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Biomedical subjects

Andreas H Weiglein

Publications and source records attributed to Andreas H Weiglein.

3 recordsLinked to original sources

Herniation of the mylohyoid muscle.

During ultrasound examinations in patients with dysphagia, deficiencies in the mylohyoid muscle with herniation of the sublingual gland were found, which may be mistaken as soft tissue tumors. Between the years 2001 and 2003, 205 half-heads used in dissection courses were examined to determine the location and contents of these gaps. In 25 of these cadaveric specimens, the hiatus (of variable size) appeared as small fissures between the divided fibers of the mylohyoid. In 18 cases (72%), the sublingual gland slipped through these deficiencies and occurred in the front part of the submandibular triangle. From the inferior surface of the muscle, the submental artery also coursed through the separated muscle fibers. The herniations of 7 specimens (28%) were found without any contents, neither with gland perforation nor with a submental artery. The following study points out the spatial relation of the salivary glands to the floor of the mouth and the clinical significance, and some factors referred to the development of herniations are discussed.

Deglutition Disorders↗

Ursodeoxycholic acid aggravates bile infarcts in bile duct-ligated and Mdr2 knockout mice via disruption of cholangioles.

BACKGROUND & AIMS: The effects of ursodeoxycholic acid (UDCA) in biliary obstruction are unclear. We aimed to determine the effects of UDCA in bile duct-ligated and in Mdr2 knockout (Mdr2(-/-)) mice with biliary strictures. METHODS: Mice fed UDCA (0.5% wt/wt) or a control diet were subjected to common bile duct ligation (CBDL), selective bile duct ligation (SBDL), or sham operation. UDCA was also fed to 2-month-old Mdr2(-/-) mice. Serum biochemistry, liver histology, and mortality rates were investigated. The biliary tract was studied by plastination, India ink injection, and electron microscopy. The effects of UDCA on biliary pressure were determined by cholangiomanometry. RESULTS: UDCA feeding in CBDL mice increased biliary pressure, with subsequent rupture of cholangioles and aggravation of hepatocyte necroses, resulting in significantly increased mortality. UDCA feeding in SBDL mice aggravated liver injury exclusively in the ligated lobe. Mdr2(-/-) mice developed liver lesions resembling sclerosing cholangitis characterized by biliary strictures and dilatations. UDCA induced bile infarcts in these animals. CONCLUSIONS: UDCA aggravates bile infarcts and hepatocyte necroses in mice with biliary obstruction via disruption of cholangioles as a result of increased biliary pressure caused by its choleretic action.

ATP Binding Cassette Transporter, Subfamily B↗