Do Patients Fear Undergoing General Anesthesia for Oral Surgery?

Many patients undergoing major surgery have more fear of the general anesthesia than the procedure. This appears to be reversed with oral surgery. Therefore, patients need to be as well informed about this aspect as the surgical operation.A study by the American Society of Anesthesiologists (ASA), reported in 2010, found that a lack of understanding and fear about general anesthesia has led to as many as 25% of patients postponing necessary surgery.¹ However, the attitude of patients about having general anesthesia specifically for oral surgery procedures has never been investigated. The purpose of this study was to determine if patients who need to undergo a general anesthetic for oral surgery have the same apprehension as those needing major surgery. It was hypothesized that a similar lack of knowledge and fear about general anesthesia would be found. If this were true, it could lead to protocols being developed that would make it possible for patients to undergo such treatment in a less stressful manner.     

Differential induction of heme oxygenase-1 in macrophages and hepatocytes during acetaminophen-induced hepatotoxicity in the rat: effects of hemin and biliverdin

Heme oxygenase-1 (HO-1), also known as heat shock protein 32, has been shown to protect against oxidant-induced tissue injury. In the present studies, we analyzed expression of this enzyme in macrophages and hepatocytes following acetaminophen administration and its potential role in hepatotoxicity. Treatment of rats with a hepatotoxic dose of acetaminophen (1 g/kg, ip) resulted in a time-dependent induction of HO-1 in the liver. This was observed within 6 h of acetaminophen administration in both hepatocytes and macrophages. Hepatocytes were found to be more sensitive than macrophages to the effects of acetaminophen on HO-1. Up regulation of HO-1 in the liver following acetaminophen administration correlated with induction of ferritin and manganese superoxide dismutase (MnSOD). To determine if HO-1 was hepatoprotective, rats were pretreated with hemin (30 micromol/kg, ip), a potent inducer of the enzyme. Following hemin treatment, we observed a time-dependent increase in HO-1 protein in the liver and in serum bilirubin levels. Pretreatment of rats with hemin was found to prevent acetaminophen-induced hepatotoxicity, as measured histologically and biochemically by decreased serum transaminase levels. This was correlated with more rapid increases in expression of hepatic ferritin and MnSOD. Heme metabolism via HO-1 generates biliverdin, which is rapidly converted to bilirubin by biliverdin reductase. Pretreatment of rats with biliverdin (40 micromol/kg, ip) was also found to block acetaminophen-induced injury. These data suggest that HO-1 is an important component of antioxidant defense during acetaminophen-induced hepatotoxicity.     

Oxygen toxicity in premature infants

Oxygen causes tissue injury through the formation of reactive oxygen intermediates and peroxidation of membrane lipids. Premature infants, who have severely reduced antioxidant defenses, are particularly sensitive to the toxic effects of oxygen. Supplemental oxygen in premature infants contributes to the development of chronic lung disease (bronchopulmonary dysplasia), characterized by dysregulated inflammation and altered expression of proteases and growth factors. This can result in fibrosis, asymmetric aeration, and respiratory insufficiency. Oxygen also induces aberrant physiologic responses that can be damaging in premature infants. For example, vasoconstriction in the retina is an early response to oxygen that can lead to vasoobliteration, neovascularization, and retinal traction (retinopathy of prematurity). Increasing knowledge of the mechanisms underlying oxygen toxicity in premature infants has suggested strategies to minimize tissue injury and to optimize long-term medical outcomes. These include limiting oxygen supplementation and light exposure, the use of antiinflammatory agents or antioxidants, and the use of room air in neonatal resuscitation.     

The ribotoxic stress response as a potential mechanism for MAP kinase activation in xenobiotic toxicity.

The article highlighted in this issue is "Vomitoxin-InducedCyclooxygenase-2 Gene Expression in Macrophages Mediated byActivation of ERK and p38 but Not JNK Mitogen-Activated ProteinKinases," by Yuseok Moon and James J. Pestka (pp. 373–382).     

Training of the oral and maxillofacial surgeon in implantology.

This article reports the results of a survey of oral and maxillofacial surgery residency programs regarding the teaching of implantology. The findings show that although oral and maxillofacial surgery residents receive as much or more didactic training than most trainees in other dental specialties, and much more extensive surgical experience, the teaching is not uniform and there is still need for improvement in some areas.     

First-line treatment for advanced non-small-cell lung cancer

With best supportive care alone, patients with metastatic non-small-cell lung cancer (NSCLC) have a median survival of 4 to 5 months and a 1-year survival rate of approximately 10%. Trials carried out in the 1980s and 1990s comparing chemotherapy to best supportive care reported variable efficacy results; however, a pivotal meta-analysis of these data indicated that cisplatin-based chemotherapy provided a survival benefit in advanced NSCLC. In the past decade newer agents such as gemcitabine (Gemzar), vinorelbine, paclitaxel, and docetaxel (Taxotere) have all demonstrated activity in NSCLC as single agents; consequently these agents have been combined with cisplatin or carboplatin. Randomized phase III trials comparing these "newer" platin-based doublets have failed to identify an optimal platinum-based doublet therapy regimen. Though it is clear that chemotherapy is an appropriate treatment for many patients with lung cancer, there a sense in which the use of traditional chemotherapeutic agents has reached a therapeutic plateau. Increased understanding of cancer biology has revealed numerous potential therapeutic strategies, including targeting the epidermal growth factor receptor, protein kinase C, rexinoid receptors, and the angiogenesis pathway. The Eastern Cooperative Oncology Group study E4599 comparing paclitaxel/carboplatin with/without bevacizumab is the first phase III randomized trial to show a survival advantage with the addition of a molecularly targeted agent to chemotherapy in the chemotherapy-naive patient population. Future studies will involve the evaluation of additional targeted agents plus chemotherapy as well as looking at combinations of these targeted agents alone or with chemotherapy.