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Displaying publications 21 - 29 of 29 in total

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Single-centre study of therapeutic drug monitoring of posaconazole in lung transplant recipients: factors affecting trough plasma concentrations

Jeong W, Snell GI, Levvey BJ, Westall GP, Morrissey CO, Wolfe R, et al.

J Antimicrob Chemother, 2018 Mar 01;73(3):748-756.
PMID: 29211913 DOI: 10.1093/jac/dkx440

Objectives: This study describes therapeutic drug monitoring (TDM) of posaconazole suspension and modified release (MR) tablets in lung transplant (LTx) recipients and evaluates factors that may affect posaconazole trough plasma concentration (Cmin).
Methods: A single-centre, retrospective study evaluating posaconazole Cmin in LTx recipients receiving posaconazole suspension or MR tablets between January 2014 and December 2016.
Results: Forty-seven LTx patients received posaconazole suspension, and 78 received the MR tablet formulation; a total of 421 and 617 Cmin measurements were made, respectively. Posaconazole was concurrently administered with proton pump inhibitor in ≥ 90% of patients. The median (IQR) of initial posaconazole Cmin following 300 mg daily of posaconazole tablet was significantly higher than that of 800 mg daily of posaconazole suspension [1.65 (0.97-2.13) mg/L versus 0.81 (0.48-1.15) mg/L, P tremor, lethargy, sweating, nausea/vomiting and weight loss) were reported in 3/78 (4%) patients receiving posaconazole MR tablets. Posaconazole Cmin in these three patients was determined to be 9.6, 6.2 and 2.3 mg/L.
Conclusions: The current study has provided clinically important insights into the TDM of posaconazole in LTx recipients. Routine TDM should be undertaken in LTx recipients receiving posaconazole suspension and/or MR tablets.

Matched MeSH terms: Tremor
Noncoding CGG repeat expansions in neuronal intranuclear inclusion disease, oculopharyngodistal myopathy and an overlapping disease

Ishiura H, Shibata S, Yoshimura J, Suzuki Y, Qu W, Doi K, et al.

Nat Genet, 2019 08;51(8):1222-1232.
PMID: 31332380 DOI: 10.1038/s41588-019-0458-z

Noncoding repeat expansions cause various neuromuscular diseases, including myotonic dystrophies, fragile X tremor/ataxia syndrome, some spinocerebellar ataxias, amyotrophic lateral sclerosis and benign adult familial myoclonic epilepsies. Inspired by the striking similarities in the clinical and neuroimaging findings between neuronal intranuclear inclusion disease (NIID) and fragile X tremor/ataxia syndrome caused by noncoding CGG repeat expansions in FMR1, we directly searched for repeat expansion mutations and identified noncoding CGG repeat expansions in NBPF19 (NOTCH2NLC) as the causative mutations for NIID. Further prompted by the similarities in the clinical and neuroimaging findings with NIID, we identified similar noncoding CGG repeat expansions in two other diseases: oculopharyngeal myopathy with leukoencephalopathy and oculopharyngodistal myopathy, in LOC642361/NUTM2B-AS1 and LRP12, respectively. These findings expand our knowledge of the clinical spectra of diseases caused by expansions of the same repeat motif, and further highlight how directly searching for expanded repeats can help identify mutations underlying diseases.

Matched MeSH terms: Tremor/genetics*; Tremor/pathology
Fulltext Delayed neuropsychiatric sequelae of carbon monoxide poisoning: a case report

Nurul Azreen Hashim, Norley Shuib, Salina Mohamed, Ling SL, Khariah Mat Nor

Journal of Clinical and Health Sciences, 2016;1:64-68.

Delayed neuropsychiatric sequelae is an important condition which commonly occur during recovery from acute carbon monoxide poisoning. Typical presentation would be apathy, disorientation, amnesia, hypokinesia, bizarre behavior, insomnia and neurological manifestations such as gait disturbance, hypertonia and tremor. We report here a case of a man presented with delayed neuropsychiatric sequelae one month after the carbon monoxide poisoning in his suicidal attempt. He presented with the typical presentation and diagnosis confirmed with the MRI findings. His MRI showed abnormal signal in subcortical hemisphere white matter of both temporo-fronto-parietal-occipital regions along the insula and both globus pallidus. He was treated with Olanzapine, Fluvoxamine, Chlorpromazine and Levodopa and his condition slowly improved. It is important for clinicians to recognize the symptoms and risk factors to develop delayed neuropsychiatric sequelae in patients who previously had carbon monoxide poisoning.

