Volume 3, Issue 6

Human embryo stem cells and DNA repair

Marco Durante,

https://doi.org/10.18632/aging.100337 pp 564

PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Durante M, . Human embryo stem cells and DNA repair. . 3:564-564. https://doi.org/10.18632/aging.100337

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

Type 2 Diabetes and the Aging Pancreatic Beta Cell

Uma Gunasekaran, Maureen Gannon,

https://doi.org/10.18632/aging.100350 pp 565—575

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gunasekaran U, Gannon M, . Type 2 Diabetes and the Aging Pancreatic Beta Cell. . 3:565-575. https://doi.org/10.18632/aging.100350

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gunasekaran, Uma 
                AU  - Gannon, Maureen 
                TI  - Type 2 Diabetes and the Aging Pancreatic Beta Cell
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100350
                DO  - 10.18632/aging.100350
                SP  - 565
                EP  - 575
                PY  - 
                AB  - The incidence of and susceptibility to Type 2 diabetes increases with age, but the underlying mechanism(s) within beta cells that contribute to this increased susceptibility have not been fully elucidated. Here we review how aging affects the proliferative and regenerative capacity of beta cells and how this impacts beta cell mass. In addition we review changes that occur in beta cell function with age. Although we focus on the different rodent models that have provided insight into the characteristics of the aging beta cell, the limited knowledge from non-rodent models is also reviewed. Further studies are needed in order to identify potential beta cell targets for preventing or slowing the progression of diabetes that occurs with age.
                ER  -

Click to copy this citation from the text box above or download the citation:

New comparative genomics approach reveals a conserved health span signature across species

Michael Antosh, David Fox, Stephen L. Helfand, Leon N Cooper, Nicola Neretti,

https://doi.org/10.18632/aging.100342 pp 576—583

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Antosh M, Fox D, Helfand SL, Cooper LN, Neretti N, . New comparative genomics approach reveals a conserved health span signature across species. . 3:576-583. https://doi.org/10.18632/aging.100342

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Antosh, Michael 
                AU  - Fox, David 
                AU  - Helfand, Stephen L. 
                AU  - Cooper, Leon N 
                AU  - Neretti, Nicola 
                TI  - New comparative genomics approach reveals a conserved health span signature across species
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100342
                DO  - 10.18632/aging.100342
                SP  - 576
                EP  - 583
                PY  - 
                AB  - Environmental and genetic interventions extend health span in a range of organisms by triggering changes in different specific but complementary pathways. We investigated the gene expression changes that occur across species when health span is extended via different interventions. To perform this comparison using heterogeneous datasets from different measurement platforms and organisms, we developed a novel non-parametric methodology that can detect statistical significance of overlaps in ranked lists of genes, and estimate the number of genes with a common expression profile. By comparing genetic and environmental interventions that consistently lead to increased health span in invertebrates and vertebrates we built a conserved health span signature and described how such a signature depends on tissue type. Furthermore, we examined the relationship between calorie restriction and resveratrol administration and for the first time, identified common gene and pathway changes in calorie restriction and resveratrol in both invertebrates and mammals. Our approach can thus be used to explore and better define the relationships between highly complex biological phenomena, in this case those that affect the health and longevity.
                ER  -

Click to copy this citation from the text box above or download the citation:

Error-prone nonhomologous end joining repair operates in human pluripotent stem cells during late G2

Alexandra N. Bogomazova, Maria A. Lagarkova, Leyla V. Tskhovrebova, Maria V. Shutova, Sergey L. Kiselev,

https://doi.org/10.18632/aging.100336 pp 584—596

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Bogomazova AN, Lagarkova MA, Tskhovrebova LV, Shutova MV, Kiselev SL, . Error-prone nonhomologous end joining repair operates in human pluripotent stem cells during late G2. . 3:584-596. https://doi.org/10.18632/aging.100336

