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Article ; Online: Uncommon liver lesions with multimodality imaging and pathology correlation.

Ho, A K / Girgis, S / Low, G

2017 Volume 73, Issue 2, Page(s) 191–204

Abstract: Uncommon liver lesions pose a diagnostic challenge because of unfamiliar imaging findings. For simplification, these lesions can be divided into four broad categories based on the dominant imaging feature in each: hypervascular, hypovascular, fat- ... ...

Abstract	Uncommon liver lesions pose a diagnostic challenge because of unfamiliar imaging findings. For simplification, these lesions can be divided into four broad categories based on the dominant imaging feature in each: hypervascular, hypovascular, fat-containing, or cystic lesions. In this review, we profile the radiological features of uncommon liver lesions on multimodality imaging including ultrasound (US), computed tomography (CT), magnetic resonance imaging (MRI), and nuclear medicine.
MeSH term(s)	Diagnostic Imaging/methods ; Humans ; Liver/diagnostic imaging ; Liver/pathology ; Liver Neoplasms/diagnostic imaging ; Liver Neoplasms/pathology ; Multimodal Imaging/methods
Language	English
Publishing date	2017-09-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	391227-9
ISSN	1365-229X ; 0009-9260
ISSN (online)	1365-229X
ISSN	0009-9260
DOI	10.1016/j.crad.2017.07.016
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Article ; Online: Ibrutinib-associated T-cell pseudolymphoma.

Ho, A K H / Koh, X Q / Liau, M M Q / Tan, K B / Tan, C L

Clinical and experimental dermatology

2019 Volume 44, Issue 7, Page(s) 828–830

MeSH term(s)	Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors ; Aged ; Diagnosis, Differential ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Male ; Pseudolymphoma/chemically induced ; Pseudolymphoma/pathology ; Pyrazoles/adverse effects ; Pyrazoles/therapeutic use ; Pyrimidines/adverse effects ; Pyrimidines/therapeutic use ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology ; Withholding Treatment
Chemical Substances	Pyrazoles ; Pyrimidines ; ibrutinib (1X70OSD4VX) ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2)
Language	English
Publishing date	2019-01-08
Publishing country	England
Document type	Case Reports ; Letter
ZDB-ID	195504-4
ISSN	1365-2230 ; 0307-6938
ISSN (online)	1365-2230
ISSN	0307-6938
DOI	10.1111/ced.13907
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Article ; Online: Impact of Huntington's across the entire disease spectrum: the phases and stages of disease from the patient perspective.

Ho, A K / Hocaoglu, M B

Clinical genetics

2011 Volume 80, Issue 3, Page(s) 235–239

Abstract: Although Huntington's disease (HD) is a neurodegenerative disease characterized by motor, cognitive and behavioural disturbances, there has been little empirical data examining what patients are most concerned about throughout the different stages of ... ...

Abstract	Although Huntington's disease (HD) is a neurodegenerative disease characterized by motor, cognitive and behavioural disturbances, there has been little empirical data examining what patients are most concerned about throughout the different stages of disease, which can span many years. Semi-structured face-to-face interviews were individually conducted with 31 people living with different stages of Huntington's, from pre-clinical gene carriers to advanced stage. We examined how often participants raised issues and concerns regarding the impact of Huntington's on everyday life. The Physical/functional theme hardly featured pre-clinically, but was strongly present from Stage 1, rose steadily and peaked at Stage 5. There were no significant changes between stages for the Emotional, Social, and Self themes that all featured across all stages, indicating that these issues were not raised more frequently over the course of the disease. Likewise, the more rarely mentioned Financial and Legal themes also remained similar across stages. However, the Cognitive theme only featured between Stages 1 and 4, and hardly at all pre-clinically and at Stage 5. These findings provide insight into patients' important and unique perspective and have implications for the management and development of interventions across the spectrum of HD stages.
MeSH term(s)	Adaptation, Psychological ; Adult ; Aged ; Aged, 80 and over ; Cognition ; Disease Progression ; Emotions ; Female ; Humans ; Huntington Disease/genetics ; Huntington Disease/physiopathology ; Huntington Disease/psychology ; Interview, Psychological/methods ; Male ; Middle Aged ; Quality of Life/psychology ; Severity of Illness Index ; Social Conformity ; Social Desirability ; Statistics, Nonparametric
Language	English
Publishing date	2011-08-04
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	221209-2
ISSN	1399-0004 ; 0009-9163
ISSN (online)	1399-0004
ISSN	0009-9163
DOI	10.1111/j.1399-0004.2011.01748.x
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Article ; Online: Speech and oro-motor function in children with developmental coordination disorder: a pilot study.

