Ingestion of a row of artificial dentures in an adult: A case report and review of the literature.

RATIONALE: Foreign body (FB) ingestion is a common clinical emergency, although in most cases, the FB can pass safely through the entire gastrointestinal tract without causing any damage. However, ingestion of large dentures is very rare and alarming, as it can threaten the intestinal mucosa and cause perforation of the gastrointestinal tract, among other complications. PATIENT CONCERNS: A 64-year-old Chinese male was referred to our hospital for removal of a FB, which was a large denture. Clinical symptoms included chest and upper abdominal pain. He had no cough or dyspnea. Medical history included a recent cerebral infarction, craniocerebral surgery, and being bedridden for a long term. DIAGNOSES: We initially suspected a single and smooth denture, complicated by pharyngeal and esophageal mucosal injury. Radiographic examination however showed a 70-mm long opaque object located in the middle and upper esophagus, close to the trachea and aorta. INTERVENTIONS: Multiple dentures and metal hooks were removed via endoscopy using a net, grasping forceps, and rubber jacket. OUTCOMES: The patient recovered well and experienced no postoperative complications. The patient was discharged 5 days after endoscopic therapy. LESSONS: Our case showed that endoscopy was effective for the retrieval of an esophageal FB. For sharp FBs, the use of a net and rubber jacket is a good choice. However, we advocate for appropriate surgery in patients in whom endoscopy is not possible after an accurate diagnosis or those with severe complications.

Lipopolysaccharide (LPS) detoxification of analogue peptides derived from limulus anti-LPS factor.

Lipopolysaccharide (LPS) plays a critical role in the pathogenesis of sepsis due to gram-negative bacterial infections. Therefore, LPS-neutralizing molecules could have important clinical applications. Our previous work showed, CLP19, an analogue peptide derived from limulus anti-LPS factor (LALF), possessed the capacity to neutralize LPS and thereby inhibit the LPS-induced responses. However, potential cytotoxicity of CLP19 was also found, especially when added to human red blood cells. Accordingly we further developed two peptides (designated as CLP19-1 and CLP19-2) by single- and double-point amino acid substitution of CLP19, respectively, in order to reduce its toxicity and meanwhile retain the anti-LPS activity. In this study, the LPS-detoxifying effectiveness of these peptides was evaluated both in vitro and in vivo. CLP19-1 was found to dose-dependently neutralize LPS in vitro, with significantly lower hemolysis of red blood cells as compared with CLP19. Further in vivo tests verified that CLP19-1 exerted significant protective effects on mice against LPS, characterized by significantly improved survival, decreasing of tumor necrosis factor alpha (TNF-α) serum level and alleviation of tissue injury. Our work indicates that CLP19-1 is worthy of further study as potential anti-LPS agents for the management of sepsis.

[Study of in vitro endotoxin neutralization effect and antibacterial activity of limulus anti-lipopolysaccharide factor simulated peptide REMP2].

OBJECTIVE: To investigate the role of REMP2 derived from limulus anti-lipopolysaccharide factor in neutralizing endotoxin in vitro and its antibacterial activity. METHODS: (1) REMP2 and PMB in the concentrations of 100.00, 10.00, 1.00, 0.10, 0.01 micromol/L were respectively mixed with LPS (lEU/mL), with PMB as positive control. The LPS concentrations in different specimens were determined by routine method, and the neutralizing percentage was respectively calculated. (2) After adding isotonic saline (NS), the final concentrations of REMP2 and PMB were 10, 20, 40, 80 micromol/L, and the concentration of LPS was 100 microg/L. The murine monocytic macrophages were stimulated with LPS, then cultured with REMP2 and PMB, with NS in culture as negative control. The content of tumor necrosis factor (TNF)-alpha was determined by ELISA kit. (3) The morphologic changes of Escherichia coli. was observed under electron microscope at 10, 20 and 40 minutes after addition of REMP2 to Escherichia coli suspension (with terminal concentration of REMP2 at 40 micromol/L). RESULTS: There were no significant difference in endotoxin-neutralizing percentages between PMB and REMP2 in concentrations of 0.10, 10.00, 100.00 micromol/L (P > 0.05). The contents of TNF-alpha were 1175 +/- 162, 859 +/- 122, 645 +/- 142, 489 +/- 102 ng/L, respectively,after treatment of 10, 20, 40, 80 micromol/L REMP2, which were obviously lower than that of NS (3463 +/- 218 ng/L, P < 0.01). Under transmission electron microscope, the outer and interior membranes of Escherichia coli were obscure and rough, bacterial bodies were swollen with vacuoles in cytoplasm after treatment with REMP2. CONCLUSION: REMP2 has ability of neutralizing endotoxin and also antibacterial activity.

A synthetic cyclic peptide derived from Limulus anti-lipopolysaccharide factor neutralizes endotoxin in vitro and in vivo.

