Oxygen-derived free radicals and postischemic myocardial reperfusion: therapeutic implications

Oxygen-derived free radicals have been implicated in the pathogenesis of various disease states, including myocardial ischemia and reperfusion. In this article, we review 1) the evidence linking free radical production and myocardial injury during myocardial ischemia and reperfusion and 2) results of studies of the effects of the pharmacological therapies available potentially to prevent free radical-mediated injury. Free radicals can be produced during ischemia and reperfusion by several different biochemical pathways. Of these, the xanthine oxidase reaction and the output of free radicals by neutrophils that have accumulated in damaged tissue have been studied extensively. When produced, free radicals can potentially damage myocytes or endothelial cells through peroxidation of membrane lipids or damage to proteins or nucleic acids. Using electron spin resonance spectroscopy, several studies have shown a 'burst' of oxygen free radicals immediately after reperfusion. Moreover, exogenous generation of intravascular free radicals has been shown to produce marked vascular and myocyte damage, as well as contractile dysfunction. 'Anti-free radical' interventions, such as xanthine oxidase inhibitors and free radical scavengers have been reported to prevent contractile dysfunction and reperfusion-induced arrhythmias after an episode of reversible ischemic injury. However, after more severe episodes of ischemia, such interventions have had conflicting effects on myocardial infarct size. 'Anti-free radical' interventions could be of potential use in situations where reversible ischemic injury occurs. In situations where reperfusion is achieved after irreversible ischemic injury has occurred, the potential beneficial effect of these treatments on infarct size is more doubtful.     

Intravascular signal in MR imaging: use of phase display for differentiation of blood-flow signal from intraluminal disease

Intravascular signal from flowing blood is frequently observed on magnetic resonance (MR) images and may be indistinguishable from partial or complete vascular occlusion caused by thrombus or tumor. With a phase-display reconstruction method, qualitative assessment of large-vessel patency within the abdomen was undertaken in 15 healthy subjects and 12 patients with angiographically or surgically documented intravascular thrombus or tumor. Computed tomographic (CT) scans were available in all patients for correlation. MR studies were performed with a multisection spin-echo pulse sequence and two-dimensional Fourier transform spatial encoding. Data acquired from a single sequence was reconstituted in two ways to provide both routine anatomic images and a pictorial representation of large-vessel flow on a phase-sensitive image. With this method, reliable and easy differentiation of intraluminal thrombus and tumor from blood flow signal within large vessels was achieved. Information from these phase-display images compared favorably with findings from angiography and contrast-enhanced CT in the determination of luminal patency and obstruction.     

Incidental detection of bilateral elastofibroma dorsi with F-18 FDG PET/CT

An 83-year-old asymptomatic woman with a history of breast cancer treated with resection, radiation, and chemotherapy was studied with F-18 FDG positron emission tomography/computed tomography (PET/CT) for staging purposes. The whole-body F-18 FDG PET/CT images revealed poorly circumscribed, bilateral soft tissue masses between the inferior tips of the scapulae and chest wall with a moderate degree of F-18 FDG accumulation. The maximum standardized uptake values were 2.8 for both the left and right lesions. A biopsy or further imaging was not recommended because the lesions were asymptomatic, bilateral, and their imaging features were diagnostic for elastofibroma dorsi. Comparison to a CT scan performed 2 years earlier demonstrated stability of the lesions, further supporting our diagnosis. Recognition of this moderately metabolic benign entity in oncologic patients will avoid unnecessary medical, radiologic, or surgical interventions.     

Modification of human hearing loss by plasma-membrane calcium pump PMCA2

Five adult siblings presented with autosomal recessive sensorineural hearing loss: two had high-frequency loss, whereas the other three had severe-to-profound loss affecting all frequencies. Genetic evaluation revealed that a homozygous mutation in CDH23 (which encodes cadherin 23) caused the hearing loss in all five siblings and that a heterozygous, hypofunctional variant (V586M) in plasma-membrane calcium pump PMCA2, which is encoded by ATP2B2, was associated with increased loss in the three severely affected siblings. V586M was detected in two unrelated persons with increased sensorineural hearing loss, in the other caused by a mutation in MYO6 (which encodes myosin VI) in one and by noise exposure, suggesting that this variant may modify the severity of sensorineural hearing loss caused by a variety of factors.     

Genotypic and Phenotypic Evidence of Different Drug-Resistance Mutation Patterns between B and Non-B Subtype Isolates of Human Immunodeficiency Virus Type 1 found in Brazilian Patients Failing HAART

We have investigated the phenotypic and genotypic susceptibility of 14 HIV-1 strains isolated from individuals failing HAART therapy to protease inhibitors (PI). Proviral and plasma viral pol gene fragment were amplified, sequenced and subtyped. Nine samples clustered with protease subtype B reference strains and the remaining samples were classified as non-B subtype corresponding to subtype F (n=4) and subtype A (n=1). Although all patients were treated with similar PI drug regimen, the non-B subtype isolates did not present the L90M and I84V mutations and used mainly G48V and V82A/F to achieve drug resistance. A strong cross-resistance phenotype among all four PI was associated with the mutation L90M in the subtype-B isolates, and with G48V and V82A/F in the non-B counterparts. This observation revealed that the non-B viruses tested had specific genotypic characteristics contrasting with the subtype-B isolates.     

Capsule endoscopic features of Crohn's disease

Background: Crohn's disease (CD) is becoming increasingly recognized in Indian patients. As this disease often affects the small bowel, capsule endoscopy can help diagnose this disease and add valuable information regarding the extent of the disease. Our aim is to report our experience with the wireless capsule endoscope in patients with either known or suspected CD. Methods: Patients referred for capsule endoscopy with known or suspected CD were studied. All patients underwent precapsule endoscopy colonoscopy and small bowel series examination. After an overnight fast and bowel preparation, the capsule was ingested and the data were recorded for 8 h on the external recording device. A gastroenterologist experienced in reading capsule endoscopy interpreted images. Results: Eleven patients (mean age 42 years [range 14–70], 7 males) underwent capsule examination. Seven patients had symptoms suggestive of CD with no precapsule evidence of the disease, one had suspected small bowel pseudo‐obstruction and three had known CD. All patients had lesions in the small intestine consistent with CD. Two patients had strictures that led to a retained capsule, despite precapsule small bowel series. Conclusions: Capsule endoscopy is emerging as a small bowel imaging modality that can greatly assist in making the diagnosis of CD. Small bowel radiology is unreliable in excluding strictures that may cause capsule retention.     

等离子低温扁桃体消融术治疗阻塞性睡眠呼吸暂停综合征

目的：探讨等离子低温射频扁桃体消融术治疗阻塞性睡眠呼吸暂停低通气综合征的效果。方法：用等离子低温扁桃体消融术治疗阻塞性睡眠呼吸暂停低通气综合征(OSAHS)45例，于术前及术后12周行多导睡眠仪监测和Epworth嗜睡程度评分以确定治疗效果。结果：术后随访3-6个月，患者均取得了满意的疗效。与治疗前比较，最低血氧饱和度(LSPO2)显著提高(P＜0．05)；呼吸暂停低通气指数减低，差异有高度显著性(P＜0．01)。扁桃体缩小及鼾声评级降低程度与治疗前差异有高度显著性(P＜0．01)，Epworth嗜睡程度评分亦明显降低(P＜0．01)。结论：等离子低温扁桃体射频消融术具有较好的临床疗效，且方便、安全、微创，无不良反应，有较好的应用前景。