Competition and Combative Advertising: An Historical Analysis

Fred K. Beard (PhD, University of Oklahoma) is a professor of advertising in the Gaylord College of Journalism and Mass Communication, University of Oklahoma. His research interests include comparative advertising, advertising humor, and advertising history. His work has appeared in the Journal of Advertising, the Journal of Advertising Research, the Journal of Business Ethics, the Journal of Business Research, Journalism History, the Journal of Historical Research in Marketing, the Journal of Macromarketing, and the Journal of Marketing Communications, among others.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Evaluation of potential changes in liver and lung tissue of rats in an ischemia-reperfusion injury model (modified pringle maneuver).

In surgical procedures involving the liver, such as transplantation, resection, and trauma, a temporary occlusion of hepatic vessels may be required. This study was designed to analyze the lesions promoted by ischemia and reperfusion injury of the hepatic pedicle, in the liver and lung, using histopathological and immunohistochemical techniques. In total, 39 Wistar rats were divided into four groups: control group (C n = 3) and ischemia groups subjected to 10, 20, and 30 minutes of hepatic pedicle clamping (I10, n = 12; I20, n = 12; I30, n = 12). Each ischemia group was subdivided into four subgroups of reperfusion (R15, n = 3; R30, n = 3; R60, n = 3; R120, n = 3), after 15, 30, 60, and 120 minutes of reperfusion, respectively. Significant differences were observed in the liver parenchyma (P 0.05). In the lung parenchyma, a significant difference was observed (P 0.05) at different times of ischemia and reperfusion. In the pulmonary parenchyma, the immunoreactivity was not specific, and was not quantified. This study demonstrated that the longer the duration of ischemia and reperfusion, the greater are the morphological lesions found in the hepatic and pulmonary parenchyma

Photomicrographs of the hepatic parenchyma of Wistar rats subjected to ischemia and reperfusion.

<p>Groups (10, 20, and 30 minutes ischemia) and subgroups (15, 30, 60 and 120 minutes reperfusion): I10 and R15 (A), I10 and R30 (B), I10 and R60 (C), I10 and R120 (D), I20 and R15 (E), I20 and R30 (F), I20 and R60 (G), I20 and R120 (H), I30 and R15 (I), I30 and R30 (J), I30 and R60 (K) e I30 and R120 (L). Note the positive immunoreactivity for caspase-3 protein (brown coloration).</p

Photomicrographs of the pulmonary parenchyma of control group animals (C).

<p>Note: alveolar septum, alveolar duct, alveolar sac, alveoli, and bronchioles. Hematoxylin-eosin staining (HE).</p

Photomicrographs of the pulmonary parenchyma of Wistar rats subjected to ischemia and reperfusion.

<p>Groups (10, 20, and 30 minutes ischemia) and subgroups (15, 30, 60, and 120 reperfusion): I10 and R15 (A), I10 and R30 (B), I10 and R60 (C), I10 and R120 (D), I20 and R15 (E), I20 and R30 (F), I20 and R60 (G), I20 and R120 (H), I30 and R15 (I), I30 and R30 (J), I30 and R60 (K), I30 and R120 (L). Note: vascular congestion, degeneration of bronchial epithelium, alveolar septal thickening, interstitial edema, and hemorrhage. Hematoxylin-eosin staining (HE).</p

Liver parenchyma photomicrographs of Wistar rats subjected to ischemia and reperfusion.

<p>Groups (10, 20, and 30 minutes ischemia) and subgroups (15, 30, 60, and 120 reperfusion): I10 and R15 (A), I10 and R30 (B), I10 and R60 (C), I10 and R120 (D), I20 and R15 (E), I20 and R30 (F), I20 and R60 (G), I20 and R120 (H), I30 and R15 (I), I30 and R30 (J), I30 and R60 (K) e I30 and R120 (L). Note: vascular congestion, microvesicles, hydropic degeneration, necrosis, and pyknotic nuclei. Hematoxylin-eosin staining (HE).</p

Photomicrographs of the hepatic parenchyma in control group animals: Negative control (C-) and positive control (C+).

<p>Note the positive immunoreactivity for caspase-3 in the C+ group (brown coloration).</p

Photomicrographs of the liver parenchyma of control group animals (C).

<p>Note: central vein, hepatocytes, and sinusoidal capillaries. Hematoxylin-eosin staining (HE).</p

Mean values of vascular congestion (A), microvesicles (B), hydropic degeneration (C), necrosis (D), and pyknotic nuclei (E) in the liver parenchyma of the ischemia (I), reperfusion (R), and control (C) group animals.

<p>The data were recorded by optical microscopy after hematoxylin-eosin staining (HE). Ischemic groups: I10–10 minutes of ischemia, I20–20 minutes of ischemia and I30–30 minutes of ischemia. Reperfusion subgroups: R15–15 minutes of reperfusion, R30–30 minutes of reperfusion, R60–60 minutes of reperfusion and R120–120 minutes of reperfusion (*P < 0.05).</p