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Dive into the research topics where Alfreda Stadlin is active.

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Featured researches published by Alfreda Stadlin.


Neuroreport | 2001

Association between mu opioid receptor gene polymorphisms and Chinese heroin addicts.

Carol Y. K. Szeto; Nelson L.S. Tang; Dominic T. S. Lee; Alfreda Stadlin

Mu opioid receptor (MOR) has been shown to be associated with alcoholism and opioid dependence. The present study examined the involvement of a polymorphism in A118G in exon 1 and C1031G in intron 2 of the MOR gene in 200 Chinese heroin-dependent and 97 control subjects. Results showed a significant association for both A118G and C1031G polymorphisms and opioid dependence. The G allele is more common in the heroin-dependent group (39.5% and 30.8% for A118G and C1031G polymorphisms, respectively) when compared to the controls (29.4% and 21.1% for A118G and C1031G polymorphisms, respectively). This study suggests that the variant G allele of both A118G and C1031G polymorphisms may contribute to the vulnerability to heroin dependence.


Drug and Alcohol Dependence | 2008

Impulsivity in Hong Kong-Chinese club-drug users

Natalie J. Loxton; Venice L.-N. Wan; Ada Man Choi Ho; B. K. L. Cheung; Nicole Tam; Freedom Leung; Alfreda Stadlin

To investigate the relationship between personality, club-drug use and high-risk drug-related behaviour, 360 club-drug users and 303 non-drug users in Hong Kong were assessed on measures of two impulsivity dimensions, reward drive and rash impulsivity, and a related trait of punishment sensitivity. The most frequently used drugs were ketamine, ecstasy, and cannabis, with the majority of participants using two or more drugs on any one occasion. Club-drug users were more rash-impulsive and reward-driven, and less punishment-sensitive than non-drug users (p<0.001). Rash impulsivity, but not reward drive or punishment sensitivity, was significantly (p<0.001) associated with risky drug-related behaviour. There was no association between any personality traits and preferred drug. These findings suggest that, while those who use club drugs are generally more impulsive and less punishment-sensitive, some discrete facets of impulsivity are associated with differing patterns of drug-use behaviour.


Annals of the New York Academy of Sciences | 2000

Methamphetamine-induced oxidative stress in cultured mouse astrocytes.

Josephine W.S. Lau; Solomon S. Senok; Alfreda Stadlin

Methamphetamine (METH) is a monoaminergic toxin that destroys dopamine terminals and causes astrogliosis in vivo. Oxidative stress has been shown to play an important role in the toxic effects of METH. In the present study, we sought to determine whether astrocytes are involved in METH‐induced oxidative stress. Reactive oxygen species (ROS), ATP, and change in mitochondria membrane potential (ΔΨm) were examined in cultured striatal, mesencephalic, and cortical astrocytes after 4 to 48 h of 4 mM METH treatment. Results showed that only striatal and mesencephalic astrocytes showed a significant increase in ROS formation from 8 and 12 h, respectively. At 48 h treatment, there was a 55 and 53% increase in ROS content in striatal and mesencephalic astrocytes, respectively, whereas cortical astrocytes showed only a 25% (not significant) increase. JC‐1, a ΔΨm‐sensitive dye, showed a decrease in ΔΨm at 8 h treatment for striatal and mesencephalic astrocytes and at 12 h for cortical astrocytes. Astrocytes from all three regions showed a similar pattern of initial increase followed by a decrease in ATP content, with striatal astrocytes resulting in a maximum depletion (39% of control value) at 48 h treatment. These findings showed that METH treatment resulted in the formation of ROS in the order of striatal > mesencephalic > cortical astrocytes. Although the formation of ROS did not severely interfere with ATP production, a depolarization of mitochondria was observed. The present study suggested that astrocytes may be an important element governing the selective vulnerability to the striatum to METH‐induced oxidative stress.


Brain Research | 1999

Oxidative stress induced by MPTP and MPP+: selective vulnerability of cultured mouse astrocytes

