Brief Reports should be submitted online to www.editorialmanager.com/ amsurg. (See details online under ''Instructions for Authors''.) They should be no more than 4 double-spaced pages with no Abstract or sub-headings, with a maximum of four (4) references. If figures are included, they should be limited to two (2). The cost of printing color figures is the responsibility of the author.In general, authors of case reports should use the Brief Report format.

Injection drug use has been recognized as a major risk factor for AIDS from the outset of the epidemic. Cocaine, one of the most widely abused drugs in the United States can both impair the functions of macrophages & CD4 + lymphocytes and also activate HIV-1 expression in these cells. Cocaine is a multifactorial agent that acts globally to impair the functioning of brain resident cells through multiple pathways. The drug not only promotes virus replication in macrophages, microglia and astrocytes, but can also upregulate CCR5 coreceptor, and reciprocally inhibit its ligands, thereby increasing virus infectivity. Cocaine is known to modulate astroglial function and activation. Cocaine causes a myriad of toxic responses in the neurons: a) it synergizes with viral proteins, Tat and gp120 resulting in exacerbated neuronal apoptosis, b) it causes calcium mobilization and, c) generation of reactive oxygen species. Additionally, cocaine also exerts potent effects on microvascular permeability, thereby impacting the influx of virus-infected inflammatory cells in brain parenchyma. By amplifying the various arms of the toxic responses that characterize HIV-associated dementia (HAD), cocaine skews the balance in favor of the virus leading to accelerated progression and severity of dementia.

An estimated 70% to 80% of all HCCs arise from cirrhotic liver, especially postchronic HBV or HCV infection. Identifying WD HCC arising in the background of cirrhosis is challenging on morphology in core biopsies. In addition, presence of dysplasia (micro/macro) in cirrhotic nodules makes the task more difficult. In HCC, miRNAs have aberrant expression profiles, with possible applications in diagnosis, especially for early, presymptomatic disease, and prognosis of HCC. Multiple studies have consistently demonstrated that along with other mi-RNAs, there is increased expression of mir-21 in HCC. Similar studies have shown mir-21 simultaneously regulates multiple programs that enhance cell proliferation, apoptosis, or tumor invasiveness in HCC. Methods of subcellular and tissue localization of mi-RNAs are essential to understand their biological roles and their contribution to disease along with diagnosis. The aim of this study is to evaluate the utility of mir-21 detection by CISH as a diagnostic tool in the setting of well and moderately differentiated (MD) HCCs. Archival blocks were retrieved and slides were reviewed with clinical information on 8 HCC and 5 normal liver resections. In 8 HCC, 5 cases were HBV and HCV infected with cirrhosis. Manufacturer's guidelines were followed for CISH (NAR-I, FAM-labeled Hsa-miR-21 probe, BioGenex). Nuclear mir-21 CISH stain was graded as: negative (-), weak (1+), moderate (2+) or strong (3+) and distribution was focal (50%). Neoplastic cells in HCC showed strong (2-3) multifocal to diffuse nuclear staining for miR-21 in 8/8 (100%) compared with the staining seen in normal liver cells. Currently other than morphology on H&E, there are no definite helpful immunohistochemical markers aiding in differentiating dysplasia (micro/macro) vs WD HCC on a core biopsy in a postinfectious cirrhotic liver. Here we offer a rapid CISH technique which can clearly identify increased nuclear expression of mir-21.

Brief Reports should be submitted online to www.editorialmanager.com/ amsurg. (See details online under ''Instructions for Authors''.) They should be no more than 4 double-spaced pages with no Abstract or sub-headings, with a maximum of four (4) references. If figures are included, they should be limited to two (2). The cost of printing color figures is the responsibility of the author.