外伤性主动脉破裂致全程胸主动脉夹层1例

抢救1例因摩托车事故急诊入院男病人。X线胸片发现病人右气管旁外侧纹理和左纵隔影异常增宽，并扩展至主动脉弓水平。经食管心脏超声检查发现围绕主动脉根部和升主动脉的壁间水肿。延伸至主动脉弓和左横膈下水平的全程降主动脉；左锁骨下动脉起始点远端降主动脉上端全层断裂。急诊手术行降主动脉上端端端吻合，终因心跳骤停未及手术死亡。尸检证实全程胸主动脉自破裂处向前和逆向延伸，引起双向主动脉夹层。     

Escherichia coli Nissle 1917-derived factors reduce cell death and late apoptosis and increase transepithelial electrical resistance in a model of 5-fluorouracil-induced intestinal epithelial cell damage

We evaluated the capacity for supernatants (SNs) derived from Escherichia coli Nissle 1917 (EcN), cultured under different growth conditions, to prevent 5-fluorouracil (5-FU)-induced intestinal epithelial cell damage. EcN was cultured in: Luria Bertani (LB) broth, tryptone soya broth (TSB), de Man Rogosa Sharpe (MRS) broth, and M17 broth supplemented with 10% (v/v) lactose solution (M17). Intestinal epithelial cells (IEC-6) were treated with the following EcN SNs: LB⁺, TSB⁺, MRS⁺, and M17⁺ in the presence and absence of 5-FU (1.5 or 5 μM). Cell viability, apoptotic activity and cell monolayer permeability were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and transepithelial electrical resistance (TER) assays, respectively. 5-FU significantly reduced cell viability (P < 0.05) at both 24 and 48 h. However, only EcN SN produced from LB and M17 growth media significantly decreased cell death induced by 5-FU (by approximately 10% after 24 and 48 h; and 10% after 24 h, respectively [P < 0.05]). When measured by flow cytometry all EcN SNs in the presence of 5-FU increased the proportion of viable cells (by 3–5% for 24 h, 3–7% for 48 h, P < 0.05) and reduced late-apoptotic cells after 24 and 48 h, compared with 5-FU control. Moreover, all EcN SNs significantly reduced the disruption of IEC-6 cell barrier function induced by 5-FU by 7–10% (P < 0.05), compared with DMEM control. We conclude that EcN derived factors could potentially reduce the severity of intestinal mucositis.     

Brain mineralocorticoid receptors: orchestrators of hypertension and end-organ disease

PURPOSE OF REVIEW: 'New' tasks have been discovered for aldosterone and its receptor, the mineralocorticoid receptor, within both epithelial tissues of vectorial ion and water transport, such as the kidney, and non-epithelial organs, including the brain, heart and vessels. Promising results of clinical trials using low doses of mineralocorticoid receptor antagonists to forestall end-organ disease is resulting in an increase in their use, yet the biology of the mineralocorticoid receptor is far from clear. RECENT FINDINGS: Mineralocorticoid receptors within the kidney, heart and blood vessels mediate direct effects of aldosterone, including tissue inflammation, hypertrophy and fibrosis, that are independent of blood pressure. Activation, by aldosterone, of mineralocorticoid receptors in the brain increases central sympathetic nervous system drive to the periphery, thereby producing hypertension through multiple mechanisms, and increases levels of proinflammatory cytokines in both the circulation and peripheral tissues. Blocking of the mineralocorticoid receptor of the forebrain lowers the levels of peripheral tissue cytokines, including those induced by ischemic injury in the heart. Aldosterone is produced within the heart, blood vessels and brain, potentially liberating regulation of local concentrations of the steroid from peripheral mechanisms of control. A conundrum yet to be explained is the ligand-dependent functional specificity of the mineralocorticoid receptor in some non-epithelial tissues, which may be crucial to our understanding the end-organ pathophysiology of hypertension. SUMMARY: New technology is rapidly adding layers of complexity to, rather than simplifying, our understanding of the facile terms 'hemodynamic homeostasis' and 'end-organ' disease, but within this new knowledge lies the promise of better, more precise treatment of hypertension and its sequelae.     

Mineralocorticoid activity of 16beta-hydroxydehydroepiandrosterone and related steroids.

16beta-Hydroxydehydroepiandrosterone (16beta-OH-DHEA) and related C19-steroids have recently been reported to be etiologic in low-renin essential hypertension. The mineralocorticoid potency of 16beta-OH-DHEA and several C19-steroids (16-oxo-A-diol, 16-oxo-testosterone, 16beta-OH-epiandrosterone, 5-androstene-3beta, 16beta,17beta-triol, 19beta-OH-testosterone, 18-OH-DHEA, and 16alpha-OH-DHEA) were investigated in two different rat bioassay systems under a variety of experimental conditions. In all but one instance, only negligible mineralocorticoid activity was observed, usually less than 0.1 per cent that of aldosterone. Since 16beta-OH-DHEA has negligible mineralocorticoid activity in the rat bioassay and the toad bladder assay (as reported by others), does not cause hypertension when injected chronically into the rat, and does not displace aldosterone from its renal receptors, it appears unlikely to be etiologic in low-renin essential hypertension. On the other hand, when 16-oxo-testosterone was injected intraperitoneally instead of subcutaneously, it demonstrated a slight increase in mineralocorticoid activity (from less than 0.1 per cent to 0.2 per cent) which equaled that of 18-hydroxydeoxycorticosterone (18-OH-DOC) injected subcutaneously. Thus, the possibility remains that 16-oxo-testosterone or a closely related metabolite may have sufficient mineralocorticoid activity to be involved in certain forms of hypertension in man.