ABSTRACT
Medical photographic image capture and data management has undergone a rapid and compelling change in complexity over the last 20 years. This is because of multiple factors, including significant advances in ease of photograph capture, alongside an evolution of mechanisms of data portability/dissemination, combined with governmental focus on health information privacy. Literature to guide medical, legal, governmental and business professionals when dealing with issues related to medical photography is virtually nonexistent. Herein, we will address the breadth of uses of medical photography, device properties/specific devices utilised for image capture, methods of data transfer and dissemination and patient perceptions and attitudes regarding photography in a medical setting. In addition, we will address the legal implications, including legal precedent, copyright and privacy law, informed consent, protected health information and the Health Insurance Portability and Accountability Act (HIPAA), as they pertain to medical photography.
Subject(s)
Data Collection/methods , Medical Records , Photography/methods , Computer Security/legislation & jurisprudence , Data Collection/legislation & jurisprudence , Humans , Informed Consent/legislation & jurisprudence , Medical Records/legislation & jurisprudence , Photography/legislation & jurisprudence , Privacy/legislation & jurisprudenceABSTRACT
Orofacial inflammation is associated with prostaglandin release and the sensitization of nociceptive receptors such as the transient receptor potential subtype V(1) (TRPV(1)). We hypothesized that certain PGE(2) receptor subtypes (EP1-EP4) are co-expressed with TRPV(1) in trigeminal nociceptors and sensitize responses to a TRPV(1) agonist, capsaicin. Accordingly, combined in situ hybridization was performed with immunohistochemistry on rat trigeminal ganglia. We next evaluated the effects of specific EP2 and EP3 agonists (butaprost and sulprostone) in cultured trigeminal ganglia neurons. The results showed that EP2 and EP3 are expressed in trigeminal neurons (58% and 53% of total neurons, respectively) and are co-expressed in TRPV(1)-positive neurons (64% and 67 % of TRPV(1)-positive neurons, respectively). Moreover, most of the cells expressing EP2 or EP3 mRNA were of small to medium diameter (< 30 microm). The application of butaprost and sulprostone triggered neuropeptide exocytosis, and butaprost sensitized capsaicin responses. Analysis of these data, collectively, supports the hypothesis that prostaglandins regulate trigeminal TRPV(1) nociceptors via activation of the EP2 and EP3 receptors.
