalimbali, wimbo wa “Enjoy” unaonesha kuwa suluhisho ni kuamua “ku-enjoy” (kuyafurahia tu) kwa kadri mtu anavyoweza baada ya kupata nafasi ya kufanya hivyo. Hii ni tofauti na ilivyo katika kazi zingine za kidhanaishi, hususani kazi za Kezilahabi, ambazo zinaonesha kuwa suluhisho ni kujiua. Nadharia ya Udhanaishi iliongoza katika uchambuzi wa matini teule. Mbinu ya usampulishaji lengwa ilitumika katika kupata data zilizofanikisha makala hii. Data zilikusanywa kwa kutumia mbinu ya uchambuzi matini. Matokeo ya utafiti uliozaa makala hii yanaonesha kuwa maisha ayaishiyo mwanadamu ni mafupi, mwanadamu anao uhuru wake binafsi, kuna kukata tamaa kunakosababishwa na masuala ya mapenzi, dunia ni uwanja wa fujo—kila mtu amekuja kufanya fujo zake na mwisho atajiondokea, na, mwisho, masuala ya mahusiano ya kimapenzi ni huzuni tupu. Makala inahitimisha kwa kutoa mapendekezo kuwa suluhu ya kukata tamaa maishani siyo kujiua bali kuyafurahia maisha kwa kadri mtu awezavyo kwani kujiua hakutatui tatizo husika bali huweza kusababisha tatizo ama matatizo mengine. Aidha, iwapo mwanadamu ataamua kufanya fujo zake, ni vema afanye fujo za amani zisizowaathiri wengine. Uhuru binafsi uzingatie mipaka, kwani kila kitu kinapopitiliza huweza kuwa na madhara
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