Ho, A K / Wilmut, K

Human movement science

2010 Volume 29, Issue 4, Page(s) 605–614

Abstract: The protracted maturation and development of speech articulation underlies the complexity of the skill, and suggests it may be an area susceptible to a general deficit in motor control. Recent research suggests a high co-occurrence between Developmental ... ...

Abstract	The protracted maturation and development of speech articulation underlies the complexity of the skill, and suggests it may be an area susceptible to a general deficit in motor control. Recent research suggests a high co-occurrence between Developmental Coordination Disorder (DCD) and disordered speech production. Despite this there has been no systematic investigation of speech motor control in children with DCD. We conducted a pilot study which looked at speech motor control in a group of children with DCD (N=5) and a group typically developing (TD) children (N=5). Movements of the upper and lower lip were recorded during non-verbal movements, single words, syllable sequences, and sentence repetition. In the baseline conditions (normal talking speed or an isolated utterance) children with DCD demonstrated a typical pattern of movement, albeit a slower and shorter movement. In contrast, when task complexity was increased the children with DCD showed an atypical pattern of movement. It was concluded that children with DCD demonstrate inferior motor control for complex speech gestures, suggesting that the motor deficit in DCD may indeed be a more generalized phenomenon affecting the speech motor system.
MeSH term(s)	Adolescent ; Biomechanical Phenomena ; Child ; Dysarthria/diagnosis ; Dysarthria/physiopathology ; Female ; Humans ; Lip/physiopathology ; Male ; Motor Skills Disorders/diagnosis ; Motor Skills Disorders/physiopathology ; Phonation/physiology ; Pilot Projects ; Speech Articulation Tests ; Verbal Behavior/physiology
Language	English
Publishing date	2010-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	601851-8
ISSN	1872-7646 ; 0167-9457
ISSN (online)	1872-7646
ISSN	0167-9457
DOI	10.1016/j.humov.2010.01.007
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Article ; Online: The adrenergic-regulated CRTC1 and CRTC2 phosphorylation and cellular distribution is independent of endogenous SIK1 in the male rat pinealocyte.

McTague, J / Ferguson, M / Chik, C L / Ho, A K

Molecular and cellular endocrinology

2015 Volume 414, Page(s) 156–167

Abstract: Salt inducible kinase 1 (SIK1) has been reported to repress cAMP-response element binding protein (CREB)-mediated gene transcription by causing the nuclear export of CREB-regulated transcription coactivators (CRTCs) through phosphorylation. Although the ... ...

Abstract	Salt inducible kinase 1 (SIK1) has been reported to repress cAMP-response element binding protein (CREB)-mediated gene transcription by causing the nuclear export of CREB-regulated transcription coactivators (CRTCs) through phosphorylation. Although the repressor role of SIK1 in suppressing the expression of arylalkylamine N-acetyltransferase, the enzyme that controls the daily rhythm in melatonin production in the rat pineal gland, has been established, whether SIK1 regulates the phosphorylation and localization of CRTC1 and CRTC2 in this tissue remains unclear. The present study found that overexpressing SIK1 in NE-stimulated rat pinealocytes could increase the phosphorylation of CRTC1 and CRTC2, reduced selectively the nuclear level of CRTC2 (but not that of CRTC1), and elevated the cytosolic levels of both CRTC1 and CRTC2. In contrast, transient knockdown of endogenous SIK1 had no effect on the phosphorylation or distribution of CRTC1 and CRTC2 in norepinephrine (NE)-stimulated pinealocytes. Our results also showed that adrenergic blockade during NE stimulation led to a rapid rephosphorylation and decline in the nucleus levels of CRTC1 and CRTC2; however SIK1 knockdown had no effect on this rapid rephosphorylation. Moreover, studies with kinase inhibitors revealed that kinase(s) sensitive to KT5823 appeared to be involved in this rapid rephosphorylation. Together, these results indicate that although overexpressing SIK1 can phosphorylate CRTC1 and CRTC2 in the NE-stimulated pinealocyte, the endogenous SIK1, in spite of its induction by NE, does not appear to be the main regulator of the phosphorylation and intracellular localization of these two coactivators.
MeSH term(s)	Adrenergic alpha-Agonists/pharmacology ; Animals ; Cell Nucleus/drug effects ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytosol/drug effects ; Cytosol/metabolism ; Gene Expression Regulation/drug effects ; Male ; Norepinephrine/pharmacology ; Phosphorylation/drug effects ; Pineal Gland/cytology ; Pineal Gland/drug effects ; Pineal Gland/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Adrenergic alpha-Agonists ; CRTC2 protein, rat ; Crtc1 protein, rat ; Trans-Activators ; Transcription Factors ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Sik1 protein, rat (EC 2.7.11.1) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2015-10-15
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2015.07.021
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Article: Success rate of resuscitation after out-of-hospital cardiac arrest.

