Comparison of Buccal Infiltration of 4% Articaine With 1?:?100,000 and 1?:?200,000 Epinephrine for Extraction of Maxillary Third Molars With Pericoronitis: A Pilot Study

We compared the buccal infiltration of 4% articaine with 1 : 100,000 or 1 : 200,000 epinephrine without a palatal injection for the extraction of impacted maxillary third molars with chronic pericoronitis. This prospective, double-blind, controlled clinical trial involved 30 patients between the ages of 15 and 46 years who desired extraction of a partially impacted upper third molar with pericoronitis. Group 1 (15 patients) received 4% articaine with 1 : 100,000 epinephrine and group 2 (15 patients) received 4% articaine with 1 : 200,000 epinephrine by buccal infiltration. None of the patients in group 1 reported pain, but 3 patients in group 2 reported pain, which indicated a need for a supplementary palatal injection. The palatal injections were all successful in eliminating the pain. Two additional patients in group 2 experienced pain when the suture needle penetrated their palatal mucosa. Based on these results, 4% articaine with 1 : 100,000 epinephrine was found to be more effective for the removal of upper third molars in the presence of pericoronitis than 4% articaine hydrochloride with 1 : 200,000 epinephrine when only a buccal infiltration was used.Key Words: Articaine, Epinephrine, Molar extractionMaxillary third molar extraction is generally straightforward, due to the plasticity of the maxillary bone and to the low resistance to extraction movements. Nevertheless, the anesthetic technique needed for such extraction may be extremely uncomfortable because it requires palatal mucosal anesthesia.^1,2Studies have suggested that articaine has good diffusion through the hard and soft tissues, eliminating the need for the palatal injection in maxillary third molar extractions.^3–6 However, the anesthetic effect may be decreased or neutralized because the inflammation and low tissue pH affects tissue diffusion of the anesthetic, making the drug less effective.^7–9Pericoronitis is the most frequent inflammatory pathology associated with third molars and is caused by a combination of factors including trauma and food impaction with subsequent bacterial colonization and infection.^1,10–13 Clinically, it is characterized by the presence of erythema, swelling, and even ulceration in some cases.^1,14 The management of pericoronitis varies. Many authors have recommended using antibiotic therapy when there are signs of acute infection with systemic involvement such as fever. In cases of chronic or nonacute clinical manifestations, treatment should be limited to antiseptic mouthwashes, irrigation, and anti-inflammatory and/or anesthetic medication. Surgically, the usual treatment is the extraction of the impacted tooth.^1,11–15The aim of the present study was to evaluate the differences between articaine hydrochloride with 1 : 100,000 and 1 : 200,000 epinephrine (adrenaline) administered by buccal infiltration alone (without palatal infiltration) for the removal of impacted upper third molar teeth with pericoronitis.     

Rhein Protects Pancreatic β-Cells From Dynamin-Related Protein-1–Mediated Mitochondrial Fission and Cell Apoptosis Under Hyperglycemia