Matched MeSH terms: Tremor
Neuropharmacological potentials of β-carboline alkaloids for neuropsychiatric disorders

Ayipo YO, Mordi MN, Mustapha M, Damodaran T

Eur J Pharmacol, 2021 Feb 15;893:173837.
PMID: 33359647 DOI: 10.1016/j.ejphar.2020.173837

Neuropsychiatric disorders are diseases of the central nervous system (CNS) which are characterised by complex pathomechanisms that including homeostatic failure, malfunction, atrophy, pathology remodelling and reactivity anomaly of the neuronal system where treatment options remain challenging. β-Carboline (βC) alkaloids are scaffolds of structurally diverse tricyclic pyrido[3,4-b]indole alkaloid with vast occurrence in nature. Their unique structural features which favour interactions with enzymes and protein receptor targets account for their potent neuropharmacological properties. However, our current understanding of their biological mechanisms for these beneficial effects, especially for neuropsychiatric disorders is sparse. Therefore, we present a comprehensive review of the scientific progress in the last two decades on the prospective pharmacology and physiology of the βC alkaloids in the treatment of some neuropsychiatric conditions such as depression, anxiety, Alzheimer's disease, Parkinson's disease, brain tumour, essential tremor, epilepsy and seizure, licking behaviour, dystonia, agnosia, spasm, positive ingestive response as demonstrated in non-clinical models. The current evidence supports that βC alkaloids offer potential therapeutic agents against most of these disorders and amenable for further drug design.

Matched MeSH terms: Essential Tremor
Fulltext MicroRNA Dysregulation in Parkinson's Disease: A Narrative Review

Nies YH, Mohamad Najib NH, Lim WL, Kamaruzzaman MA, Yahaya MF, Teoh SL

Front Neurosci, 2021;15:660379.
PMID: 33994934 DOI: 10.3389/fnins.2021.660379

Parkinson's disease (PD) is a severely debilitating neurodegenerative disease, affecting the motor system, leading to resting tremor, cogwheel rigidity, bradykinesia, walking and gait difficulties, and postural instability. The severe loss of dopaminergic neurons in the substantia nigra pars compacta causes striatal dopamine deficiency and the presence of Lewy bodies indicates a pathological hallmark of PD. Although the current treatment of PD aims to preserve dopaminergic neurons or to replace dopamine depletion in the brain, it is notable that complete recovery from the disease is yet to be achieved. Given the complexity and multisystem effects of PD, the underlying mechanisms of PD pathogenesis are yet to be elucidated. The advancement of medical technologies has given some insights in understanding the mechanism and potential treatment of PD with a special interest in the role of microRNAs (miRNAs) to unravel the pathophysiology of PD. In PD patients, it was found that striatal brain tissue and dopaminergic neurons from the substantia nigra demonstrated dysregulated miRNAs expression profiles. Hence, dysregulation of miRNAs may contribute to the pathogenesis of PD through modulation of PD-associated gene and protein expression. This review will discuss recent findings on PD-associated miRNAs dysregulation, from the regulation of PD-associated genes, dopaminergic neuron survival, α-synuclein-induced inflammation and circulating miRNAs. The next section of this review also provides an update on the potential uses of miRNAs as diagnostic biomarkers and therapeutic tools for PD.

Matched MeSH terms: Tremor
Fulltext Congenital biliary anomaly with secondary cholangiohepatitis in a Siamese cross kitten

Yiew, X.T., Leong, Z.P., Rahman, N., Watanabe, M., Noordin, M.M., Khor, K.H.