Ho, A M H / Mizubuti, G B / Ho, A K / Wan, S / Sydor, D / Chung, D C

Hong Kong medical journal = Xianggang yi xue za zhi

2019 Volume 25, Issue 3, Page(s) 254–256

MeSH term(s)	Cardiopulmonary Resuscitation ; Emergency Medical Services ; Hong Kong ; Humans ; Out-of-Hospital Cardiac Arrest
Language	English
Publishing date	2019-06-10
Publishing country	China
Document type	Journal Article ; Comment
ZDB-ID	1239255-8
ISSN	1024-2708
ISSN	1024-2708
DOI	10.12809/hkmj187596
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Article ; Online: The Huntington's Disease health-related Quality of Life questionnaire (HDQoL): a disease-specific measure of health-related quality of life.

Hocaoglu, M B / Gaffan, E A / Ho, A K

Clinical genetics

2012 Volume 81, Issue 2, Page(s) 117–122

Abstract: Huntington's disease (HD) is a genetic neurodegenerative disorder characterized by motor, cognitive and psychiatric disturbances, and yet there is no disease-specific patient-reported health-related quality of life outcome measure for patients. Our aim ... ...

Abstract	Huntington's disease (HD) is a genetic neurodegenerative disorder characterized by motor, cognitive and psychiatric disturbances, and yet there is no disease-specific patient-reported health-related quality of life outcome measure for patients. Our aim was to develop and validate such an instrument, i.e. the Huntington's Disease health-related Quality of Life questionnaire (HDQoL), to capture the true impact of living with this disease. Semi-structured interviews were conducted with the full spectrum of people living with HD, to form a pool of items, which were then examined in a larger sample prior to data-driven item reduction. We provide the statistical basis for the extraction of three different sets of scales from the HDQoL, and present validation and psychometric data on these scales using a sample of 152 participants living with HD. These new patient-derived scales provide promising patient-reported outcome measures for HD.
MeSH term(s)	Adult ; Aged ; Female ; Humans ; Huntington Disease/epidemiology ; Huntington Disease/psychology ; Male ; Middle Aged ; Psychometrics ; Quality of Life ; Reproducibility of Results ; Surveys and Questionnaires
Language	English
Publishing date	2012-01-18
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	221209-2
ISSN	1399-0004 ; 0009-9163
ISSN (online)	1399-0004
ISSN	0009-9163
DOI	10.1111/j.1399-0004.2011.01823.x
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Article ; Online: Sustained adrenergic stimulation is required for the nuclear retention of TORC1 in male rat pinealocytes.

McTague, J / Ferguson, M / Chik, C L / Ho, A K

Endocrinology

2013 Volume 154, Issue 9, Page(s) 3240–3250

Abstract: The process involved in relocation of the coactivator, transducer of regulated cAMP-regulated element-binding protein (TORC) to the cytoplasm, unlike its activation, is not well understood. Using cultured pineal cells prepared from male rats, we found ... ...