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Bogomazova, Alexandra N. 
                AU  - Lagarkova, Maria A. 
                AU  - Tskhovrebova, Leyla V. 
                AU  - Shutova, Maria V. 
                AU  - Kiselev, Sergey L. 
                TI  - Error-prone nonhomologous end joining repair operates in human pluripotent stem cells during late G2
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100336
                DO  - 10.18632/aging.100336
                SP  - 584
                EP  - 596
                PY  - 
                AB  - Genome stability of human embryonic stem cells (hESC) is an important issue because even minor genetic alterations can negatively impact cell functionality and safety. The incorrect repair of DNA double-stranded breaks (DSBs) is the ultimate cause of the formation of chromosomal aberrations. Using G2 radiosensitivity assay, we analyzed chromosomal aberrations in pluripotent stem cells and somatic cells. The chromatid exchange aberration rates in hESCs increased manifold 2 hours after irradiation as compared with their differentiated derivatives, but the frequency of radiation-induced chromatid breaks was similar. The rate of radiation-induced chromatid exchanges in hESCs and differentiated cells exhibited a quadratic dose response, revealing two-hit mechanism of exchange formation suggesting that a non-homologous end joining (NHEJ) repair may contribute to their formation. Inhibition of DNA-PK, a key NHEJ component, by NU7026 resulted in a significant decrease in radiation-induced chromatid exchanges in hESCs but not in somatic cells. In contrast, NU7026 treatment increased the frequency of radiation-induced breaks to a similar extent in pluripotent and somatic cells. Thus, DNA-PK dependent NHEJ efficiently participates in the elimination of radiation-induced chromatid breaks during the late G2 in both cell types and DNA-PK activity leads to a high level of misrejoining specifically in pluripotent cells.
                ER  -

Click to copy this citation from the text box above or download the citation:

Tunneling nanotubes mediate rescue of prematurely senescent endothelial cells by endothelial progenitors: exchange of lysosomal pool

Kaoru Yasuda, Anupama Khandare, Leonid Burianovskyy, Shoichi Maruyama, Frank Zhang, Alberto Nasjletti, Michael S Goligorsky,

https://doi.org/10.18632/aging.100341 pp 597—608

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Yasuda K, Khandare A, Burianovskyy L, Maruyama S, Zhang F, Nasjletti A, Goligorsky MS, . Tunneling nanotubes mediate rescue of prematurely senescent endothelial cells by endothelial progenitors: exchange of lysosomal pool. . 3:597-608. https://doi.org/10.18632/aging.100341

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Yasuda, Kaoru 
                AU  - Khandare, Anupama 
                AU  - Burianovskyy, Leonid 
                AU  - Maruyama, Shoichi 
                AU  - Zhang, Frank 
                AU  - Nasjletti, Alberto 
                AU  - Goligorsky, Michael S 
                TI  - Tunneling nanotubes mediate rescue of prematurely senescent endothelial cells by endothelial progenitors: exchange of lysosomal pool
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100341
                DO  - 10.18632/aging.100341
                SP  - 597
                EP  - 608
                PY  - 
                AB  - Although therapeutic effect of adoptive transfer of endothelial progenitor cells (EPC) has been well-substantiated, the actual engraftment is relatively low compared to a robust functional improvement of vasculopathy. Cellular mechanisms governing this action remain elusive. A recently discovered cell-cell communication via tunneling nanotube (TNT) formation is capable of transferring mitochondria and lysosomes between the cells – “organellar diakinesis”. Based on the previous demonstration of lysosomal dysfunction in endothelial cells exposed to AGE-modified collagen I, we inquired whether TNT mechanism may be involved in EPC-mediated repair of stressed endothelial cells. Here we demonstrate that EPC selectively and multiplicatively establish TNT communication with stressed endothelia. The guidance cues for the selectivity are provided by exofacially exposed phosphatidylserine moieties. Lysosomal transfer is associated with the preservation of lysosomal pH gradient, functionally reconstituting lysosomal pool of stressed cells and improving endothelial cell viability, reducing premature senescence and apoptosis. In vivo, adoptive transfer of EPC to streptozotocin-diabetic mice results in a TNT-dependent reduction of senescent endothelial cells and correction of endothelium-dependent vasorelaxation. Collectively, these data establish a selective multiplicative effect of TNT between EPC and stressed endothelia, reconstitution of the lysosomal pool, and improved viability and function of stressed endothelia.
                ER  -

Click to copy this citation from the text box above or download the citation:

Induction and persistence of radiation-induced DNA damage is more pronounced in young animals than in old animals

Darryl Hudson, Igor Kovalchuk, Igor Koturbash, Bryan Kolb, Olga A. Martin, Olga Kovalchuk,

https://doi.org/10.18632/aging.100340 pp 609—620

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Hudson D, Kovalchuk I, Koturbash I, Kolb B, Martin OA, Kovalchuk O, . Induction and persistence of radiation-induced DNA damage is more pronounced in young animals than in old animals. . 3:609-620. https://doi.org/10.18632/aging.100340