Rhein, an anthraquinone compound isolated from rhubarb, has been shown to improve glucose metabolism disorders in diabetic mice. The mechanism underlying the protective effect of rhein, however, remains unknown. Here, we demonstrate that rhein can protect the pancreatic β-cells against hyperglycemia-induced cell apoptosis through stabilizing mitochondrial morphology. Oral administration of rhein for 8 or 16 weeks in db/db mice significantly reduced fasting blood glucose (FBG) level and improved glucose tolerance. Cell apoptosis assay using both pancreatic sections and cultured pancreatic β-cells indicated that rhein strongly inhibited β-cell apoptosis. Morphological study showed that rhein was mainly localized at β-cell mitochondria and rhein could preserve mitochondrial ultrastructure by abolishing hyperglycemia-induced mitochondrial fission protein dynamin-related protein 1 (Drp1) expression. Western blot and functional analysis confirmed that rhein protected the pancreatic β-cells against hyperglycemia-induced apoptosis via suppressing mitochondrial Drp1 level. Finally, mechanistic study further suggested that decreased Drp1 level by rhein might be due to its effect on reducing cellular reactive oxygen species. Taken together, our study demonstrates for the first time that rhein can serve as a novel therapeutic agent for hyperglycemia treatment and rhein protects pancreatic β-cells from apoptosis by blocking the hyperglycemia-induced Drp1 expression.Rhein (4,5-dihydroxyanthraquinone-2-carboxylic acid) is an anthraquinone compound isolated from rhubarb that has been used for more than 2,000 years in China to treat constipation, gastrointestinal hemorrhage, and ulcers (1). In our previous work, we found that rhein could improve glucose metabolism disorders in diabetic mice, and its effect on reducing blood glucose level was even stronger than rosiglitazone and benazepril (2,3). Moreover, rhein also inhibited apoptosis of islet cells and protected islet function (4). Using mouse nonalcoholic fatty liver disease as an animal model associated with obesity, insulin resistance, and inflammatory disorders, Sheng et al. (5) reported that rhein could ameliorate fatty liver disease in diet-induced obese mice via negative energy balance, hepatic lipogenous regulation, and immunomodulation. Recent antihyperglycemic study by Chatterjee et al. (6) suggests that rhein, as well as other natural inhibitors such as aloins and capparisine, may be a foundation for a better antidiabetic therapy. However, the mechanism underlying these protective effects of rhein remains unclear.Increasing evidence suggests that β-cell failure is the mainstay of the pathogenesis of type 2 diabetes (7). Although the precise mechanisms underlying the β-cell dysfunction in type 2 diabetes are not fully understood, hyperglycemia has been shown as a major factor to cause the β-cell apoptosis. Once hyperglycemia develops, the pancreatic β-cell is exposed to increased metabolic flux and associated cellular stress, leading to impairment of β-cell function and survival, a process called glucotoxicity (8,9). In type 2 diabetes, hyperglycemia is commonly associated with deregulation of lipid metabolism and elevation of free fatty acids, which also contribute to β-cell dysfunction (8,10). Moreover, high levels of glucose can also amplify lipotoxicity (10). The thiazolidinedione peroxisome proliferator–activated receptor-γ activator drugs, rosiglitazone and pioglitazone, have been widely used to suppress insulin resistance in type 2 diabetic patients (11). Although rhein shows a similar or even better effect on reducing mouse blood glucose level than rosiglitazone, the underlying mechanism remains unclear. It has been known that mitochondrial fission and fusion modulators, dynamin-related protein 1 (Drp1) (12), optic atrophy protein 1 (Opa1) (13), prohibitin (14), and mitofusin (15), collectively control the dynamic balance of mitochondria fission and fusion processes and consequent mitochondria functions. Previous studies have demonstrated that Drp1 plays an important role in promoting hyperglycemia-induced apoptosis of β-cells and neurons (12,16,17). Drp1 expression was increased drastically in islet β-cells under hyperglycemia conditions. Estaquier and Arnoult (18) further demonstrated that inhibiting Drp1-mediated mitochondrial fission could selectively prevent the release of cytochrome c, a mediator of apoptosis, from mitochondria. In contrast to the mitochondria fission modulators, which are upregulated or activated by stress factors such as high concentration of glucose (HG), mitochondria fusion modulators are generally reduced when cells are challenged with proapoptotic insults. Recent studies by Kushnareva et al. (19) and Leboucher et al. (15) showed that stress-induced loss of Opa1 and mitofusin can facilitate mitochondrial fragmentation and cell apoptosis. However, it remains to be determined whether rhein executes its protective role in pancreatic β-cells through regulating the expression or activation of these mitochondria fission/fusion modulators.In the current study, we used db/db mice and a pancreatic β-cell line (NIT-1) to study the protective effect of rhein. Our results showed that rhein largely localized at mitochondria in the β-cells and that it strongly protected pancreatic β-cells from hyperglycemia-induced apoptosis through suppressing Drp1 activation and Drp1-mediated mitochondria fission.     

