The cochlea also mounts a significant inflammatory response following  terjemahan - The cochlea also mounts a significant inflammatory response following  Bahasa Indonesia Bagaimana mengatakan

The cochlea also mounts a significa

The cochlea also mounts a significant inflammatory response following noise
exposure. Infiltration of inflammatory cells including macrophages as well as
activation of inherent macrophages in the cochlea occurs in the period after acute
noise exposure18. Whilst this inflammatory response is likely part of the reparative
processes in the cochlea following noise, it is conceivable that they may exacerbate or contribute to the ongoing injury, especially chronic injury. This needs to be further
investigated.
Adaptation to noise—The response of the cochlea to noise exposure is complicated
by the fact that its reaction is not purely “passive” as it clearly adapts to excessive
sound exposure (eg. Housley et al.19).
Exposure to a non-traumatic noise or to hypoxia provides some protection to the ear
from a subsequent traumatic noise exposure (eg. Canlon and Fransson20). This
phenomenon, known as sound conditioning may relate to mobilisation of inherent
protective processes, particularly oxidative enzymes and antioxidants.21 Noise
exposure also upregulates the expression of a variety of proteins 22-24 including
protective (eg Yamamoto et al.25) and repair proteins. The cochlea receives a
descending or efferent innervation that arises in the Superior Olivary Complex in the
brainstem and innervates both the OHC and the boutons of the type I neurons
innervating IHC. Activation of these pathways appears to dampen the cochlear
response to noise and hence may also provide some “protection” from noise exposure.
The role of such a variety of active reactions of the cochlea to excessive sound
exposure in the human response to noise exposure has not been established or well
considered. However, variations in these across the population could affect the
characteristic susceptibility of individuals to noise-induced hearing loss.
Consequences for tinnitus—Clearly there are considerable pathological changes in
the cochlea that are associated with noise exposure and noise-induced hearing loss
that could underly the tinnitus observed after noise. The changes to the hair cells,
neurons and supporting structures will lead to significant alterations in functional
input to the central nervous system and alter the pattern of driven and standing
activity in central auditory nuclei. Many of the functional changes in the central
auditory pathways following noise exposure have been well characterised (eg
cochlear nucleus, inferior colliculus and cortex) and will be discussed by others in this
symposium. However, mostly these central changes have been correlated to the
substantial hair cell and neuronal loss. How injury or loss of some of the supporting
and accessory structures such as the lateral wall tissues are manifest centrally has not been established.
Important to the consideration of the relationship of cochlear noise-induced injury and
tinnitus is that the cochlear pathologies, and indeed the adaptive reaction to noise, are very different among individuals and also show substantial variation with different
noise exposures. There is an implicit assumption that the injury is of hair cell, and to
some extent neuronal origin, but clearly there are many other pathologies which
would not be distinguishable in humans using standard clinical functional assessment
methods such as the pure tone audiogram. The evidence of neuronal injury without
any change in auditory thresholds, in animals, further indicates that the pure tone
audiogram will not provide a suitable index of all cochlear injury.
Injury to the cochlea after noise may also not be static as indicated by the ongoing
degeneration that can occur (eg. Kujawa and Liberman8) and the impact of a
continued inflammatory reaction in the ear from chronic cochlear injury on auditory
function is also not known. Thus it is important to acknowledge that the response of
the cochlea to noise exposure is complicated and varies across individuals. This may
account for substantial differences in the extent to which noise may influence the
generation of tinnitus across individuals.
