Protecting the small: preliminary investigation of bryozoan community change in New Zealand’s oldest marine reserve

Author(s):  
Hannah L. Mello ◽  
Dennis P. Gordon ◽  
John S. Ryland ◽  
Abigail M. Smith
Author(s):  
R.P. Apkarian ◽  
J.S. Sanfilippo

The synthetic androgen danazol, is an isoxazol derivative of ethisterone. It is utilized in the treatment of endometriosis, fibrocystic breast disease, and has a potential use as a contraceptive. A study was designed to evaluate the ultrastructural changes associated with danazol therapy in a rat model. The preliminary investigation of the distal segment of the rat uterine horn was undertaken as part of a larger study intended to elucidate the effects of danazol on the female reproductive tract.Cross-sections (2-3 mm in length) of the distal segment of the uterine horn from sixteen Sprague-Dawley rats were prepared for SEM. Ten rats in estrus served as controls and six danazol treated rats were noted to have alterations of the estrus cycle i.e. a lag in cycle phase or noncycling patterns. Specimens were fixed in 3% glutaraldehyde in 0.05M phosphate buffer containing CaCl2 at pH 7.0-7.4 and chilled to 4°C. After a brief wash in distilled water, specimens were passed through a graded series of ethanol, critical point dryed in CO2 from absolute ethanol, and coated with 6nm Au. Observations were made with an IS1-40 SEM operated at 15kV.


Author(s):  
Becky Jackson

Preliminary investigation has indicated similarity in hepatic ultrastructural morphology in nutritional deprivation, and cyanide induced hepatic necrosis. Analysis of hepatic tissue has indicated disruption of intracellular membranes, specifically, reduction in rough endoplasmic reticulum (RER) mitochondrial integrity, and glycogen stores. An increase in smooth endoplasmic reticulum (SER) portion was observed.To further investigate the apparent equivalence of necrotic morphology, ultrastructura1ly, BDF1 mice were subjected to senescence, nutritional deprevation, potassium cyanide (KCN) induced toxemia, and acetaminophen induced toxemia. Controls were utilized to ellucidate non-necrotic hepatocellular normals. U1trastructura1 investigation of controls (Fig. 1) shows densely granular RER, abundant glycogen stores, and morphologically normal mitochondria. Subjects with acetaminophen induced necrosis exhibit reduced normal RER with increased levels of dialated, vesicular RER in apparent conversion to SER (Fig. 2), loss of mitochondrial integrity, and glycogen store reduction. Senescent subjects exhibit a pronounced increase in SER and loss of glycogen store. (Fig. 3). Investigation of the senescent SER at high magnification (Fig. 5) indicates that the SER is arising from degranulating and vesiculating RER.


Author(s):  
Richard L. Klein ◽  
Åsa K. Thureson-Klein ◽  
Harihara M. Mehendale

KeponeR (decachlorooctahydro-1,3,4-metheno-2H-cyclobuta[cd]pentalen-2-one) is an insecticide effective against ants and roaches. It can cause severe toxicity in fishes, birds, rodents and man. Prominent effects include hepatic lipid deposition and hypertrophy, impairment of reproductive capacity and neurological disorders. Mitochondrial oligomycin-sensitive Mg2+-ATPase is also inhibited. The present study is a preliminary investigation of tissue ultrastructural changes accompanying physiological signs of acute toxicity, which after two days treatment include: pronounced hypersensitivity and tremor, various degrees of anorexia and adipsia, and decreased weight gain.Three different series of adult male Sprague-Dawley rats (Charles River or CD-I) were treated by intubation with Kepone in corn oil at a dose of 50 mg per kg for 3 successive days or at 200 ppm in food for 8 days. After ether anesthesia, rats were immediately perfused via a cannula in the left ventricle with 4% p-formaldehyde and 0.5% glutaraldehyde in Millonig's phosphate buffer at pH 7.2 for 20-30 min at 22°C.


2005 ◽  
Author(s):  
Brian D. Lyons ◽  
John W. Michel ◽  
Brian J. Hoffman

2008 ◽  
Author(s):  
Jenny L. Collier ◽  
Laura A. Glass ◽  
Joseph J. Ryan ◽  
Tara S. Duckworth

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