Substance Use Disorders and Adoption: Findings From a National Sample.

Substance use disorders and adoption: findings from a national sample.

Filed under: Drug and Alcohol Rehabilitation

PLoS One. 2012; 7(11): e49655
Yoon G, Westermeyer J, Warwick M, Kuskowski MA

Prior research has shown that adoptees have a higher rate of substance use disorders (SUDs) than nonadoptees. But these findings have not been verified with a population-based sample of adult adoptees in the United States. Also, no previous adoption study has measured the prevalence of each specific substance use disorder (SUD). We aimed to compare lifetime prevalence rates and odds ratios of SUDs in adopted and nonadopted adults.The data come from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). The main outcome measure was the prevalence of lifetime SUDs in adopted (n?=?378) and nonadopted adults (n?=?42503). Adoptees and nonadoptees were compared to estimate the odds of lifetime SUDs using logistic regression analysis. Adoptees had higher prevalence rates of lifetime SUDs than nonadoptees. Overall, adoptees had a 1.87-fold increase (adjusted odds ratio [AOR] 1.87, 95% CI 1.51-2.31) in the odds of any lifetime SUD compared to nonadoptees. For each SUD, adoptees had higher odds for alcohol abuse/dependence (AOR 1.84), nicotine dependence (AOR 1.78), cannabis abuse/dependence (AOR 1.77), cocaine abuse/dependence (AOR 2.54), amphetamine abuse/dependence (AOR 3.14), hallucinogen abuse/dependence (AOR 2.85), opioid abuse/dependence (AOR 2.21), and other drug abuse/dependence (AOR 2.87) compared to nonadoptees. This study also identified two adoption-specific risk factors (Hispanic, never married) associated with any lifetime SUD.This study demonstrated an increased risk of lifetime SUDs in adopted adults. The findings can be useful for clinicians and policy makers to provide education, prevention, and support for adoptees and their families.
HubMed – drug


Aristolochia Manshuriensis Kom Inhibits Adipocyte Differentiation by Regulation of ERK1/2 and Akt Pathway.

Filed under: Drug and Alcohol Rehabilitation

PLoS One. 2012; 7(11): e49530
Kwak DH, Lee JH, Kim T, Ahn HS, Cho WK, Ha H, Hwang YH, Ma JY

Aristolochia manshuriensis Kom (AMK) is a traditional medicinal herb used for the treatment of arthritis, rheumatism, hepatitis, and anti-obesity. Because of nephrotoxicity and carcinogenicity of AMK, there are no pharmacological reports on anti-obesity potential of AMK. Here, we showed AMK has an inhibitory effect on adipocyte differentiation of 3T3-L1 cells along with significantly decrease in the lipid accumulation by downregulating several adipocyte-specific transcription factors including peroxisome proliferation-activity receptor ? (PPAR-?), CCAAT/enhancer binding protein ? (C/EBP-?) and C/EBP-?, which are critical for adipogenesis in vitro. AMK also markedly activated the extracellular signal-regulated protein kinase 1/2 (ERK1/2) pathway including Ras, Raf1, and mitogen-activated protein kinase kinase 1 (MEK1), and significantly suppressed Akt pathway by inhibition of phosphoinositide-dependent kinase 1 (PDK1). Aristolochic acid (AA) and ethyl acetate (EtOAc) fraction of AMK with AA were significantly inhibited TG accumulation, and regulated two pathway (ERK1/2 and Akt) during adipocyte differentiation, and was not due to its cytotoxicity. These two pathways were upstream of PPAR-? and C/EBP? in the adipogenesis. In addition, gene expressions of secreting factors such as fatty acid synthase (FAS), adiponectin, lipopreotein lipase (LPL), and aP2 were significantly inhibited by treatment of AMK during adipogenesis. We used the high-fat diet (HFD)-induced obesity mouse model to determine the inhibitory effects of AMK on obesity. Oral administration of AMK (62.5 mg/kg/day) significantly decreased the fat tissue weight, total cholesterol (TC), and low density lipoprotein-cholesterol (LDL-C) concentration in the blood. The results of this study suggested that AMK inhibited lipid accumulation by the down-regulation of the major transcription factors of the adipogensis pathway including PPAR-? and C/EBP-? through regulation of Akt pathway and ERK 1/2 pathway in 3T3-L1 adipocytes and HFD-induced obesity mice, and AA may be main act in inhibitory effects of AMK during adipocyte differentiation.
HubMed – drug


Identification of novel translational urinary biomarkers for acetaminophen-induced acute liver injury using proteomic profiling in mice.

