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Only five patients diagnosed with transverse myelitis (TM) associated with primary biliary cirrhosis (PBC) have been reported in the literature to date. We report two additional patients with TM associated with PBC at our hospital and review all seven cases.

An association between neuromyelitis optic spectrum disease (NMOSD) and PBC is reported for the first time in one of our patients. The second patient was diagnosed with TM associated with PBC without Sjögren's syndrome (SS). A literature review was performed using the PubMed database.

All patients diagnosed with TM associated with PBC were female with a median age of 53 years. TM was associated with SS in 71.4% of the patients. Complete TM and incomplete TM were diagnosed in 71.4% and 28.6% of the patients. The erythrocyte sedimentation rate was increased in 83.3% of patients. All patients were positive for anti-mitochondrial antibodies. Other autoantibodies, including anti-nuclear antibodies, rheumatoid factor, anti-SSA antibody, were detected in some patients. Cerebrospinal fluid analysis was abnormal in 83.3% of patients. CDK inhibitor The spinal cord lesions involved more than three vertebral segments in 85.7% of patients. Glucocorticoids were administered in 85.7% of patients, and good responses were observed.

The association between TM and PBC may be missed by neurologists. More attention should be paid to the association between NMOSD and PBC. Most patients show SS and may experience relapse, and there is a good rationale for early commencement of immunosuppressive therapy.

The association between TM and PBC may be missed by neurologists. More attention should be paid to the association between NMOSD and PBC. Most patients show SS and may experience relapse, and there is a good rationale for early commencement of immunosuppressive therapy.

The current study aimed to extend findings of a study comparing two psychosocial treatments for ADHD in Latinx youth by examining if parental ADHD knowledge improves following treatment and if parental gender differences in ADHD knowledge exist.

Following a comprehensive ADHD assessment, 58 Latinx families of school-aged children (mean age of 8 years) were randomly assigned to either culturally-adapted treatment (CAT) or standard evidence-based treatment (EBT). Parents completed an ADHD Knowledge measure both pre- and post-treatment.

Latinx mothers demonstrated greater knowledge of ADHD symptomatology than fathers at pre-treatment. CAT resulted in improvements in parental knowledge of ADHD for both mothers and fathers, whereas standard EBT resulted in no change in maternal knowledge and reduced paternal knowledge of ADHD symptomatology. Clinical implications will be discussed.

Latinx mothers demonstrated greater knowledge of ADHD symptomatology than fathers at pre-treatment. CAT resulted in improvements in parental knowledge of ADHD for both mothers and fathers, whereas standard EBT resulted in no change in maternal knowledge and reduced paternal knowledge of ADHD symptomatology. Clinical implications will be discussed.

Cocaine addiction is a global health issue with limited therapeutic options and a high relapse rate. Attentional bias towards substance-related cues may be an important factor for relapse. However, it has never been compared in former and current cocaine-dependent patients.

Attentional bias towards cocaine-related words was assessed using an emotional Stroop task in cocaine-dependent patients (

= 40), long-term abstinent former cocaine-dependent patients (

= 24; mean abstinence 2 years) and control subjects (

= 28). Participants had to name the colour of cocaine-related words, neutral words and colour names. We assessed response times using an automatic voice-onset detection method we developed and we measured attentional bias as the difference in response times between cocaine-related and neutral conditions.

There was an overall group effect on attentional bias towards cocaine, but no group effect on the colour Stroop effect. Two-by-two comparison showed a difference in attentional bias between cr as an absence of attentional bias predicting success in maintaining abstinence, or as attentional bias being able to disappear with long-term cocaine abstinence. Further research is needed to distinguish the role of attentional bias in maintaining abstinence.

Regulator of G protein Signaling (RGS) proteins inhibit G protein-coupled receptor (GPCR) signaling, including the signals that arise from neurotransmitter release. We have shown that RGS12 loss diminishes locomotor responses of C57BL/6J mice to dopamine transporter (DAT)-targeting psychostimulants. This diminution resulted from a brain region-specific upregulation of DAT expression and function in RGS12-null mice. This effect on DAT prompted us to investigate whether the serotonin transporter (SERT) exhibits similar alterations upon RGS12 loss in C57BL/6J mice.

Does RGS12 loss affect (a) hyperlocomotion to the preferentially SERT-targeting psychostimulant 3,4-methylenedioxymethamphetamine (MDMA), (b) SERT expression and function in relevant brain regions, and/or (c) serotonergically modulated behaviors?

Open-field and spontaneous home-cage locomotor activities were quantified. 5-HT, 5-HIAA, and SERT levels in brain-region homogenates, as well as SERT expression and function in brain-region tissue preparations, were measured using appropriate biochemical assays. Serotonergically modulated behaviors were assessed using forced swim and tail suspension paradigms, elevated plus and elevated zero maze tests, and social interaction assays.

RGS12-null mice displayed no hyperlocomotion to 10 mg/kg MDMA. There were brain region-specific alterations in SERT expression and function associated with RGS12 loss. Drug-naïve RGS12-null mice displayed increases in both anxiety-like and anti-depressive-like behaviors.

RGS12 is a critical modulator of serotonergic neurotransmission and serotonergically modulated behavior in mice; lack of hyperlocomotion to low dose MDMA in RGS12-null mice is related to an alteration of steady-state SERT expression and 5-HT uptake.

RGS12 is a critical modulator of serotonergic neurotransmission and serotonergically modulated behavior in mice; lack of hyperlocomotion to low dose MDMA in RGS12-null mice is related to an alteration of steady-state SERT expression and 5-HT uptake.

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