In the management of upper type of brachial plexus injury, reconstruction to restore shoulder function is accomplished by multiple nerve transfers. We used the accessory nerve to neurotize the suprascapular nerve in 12 patients (11 men, 1 woman) from 1989 to 2003. The average age at the time of operation was 28.1 years (range 16 to 53). The mean preoperative time was 3.6 months. The type of paralysis was C5-C6 type in four cases, C5-C7 type in five cases, and C5-C8 type in three cases. The average time of follow-up was 28.5 months. All the patients showed reinnervation of the supraspinatus and infraspinatus muscles that was confirmed by electromyogram. At the time of final followup, the average shoulder flexion was 70.4 degrees and abduction was 77.1 degrees. However, average shoulder external rotation was only 16.7 degrees. We compared the shoulder flexion and abduction in patients with or without paralysis of the serratus anterior muscle and found significantly better functional outcome in the latter group of patients. We, therefore, conclude that repair of long thoracic nerve is mandatory for achieving optimum shoulder function.

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Background: Proton pump inhibitors have been reported to modify the level of Helicobacter pylori gastritis. Aim: To quantitatively investigate the effect of a proton pump inhibitor on the mucosal neutrophil reaction. Methods: Forty‐six H. pylori‐infected patients (17 duodenal ulcer, 29 gastric ulcer) were enrolled. During endoscopic examination, biopsy samples were obtained from the antrum and the corpus. The tissue content of neutrophil myeloperoxidase was measured by enzyme‐linked immunoabsorbent assay, and H. pylori infection was histologically assessed. A proton pump inhibitor was administered orally for 8 weeks. Results: In the patients as a whole, antral myeloperoxidase decreased significantly after proton pump inhibitor treatment, but corpus myeloperoxidase remained largely unchanged. In duodenal ulcer patients, myeloperoxidase significantly decreased in the antrum, but increased in the corpus. In gastric ulcer patients, a significant reduction was observed in antral myeloperoxidase, but corpus myeloperoxidase remained unchanged. In the antral myeloperoxidase > corpus myeloperoxidase subgroup (n=24), antral myeloperoxidase significantly decreased, whereas corpus myeloperoxidase increased. No changes were observed at either site in the corpus myeloperoxidase > antral myeloperoxidase subgroup. Histology showed that the antral bacterial load of H. pylori decreased in all subgroups, but that it was mostly unchanged in the corpus. Conclusions: Proton pump inhibitor treatment stimulated the neutrophil reaction in the corpus mucosa of duodenal ulcer patients and of patients in whom antral neutrophil accumulation was more predominant than that of the corpus. This phenomenon may not be caused by increased bacterial density.

This study aimed to examine the behavior of stimulated leukocytes in the pulmonary microcirculation. The leukocyte-endothelium interaction was visualized under physiological shear rates in perfused rat lungs using high-speed confocal laser video microscopy. Leukocytes labeled with carboxyfluorescein were stimulated with cytokine-induced neutrophil chemoattractant (CINC/gro), which caused L-selectin shedding and inverse upregulation of CD18. Neither unstimulated nor stimulated leukocytes exhibited rolling in either pulmonary arterioles or venules, whereas both were sequestered in capillaries. Approximately 50% of stimulated leukocytes showed a transient cessation of movement in pulmonary capillaries. The CINC/gro stimulation, which inhibited leukocyte rolling and adhesion to mesenteric venules, reduced leukocyte velocity and increased leukocytes in pulmonary capillaries. Pretreatment with monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1) or CD18 attenuated these changes. Confocal microfluorography revealed constitutive expression of ICAM-1 not only in venules but also abundantly in capillary networks. These results suggest that selectin-independent, CD18-ICAM-1-dependent capillary sequestration is one of the major mechanisms by which activated leukocytes accumulate in the lungs.

Aim: To examine whether proton pump inhibitors modify the production of oxygen‐derived free radicals and related cytokines in the human gastric mucosa infected with H. pylori. Methods: Thirty‐four H. pylori‐positive peptic ulcer patients (23 gastric ulcer, 11 duodenal ulcer) were enrolled. Biopsy tissue samples were obtained endoscopically from the antrum and corpus. Tissue content of neutrophil myeloperoxidase (myeloperoxidase) and IL‐8 was measured by ELISA. Mucosal production of oxygen‐derived free radical was measured using luminol‐dependent chemiluminescence (ChL). A proton pump inhibitor (either lansoprazole 30 mg, omeprazole 20 mg, or rabeprazole 10 mg) was administered daily by mouth to all patients for 8 weeks. Endoscopic examination was then repeated, and biochemical analysis was performed. Results: Antral myeloperoxidase decreased significantly after proton pump inhibitor treatment (5.23 ± 7.00–2.76 ± 5.11 ng/mg, P < 0.02), but corpus myeloperoxidase was unchanged. IL‐8 was also modified by proton pump inhibitors and these changes were parallel to those of myeloperoxidase. Corpus ChL was significantly increased from 88.5 ± 69.8–159 ± 172 counts/10 s/mg after proton pump inhibitor treatment, whereas antrum ChL was not altered. H. pylori infection rate was decreased in the antrum as well as the corpus. Conclusions: Proton pump inhibitor treatment stimulated oxygen‐derived free radical production in the corpus mucosa.