Steve S Wong; Raymond H.Y. Li; Alfreda Stadlin

Oxidative stress has been implicated in the pathogenesis of Parkinsons disease. In the present study, reactive oxygen species (ROS) formation and antioxidant enzyme superoxide dismutase (SOD) activities were examined in cultured cortical, striatal and mesencephalic mouse astrocytes after 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP) or 1-methyl-4-phenylpyridinium (MPP(+)) treatment. Linear regression analysis showed that control mesencephalic (slope coefficient=0.01) astrocytes had a three-fold (F-test, p<0.05) greater rate of change in ROS production when compared to cortical (0.003) or striatal (0.003) astrocytes. However, when treated with 500 microM MPTP for 120 min, mesencephalic and striatal astrocytes demonstrated a decreased and increased rate of change in ROS production respectively. On the other hand, when treated with 10 microM MPP(+), a significant increase in the rate of change in ROS formation was observed in both mesencephalic and striatal astrocytes, with mesencephalic astrocytes producing a four-fold greater increase when compared to striatal astrocytes. Cortical astrocytes did not show any significant changes in ROS production when treated with MPTP or MPP(+). When astrocytes were treated with MPTP over a 24 h period, striatal astrocytes demonstrated significant increases in SOD activity to 12 h, followed by a return towards control levels after 8 h treatment. In contrast, mesencephalic astrocytes showed trends for a decrease in SOD production as well as a significant decrease in ATP levels by 24 h MPTP treatment. The present results suggested that mesencephalic astrocytes are more vulnerable to oxidative stress when compared to striatal astrocytes, given their greater rates of ROS production at basal and MPP(+) conditions. Striatal astrocytes, on the other hand, may have a more protective capacity against oxidative stress by producing greater SOD activities.


Neurochemistry International | 2001

Effects of tumor necrosis factor alpha on taurine uptake in cultured rat astrocytes.

Raymond Chuen-Chung Chang; Alfreda Stadlin; D. Tsang

Taurine is known to play a major role in volume regulation in astrocytic swelling associated with stroke and brain trauma. Apart from brain edema, the severity of brain injury is related to the levels of inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha). TNFalpha had been shown to be closely associated with brain edema formation since the neutralization of TNFalpha reduced brain edema. Considering taurine has osmoregulatory functions in astrocytes, experiments were performed to study the effects of TNFalpha on taurine uptake in cultured astrocytes. Astrocytes exposed to 20 ng/ml of TNFalpha for 48 h showed a 91% increase in taurine uptake and significant increase was observed after 24 h exposure. This cytokine caused neither significant changes in cell volume nor taurine release. The increased in taurine uptake induced by TNFalpha was unlikely resulted from the modification of Na(+) movement because TNFalpha decreased tyrosine uptake, Na(+)-dependent transport system. In contrast to TNFalpha, interferon-gamma (IFNgamma) did not significantly affect taurine uptake. Taken together, our results did not support a suggestion that TNFalpha affects cell volume regulation via modulating taurine uptake in astrocytes. Increasing lines of evidence have demonstrated that taurine has anti-inflammatory and anti-oxidative effects, these findings therefore suggested that the increase in taurine uptake might be an adaptive response or a tool for astrocytes against oxidative stress.


Annals of the New York Academy of Sciences | 1998

A Selective Regional Response of Cultured Astrocytes to Methamphetaminea

Alfreda Stadlin; Josephine W.S. Lau; Y. K. Szeto

ABSTRACT: Methamphetamine (METH) has long‐lasting neurotoxic effects on the dopamine and forebrain serotonin systems. It was reported that METH would induce the release of glutamate within the striatum and that it also caused astrogliosis. The mechanisms of this release and subsequent neurotoxicity are not well defined. The aim of this study was to examine the response of cultured astrocytes after METH‐induced injury. Astrocytes were cultured from neonatal C57B1/6 mice brains. Cells were obtained from the mesencephalon, striatum and cortex in order to examine any regional differences. Cells were treated with 4 mM METH for 4, 8, 12, 24 and 48 hr. Lactate dehydrogenase (LDH) levels were used as a measure of cell viability. At various time points, Western blot analyses were performed to study the change in GFAP and vimentin (markers for astrogliosis) levels. Change in glutamine synthase (GS), the enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia in astrocytes, was also examined. The results showed that METH caused marked astrogliosis in striatal and mesencephalic astrocytes. Cells were transformed from protoplasmic (inactive) to fibrous (reactive) form after 48 hr treatment. There were also large amounts of vacuoles present in the cytoplasm of these cells. LDH results showed that there was only slight increase in enzyme levels after 48 hr treatment suggesting that the astrogliosis observed was not due to the decrease in cell viability. The amount of GS were depleted more rapidly in striatal astrocytes (50% of control by 8 hr treatment) followed by mesencephalic astrocytes (reaching 10% of control by 48 hr treatment). Cortical astrocytes showed only a 48% depletion by 48 hr treatment, indicating that they are more resistant to METH‐induced toxicity. The rapid depletion of GS obtained in striatal and mesencephalic astrocytes suggested that astrocytes of the dopaminergic system are more sensitive to METH‐induced injury. This may be due to the direct effects of METH‐induced oxidative stress on the mitochondria of these cells resulting in GS depletion and astrogliosis.


