Eosinophilic enteritis is a rare disease which may mimic acute abdominal emergency. Two sonographically documented cases are presented, which were subsequently proven at operation. Although the sonographic features of severe echolucent bowel wall thickening were not specific, combination with clinical and laboratory data may suggest the correct diagnosis.

Cerebral demyelination is possibly one of the main pathological factors involved in the development of schizophrenia. Our previous studies have showed that Areca catechu nut extract could ameliorate cognitive decline by facilitating myelination processes in the frontal cortex in a cuprizone (CPZ)-induced mouse model of schizophrenia. The aim of the present study was to evaluate the effects of arecoline, one of the alkaloids in A. catechu nut extract, on memory impairment and cerebral demyelination in CPZ-treated mice. Mice were treated with CPZ (0 or 0.2%) in chow food and arecoline hydrobromide (0, 2.5, or 5 mg/kg/day) in drinking water for 12 weeks before Y-maze behavioral test. After the behavioral test, the mice were sacrificed for the measurement of myelin basic protein in the frontal cortex. We showed that arecoline-attenuated spatial working memory impairment, concurrent with attenuated demyelination related to vehicle-treated CPZ mice for the first time. Arecoline is one of the primary active ingredients in A. catechu nut responsible for attenuating memory impairment and demyelination in CPZ mice, cerebral demyelination may have a role in memory impairment, and modulation of cerebral demyelination could be a useful strategy in schizophrenia treatment.

Background Bipolar disorder is a severe psychiatric illness with poor prognosis and problematic and suboptimal treatments. Understanding the pathoetiologic mechanisms may improve treatment and outcomes. Discussion Dysregulation of cationic homeostasis is the most reproducible aspect of bipolar pathophysiology. Correction of ionic balance is the universal mechanism of action of all mood stabilizing medications. Recent discoveries of the role of endogenous sodium pump modulators (which include ‘endogenous ouabain’) in regulation of sodium and potassium distribution, inflammation, and activation of key cellular second messenger systems that are important in cell survival, and the demonstration that these stress-responsive chemicals may be dysregulated in bipolar patients, suggest that these compounds may be candidates for the coupling of environmental stressors and illness onset. Specifically, individuals with bipolar disorder appear to be unable to upregulate endogenous ouabain under conditions that require it, and therefore may experience a relative deficiency of this important regulatory hormone. In the absence of elevated endogenous ouabain, neurons are unable to maintain their normal resting potential, become relatively depolarized, and are then susceptible to inappropriate activation. Furthermore, sodium pump activity appears to be necessary to prevent inflammatory signals within the central nervous system. Nearly all available data currently support this model, but additional studies are required to solidify the role of this system. Conclusion Endogenous ouabain dysregulation appears to be a reasonable candidate for understanding the pathophysiology of bipolar disorder.

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Brain demyelination is possibly one of the main pathological factors involved in schizophrenia, and targeting on myelination may be a useful strategy for schizophrenia treatment. Quetiapine, a widely used atypical antipsychotic drug for schizophrenia treatment, has been reported to have neuroprotective effects on cerebral myelination in a demyelination animal model. The objective of the present study was to evaluate the effect and underlying neuroprotective mechanism of quetiapine on the schizophrenia-like behaviors and possible cerebral demyelination induced by MK-801, an N-methyl-Daspartate glutamate receptor antagonist. Mice were treated with chronic quetiapine (10 mg/kg/day, intraperitoneally) for 28 days. From day 22 to 28, 1 h after the administration of quetiapine, the mice were administered MK-801 (2 mg/kg/day, subcutaneously). The positive symptom of schizophrenia was measured in a locomotor activity test on day 29, the memory was evaluated by a Y-maze test on day 30, and the sensorimotor gating deficit in mice was measured by prepulse inhibition test on day 31. After the behavioral tests, the protein expression of myelin basic protein (MBP) was measured by Western Blot, and the protein expression of brain-derived neurotrophic factor (BDNF) was measured by ELISA in the frontal cortex of mice. Our results showed quetiapine attenuated schizophrenia-like behaviors including hyperactivity, memory impairment, and sensorimotor gating deficit in the MK-801 mice. In the same time, quetiapine attenuated demyelination, concurrent with attenuated BDNF decrease in the brain of MK-801-injected mice. These results suggest that the beneficial effects of quetiapine on schizophrenia might be partly related to its neuroprotective effect on brain myelin basic protein and its upregulating neuroprotective proteins such as BDNF, and indicate that modulation of cerebral demyelination could be a novel treatment target of schizophrenia.