摘要:

Fibroblast accumulation in a cutaneous wound requires phenotypic modulation of fibroblasts. In response to injury, resident fibroblasts in the surrounding tissue proliferate for the first 3 days and then at day 4 migrate into the wounded site. Once within the wound, they produce type I procollagen as well as other matrix molecules and deposit these extracellular matrix molecules in the local milieu. By day 7, abundant extracellular matrix has accumulated and fibroblasts switch to a myofibroblast phenotype replete with actin bundles along the cytoplasmic face of the plasma membrane. Wound contraction occurs as these myofibroblast gather in the wound extracellular matrix by extending pseudopodia, attaching to extracellular matrix molecules, such as fibronectin and collagen, then retracting the pseudopodia. Once these processes have been accomplished, the fibroblasts appear to undergo apoptosis. Therefore, during cutaneous wound repair, fibroblasts appear to progress through four phenotypes: first proliferating, second migrating, third synthesizing extracellular matrix molecules, and fourth expressing thick actin bundles as myofibroblasts.

ISSN:0002-9629    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Flumazenil is a central antagonist of the sedative effects of benzodiazepines. It has been used to reverse benzodiazepine effects in conscious sedation, general anesthesia, and overdose with restoration of alertness and psychomotor function within minutes of administration. Seizures have followed the use of flumazenil. Overdose patients who have co-ingested cyclic antidepressants are especially at risk for this complication. Flumazenil is administered intravenously in small, incremental doses.

ISSN:0002-9629    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

The cardinal features of the nephrotic syndrome are albuminuria, hypoalbuminemia, and edema. Traditionally, albuminuria was thought to be responsible primarily for the development of hypoalbuminemia. A decreased plasma-albumin concentration accompanied by a decreased plasma-oncotic pressure was thought responsible for the development of edema and secondary salt retention by the kidney. However, new findings have prompted a reevaluation of these relationships. For example, increased renal catabolism and blunted hepatic synthesis appear to play major roles in the development of hypoalbuminemia. Evidence suggests that primary, rather than secondary, salt retention by the kidney and activation of mechanisms that limit fluid movement across the capillary wall participate in the pathogenesis of the nephrotic syndrome and related edema. The treatment of patients with the nephrotic syndrome should limit proteinuria. This can be accomplished by administering angiotensin-converting enzyme inhibitors, lowering the protein content of the diet, and cautiously using non-steroidal antiinflammatory agents.

ISSN:0002-9629    

出版商:OVID    

年代:1993

数据来源: OVID