Filed under: Drug and Alcohol Rehabilitation

PLoS One. 2012; 7(11): e49524
van Swelm RP, Laarakkers CM, van der Kuur EC, Morava-Kozicz E, Wevers RA, Augustijn KD, Touw DJ, Sandel MH, Masereeuw R, Russel FG

Drug-induced liver injury (DILI) is the leading cause of acute liver failure. Currently, no adequate predictive biomarkers for DILI are available. This study describes a translational approach using proteomic profiling for the identification of urinary proteins related to acute liver injury induced by acetaminophen (APAP). Mice were given a single intraperitoneal dose of APAP (0-350 mg/kg bw) followed by 24 h urine collection. Doses of ?275 mg/kg bw APAP resulted in hepatic centrilobular necrosis and significantly elevated plasma alanine aminotransferase (ALT) values (p<0.0001). Proteomic profiling resulted in the identification of 12 differentially excreted proteins in urine of mice with acute liver injury (p<0.001), including superoxide dismutase 1 (SOD1), carbonic anhydrase 3 (CA3) and calmodulin (CaM), as novel biomarkers for APAP-induced liver injury. Urinary levels of SOD1 and CA3 increased with rising plasma ALT levels, but urinary CaM was already present in mice treated with high dose of APAP without elevated plasma ALT levels. Importantly, we showed in human urine after APAP intoxication the presence of SOD1 and CA3, whereas both proteins were absent in control urine samples. Urinary concentrations of CaM were significantly increased and correlated well with plasma APAP concentrations (r?=?0.97; p<0.0001) in human APAP intoxicants, who did not present with elevated plasma ALT levels. In conclusion, using this urinary proteomics approach we demonstrate CA3, SOD1 and, most importantly, CaM as potential human biomarkers for APAP-induced liver injury. HubMed – drug


Evaluation of Genotype MTBDRsl Assay to Detect Drug Resistance Associated with Fluoroquinolones, Aminoglycosides and Ethambutol on Clinical Sediments.

Filed under: Drug and Alcohol Rehabilitation

PLoS One. 2012; 7(11): e49433
Ajbani K, Nikam C, Kazi M, Gray C, Boehme C, Balan K, Shetty A, Rodrigues C

The emergence of resistant tuberculosis (TB) is a major setback to the global control of the disease as the treatment of such resistance is complex and expensive. Use of direct detection of mutations by molecular methods could facilitate rapid diagnosis of resistance to offset diagnostic delays. We evaluated the performance of the Genotype MTBDRsl (Hain Life Sciences) for the detection of second line resistant TB directly from stored smear positive sputum sediments.The assay showed a diverse range of sensitivity and specificity, 91.26% [95% CI, 84-96] and 95.5% [95% CI, 87-99] for FQ (PPV ?97% & NPV ? 87.67%), 56.19% [95%CI, 46-66] and 81% [95%CI, 66-91] for EMB (PPV ? 88.06% & NPV ? 43.21%) and 100% for SLD. Diagnostic accuracy for FQ, SLD and EMB was 94%, 100% and 63.51%, respectively. 1.17% (2/170) were heteroresistance strains, where the heteroresistance was linked to rrs gene. A varying rate of validity was observed 100% (170/170) for FQ, 94.11% (160/170) for EMB, 88.23% (150/170) for SLD.Genotype MTBDRsl is simple, rapid, economical assay that can be used to detect commonly known resistance associated with Fluoroquinolone, second line injectable drugs and ethambutol. The assay detects the targeted resistance in less time as compared to phenotypic DST. But due to low NPV to FQ (88%) and EMB (43.21%), the assay results must be interpreted in coordination with the phenotypic DST.
HubMed – drug



Dwight Muhammad Qawi vs. Eddie Davis – Background Qawi, then known as Dwight Braxton, was born in Baltimore, Maryland, but grew up in Camden, New Jersey, where he got involved with crime at a young age. He was eventually convicted of armed robbery and spent around five years in prison.[2] It was at Rahway that Braxton found his place in life. The prison had an extensive boxing program and one of its inmates, James Scott, was a light heavyweight title contender who fought several times inside the prison itself. Braxton took up the sport, and when he was released from prison in 1978, immediately became a professional boxer. Qawi’s style was most often likened to Joe Frazier and with good reason as he had trained in Fraziers Philadelphia gym as a professional. [edit] Professional career He went 1-1-1 in his first three pro fights, but then reeled off 14 straight victories to move into the world rankings at light heavyweight. The last of those wins came on September 5, 1981, when Braxton returned to Rahway to fight Scott, with the winner promised a shot at Matthew Saad Muhammad’s WBC world championship belt. Braxton won a unanimous 10-round decision. On December 19 of the same year, Braxton faced Saad Muhammad in Atlantic City. The ex-convict was the underdog against Saad, one of the most popular fighters of his generation and a fellow Hall of Famer, but Braxton defeated him on a 10th-round technical knockout and became a world champion for the first time.[3] It was shortly after this that he announced his


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