Esophageal foreign body-induced esophageal perforation is a lethal complication and its treatment very complex. We had reviewed 1,428 patients with esophageal foreign body, who were hospitalized and treated over the past 25 years. A classification summary was made of 121 patients (of these 1,428 cases) who presented with esophageal foreign body-induced perforation and complicated cervical abscess, mediastinitis, and mediastinal abscess. This summary considered foreign body types, location and lodging duration, complications, and surgical approaches. Among these 121 patients, esophageal foreign bodies in 81 patients were successfully extracted via esophagoscope or fiber optic esophagoscope. Cervical esophageal foreign bodies in 22 patients were extracted by esophagoscope and lateral cervical incision (n = 6) and simple lateral cervical incision (n = 16). Thoracotomy was performed to remove thoracic esophageal foreign bodies in 18 patients with 10 successes and 8 failures. Of the 121 patients, 67 patients with cervical abscess were cured by means of lateral cervical abscess incision and drainage, esophageal stent placement, and esophageal perforation repair with pedicle myolemma or pedicle muscular periosteum flap. 54 patients with mediastinitis and/or abscess were all cured, except one mortality, by means of mediastinotomy and drainage or/and closed-chest drainage, simple esophageal repair, esophageal repair with pedicle myolemma or pedicle muscular periosteum flap and stent placement for esophageal perforation, and esophageal exclusion plus two-stage gastric-pharyngeal anastomosis. In the treatment of esophageal foreign body-induced severe complications, various therapies should be applied simultaneously. Lateral cervical incision should be made immediately to remove the foreign bodies if the foreign body extraction under esophagoscope proves to be a failure after repeated attempts, or esophageal perforation develops during the procedure, or should cervical abscess develop. Mediastinotomy and drainage or/and closed-chest drainage should be carried out as early as possible when mediastinitis and/or mediastinal abscess develops after esophageal foreign body ingestion.

A complete tricarboxylic acid (TCA) cycle is generally considered necessary for energy production from the dicarboxylic acid substrates malate, succinate, and fumarate. However, a Bradyrhizobium japonicum sucA mutant that is missing ␣-ketoglutarate dehydrogenase is able to grow on malate as its sole source of carbon. This mutant also fixes nitrogen in symbiosis with soybean, where dicarboxylic acids are its principal carbon substrate. Using a flow chamber system to make direct measurements of oxygen consumption and ammonium excretion, we confirmed that bacteroids formed by the sucA mutant displayed wild-type rates of respiration and nitrogen fixation. Despite the absence of ␣-ketoglutarate dehydrogenase activity, whole cells of the mutant were able to decarboxylate ␣-[U-14 C]ketoglutarate and [U-14 C]glutamate at rates similar to those of wild-type B. japonicum, indicating that there was an alternative route for ␣-ketoglutarate catabolism. Because cell extracts from B. japonicum decarboxylated [U-14 C]glutamate very slowly, the ␥-aminobutyrate shunt is unlikely to be the pathway responsible for ␣-ketoglutarate catabolism in the mutant. In contrast, cell extracts from both the wild type and mutant showed a coenzyme A (CoA)-independent ␣-ketoglutarate decarboxylation activity. This activity was independent of pyridine nucleotides and was stimulated by thiamine PP i . Thin-layer chromatography showed that the product of ␣-ketoglutarate decarboxylation was succinic semialdehyde. The CoA-independent ␣-ketoglutarate decarboxylase, along with succinate semialdehyde dehydrogenase, may form an alternative pathway for ␣-ketoglutarate catabolism, and this pathway may enhance TCA cycle function during symbiotic nitrogen fixation.

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