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Hudson, Darryl 
                AU  - Kovalchuk, Igor 
                AU  - Koturbash, Igor 
                AU  - Kolb, Bryan 
                AU  - Martin, Olga A. 
                AU  - Kovalchuk, Olga 
                TI  - Induction and persistence of radiation-induced DNA damage is more pronounced in young animals than in old animals
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100340
                DO  - 10.18632/aging.100340
                SP  - 609
                EP  - 620
                PY  - 
                AB  - Younger individuals are more prone to develop cancer upon ionizing radiation (IR) exposure. Radiation-induced tumors are associated with inefficient repair of IR-induced DNA damage and genome instability. Phosphorylation of histone H2AX (γ-H2AX) is the initial event in repair of IR-induced DNA damage on the chromatin flanking the DNA strand breaks. This step is crucially important for the repair of DNA strand breaks and for the maintenance of genome stability. We studied the molecular underpinnings of the age-related IR effects using an animal model. By assaying for IR-induced γ-H2AX foci we analyzed the induction and repair of the DNA strand breaks in spleen, thymus, liver, lung, kidney, cerebellum, hippocampus, frontal cortex and olfactory bulb of 7, 14, 24, 30 and 45 days old male and female mice as a function of age. We demonstrate that tissues of younger animals are much more susceptible to IR-induced DNA damage. Younger animals exhibited higher levels of γ-H2AX formation which partially correlated with cellular proliferation and expression of DNA repair proteins. Induction and persistence of γ-H2AX foci was the highest in lymphoid organs (thymus and spleen) of 7 and 14 day old mice. The lowest focal induction was seen in lung and brain of young animals. The mechanisms of cell and tissue-specificity of in vivo IR responses need to be further dissected. This study provides a roadmap for the future analyses of DNA damage and repair induction in young individuals.
                ER  -

Click to copy this citation from the text box above or download the citation:

Store-Operated Ca²⁺ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle

Angela M Thornton, Xiaoli Zhao, Noah Weisleder, Leticia S. Brotto, Sylvain Bougoin, Thomas M. Nosek, Michael Reid, Brian Hardin, Zui Pan, Jianjie Ma, Jerome Parness, Marco Brotto,

https://doi.org/10.18632/aging.100335 pp 621—634

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Thornton AM, Zhao X, Weisleder N, Brotto LS, Bougoin S, Nosek TM, Reid M, Hardin B, Pan Z, Ma J, Parness J, Brotto M, . Store-Operated Ca²⁺ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle. . 3:621-634. https://doi.org/10.18632/aging.100335

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Thornton, Angela M 
                AU  - Zhao, Xiaoli 
                AU  - Weisleder, Noah 
                AU  - Brotto, Leticia S. 
                AU  - Bougoin, Sylvain 
                AU  - Nosek, Thomas M. 
                AU  - Reid, Michael 
                AU  - Hardin, Brian 
                AU  - Pan, Zui 
                AU  - Ma, Jianjie 
                AU  - Parness, Jerome 
                AU  - Brotto, Marco 
                TI  - Store-Operated Ca<sup>2+</sup> Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100335
                DO  - 10.18632/aging.100335
                SP  - 621
                EP  - 634
                PY  - 
                AB  - Muscle atrophy alone is insufficient to explain the significant decline in contractile force of skeletal muscle during normal aging. One contributing factor to decreased contractile force in aging skeletal muscle could be compromised excitation-contraction (E-C) coupling, without sufficient available Ca2+ to allow for repetitive muscle contractility, skeletal muscles naturally become weaker. Using biophysical approaches, we previously showed that store-operated Ca2+ entry (SOCE) is compromised in aged skeletal muscle but not in young ones. While important, a missing component from previous studies is whether or not SOCE function correlates with contractile function during aging. Here we test the contribution of extracellular Ca2+ to contractile function of skeletal muscle during aging. First, we demonstrate graded coupling between SR Ca2+ release channel-mediated Ca2+ release and activation of SOCE. Inhibition of SOCE produced significant reduction of contractile force in young skeletal muscle, particularly at high frequency stimulation, and such effects were completely absent in aged skeletal muscle. Our data indicate that SOCE contributes to the normal physiological contractile response of young healthy skeletal muscle and that defective extracellular Ca2+ entry through SOCE contributes to the reduced contractile force characteristic of aged skeletal muscle.
                ER  -

