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We describe a patient with Guillain-Barré syndrome (GBS) following Campylobacter jejuni enteritis, accompanied with severe cramping pain and a marked increase in serum creatine kinase (CK) levels. Both conditions became evident three weeks after the onset of GBS and continued for longer than one month. In this patient, it is possible that rapid extensive denervation due to severe axonal degeneration of motor nerve terminals might have caused hyperexcitability in regional muscles, leading to recurrent muscle cramps and persistent release of muscular CK.

SummaryTo evaluate the immunological development of preterm infants, especially in early infancy, we examined the serum cytokine levels and the expression of Th2 and Th1 chemokine receptors, CCR4 and CCR5, on days 0, 14 and 28 in 16 low birth weight infants (1720·38 ± ± ± ± 502·80 g) born at less than 37 (33·63 ± ± ± ± 3·29) weeks of gestation. Using an enzyme-linked immunosorbent assay (ELISA), serum interleukin (IL)-4 levels exhibited an increase on day 14, but decreased to the initial level on day 28 ( P < < < < 0·05). The significant elevation of serum transforming growth factor (TGF)-b b b b levels was confirmed on day 14 ( P < < < < 0·05) but decreased to the initial level on day 28 ( P < < < < 0·05). The expression of CCR4 and CCR5 were examined using reverse transcriptionpolymerase chain reaction (RT-PCR) and flow cytometric analysis. The RT-PCR confirmed the expression of CCR5-mRNA soon after birth, while there was no expression of CCR4-mRNA. Thereafter, the expression of CCR4-mRNA increased significantly and reached the level of CCR5-mRNA expression on day 28 ( P < < < < 0·05). Flow cytometric analysis, however, revealed that the expression levels of both CCR4 and CCR5 were low at birth. Thus, CCR4

Background: Neonatal necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in premature infants. The mortality rate associated with NEC is quite high and in most reports ranges from 20 to 30%. Despite extensive studies, the pathogenesis of NEC remains poorly understood. Objectives: To investigate the mechanisms of NEC in terms of inflammatory signaling in the intestine. Methods: A new enterocolitis model was established and examined the expression of inflammatory and anti-inflammatory signals in the intestines of rat pups. The premature rat pups, delivered by abdominal incision on day 20 of gestation (day 21 is considered as full term), were divided into three groups, and they were given a single administration of 0.05, 0.1, and 0.15 ml of formula milk via an orogastric catheter. After 24 h, the development of enterocolitis was evaluated by the presence of hemorrhagic enterocolitis, and the expression of signaling molecules, inhibitor of nuclear factor-ĸB (IĸB)-α/β and peroxisome proliferator-activated receptor (PPAR)-γ mRNA was examined by reverse transcription-polymerase chain reaction from inflamed and non-inflamed intestinal samples. Results: The incidence of enterocolitis increased with the volume of milk, and 50% of rat pups showed enterocolitis with a volume of 0.15 ml of milk. Expression of IĸB-α/β and PPAR-γ mRNA increased in inflamed intestine. Conclusions: Increased expression of IĸB-α/β suggested that the inflammatory mediator nuclear factor-ĸB is deeply involved in the pathogenesis of enterocolitis that can be easily introduced by overfeeding of milk ingestion in premature rat pups which mimic those seen in NEC. Increased expression of PPAR-γ may possibly regulate further development of enterocolitis in this system.