Author information: Peter R Thorne, Section of Audiology, The University of
Auckland, Auckland, New Zealand
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The cochlea also mounts a significant inflammatory response following noiseexposure. Infiltration of inflammatory cells including macrophages as well asactivation of inherent macrophages in the cochlea occurs in the period after acutenoise exposure18. Whilst this inflammatory response is likely part of the reparativeprocesses in the cochlea following noise, it is conceivable that they may exacerbate or contribute to the ongoing injury, especially chronic injury. This needs to be furtherinvestigated.Adaptation to noise—The response of the cochlea to noise exposure is complicatedby the fact that its reaction is not purely “passive” as it clearly adapts to excessivesound exposure (eg. Housley et al.19).Exposure to a non-traumatic noise or to hypoxia provides some protection to the earfrom a subsequent traumatic noise exposure (eg. Canlon and Fransson20). Thisphenomenon, known as sound conditioning may relate to mobilisation of inherentprotective processes, particularly oxidative enzymes and antioxidants.21 Noiseexposure also upregulates the expression of a variety of proteins 22-24 includingprotective (eg Yamamoto et al.25) and repair proteins. The cochlea receives adescending or efferent innervation that arises in the Superior Olivary Complex in thebrainstem and innervates both the OHC and the boutons of the type I neuronsinnervating IHC. Activation of these pathways appears to dampen the cochlearresponse to noise and hence may also provide some “protection” from noise exposure.The role of such a variety of active reactions of the cochlea to excessive soundexposure in the human response to noise exposure has not been established or wellconsidered. However, variations in these across the population could affect thecharacteristic susceptibility of individuals to noise-induced hearing loss.Consequences for tinnitus—Clearly there are considerable pathological changes inthe cochlea that are associated with noise exposure and noise-induced hearing lossthat could underly the tinnitus observed after noise. The changes to the hair cells,neurons and supporting structures will lead to significant alterations in functionalinput to the central nervous system and alter the pattern of driven and standingactivity in central auditory nuclei. Many of the functional changes in the centralauditory pathways following noise exposure have been well characterised (egcochlear nucleus, inferior colliculus and cortex) and will be discussed by others in thissymposium. However, mostly these central changes have been correlated to thesubstantial hair cell and neuronal loss. How injury or loss of some of the supportingand accessory structures such as the lateral wall tissues are manifest centrally has not been established.Important to the consideration of the relationship of cochlear noise-induced injury andtinnitus is that the cochlear pathologies, and indeed the adaptive reaction to noise, are very different among individuals and also show substantial variation with different
noise exposures. There is an implicit assumption that the injury is of hair cell, and to
some extent neuronal origin, but clearly there are many other pathologies which
would not be distinguishable in humans using standard clinical functional assessment
methods such as the pure tone audiogram. The evidence of neuronal injury without
any change in auditory thresholds, in animals, further indicates that the pure tone
audiogram will not provide a suitable index of all cochlear injury.
Injury to the cochlea after noise may also not be static as indicated by the ongoing
degeneration that can occur (eg. Kujawa and Liberman8) and the impact of a
continued inflammatory reaction in the ear from chronic cochlear injury on auditory
function is also not known. Thus it is important to acknowledge that the response of
the cochlea to noise exposure is complicated and varies across individuals. This may
account for substantial differences in the extent to which noise may influence the
generation of tinnitus across individuals.
Author information: Peter R Thorne, Section of Audiology, The University of
Auckland, Auckland, New Zealand
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Koklea juga mount respon inflamasi yang signifikan berikut kebisingan
paparan. Infiltrasi sel inflamasi termasuk makrofag serta
aktivasi makrofag yang melekat dalam koklea terjadi pada periode setelah akut
exposure18 kebisingan. Sementara respon inflamasi ini mungkin bagian dari reparatif
proses dalam koklea berikut kebisingan, dapat dibayangkan bahwa mereka dapat memperburuk atau berkontribusi pada cedera berkelanjutan, terutama cedera kronis. Hal ini perlu lebih
diteliti.
Adaptasi terhadap suara-Respon koklea paparan kebisingan rumit
oleh fakta bahwa reaksi yang tidak murni "pasif" karena jelas menyesuaikan dengan berlebihan
paparan suara (Housley et al.19 misalnya.) .
