Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The corneal endothelium transports solute from the stroma to the aqueous humor, maintaining corneal hydration. Currently, little is known about how this active transport system is controlled. The purpose of this study is to investigate in greater detail the corneal response to small NaCl osmotic perturbations using a more refined automatic thickness measurement system in a search for response signatures of transport control. Adult New Zealand White rabbit corneas were debrided of their epithelium, excised and mounted in perfusion chambers. The endothelium, thus isolated, was bathed in isotonic Glutathione Bicarbonate Ringer's (GBR) solution and the bare anterior stroma was covered with silicone oil. Following stabilization in isotonic GBR, the endothelial perfusate was altered by +/-15 mOsm or+/-45 mOsm for 1 hr and 45 min by addition or removal of NaCl and returned (reversal) to GBR for 1 hr and 45 min. An enhanced, automatic scanning specular microscope monitored stromal thickness. The effective membrane transport coefficients were determined from the stromal thickness vs. time curves using an established numerical model of corneal hydration dynamics. It was found that the small (+/-15 mOsm) NaCl perturbations of the rabbit corneal endothelium resulted in a rapid trans-endothelial stromal volume control response that was not reversible after return to GBR. Long after the expected dissipation of the induced transients, this thickness 'controlling' response ultimately resulted in a sustained net thinning of 14 microm following the hypotonic perturbation and reversal, and a net swelling of 16 microm following the hypertonic perturbation and reversal. Model calculations indicated that the change induced by the perturbation could be explained by an immediate and persistent reduction of the passive endothelial NaCl permeability by 26% for the -15 mOsm perturbation compared to the +15 mOsm perturbation. This change persisted even after return to GBR. In contrast, the larger (+/-45 mOsm) perturbations did not elicit a similar response consistently. Our data suggest that trans-endothelial fluid transport can be rapidly modulated to control stromal hydration in response to small NaCl osmotic stresses in a way that cushions the shock and reduces the change in corneal thickness. Moreover, this behavior is not reversible in the short term, and may assist the regulation of corneal hydration homeostatically.
 ...
PMID:NaCl osmotic perturbation can modulate hydration control in rabbit cornea. 1257 64

In the present study, female Chinese rare minnows (Gobiocypris rarus) were used as in vivo models and exposed to nonylphenol (NP) at concentrations of 1 to 200 microg/L for 21 d under semistatic conditions. Molecular biomarkers of oxidative stress were measured in unfertilized eggs and included reactive oxygen species (ROS), lipid peroxidation products (thiobarbituric acid- reactive substances [TBARS] and protein carbonyl), superoxide dismutase activity, and glutathione. Cathepsin D activity as an indicator of egg viability also was assayed. Nonylphenol induced ROS formation in unfertilized eggs in all exposed groups compared to the controls. The levels of protein carbonyl and TBARS in unfertilized eggs were significantly increased (p < 0.05) at 10 to 200 and 100 to 200 microg/L, respectively. Good positive correlations were shown between ROS induction and levels of TBARS and protein carbonyl in eggs (R = 0.918, p < 0.05 and R = 0.784, p < 0.05, respectively). Superoxide dismutase activity in eggs was significantly inhibited (p < 0.05) in the 50 to 200 microg/L exposure groups. Glutathione levels in eggs were significantly depleted (p < 0.05) at 100 to 200 microg/L concentrations. In addition, ROS induction resulted in oxidative damage to lipid and protein in chorions. Significant reductions (p < 0.05) of the protein and lipid contents in chorions were both found in the 50 to 200 microg/L exposure groups. A previous study found that NP exposure could lead to chorion thinning in zebra fish. Thus, the reductions in protein and lipid contents in chorion could be the reason for chorion thinning by NP exposure. Meanwhile, cathepsin D activity was significantly inhibited (p < 0.05) in all exposure groups. The results demonstrated that NP-induced oxidative stress could damage the chorion of unfertilized eggs and lead to a decline in gamete quality in female Chinese rare minnow.
 ...
PMID:Oxidative damage in unfertilized eggs of Chinese rare minnow (Gobiocypris rarus) exposed to nonylphenol. 1809 62

In the current study, effects of oral phenytoin on hair growth in cyclophosphamide-treated rats were assessed with the goal of evaluating the ability of phenytoin to suppress chemotherapy-induced hair loss. Thirty-six rats were randomly assigned to six groups (1k6) of six each (n=6). In all groups, anagen was induced in flank skin of rats by depilation. On day 9 (anagen VI), rats were injected once with either distilled water (groups 1-3) or cyclophoshamide (groups 4-6). From day 10, rats in group 1 and 4 received oral vehicle (distilled water), groups 2 and 5 received oral phenytoin (50mg/kg), while groups 3 and 6 also received oral phenytoin (100mg/kg). Drug or vehicle was administered daily for a period of 28days. The flank area was serially photographed. At the end of the experimental period, rats were sacrificed to correlate visible hair growth with a histological profile of follicle response and recovery. Glutathione (GSH), glutathione peroxidase (GPX) and lipid peroxidation status were assessed. Cyclophosphamide (CYP) treatment was associated with gross morphologic and histological evidence of hair loss in the flanks, microscopic evidence of hair-shaft thinning, increased skin lipid peroxidation, decreased GSH level, and reduction in GPX activities. Phenytoin co-administration was associated with evidence of improved hair growth, increased hair-shaft thickness, reduced skin lipid peroxidation, increased GSH level, and increased GPX activities. This study showed that oral phenytoin can suppress hair loss due to CYP therapy in rats; however, further studies are needed to evaluate its potential application in chemotherapy-induced alopecia.
 ...
PMID:Oral phenytoin protects against experimental cyclophosphamide-chemotherapy induced hair loss. 2921 84