Interstitial incisional hernia of greater omentum: An incidental finding during routine cadaveric dissection.

Omental herniation, located between the rectus abdominis muscle and the anterior blade of the rectus sheath, can be triggered after a transverse suprapubic incision. It causes the development of an incisional interstitial hernia (IIH), which is an extremely rare and poorly understood condition. Based on this information, our work presents the first anatomical description of incisional interstitial hernia found during routine dissection at the Human Anatomy Laboratory of the Federal University of Ceará in a formalized female corpse.

Immature Stages, Natural History, Systematics and Conservation of an Endangered Neotropical Butterfly: the Case of Scada karschina delicata (Nymphalidae: Ithomiini).

The endangered butterfly Scada karschina delicata Talbot, 1932 (Nymphalidae: Danainae: Ithomiini) is endemic to northeastern Brazil, occurring in very few forest remnants of the 'Pernambuco Center of Endemism'. Larvae feed on Solanaceae and are very similar to those of other species in the subtribe Mechanitina, with lateral projections on body, one of the main synapomorphies of this subtribe. Based on molecular data, S. k. delicata clustered together with S. karschina karschina, as a monophyletic group sister to the amazon clade of S. reckia. Based on all available data, S. k. delicata is known from only five localities of mid- to high-altitude forests (from 500 to 1000 m of altitude) in northeastern Brazil. Grounded on available data, a new assessment of extinction risk is proposed, and S. k. delicata is now considered Vulnerable (VU) taxon.

Pro-inflammatory effects of cholera toxin: role of tumor necrosis factor alpha.

Cholera toxin has been traditionally described as the one that does not induce inflammation. It has, however, potent adjuvant and immuno-modulatory activities. Since the adjuvanticity of other compounds is linked to their capacity to induce inflammation, in the present study the pro-inflammatory activity of cholera toxin was investigated. We studied this activity in the following rat models of inflammation: paw edema and neutrophil migration into the peritoneal cavity, and evaluated cholera toxin's effect on tumor necrosis factor alpha (TNF-alpha) production by mouse macrophages. We, also, explored the effects of dexamethasone (DEXA) and of two inhibitors of TNF-alpha production, thalidomide (TAL) and pentoxifylline, on paw swelling. Cholera toxin-induced significant and dose-dependent paw edema, which peaked 48 h after toxin challenge (Cholera toxin(2.5 microg): 2.39 +/- 0.22 ml). Cholera toxin B subunit did not show edematogenic activity. DEXA, TAL and pentoxifylline significantly reduced cholera toxin-induced edema (DEXA(0.5 mg/kg): 42.6% of inhibition; TAL(45 mg/kg): 36% of inhibition; pentoxifylline (45 mg/kg): 61% of inhibition). Neither cholera toxin nor its B subunit induced neutrophil migration into peritoneal cavities. Cholera toxin stimulated the release of TNF-alpha by macrophages (cholera toxin(10 microg): 11.46 +/- 0.44 UI/ml). These data provide evidences that cholera toxin exhibits significant pro-inflammatory activity. It also indicates the role of TNF-alpha upon the pathophysiology of this event based on the inhibitory action of DEXA, TAL and pentoxifylline, and on TNF-alpha secretion induced by cholera toxin.