The sternoclavicular joint (SCJ) is anatomically and clinically significant considering its proximity to important neuro-vascular structures like the subclavian vessels and the phrenic nerve. Infections of this joint masquerade multiple disorders, delay diagnosis and spread to the bone and deep tissues. There is no standardized workup and treatment protocol for sternoclavicular joint infections (SCJI) as defined in literature. Here, we review the existing literature to understand the current knowledge of the diagnosis and treatment of SCJI. We searched English publications in PubMed and included clinical trials, case reports, case series, retrospective cohort studies, literature and systematic reviews after excluding non-infectious etiology of SCJ pathologies. There are many risk factors for SCJI, such as immunocompromised status, intravenous drug use, trauma and arthropathies. But a large percentage of patients with disease have none of these risk factors. SCJIs can present with fever, joint swelling, immobility, and rarely with vocal cord palsy or dysphagia. While Staphylococcus aureus causes over 50% of SCJI cases, other pathogens such as Pseudomonas and Mycobacterium are frequently seen. When diagnosed early, the infection can be medically managed with antibiotics or joint aspirations. Most cases of SCJI, however, are diagnosed after extensive spread to soft tissue and bones requiring en-bloc resection with or without a muscle flap. Complications of undertreatment can range from simple abscess formation to mediastinitis, even sepsis. SCJIs are rare but serious infections prompting early detection and interventions. Most cases of SCJI treated adequately show complete resolution in months while retaining maximum functionality. Key features of proper healing include aggressive physiotherapy to prevent adhesive shoulder capsulitis and decreased range of motion.

Distance from an LTC is a risk factor of mortality on the waitlist for OLT, whereas RUCA classification is not a significant factor.

Introduction: Primary liver cancer is a significant cause of cancer-related death in both the United States and the world at large. Hepatocellular carcinoma comprises 90% of these primary liver cancers and has numerous known etiologies. Evaluation of these identified etiologies and other traditional risk factors cannot explain the high incidence rates of hepatocellular carcinoma in Texas. Texas is home to the second largest petrochemical industry and agricultural industry in the nation; industrial activity and exposure to pathogenic chemicals have never been assessed as potential links to the state's increased incidence rate of hepatocellular carcinoma. Methods: The association between the county-level concentrations of 4 air pollutants known to be linked to liver cancer, vinyl chloride, arsenic, benzene, and 1,3-butadiene, and hepatocellular carcinoma rates was evaluated using nonparametric generalized additive logistic regression and gamma regression models. Hepatocellular carcinoma incidence rates for 2000-2013 were evaluated in comparison to 1996 and 1999 pollution concentrations and hepatocellular carcinoma rates for the subset of 2006-2013 were evaluated in comparison to 2002 and 2005 pollution concentrations, respectively. Results: The analysis indicates that the relationship between the incidence of liver cancer and air pollution and risk factors is nonlinear. There is a consistent significant positive association between the incidence of liver cancer and hepatitis C prevalence rates (gamma all years, p < 0.05) and vinyl chloride concentrations (logistic 2002 and 2005, p < 0.0001; gamma 2002 and 2005, p < 0.05). Conclusions: This study suggests that vinyl chloride is a significant contributor to the incidence of liver cancer in Texas. The relationship is notably nonlinear. Further, the study supports the association between incidence of liver cancer and prevalence of hepatitis B.

Glypican-3 (GPC-3), a transmembrane heparan sulfate proteoglycan (HSPG), has recently been investigated as a player in tissue-dependent cellular signaling, specifically as a regulator of growth. Noteworthy, the regulatory protein has been implicated in both stimulatory and inhibitory pathways involving cell growth. Initially, GPC-3 was thought to act as a cell cycle regulator, as a loss-of-function mutation in the gene caused a hyper-proliferative state known as Simpson-Golabi-Behmel (SGB) overgrowth syndrome. Additionally, certain cancer types have displayed a downregulation of GPC-3 expression. More recently, the protein has been evaluated as a useful marker for hepatocellular carcinoma (HCC) due to its increased expression in the liver during times of growth. In contrast, the GPC-3 marker is not detectable in normal adult liver. Immunotherapy that targets GPC-3 and its affiliated proteins is under investigation as these new biomarkers may hold potential for the detection and treatment of HCC and other diseases in which GPC-3 may be overexpressed. Studies have reported that an overexpression of GPC-3 in HCC predicts a poorer prognosis. This prognostic value further pushes the question regarding GPC-3's role in the regulation and progression of HCC. This review will summarize the current knowledge regarding the clinical aspects of GPC-3, while also synthesizing the current literature with the aim to better understand this molecule's biological interactions at a molecular level, not only in the liver, but in the rest of the body as well. Due to the existing gap in the literature surrounding GPC-3, we believe further investigation of function, structure and domains, cellular localization, and other subfields is warranted to evaluate the protein as a whole, as well as its part in the study of HCC.

Our data reveal new aspects of the role of GPC3 in early hepatocyte transformation. In addition we conclude that GPC3 may serve as a new HCC immune-therapeutic target.