新型频域相关断层扫描对健康年轻人视网膜各参数的测量分析

目的：采用新型频域相关断层扫描测量分析健康年轻人中视网膜各参数生理的不对称性。方法：对146名健康年轻人进行横断面观察研究,采用新型频域相关断层扫描对其双眼视网膜参数（视网膜神经纤维层厚度、视盘、黄斑）进行扫描。通过右眼减去左眼所得参数值的平均差进行配对t检验。两眼间的差异采用2．5％～97．5％之间进行评估。视网膜参数相关。通过回归分析,评价性别和血压对视网膜参数的影响。结果：两眼的视网膜神经纤维层平均厚度无统计学差异（＋0．7μm,P＝0．09）。两眼视网膜颞侧象限（＋2．51μm,P＝0．02）,鼻侧象限（＋2．50μm,P＝0．04）,钟表位右眼2点与左眼10点（＋5．85μm,P＝0．002）,右眼3点与左眼9点（＋3．20μm,P＝0．005）,右眼11点与左眼1点（＋3．80μm,P＝0．024）,平均厚度（－0．034μm,P＝0．013）和垂直方向杯盘比（－0．028μm,P＝0．008）,黄斑部鼻侧象限（＋7．76μm,P＝0．003）。左眼上方视网膜明显较薄（－2．40μm, P＝0．03）。平均视网膜神经纤维层厚度和黄斑厚度分别为11μm和18μm。视网膜参数在双眼有中度的相关性（0．41～0．6）,而两眼视网膜参数与性别、血压不相关（P＜0．05）。研究表明通过新型频域相关断层扫描发现健康年轻人的视网膜神经纤维层厚度和黄斑厚度两眼间的差异分别不应超过11μm和18μm。结论：视网膜参数的不对称性存在于健康视网膜,并对早期视网膜病变的诊断提供有价值的评估。     

Mitochondria play a central role in nonischemic cardiomyocyte necrosis: common to acute and chronic stressor states

The survival of cardiomyocytes must be ensured as the myocardium adjusts to a myriad of competing physiological and pathophysiological demands. A significant loss of these contractile cells, together with their replacement by stiff fibrillar collagen in the form of fibrous tissue accounts for a transition from a usually efficient muscular pump into one that is failing. Cellular and subcellular mechanisms involved in the pathogenic origins of cardiomyocyte cell death have long been of interest. This includes programmed molecular pathways to either necrosis or apoptosis, which are initiated from ischemic or nonischemic origins. Herein, we focus on the central role played by a mitochondriocentric signal-transducer-effector pathway to nonischemic cardiomyocyte necrosis, which is common to acute and chronic stressor states. We begin by building upon the hypothesis advanced by Albrecht Fleckenstein and coworkers some 40?years ago based on the importance of calcitropic hormone-mediated intracellular Ca²⁺ overloading, which predominantly involves subsarcolemmal mitochondria and is the signal to pathway activation. Other pathway components, which came to be recognized in subsequent years, include the induction of oxidative stress and opening of the mitochondrial inner membrane permeability transition pore. The ensuing loss of cardiomyocytes and consequent replacement fibrosis, or scarring, represents a disease of adaptation and a classic example of when homeostasis begets dyshomeostasis.     