Click to copy this citation from the text box above or download the citation:

SIRT1 and SIRT3 Deacetylate Homologous Substrates: AceCS1,2 and HMGCS1,2

Matthew D. Hirschey, Tadahiro Shimazu, John A. Capra, Katherine S. Pollard, Eric Verdin,

https://doi.org/10.18632/aging.100339 pp 635—642

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Hirschey MD, Shimazu T, Capra JA, Pollard KS, Verdin E, . SIRT1 and SIRT3 Deacetylate Homologous Substrates: AceCS1,2 and HMGCS1,2. . 3:635-642. https://doi.org/10.18632/aging.100339

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Hirschey, Matthew D. 
                AU  - Shimazu, Tadahiro 
                AU  - Capra, John A. 
                AU  - Pollard, Katherine S. 
                AU  - Verdin, Eric 
                TI  - SIRT1 and SIRT3 Deacetylate Homologous Substrates: AceCS1,2 and HMGCS1,2
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100339
                DO  - 10.18632/aging.100339
                SP  - 635
                EP  - 642
                PY  - 
                AB  - SIRT1 and SIRT3 are NAD+-dependent protein deacetylases that are evolutionarily conserved across mammals. These proteins are located in the cytoplasm/nucleus and mitochondria, respectively. Previous reports demonstrated that human SIRT1 deacetylates Acetyl-CoA Synthase 1 (AceCS1) in the cytoplasm, whereas SIRT3 deacetylates the homologous Acetyl-CoA Synthase 2 (AceCS2) in the mitochondria. We recently showed that 3-hydroxy-3-methylglutaryl CoA synthase 2 (HMGCS2) is deacetylated by SIRT3 in mitochondria, and we demonstrate here that SIRT1 deacetylates the homologous 3-hydroxy-3-methylglutaryl CoA synthase 1 (HMGCS1) in the cytoplasm. This novel pattern of substrate homology between cytoplasmic SIRT1 and mitochondrial SIRT3 suggests that considering evolutionary relationships between the sirtuins and their substrates may help to identify and understand the functions and interactions of this gene family. In this perspective, we take a first step by characterizing the evolutionary history of the sirtuins and these substrate families.
                ER  -

Click to copy this citation from the text box above or download the citation:

Aging-Associated Changes in Hematopoiesis and Leukemogenesis: What's the Connection?

Curtis J. Henry, Andriy Marusyk, James DeGregori,

https://doi.org/10.18632/aging.100351 pp 643—656

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Henry CJ, Marusyk A, DeGregori J, . Aging-Associated Changes in Hematopoiesis and Leukemogenesis: What's the Connection?. . 3:643-656. https://doi.org/10.18632/aging.100351

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Henry, Curtis J. 
                AU  - Marusyk, Andriy 
                AU  - DeGregori, James 
                TI  - Aging-Associated Changes in Hematopoiesis and Leukemogenesis: What's the Connection?
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100351
                DO  - 10.18632/aging.100351
                SP  - 643
                EP  - 656
                PY  - 
                AB  - Aging is associated with a marked increase in a number of diseases, including many types of cancer. Due to the complex and multi-factorial nature of both aging and cancer, accurate deciphering of causative links between aging and cancer remains a major challenge. It is generally accepted that initiation and progression of cancers are driven by a process of clonal evolution. In principle, this somatic evolution should follow the same Darwinian logic as evolutionary processes in populations in nature: diverse heritable types arising as a result of mutations are subjected to selection, resulting in expansion of the fittest clones. However, prevalent paradigms focus primarily on mutational aspects in linking aging and cancer. In this review, we will argue that age-related changes in selective pressures are likely to be equally important. We will focus on aging-related changes in the hematopoietic system, where age-associated alterations are relatively well studied, and discuss the impact of these changes on the development of leukemias and other malignancies.
                ER  -

Click to copy this citation from the text box above or download the citation:

Besides Huntington's disease, does brain-type creatine kinase play a role in other forms of hearing impairment resulting from a common pathological cause?

