A case of ileus surgery using the water pressure method against ileus caused by incarceration into the inverted bladder diverticulum.

BACKGROUND: Ileus is quite a common disease, but is associated with various causes. As far as we know, there have only been one case of ileus due to inverted bladder diverticulum, which is extremely rare. CASE PRESENTATION: The patient was a 53-year-old male. He made an emergency visit to our hospital with a chief complaint of left lower quadrant pain. He underwent right inguinal hernia surgery at 2 years of age with no history of laparotomy. An abdominal enhanced CT revealed inversion of the bladder left side wall where part of enlarged small intestine was found. Ascites were also found between the incarcerated small intestine and the bladder, leading to a diagnosis of strangulation ileus due to internal hernia and subsequent emergency surgery. A laparotomy revealed incarceration of the small intestine in the bladder left wall as a Richter type. The incarceration was rigid. We believed it would be difficult to pull out by extraction. Therefore, we inserted a Nelaton catheter between the incarcerated small intestine and the bladder and carried out the water pressure method to release the ileus. We did not perform an enterectomy since no manifest necrosis or perforation of the small intestine was found. The inverted bladder wall was a partial depression. We interpreted it to be a bladder diverticulum. We made a suture for occlusion with the bladder diverticulum inverted. Ileus arising from inverted bladder diverticulum is a very rare disease state. We hereinafter report on this case along with bibliographical considerations. CONCLUSIONS: We experienced a case of small intestine ileus due to inverted bladder diverticulum, which is very rare. In terms of preservation of the bowel, we believed the water pressure method to release the ileus was useful.

Nervous system disruption and swimming abnormality in early-hatched pufferfish (Takifugu niphobles) larvae caused by pyrene is independent of aryl hydrocarbon receptors.

Pyrene, a member of the polycyclic aromatic hydrocarbons (PAHs), contributes to abnormality in the size of the brain and the swimming behavior of pufferfish (Takifugu niphobles) larvae. We hypothesized that the aryl hydrocarbon receptor (AHR) may mediate pyrene-induced toxic effects because AHR is assumed to be a candidate for the downstream target of PAHs in many cases. To identify the contribution of AHR on developing pufferfish, we performed exposure experiments using ß-naphthoflavone, an agonist of AHR. We found that the toxic effects of pyrene and ß-naphthoflavone in pufferfish larvae are fundamentally different. Pyrene specifically induced problems in the developing midbrain and in swimming behavior, while ß-naphthoflavone affected the heartbeat rate and the size of the yolk. These results suggest that the behavioral and morphological abnormality caused by pyrene exposure is mediated by an AHR-independent pathway. Alternatively, defects caused by pyrene may be attributed to the inhibition of the FGF signal.

In vitro cytotoxicity induced by Clostridium perfringens isolate carrying a chromosomal cpe gene is exclusively dependent on sporulation and enterotoxin production.

Clostridium perfringens type A is a common source of food poisoning (FP) and non-food-borne (NFB) gastrointestinal diseases in humans. In the intestinal tract, the vegetative cells sporulate and produce a major pathogenic factor, C. perfringens enterotoxin (CPE). Most type A FP isolates carry a chromosomal cpe gene, whereas NFB type A isolates typically carry a plasmid-encoded cpe. In vitro, the purified CPE protein binds to a receptor and forms pores, exerting a cytotoxic activity in epithelial cells. However, it remains unclear if CPE is indispensable for C. perfringens cytotoxicity. In this study, we examined the cytotoxicity of cpe-harboring C. perfringens isolates co-cultured with human intestinal epithelial Caco-2 cells. The FP strains showed severe cytotoxicity during sporulation and CPE production, but not during vegetative cell growth. While Caco-2 cells were intact during co-culturing with cpe-null mutant derivative of strain SM101 (a FP strain carrying a chromosomal cpe gene), the wild-type level cytotoxicity was observed with cpe-complemented strain. In contrast, both wild-type and cpe-null mutant derivative of the NFB strain F4969 induced Caco-2 cell death during both vegetative and sporulation growth. Collectively, the Caco-2 cell cytotoxicity caused by C. perfringens strain SM101 is considered to be exclusively dependent on CPE production, whereas some additional toxins should be involved in F4969-mediated in vitro cytotoxicity.

Pyrene induces a reduction in midbrain size and abnormal swimming behavior in early-hatched pufferfish larvae.

Spills of heavy oil (HO) have an adverse effect on marine life. We have demonstrated previously that exposure to HO by fertilized eggs of the pufferfish (Takifugu rubripes) induces neural disruption and behavioral abnormality in early-hatched larvae. Here, two kinds of polycyclic aromatic hydrocarbons, pyrene and phenanthrene, were selected to examine their toxic effects on larval behavior of another pufferfish species (T. niphobles). Larvae exposed to pyrene or phenanthrene exhibited no abnormalities in morphology. However, those exposed to pyrene but not phenanthrene swam in an uncoordinated manner, although their swimming distance and speed were normal. The optic tectum, a part of the midbrain, of pyrene-exposed larvae did not grow to full size. Thus, these findings are indicated that pyrene might be a contributor to the behavioral and neuro-developmental toxicity, although there is no indication that it is the only compound participating in the toxicity of the heavy oil mixture.

Nervous system disruption and concomitant behavioral abnormality in early hatched pufferfish larvae exposed to heavy oil.

BACKGROUND AND OBJECTIVE: Spills of heavy oil (HO) over the oceans have been proven to have an adverse effect on marine life. It has been hypothesized that exposure of early larvae of sinking eggs to HO leads largely to normal morphology, whereas abnormal organization of the developing neural scaffold is likely to be found. HO-induced disruption of the nervous system, which controls animal behavior, may in turn cause abnormalities in the swimming behavior of hatched larvae. To clarify the toxicological effects of HO, we performed exposure experiments and morphological and behavioral analyses in pufferfish (Takifugu rubripes) larvae. EXPERIMENTAL PROCEDURE: Fertilized eggs of pufferfish were exposed to 50 mg/L of HO for 8 days and transferred to fresh seawater before hatching. The hatched larvae were observed for their swimming behavior, morphological appearance, and construction of muscles and nervous system. RESULTS AND DISCUSSION: In HO-exposed larvae, we did not detect any anomaly of body morphology. However, they showed an abnormal swimming pattern and disorganized midbrain, a higher center controlling movement. Our results suggest that HO-exposed fishes suffer developmental disorder of the brain that triggers an abnormal swimming behavior and that HO may be selectively toxic to the brain and cause physical disability throughout the life span of these fishes.