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1.  Methodological Dimensions of Transcranial Brain Stimulation with the Electrical Current in Human 
Basic and Clinical Neuroscience  2013;4(3):190-208.
Transcranial current stimulation (TCS) is a neuromodulation method in which the patient is exposed to a mild electric current (direct or alternating) at 1-2 mA, resulting in an increase or a decrease in the brain excitability. This modification in neural activities can be used as a method for functional human brain mapping with causal inferences. This method might also facilitate the treatments of many neuropsychiatric disorders based on its inexpensive, simple, safe, noninvasive, painless, semi-focal excitatory and inhibitory effects. Given this, a comparison amongst different brain stimulation modalities has been made to determine the potential advantages of the TCS method. In addition, considerable methodological details on using TCS in basic and clinical neuroscience studies in human subjects have been introduced. Technical characteristics of TCS devices and their related accessories with regard to safety concerns have also been well articulated. Finally, some TCS application opportunities have been emphasized, including its potential use in the near future.
PMCID: PMC4202570  PMID: 25337348
Transcranial Electrical Stimulation (tES); Transcranial Direct Current Stimulation (tDCS); Transcranial Alternating Current Stimulation (tACS); Non Invasive Brain Stimulation (NIBS)
2.  Aberrant basal ganglia metabolism in fragile X syndrome: a magnetic resonance spectroscopy study 
The profile of cognitive and behavioral variation observed in individuals with fragile X syndrome (FXS), the most common known cause of inherited intellectual impairment, suggests aberrant functioning of specific brain systems. Research investigating animal models of FXS, characterized by limited or lack of fragile X mental retardation protein, (FMRP), has linked brain dysfunction to deficits in the cholinergic and glutamatergic systems. Thus, we sought to examine in vivo levels of neurometabolites related to cholinergic and glutamatergic functioning in males and females with FXS.
The study participants included 18 adolescents and young adults with FXS, and a comparison group of 18 individuals without FXS matched for age, sex and general intellectual functioning. Proton magnetic resonance spectroscopy (MRS) was used to assess neurometabolite levels in the caudate nucleus, a region known to be greatly enlarged and involved in abnormal brain circuitry in individuals with FXS. A general linear model framework was used to compare group differences in metabolite concentration.
We observed a decrease in choline (P = 0.027) and in glutamate + glutamine (P = 0.032) in the caudate nucleus of individuals with FXS, relative to individuals in the comparison group.
This study provides evidence of metabolite differences in the caudate nucleus, a brain region of potential importance to our understanding of the neural deficits underlying FXS. These metabolic differences may be related to aberrant receptor signaling seen in animal models. Furthermore, identification of the specific neurometabolites involved in FXS dysfunction could provide critical biomarkers for the design and efficacy tracking of disease-specific pharmacological treatments.
PMCID: PMC3766683  PMID: 23981510
Fragile X syndrome; Magnetic resonance spectroscopy; Choline; Glutamate; Caudate nucleus
3.  Specific-mutational patterns of p53 gene in bladder transitional cell carcinoma among a group of Iraqi patients exposed to war environmental hazards 
BMC Research Notes  2012;5:466.
To unfold specific-mutational patterns in TP53 gene due to exposures to war environmental hazards and to detect the association of TP53 gene alteration with the depth of bladder cancer.
Twenty-nine bladder carcinomas were analyzed for TP53 alterations. PCR-single strand conformational polymorphism analysis, DNA sequencing and immunohistochemical analysis using monoclonal mouse anti-human p53 antibody (Clone DO-7) were employed.
TP53 gene mutations occurred in 37.9% of the cases while TP53 overexpression occurred in 58.6%. Both of them were associated with deep invasive-tumors. Single mutations were seen in 63.6%, whereas only 27.3% have shown double mutations. Four mutations were frameshifted (30.8%); two of them showed insertion A after codon 244. There was no significant association between TP53 mutations and protein overexpression (P>0.05), while a significant association was observed between TP53 alterations and tumors progression (P ≤ 0.01).
The infrequent TP53mutations, especially insertion A and 196 hotspot codon, may represent the specific-mutational patterns in bladder carcinoma among the Iraqi patients who were exposed to war environmental hazards. TP53 alteration associated with bladder cancer progression should be analyzed by both mutational and protein expression analysis.
PMCID: PMC3439300  PMID: 22929185
Bladder cancer; TP53 alteration; Specific mutation; Immunohistochemistry
4.  1-(4-Meth­oxy­phen­yl)-4-(4-methyl­phen­yl)-3-phen­oxy­azetidin-2-one 
The central β-lactam ring of the title compound, C23H21NO3, is almost planar (r.m.s. deviation = 0.032Å). The meth­oxy­benzene ring is almost coplanar with the β-lactam ring [dihedral angle = 1.87 (11)°], whereas the tolyl ring is almost normal to it [75.73 (12)°]. The dihedral angle between the β-lactam ring and the O-bonded phenyl ring is 51.95 (12)°. An intra­molecular C—H⋯O inter­action generates an S(6) ring. The crystal structure features inter­molecular C—H⋯O hydrogen bonds, forming layers parallel to (011), and weak C—H⋯π inter­actions. Two aromatic π–π stacking inter­actions [centroid–centroid distances = 3.6744 (12) and 3.6799 (11) Å] are also observed.
PMCID: PMC3051730  PMID: 21523012

Results 1-4 (4)