Abstract	The process involved in relocation of the coactivator, transducer of regulated cAMP-regulated element-binding protein (TORC) to the cytoplasm, unlike its activation, is not well understood. Using cultured pineal cells prepared from male rats, we found that although both α- and β-adrenergic stimulation could cause TORC1 dephosphorylation, only α-adrenergic stimulation was effective in the norepinephrine (NE)-mediated translocation of TORC1 into the nucleus. In contrast, blockade of either the α- or the β-adrenergic receptor after NE stimulation was effective in causing the rephosphorylation and rapid relocation of TORC1 into the cytoplasm. Studies with phosphoprotein phosphatase (PP) inhibitors indicated that although both PP2A and PP2B could dephosphorylate TORC1, only PP2B could cause translocation into the nucleus. However, after NE stimulation, treatment with either PP2A or PP2B inhibitors could cause the rephosphorylation and cytoplasmic relocation of TORC1. These results indicate a requirement of continuous activation of both α- and β-adrenergic receptors as well as PP2A and PP2B activities for the nuclear retention of TORC1 during NE stimulation. Knockdown of salt-inducible kinase 1 (SIK1) had no effect on the phosphorylation or localization of TORC1. Although overexpressing SIK1 could induce TORC1 phosphorylation in the nucleus, it did not reduce TORC1 level in the nucleus, indicating that SIK1-mediated TORC1 phosphorylation may not be sufficient for its relocation into the cytoplasm. Together, these results demonstrate that, in the rat pineal gland, different mechanisms are involved in regulating the nuclear entry and exit of TORC1 and that the SIK1-mediated phosphorylation of TORC1 may not lead to its nuclear exit.
MeSH term(s)	Adrenergic Agonists/pharmacology ; Adrenergic Antagonists/pharmacology ; Animals ; Biological Transport/drug effects ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytoplasm/drug effects ; Cytoplasm/metabolism ; Enzyme Inhibitors/pharmacology ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/metabolism ; Male ; Mechanistic Target of Rapamycin Complex 1 ; Multiprotein Complexes/metabolism ; Nerve Tissue Proteins/agonists ; Nerve Tissue Proteins/antagonists & inhibitors ; Nerve Tissue Proteins/metabolism ; Neuroendocrine Cells/cytology ; Neuroendocrine Cells/drug effects ; Neuroendocrine Cells/metabolism ; Norepinephrine/metabolism ; Phosphorylation/drug effects ; Pineal Gland/cytology ; Pineal Gland/drug effects ; Pineal Gland/metabolism ; Protein Phosphatase 2/antagonists & inhibitors ; Protein Phosphatase 2/metabolism ; Protein Processing, Post-Translational/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, alpha/chemistry ; Receptors, Adrenergic, alpha/metabolism ; Receptors, Adrenergic, beta/chemistry ; Receptors, Adrenergic, beta/metabolism ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Adrenergic Agonists ; Adrenergic Antagonists ; Enzyme Inhibitors ; Isoenzymes ; Multiprotein Complexes ; Nerve Tissue Proteins ; Receptors, Adrenergic, alpha ; Receptors, Adrenergic, beta ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Protein Phosphatase 2 (EC 3.1.3.16) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2013-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2013-1293
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Article ; Online: Different signaling mechanisms are involved in the norepinephrine-stimulated TORC1 and TORC2 nuclear translocation in rat pinealocytes.

McTague, J / Amyotte, N / Kanyo, R / Ferguson, M / Chik, C L / Ho, A K

Endocrinology

2012 Volume 153, Issue 8, Page(s) 3839–3849

Abstract: The distribution of transducers of regulated cAMP-response element-binding protein activity (TORC) between the cytoplasm and the nucleus is tightly regulated and represents one of the main mechanisms whereby the cAMP response element activation ... ...

Abstract	The distribution of transducers of regulated cAMP-response element-binding protein activity (TORC) between the cytoplasm and the nucleus is tightly regulated and represents one of the main mechanisms whereby the cAMP response element activation activities of TORC are controlled. Whereas both cAMP and Ca(2+) pathways can cause translocation of TORC, the relative importance of these two pathways in regulating different TORC within the same cell is unclear. In this study, we determined the mechanism that regulated TORC1 translocation and compared it with that of TORC2 in rat pinealocytes. Stimulation of pinealocytes with norepinephrine (NE), although having no effect on Torc1 transcription, caused rapid dephosphorylation of TORC1. Although NE also caused rapid dephosphorylation of TORC2, pharmacological studies revealed that TORC1 dephosphorylation could be induced by both β-adrenoceptor/cAMP and α-adrenoceptor/intracellular Ca(2+) pathways contrasting with TORC2 dephosphorylation being induced mainly through the β-adrenoceptor/cAMP pathway. PhosTag gel indicated a different pattern of TORC1 desphosphorylation resulting from the selective activation of α- or β-adrenoceptors. Interestingly, only the α-adrenoceptor/intracellular Ca(2+)-mediated dephosphorylation could translocate TORC1 to the nucleus, whereas the β-adrenoceptor/cAMP-mediated dephosphorylation of TORC1 was ineffective. In comparison, translocation of TORC2 was induced predominantly by the β-adrenoceptor/cAMP pathway. Studies with different protein phosphatase (PP) inhibitors indicated that the NE-mediated translocation of TORC1 was blocked by cyclosporine A, a PP2B inhibitor, but that of TORC2 was blocked by okadaic acid, a PP2A inhibitor. Together these results highlight different intracellular signaling pathways that are involved in the NE-stimulated dephosphorylation and translocation of TORC1 and TORC2 in rat pinealocytes.
MeSH term(s)	Animals ; Blotting, Western ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cells, Cultured ; Male ; Norepinephrine/pharmacology ; Pineal Gland/cytology ; Protein Transport/drug effects ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	CRTC2 protein, rat ; Crtc1 protein, rat ; Trans-Activators ; Transcription Factors ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2012-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2012-1315
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Article ; Online: Salt-inducible kinase 1 in the rat pinealocyte: adrenergic regulation and role in arylalkylamine N-acetyltransferase gene transcription.