The short- and medium-term results of transcatheter closure of atrial septal defect with severe pulmonary arterial hypertension

We investigated the short-term and medium-term results in patients with pulmonary arterial hypertension (PAH) associated with atrial septal defect (ASD) undergoing transcatheter closure. Fifteen patients with severe PAH associated with ASD who underwent successful occluder implantation from 2007 to 2010 were included. Clinical, echocardiographic, and hemodynamic data were reviewed. Severe PAH was defined as pulmonary arterial systolic pressure measured by catheterization was ≥60 mmHg and pulmonary vascular resistance (PVR) ≥6 Wood Units (WU). Compared with baseline, the 6-minwalking distance significantly increased by 29.7 ± 26.3 m (P < 0.001) at 3 months (short-term) and 65.4 ± 63.6 m (P < 0.001) at 23.4 ± 9.7 months (medium-term), World Health Organization function class considerably improved after postclosure short-term and medium-term. Repeat cardiac catheterization (n = 7) showed that mean pulmonary arterial pressure decreased from 51.6 ± 9.4 mmHg at baseline to 21.0 ± 3.8 mmHg (P < 0.001) at follow-up of 12 months. The PVR decreased by 5.6 ± 1.1 WU (P < 0.001). Through carefully selected patients with severe PAH associated with ASD, transcatheter closure can be safely performed with a promising short-term and medium-term outcome. Trial occlusion is an effective way for deciding the reversibility of severe PAH in ASD patients. The role of aerosolized iloprost for pulmonary vasoreactivity testing in patients with severe PAH secondary to ASD requires further investigation.     

Cutaneous phaeohyphomycosis caused by Exophiala spinifera in a patient with systemic lupus erythematosus

Exophiala spinifera can induce both phaeohyphomycosis and chromomycosis. To date there have been 18 human infections caused by E. spinifera in the English literature. A case of E. spinifera-induced phaeohyphomycosis in a patient with systemic lupus erythematosus (SLE) is described. Direct microscopic examination of the pus showed branched, septate and chained hyphae and spores. A dark green velvety colony grew on Sabouraud dextrose agar. Slide culture showed branched, septate hyphae and spine-like annellated conidiophores. Histopathological biopsy revealed yellowish brown hyphae and spores. The isolate was identified as E. spinifera by DNA sequence analysis. The strain was unable to liquefy gelatin, grew at 25°C to 39°C, and was sensitive to itraconazole, amphotericin B, and terbinafine. To our knowledge, this is the first case of cutaneous phaeohyphomycosis caused by E. spinifera in SLE patients.     

Relationship between the angiotensin Ⅱ type 2 receptor polymorphism and antihypertensive effect of valartan/Hydrochlorothiazide

目的 探讨原发性高血压患者α-内收蛋白基因单核苷酸多态性与原发性高血压及复方缬沙坦治疗疗效的关系.方法 应用直接测序方法对80例原发性高血压、80例肾性高血压及40例正常人群α-内收蛋白基因进行单核苷酸多态性分析.结果 α-内收蛋白G/T基因型及等位基因在3组中分布无显著差异(P＞0.05);复方缬沙坦对原发性高血压TT和GT基因型患者用药后血压的下降幅度比较差异有统计学意义(P＜0.05).结论 复方缬沙坦对原发性高血压患者的降压作用可能与a-内收蛋白基因多态性有关.     

以心血管系统病变为主要表现的双硫仑样反应32例报道

目的探讨使用头孢菌素类抗生素(头孢菌素)与饮酒相互作用导致的以心血管系统病变为主要表现的双硫仑样反应及其救治方法。方法对诊断为双硫仑样反应且主要表现为心血管系统病变的32例患者的临床资料进行回顾性分析,包括涉及药物、饮酒情况、致双硫仑样反应时间、临床表现、治疗及预后。结果引起双硫仑样反应的头孢菌素以头孢哌酮加舒巴坦最为常见。双硫仑样反应多为用药后饮酒所致,致双硫仑样反应时间多发生在饮酒后5 min～1 h。心血管系统主要表现为心悸、呼吸困难、低血压、胸闷、胸痛。心电图可表现为窦性心动过速、心房颤动、室性期前收缩、ST-T改变等;容易误诊为急性冠脉综合征、急性左心力衰竭、休克。给予积极有效治疗后,多数患者于治疗后30 min～3 h缓解。无1例死亡。结论应用头孢菌素与饮酒相互作用可引起双硫仑样反应,可主要以心血管系统表现为主,表现复杂且较危重,经积极治疗大多预后良好。