Paparan suara non-traumatik atau hipoksia memberikan perlindungan untuk telinga
dari selanjutnya paparan kebisingan traumatis (misalnya. Canlon dan Fransson20). Ini
fenomena yang dikenal sebagai pengkondisian suara mungkin berhubungan dengan mobilisasi melekat
proses pelindung, enzim terutama oksidatif dan Kebisingan antioxidants.21
eksposur juga meregulasi ekspresi berbagai protein 22-24 termasuk
pelindung (misalnya Yamamoto et al.25) dan protein perbaikan . Koklea menerima
menurun atau eferen persarafan yang timbul di Kompleks unggul olivary di
batang otak dan innervates baik OHC dan boutons dari tipe I neuron
innervating Posyandu. Aktivasi jalur tersebut muncul untuk meredam koklea
respon terhadap suara dan karenanya juga dapat memberikan beberapa "perlindungan" dari paparan kebisingan.
Peran seperti berbagai reaksi aktif dari koklea ke suara berlebihan
paparan dalam respon manusia untuk paparan kebisingan belum telah didirikan atau juga
dipertimbangkan. Namun, variasi ini di seluruh populasi dapat mempengaruhi
kerentanan karakteristik individu untuk kehilangan pendengaran suara yang diinduksi.
Konsekuensi untuk tinnitus-jelas ada perubahan patologis yang cukup besar dalam
koklea yang berhubungan dengan paparan kebisingan dan gangguan pendengaran suara yang diinduksi
yang bisa mendasari tinnitus diamati setelah kebisingan. Perubahan pada sel-sel rambut,
neuron dan struktur pendukung akan menyebabkan perubahan signifikan dalam fungsional
input ke sistem saraf pusat dan mengubah pola berdiri didorong dan
aktivitas di inti pendengaran pusat. Banyak perubahan fungsional dalam pusat
jalur pendengaran berikut paparan kebisingan telah ditandai dengan baik (misalnya
inti koklea, colliculus inferior dan korteks) dan akan dibahas oleh orang lain dalam hal ini
simposium. Namun, sebagian besar perubahan sentral telah berkorelasi dengan
sel rambut besar dan hilangnya neuron. Bagaimana cedera atau kehilangan beberapa pendukung
struktur dan aksesori seperti jaringan dinding lateral nyata terpusat belum ditetapkan.
Penting untuk pertimbangan hubungan koklea noise yang disebabkan cedera dan
tinnitus adalah bahwa patologi koklea, dan memang Reaksi adaptif terhadap kebisingan, sangat berbeda antara individu dan juga menunjukkan variasi yang cukup besar dengan berbagai
eksposur suara. Ada asumsi implisit bahwa cedera adalah sel rambut, dan
beberapa batas asal saraf, tetapi jelas ada banyak patologi lain yang
tidak akan dibedakan pada manusia dengan menggunakan penilaian fungsional klinis standar
metode seperti nada audiogram murni. Bukti cedera neuronal tanpa
perubahan apapun dalam ambang pendengaran, pada hewan, lebih lanjut menunjukkan bahwa nada murni
audiogram tidak akan memberikan indeks yang cocok dari semua cedera koklea.
Cedera koklea setelah suara juga tidak statis seperti yang ditunjukkan oleh berkelanjutan
degenerasi yang dapat terjadi (misalnya. Kujawa dan Liberman8) dan dampak dari
reaksi inflamasi terus di telinga dari cedera koklea kronis pada pendengaran
fungsi juga tidak diketahui. Dengan demikian, penting untuk mengakui bahwa respon dari
koklea paparan kebisingan rumit dan bervariasi di seluruh individu. Hal ini mungkin
menjelaskan perbedaan substansial dalam sejauh mana kebisingan dapat mempengaruhi
generasi tinnitus seluruh individu.
Penulis Informasi: Peter R Thorne, Seksi Audiologi, The University of
Auckland, Auckland, Selandia Baru
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