Kanyo, R / Price, D M / Chik, C L / Ho, A K

Endocrinology

2009 Volume 150, Issue 9, Page(s) 4221–4230

Abstract: The recognition of the basic leucine zipper domain in the regulation of transcriptional activity of cAMP response element-binding protein by salt-inducible kinase (SIK) prompted our investigation of the regulatory role of this kinase in the induction of ... ...

Abstract	The recognition of the basic leucine zipper domain in the regulation of transcriptional activity of cAMP response element-binding protein by salt-inducible kinase (SIK) prompted our investigation of the regulatory role of this kinase in the induction of Aa-nat and other cAMP-regulated genes in the rat pineal gland. Here we report Sik1 expression was induced by norepinephrine (NE) in rat pinealocytes primarily through activation of beta-adrenergic receptors, with a minor contribution from activation of alpha-adrenergic receptors. Treatments with dibutyryl cAMP, and to a lesser extent, agents that elevate intracellular Ca(2+) mimicked the effect of NE on Sik1 expression. In parallel to the results of the pineal cell culture studies, a marked nocturnal induction of Sik1 transcription was found in whole-animal studies. Knockdown of Sik1 by short hairpin RNA amplified the NE-stimulated Aa-nat transcription and other adrenergic-regulated genes, including Mapk phosphatase 1, inducible cAMP repressor, and type 2 iodothyronine deiodinase in a time-dependent manner. In contrast, overexpressing Sik1 had an inhibitory effect on the NE induction of Aa-nat and other adrenergic-regulated genes. Together, our results indicate that the adrenergic induction of Sik1 in the rat pineal gland is primarily through the beta-adrenergic receptor --> protein kinase A pathway. SIK1 appears to function as part of an endogenous repressive mechanism that regulates the peak and indirectly the duration of expression of Aa-nat and other cAMP-regulated genes. These findings support a role for SIK1 in framing the temporal expression profile of Aa-nat and other adrenergic-regulated genes in the rat pineal gland.
MeSH term(s)	Animals ; Arylalkylamine N-Acetyltransferase/biosynthesis ; Bucladesine/pharmacology ; Cells, Cultured ; Circadian Rhythm ; Cycloheximide/pharmacology ; Darkness ; Dibutyryl Cyclic GMP/pharmacology ; Enzyme Induction ; Ionomycin/pharmacology ; Male ; Norepinephrine/pharmacology ; Photoperiod ; Pineal Gland/cytology ; Pineal Gland/metabolism ; Protein-Serine-Threonine Kinases/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, alpha-1/physiology ; Receptors, Adrenergic, beta-1/physiology ; Tetradecanoylphorbol Acetate/pharmacology
Chemical Substances	Receptors, Adrenergic, alpha-1 ; Receptors, Adrenergic, beta-1 ; Dibutyryl Cyclic GMP (32266-35-6) ; Ionomycin (56092-81-0) ; Bucladesine (63X7MBT2LQ) ; Cycloheximide (98600C0908) ; Arylalkylamine N-Acetyltransferase (EC 2.3.1.87) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Sik1 protein, rat (EC 2.7.11.1) ; Tetradecanoylphorbol Acetate (NI40JAQ945) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2009-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2009-0275
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