Endotoxin, also known as lipopolysaccharide (LPS), is the major mediator of septic shock due to Gram-negative bacterial infections. Recently, much attention has been focused on cationic peptides which possess the potential to detoxify LPS. Limulus anti-LPS factor (LALF), a protein found in the horseshoe crab (Limulus polyphemus), has been proved with striking anti-LPS effects. We synthesized a cyclic peptide (CLP-19), and then investigated its bioactivity both in vitro and in vivo. The ability of CLP-19 to neutralize LPS in vitro was tested using a Limulus amebocyte lysate (LAL) assay and the LPS-binding affinity was measured with an affinity biosensor method. The synthetic peptide LALF31-52 (residues 31 to 52 of LALF) was used as the positive control peptide in this study. It was found that CLP-19 exhibited the significant activity to antagonize LPS without observable cytotoxicity effect on mouse macrophages. CLP-19 directly bound to LPS, and neutralized it in a dose-dependent manner in the LAL assay. Moreover, CLP-19 also showed the remarkable ability to protect mice from lethal LPS attack and to inhibit the LPS-induced tumor necrosis factor alpha (TNF-alpha) release by decreasing serum LPS in vivo. Our work suggests that this peptide is worthy of further investigation as a potential anti-LPS agent in the treatment of septic shock.

[Reproduction of the murine endotoxin shock model in D-galactosamine-sensitized KunMing mice].

OBJECTIVE: To reproduce a Kunming murine endotoxin shock model suitable for the anti-endotoxin pharmaceutical research. METHODS: Kunming mice were challenged with an intraperitoneal (i. p.) injection of different doses of D-galactosamine (D-Gal) and endotoxin (LPS) and divided into 10 groups: i.e, group 1 [with injection of isotonic saline solution (NS) and LPS]; group 2 (with injection of NS and 90mg/kg LPS), group 3 (with injection of NS and 500mg/kg D-Gal), group 4 (with injection of 500mg/kgD-Gal and 25 microg /kg LPS), group 5 (with injection of 500mg/kg D-Gal and 50 microg/kg LPS), group 6(with injection of 500mg/kg D-Gal and 250 microg/kg LPS), group 7( with injection of NS and 600mg/ kg D-Gal), group 8 (with injection of 600mg/kg D-Gal and 10 microg/kg LPS), group 9( with injection of 600mg/kg D-Gal and 25 microg/kg LPS), group 10 (with injection of 600mg/kg D-Gal and 50 microg/kg LPS). The death of the mice were observed and the mortality rate was recorded at 48 post-injection hour (PIH). The dose of D-Gal and LPS which caused 100% lethality was chosen for the subsequent experiment to serve as control group (with injection of NS and 600mg/kg D-Gal), LPS group (with injection of 600mg/kg D-Gal and 580mg/kg LPS for later experiment). The venous blood of the mice were collected for the detection of serum content of TNF-alpha with ELISA method at 30, 75 and 120 post-injection minutes (PIM). The tissues of lung, liver, intestine were also harvested at 5 PIH for the pathological examination. RESULTS: The lethality of mice was 100% in the groups 2, 6 and 10 (P < 0.01). The serum content of TNF-alpha was maintained in a low level in control group, but it increased remarkably in LPS group, and it reached peak at 75 PIM (6365 +/- 2087ng/L, P < 0.01). Obvious inflammatory reaction was observed in the lung, liver and intestine in LPS group, while only mild inflammatory reaction was observed in liver in control group. CONCLUSION: The Kunming mice showed signs of endotoxin shock after D-galactosamine presensitizing and endotoxin challenge, and it is suitable for anti-endotoxin pharmaceutical research.

[Protective effects of bactericidal/permeability increasing protein simulated peptide on murine acute lung injury induced by lipopolysaccharide].

OBJECTIVE: To investigate the protective effects of bactericidal/permeability increasing protein simulated peptide (bactericidal neutralizing endotoxin protein, BNEP) on murine acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: A murine model of ALI was reproduced by lipopolysaccharide via intranasal instillation. The Balb/c mice were randomly divided into control (n = 20, with nasal instillation of isotonic saline), LPS instillation (n = 20, with nasal instillation of isotonic saline and LPS) and BNEP treatment (n = 20, with nasal instillation of isotonic saline plus LPS and BNEP) groups. The ratio of lung wet weight to dry weight, the permeability of pulmonary capillary vessels and the histopathology of pulmonary tissue were determined in all groups. The change in the expression of Toll-like receptor 2 and 4 (TLR2/4) in the pulmonary tissue was detected by immunohistochemistry. RESULTS: Compared with LPS instillation group, the ratio of lung wet weight to dry weight and the permeability of pulmonary capillary vessel was decreased significantly in the BNEP group, and the inflammatory infiltration in the pulmonary tissue induced by neutrophil influx was alleviated markedly with BNEP treatment. The expression of TLR2 and TLR4 in pulmonary vascular endothelial cells, macrophages and alveolar type II epithelial cells in BNEP group were lower than those in LPS group (TLR2: 128 +/- 10 vs 214 +/- 12, P < 0.01). CONCLUSION: BNEP, as a simulated peptide of BPI, exerted a remarkable protective effect on ALI induced by LPS.