Jurnal Veterinar Malaysia, 2016;28(1):7-11.
MyJurnal

A 5-month-old Siamese cross kitten was presented with jaundice and a palpable abdominal mass at the right cranial quadrant. The extra-hepatic biliary system was markedly distended upon abdominal ultrasonography. Complete bile duct obstruction was ruled out due to the presence of urobilinogen, light brown stool, and consistentlynormal alkaline phosphatase (ALP) levels. Head tremors developed on the second day of hospitalization. Tentative diagnoses of congenital biliary anomaly and hepatic encephalopathy werederived and exploratory laparotomy revealed a severely distended and tortuous bile duct indistinguishable from the gallbladder with negative duodenal filling. Modified cholechoduodenostomy was performed however the kitten did not recover from general anaesthesia. Secondary cholangiohepatitis and hepatic encephalopathy were confirmed upon histopathologic examination.Primary congenital biliary atresia or choledochal cyst with secondary cholangiohepatitis was suspected. Biliary anomalies are rare in cats with only two cases reported in the literature. These conditions are often challenging to diagnose and due to the limited treatment options, have a poor prognosis.

Matched MeSH terms: Tremor
Parkinson's disease: Cause factors, measurable indicators, and early diagnosis

Bhat S, Acharya UR, Hagiwara Y, Dadmehr N, Adeli H

Comput Biol Med, 2018 11 01;102:234-241.
PMID: 30253869 DOI: 10.1016/j.compbiomed.2018.09.008

Parkinson's disease (PD) is a neurodegenerative disease of the central nervous system caused due to the loss of dopaminergic neurons. It is classified under movement disorder as patients with PD present with tremor, rigidity, postural changes, and a decrease in spontaneous movements. Comorbidities including anxiety, depression, fatigue, and sleep disorders are observed prior to the diagnosis of PD. Gene mutations, exposure to toxic substances, and aging are considered as the causative factors of PD even though its genesis is unknown. This paper reviews PD etiologies, progression, and in particular measurable indicators of PD such as neuroimaging and electrophysiology modalities. In addition to gene therapy, neuroprotective, pharmacological, and neural transplantation treatments, researchers are actively aiming at identifying biological markers of PD with the goal of early diagnosis. Neuroimaging modalities used together with advanced machine learning techniques offer a promising path for the early detection and intervention in PD patients.

Matched MeSH terms: Tremor
Hypokalemic periodic paralysis due to Graves disease

Drakaki A, Habib M, Sweeney AT

Am J Med, 2009 Dec;122(12):e5-6.
PMID: 19958876 DOI: 10.1016/j.amjmed.2009.06.016

Hypokalemic thyrotoxic periodic paralysis is a potentially life-threatening complication of hyperthyroidism, defined by 3 characteristic features: thyrotoxicosis, hypokalemia, and acute painless muscle weakness. In this case, a 25-year-old Malaysian man presented with acute, painless lower extremity weakness immediately after a meal. His associated symptoms included palpitations, tremor, and anxiety. He also reported a 30-pound unintentional weight loss over the previous 18 months, dyspnea on exertion, and insomnia.

Matched MeSH terms: Tremor/etiology
Fulltext Pathological findings in a mouse model of Japanese encephalitis infected via the footpad

Fu, Tzeh Long, Ong, Kien Chai, Wong, Kum Thong

Neurology Asia, 2015;20(4):349-354.
MyJurnal

We have developed and characterised a mouse model of Japanese encephalitis virus (JEV) infection via
footpad inoculation in order to better mimic viral transmission by mosquito bites. Two-week-old and
5-week-old mice consistently developed signs of infection such as ruffled fur, weight loss, hunchback
posture, tremors, mask-like facies and occasionally, hindlimb paralysis at 4 days post infection (dpi)
and 11-13 dpi, respectively. Most of the animals died within 24 to 48 hours following the onset of signs
of infection, with mortalities of 100% and 33.3% in 2-week-old and 5-week-old mice, respectively.
Mild meningitis and variable parenchymal inflammation with formation of microglial nodules, focal
necrosis and neuronophagia, and perivascular cuffing by inflammatory cells were observed in the
caudate nucleus, putamen, thalamus, cerebral cortex, brainstem, and spinal cord. Viral antigens/RNA
were demonstrated by immunohistochemisty and in situ hybridization, respectively, in most of these
areas as well as in the hippocampus and cerebellum, albeit more focally. The pathological findings in
this mouse model were generally similar to human Japanese encephalitis (JE) and other established JE
models but perhaps, compared to other JEV mouse models, it demonstrates lethal encephalitic infection
more consistently. We believe that our mouse model should be useful to study the pathogenesis of JE,
and for testing anti-viral drugs and vaccines

Matched MeSH terms: Tremor