Yow-Sien Lin, Chih-Hung Wang, Yijuang Chern,

https://doi.org/10.18632/aging.100338 pp 657—662

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lin Y, Wang C, Chern Y, . Besides Huntington's disease, does brain-type creatine kinase play a role in other forms of hearing impairment resulting from a common pathological cause?. . 3:657-662. https://doi.org/10.18632/aging.100338

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lin, Yow-Sien 
                AU  - Wang, Chih-Hung 
                AU  - Chern, Yijuang 
                TI  - Besides Huntington's disease, does brain-type creatine kinase play a role in other forms of hearing impairment resulting from a common pathological cause?
                JO  - 
                JA  - 
                VL  - 3
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100338
                DO  - 10.18632/aging.100338
                SP  - 657
                EP  - 662
                PY  - 
                AB  - Hearing impairment following cochlear damage due to noise trauma, ototoxicity caused by aminoglycoside antibiotics, or age-related cochlear degeneration was linked to a common pathogenesis involving the formation of reactive oxygen species (ROS). Cochleae are more vulnerable to oxidative stress than other organs because of the high metabolic demands of their mechanosensory hair cells in response to sound stimulation. We recently showed that patients and mice with Huntington's disease (HD) have hearing impairment and that the dysregulated phosphocreatine (PCr)-creatine kinase (CK) system may account for this auditory dysfunction. Given the importance of noninvasive biomarkers and the easy access of hearing tests, the symptom of hearing loss in HD patients may serve as a useful clinical indicator of disease onset and progression of HD. We also showed that dietary creatine supplementation rescued the impaired PCr-CK system and improved the expression of cochlear brain-type creatine kinase (CKB) in HD mice, thereby restoring their hearing. Because creatine is an antioxidant, we postulated that creatine might enhance expression of CKB by reducing oxidative stress. In addition to HD-related hearing impairment, inferior CKB expression and/or an impaired PCr-CK system may also play an important role in other hearing impairments caused by elevated levels of ROS. Most importantly, dietary supplements may be beneficial to patients with these hearing deficiencies.
                ER  -

Click to copy this citation from the text box above or download the citation:

Volume 3, Issue 6

Human embryo stem cells and DNA repair

Marco Durante,

Review

Type 2 Diabetes and the Aging Pancreatic Beta Cell

Uma Gunasekaran, Maureen Gannon,

Research Papers

New comparative genomics approach reveals a conserved health span signature across species

Michael Antosh, David Fox, Stephen L. Helfand, Leon N Cooper, Nicola Neretti,

Error-prone nonhomologous end joining repair operates in human pluripotent stem cells during late G2

Alexandra N. Bogomazova, Maria A. Lagarkova, Leyla V. Tskhovrebova, Maria V. Shutova, Sergey L. Kiselev,

Tunneling nanotubes mediate rescue of prematurely senescent endothelial cells by endothelial progenitors: exchange of lysosomal pool

Kaoru Yasuda, Anupama Khandare, Leonid Burianovskyy, Shoichi Maruyama, Frank Zhang, Alberto Nasjletti, Michael S Goligorsky,

Induction and persistence of radiation-induced DNA damage is more pronounced in young animals than in old animals

Darryl Hudson, Igor Kovalchuk, Igor Koturbash, Bryan Kolb, Olga A. Martin, Olga Kovalchuk,

Store-Operated Ca²⁺ Entry (SOCE) Contributes to Normal Skeletal Muscle Contractility in young but not in aged skeletal muscle

Angela M Thornton, Xiaoli Zhao, Noah Weisleder, Leticia S. Brotto, Sylvain Bougoin, Thomas M. Nosek, Michael Reid, Brian Hardin, Zui Pan, Jianjie Ma, Jerome Parness, Marco Brotto,

Research Perspectives

SIRT1 and SIRT3 Deacetylate Homologous Substrates: AceCS1,2 and HMGCS1,2

Matthew D. Hirschey, Tadahiro Shimazu, John A. Capra, Katherine S. Pollard, Eric Verdin,

Aging-Associated Changes in Hematopoiesis and Leukemogenesis: What's the Connection?

Curtis J. Henry, Andriy Marusyk, James DeGregori,

Besides Huntington's disease, does brain-type creatine kinase play a role in other forms of hearing impairment resulting from a common pathological cause?

Yow-Sien Lin, Chih-Hung Wang, Yijuang Chern,

Explore This Issue