Addictive Behaviors | 2014

Dependent heroin use and associated risky behaviour: The role of rash impulsiveness and reward sensitivity

Lakal Odatha Dissabandara; Natalie J. Loxton; Shavindra R. Dias; P. R. Dodd; Mark Daglish; Alfreda Stadlin

Impulsive temperament has long been considered as a risk factor for substance use disorders (SUD). Considering the heterogeneity of impulsivity, a biologically-based 2-factor model incorporating reward sensitivity and rash impulsiveness facets, has been proposed. Here we report how these two facets of impulsiveness could be associated with different aspects of dependent heroin use and associated risky behaviour. Two hundred and ninety three dependent heroin users and 232 non-users were assessed on reward sensitivity, rash impulsivity, and the related trait of punishment sensitivity. After adjusting for multiple comparisons, heroin users were found to be more rash-impulsive and reward-sensitive than non-users (p<0.001). Within users, rash impulsivity was associated with high risk behaviour including escalating heroin consumption, injecting heroin use, hazardous drinking, low treatment-seeking and risky sexual behaviour. Reward sensitivity was uniquely associated with early onset of drug use. While greater impulsivity is a common trait in drug users compared with non-users, the use of a 2-factor model of impulsivity provides additional information regarding specific aspects of drug initiation and maintenance that can be targeted in the prevention and treatment of heroin dependence.


Brain Research | 1994

Postnatal changes in [3H]mazindol-labelled dopamine uptake sites in the rat striatum following prenatal cocaine exposure

Alfreda Stadlin; Heung Ling Choi; D. Tsang

The present study showed that prenatal cocaine exposure (60 mg/kg/day) has a transient effect on the [3H]mazindol-labelled dopamine uptake sites in the striatum of the rat offspring examined from postnatal week 0-32. There is a 39% and 21% decrease in the number of binding sites (Bmax) in the cocaine-exposed group at postnatal weeks 3 and 4, respectively, with a recovery to near normal values by postnatal week 8.


Life Sciences | 2001

Induction of tumor necrosis factor receptor type 2 gene expression by tumor necrosis factor-α in rat primary astrocytes

Hong Lok Lung; K.N. Leung; Alfreda Stadlin; C.M. Ma; D. Tsang

Using reverse transcription-polymerase chain reaction (RT-PCR) technique, the messenger RNA (mRNA) for tumor necrosis factor receptor type 2 (TNF-R2, 75/80 kDa) was detected in rat primary astrocytes, with much lower level of expression when compared to that for tumor necrosis factor receptor type 1 (TNF-R1, 55/60 kDa). Upon exposure to TNF-alpha (100 U/ml), the TNF-R2 mRNA level was greatly enhanced at 8 h, while TNF-R1 mRNA remained unchanged even after 24 h. The induction of TNF-R2 gene expression by TNF-alpha was dose-dependent and seemed to be unique to TNF-alpha, as interleukin-6 (IL-6) had no significant effect on TNF-R2 expression. Since TNF-R2 was reported to mediate mitogenic and gene-inducing effects in many other cell types, it is likely that the reported proliferative effect of TNF-alpha on astrocytes was also mediated by this TNF receptor subtype. Upon exposure to TNF-alpha or lipopolysaccharide (LPS), the expression of TNF-alpha gene was induced, and the LPS-induced TNF-alpha seemed to selectively enhance the TNF-R2 gene expression. Collectively, our results suggest that the TNF-alpha or LPS-induced expression of both TNF-R2 and TNF-alpha may provide a positive control mechanism to further enhance the proliferative effect of TNF-alpha in astrocytes.


American Journal of Medical Genetics | 2007

Association Analysis of GABA Receptor Subunit Genes on 5q33 With Heroin Dependence in a Chinese Male Population

E.W. Loh; Nelson L.S. Tang; D.T.S. Lee; S.I. Liu; Alfreda Stadlin

GABAA receptor subunit genes clustered on 5q33 play a role in the development of alcoholism and methamphetamine use disorder without psychosis. The present study explored the possible contribution of the same subunit genes to the development of heroin dependence. Single nucleotide polymorphisms (SNPs) of the GABAA receptor subunits GABRB2, GABRA6, GABRA1, and GABRG2 were examined in 178 male Han Chinese heroin‐dependent and 170 male control subjects. A significant difference in allele frequency for the SNP rs211014 in the GABAAγ2 receptor subunit gene between cases and controls was identified (P = 0.015). A possible mechanism for the involvement of the GABA receptor subunit genes on 5q33 in the development of heroin dependence is discussed.

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P. R. Dodd

University of Queensland

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Mark Daglish

University of Queensland

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D. Tsang

The Chinese University of Hong Kong

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Nelson L.S. Tang

The Chinese University of Hong Kong

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Heung Ling Choi

The Chinese University of Hong Kong

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