Some CPG authors failed to fully disclose all financial conflicts of interest, and most guideline development panels and chairpersons had conflicts. In addition, adherence to IOM standards for guideline development was lacking. This study is relevant to CPG panels authoring recommendations, physicians implementing CPGs to guide patient care, and the organizations establishing policies for guideline development.
Half of all applicable obstetrics trials did not report results. Furthermore, rates of compliance appeared to vary by funding source, with trials funded by the National Institutes of Health or industry appearing to have a higher rate of compliance to mandatory data reporting. Greater awareness of federal regulations is needed, and changes should be implemented to increase reporting.
Hydroxyapatite deposition disease (HADD), or calcific tendinosis, is a common cause of atraumatic pain.Radiologists can be of great diagnostic assistance using imaging and clinical data to decipher HADD from other similar presenting pathologies such as infection, gout, trauma, and tumor. The radiologist should be aware of the various diagnostic imaging pitfalls and mimics of calcific tendinosis so that they may prevent further unnecessary workup and invasive procedures. In addition, radiologists should understand the role of percutaneous image-guided interventions as treatment options for HADD. The radiologist's understanding of the clinical presentation, imaging features, and treatment options of HADD will improve diagnostic accuracy and patient outcomes.
PathophysiologyHADD is best described as pathologic deposition of calcium hydroxyapatite crystals in tendons, peritendinous
Introduction: Cervical cancer is primarily caused by the human papilloma virus (HPV), which transforms normal cervical cells into cancerous cells that are highly resistant to radiation and chemotherapy. Induction of apoptosis in transformed cells is a key strategy in successfully treating HPV-induced cervical cancer. TRAIL (tumor necrosis factor related apoptosis-inducing ligand) has been shown to selectively induce apoptosis in cancer cells by binding to death receptors and activating extrinsic pathways for apoptosis. However, certain cervical cancers-such as the cultured cell line SiHa-are remarkably resistant to TRAIL. In this study, SiHa cells were sensitized to TRAIL by using sanguinarine-derived from the plant Sanguinaria Canadensis-which is known to induce oxidative stress and lead to the upregulation of receptors for TRAIL. Methods: Cultured SiHa cells were exposed to sub-lethal doses of sanguinarine in combination with TRAIL. Cell viability changes as well as the production of reactive oxygen species (ROS) were assessed. The induction of apoptosis was investigated by assays for caspase activation. Flow cytometry was performed to analyze expression of death receptors 4/5. Results: Treatment of SiHa cells with a combination of sanguinarine and TRAIL led to a significant reduction in cell viability. Significant increase in ROS was observed and caspase activation assays confirmed the induction of apoptosis. Conclusions: The observed synergistic effect of sanguinarine and TRAIL on SiHa cells is promising for the treatment of cervical, and possibly other, HPV-induced cancers. Oxidative stress caused by sanguinarine seems to play a central role in this synergy. The precise link between reactive oxygen species and the possible upregulation of death receptors needs further investigation.
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