Mitochondria-targeted cardioprotection in aldosteronism

Chronic aldosterone/salt treatment (ALDOST) is accompanied by an adverse structural remodeling of myocardium that includes multiple foci of microscopic scarring representing morphologic footprints of cardiomyocyte necrosis. Our previous studies suggested that signal-transducer-effector pathway leading to necrotic cell death during ALDOST includes intramitochondrial Ca overloading, together with an induction of oxidative stress and opening of the mitochondrial permeability transition pore (mPTP). To further validate this concept, we hypothesized that mitochondria-targeted interventions will prove to be cardioprotective. Accordingly, 8-week-old male Sprague-Dawley rats receiving 4 weeks ALDOST were cotreated with either quercetin, a flavonoid with mitochondrial antioxidant properties, or cyclosporine A (CsA), an mPTP inhibitor, and compared with ALDOST alone or untreated, age/sex-matched controls. We monitored mitochondrial free Ca and biomarkers of oxidative stress, including 8-isoprostane and H2O2 production; mPTP opening; total Ca in cardiac tissue; and collagen volume fraction to quantify replacement fibrosis, a biomarker of cardiomyocyte necrosis, and employed terminal deoxynucleotidyl transferase dUTP nick end labeling assay to address apoptosis in coronal sections of ventricular myocardium. Compared with controls, at 4 weeks ALDOST we found a marked increase in mitochondrial H2O2 production and 8-isoprostane levels, an increased propensity for mPTP opening, and greater concentrations of mitochondrial free [Ca]m and total tissue Ca, coupled with a 5-fold rise in collagen volume fraction without any terminal deoxynucleotidyl transferase dUTP nick end labeling-based evidence of cardiomyocyte apoptosis. Each of these pathophysiologic responses to ALDOST was prevented by quercetin or cyclosporine A cotreatment. Thus, mitochondria play a central role in initiating the cellular-subcellular mechanisms that lead to necrotic cell death and myocardial scarring. This destructive cycle can be interrupted and myocardium salvaged with its structure preserved by mitochondria-targeted cardioprotective strategies.     

Keratosis Follicularis Spinulosa Decalvans Associated with Acne Keloidalis Nuchae and Tufted Hair Folliculitis

Keratosis follicularis spinulosa decalvans is a rare, X-linked disorder characterized by scarring alopecia of the scalp and eyebrows in the setting of widespread keratosis pilaris. Less frequent associations are ocular abnormalities and palmoplantar keratoderma. Acne keloidalis nuchae has previously been described in one patient with keratosis follicularis spinulosa decalvans. We report another case of keratosis follicularis spinulosa decalvans with acne keloidalis nuchae and tufted hair folliculitis, thus further establishing this association.     

Na+-H+ exchange activity in taste receptor cells

mRNA for two Na(+)-H(+)-exchanger isoforms 1 and 3 (NHE-1 and NHE-3) was detected by RT-PCR in fungiform and circumvallate taste receptor cells (TRCs). Anti-NHE-1 antibody binding was localized to the basolateral membranes, and the anti-NHE-3 antibody was localized in the apical membranes of fungiform and circumvallate TRCs. In a subset of TRCs, NHE-3 immunoreactivity was also detected in the intracellular compartment. For functional studies, an isolated lingual epithelium containing a single fungiform papilla was mounted with apical and basolateral sides isolated and perfused with nominally CO(2)/HCO(3)(-)-free physiological media (pH 7.4). The TRCs were monitored for changes in intracellular pH (pH(i)) and Na(+) ([Na(+)](i)) using fluorescence ratio imaging. At constant external pH, 1) removal of basolateral Na(+) reversibly decreased pH(i) and [Na(+)](i); 2) HOE642, a specific blocker, and amiloride, a nonspecific blocker of basolateral NHE-1, attenuated the decrease in pH(i) and [Na(+)](i); 3) exposure of TRCs to basolateral NH(4)Cl or sodium acetate pulses induced transient decreases in pH(i) that recovered spontaneously to baseline; 4) pH(i) recovery was inhibited by basolateral amiloride, 5-(N-methyl-N-isobutyl)-amiloride (MIA), 5-(N-ethyl-N-isopropyl)-amiloride (EIPA), HOE642, and by Na(+) removal; 5) HOE642, MIA, EIPA, and amiloride inhibited pH(i) recovery with K(i) values of 0.23, 0.46, 0.84, and 29 microM, respectively; and 6) a decrease in apical or basolateral pH acidified TRC pH(i) and inhibited spontaneous pH(i) recovery. The results indicate the presence of a functional NHE-1 in the basolateral membranes of TRCs. We hypothesize that NHE-1 is involved in sour taste transduction since its activity is modulated during acid stimulation.     

Inflammatory linear verrucous epidermal nevus: a case report and short review of the literature

GOAL: To understand inflammatory linear verrucous epidermal nevus (ILVEN) to better manage patients with the condition. OBJECTIVES: Upon completion of this activity, dermatologists and general practitioners should be able to: 1. Describe the presenting characteristics of ILVEN. 2. Explain the differential diagnosis of ILVEN. 3: Discuss the treatment options for ILVEN.