Serum cytokine profiling in neonates with hypoxic ischemic encephalopathy.

BACKGROUND: The fetal brain is vulnerable to severe and sustained hypoxia during and after birth, which can lead to hypoxic-ischemic encephalopathy (HIE). HIE is characterized by clinical and laboratory evidence of acute or subacute brain injury. The role of cytokines in the pathogenesis of brain injury and their relation to neurological outcomes of asphyxiated neonates are not fully understood. In this study, we investigated cytokine profile related to cerebral palsy (CP) with neonatal hypoxic ischemic encephalopathy (HIE) and HIE severity. METHODS: Eligible subjects were HIE newborns with a gestational age between 36 and 42 weeks. We included newborns who was born at our NICU and did not admit to NICU as healthy controls. The study comprised 52 newborns, including 13 with mild to severe HIE and 39 healthy control. Serum cytokine profiles were performed using a LUMINEX cytokine kit (R&D Systems). RESULTS: VEGF, MCP-1, IL-15, IL-12p70, IL-12p40, IL-1Ra, IL-2, IL-6, IL-7, IL-8, IL-10, IFN-γ, G-CSF and eotaxin in the HIE patients were significantly increased compared with the healthy neonates. In the subgroup analysis, IL-6 and G-CSF were significantly increased in CP infants (n = 5) compared with non-CP infants (n = 8). Five and eight HIE patients were classified into the mild HIE and moderate-severe HIE groups, respectively. IL-6, 10, 1Ra, and G-CSF in the moderate-severe HIE group were significantly higher than those in the mild HIE group. CONCLUSION: We demonstrated that higher serum IL-6 and G-CSF at birth in HIE patients were associated with CP and moderate-severe HIE.

[Antimicrobial susceptibility of Pseudomonas aeruginosa isolated in Fukushima Prefecture].

We investigated the susceptibility of Pseudomonas aeruginosa (isolated from the sputum of patients with respiratory infection in 4 medical institutions in Fukushima Prefecture) to 8 beta-lactam antibiotics including three carbapenems and relationships among MICs of antibiotics tested. The MIC90 values for a total of 216 strains were 6.25 micrograms/ml for meropenem, 12.5 micrograms/ml for imipenem and ceftazidime, 25 micrograms/ml for panipenem and cefsulodin, 50 micrograms/ml for cefpirome and over than 200 micrograms/ml for cefoperazone and piperacillin. The frequency of resistance of these strains to each antibiotic was as follows: The resistant strains were 19 (8.8%) for meropenem, 34 (15.7%) for imipenem and ceftazidime, 50 (23.1%) for cefsulodin, 72 (33.3%) for panipenem, 76 (35.2%) for piperacillin and 90 (41.7%) for cefpirome. Eighteen strains (18.3%) of 19 meropenem resitant straisn were resistant to imipenem and panipenem, but 16 strains of the 34 imipenem-resistant strains and 54 strains of the 72 panipenem-resistant strains were susceptible to meropenem. In investigation of isolation of multi-resistant Pseudomonas aeruginosa, the susceptibility of strains tested to 7 antibiotics except cefoperazone was as follows: The strains susceptible to all the 7 antibiotics were 92 strains (42.6%), and 33 strains (15.2%) were resistant to 2 antibiotics, 31 strains (14.4%) were resistant to 1 antibiotic, 21 strains (9.7%) were resistant to 3 antibiotics, 13 strains (6.0%) were resistant to 5 antibiotics, 9 (4.2%) were resistant to 4 and 7 antibiotics, and 8 strains (3.7%) were reistant to 6 antibiotics. Since the emergence of these multi-resistant strains is closely related to frequent use of antibiotics for nosocomial infections, special attention should be paid to the antimicrobial susceptibility of Pseudomonas aeruginosa and the situation of antibiotic resistant strains.

Effect of carnitine on decrease of branched chain amino acids and glutamine in serum of septic rats.

Blood concentrations of branched chain amino acids (BCAA; leucine, isoleucine, and valine) and glutamine (Gln) decrease markedly in sepsis. We investigated the effect of carnitine on serum concentrations of BCAA and Gln in fasted septic rats. Rats were made septic by cecal ligation and puncture. They developed extremely high blood concentrations of endotoxin, and serum concentrations of BCAA and Gln were markedly decreased 2 d after the operation. When L-carnitine was administered subcutaneously to the rats at 500 mg/kg body weight every 12 h for 2 d starting at the operation, no decrease in the serum concentrations of BCAA and Gln was observed. This indicates that the administration of carnitine can prevent the decrease of serum concentrations of BCAA and Gln in septic animals.

Beneficial effects of enteral fat administration on liver dysfunction, liver lipid accumulation, and protein metabolism in septic rats.

The purpose of this study was to examine the effect of different amounts of fat in enteral diets on liver function, liver lipid accumulation, and protein metabolism in septic rats. Sepsis was induced in Wistar rats by cecal ligation and puncture. The rats were divided into four groups and were fed enterally 0% (FO, n = 7), 10% (F10, n = 7), 20% (F20, n = 8), or 30% (F30, n = 9) of total calories as fat. The liquid diet consisted of medium-chain and long-chain triglyceride mixtures as the fat sources, casein oligopeptide, and dextrin (100 kcal/100 ml). Intraduodenum feeding was ended on the 6th day. Serum glutamic oxaloacetic transaminase and glutamic pyruvic transaminase activities, indices of liver dysfunction, were highest in the FO group, and triglycerides accumulated in the livers of that group, possibly because of the large proportion of carbohydrate in the diet. Value of nitrogen balance was highest in the F 10 group, and serum total protein and albumin concentration were higher in the F10 and F20 groups than in the FO and F30 groups. The liver protein content in the F10 and F20 groups was higher than in the FO and F30 groups. Serum triglyceride in the F30 group was about 2 times higher than in the F10 and F20 groups. These results indicate that enteral fat administration in septic rats as 30% of total calories reduced liver dysfunction and liver triglyceride accumulation, but might have been excessive for optimal protein metabolism. Therefore, the preferable amount may range from 10% to 20% of total calories.

[Clinical studies of the treatment of bladder tumor and its effects--experience in 86 cases].

Prognosis on evaluable 86 patients with primary bladder tumor seen during the 10 years up to 1985 was evaluated in relation to treatment mode and tumor stage. The majority of patients underwent multimodal therapies including surgery, chemotherapy and immunotherapy with picibanil (OK432). Transurethral resection of the tumor was performed as an initial surgical treatment in 49 patients, 9 of whom ultimately underwent total cystectomy. After leaving hospital, these patients were kept on immunotherapy with OK432 and topical chemotherapy with bladder instillation of mitomycin C or adriamycin (ADM) with or without systemic administration of Tegefur as long as possible. The overall actual 5-year survival rate for the patients treated by initial transurethral resection was 80%. Recurrence rate for these 49 patients was 35%. Total cystectomy with urinary diversion was performed in 37 patients who had been placed postoperatively on systemic administration of Tegafur and immunotherapy with OK 432 as long as possible. The overall actual 5-year survival rate for the patients treated with total cystectomy was 54%. The patients with pT2 and lower stage tumor had an actual 5 year survival rate of 72%, while the patients with pT3 and higher stage tumors had a survival of 10%. The high recurrence rate in the patients with superficial tumor and the low actual survival rate of the patients with pT3 and higher stage remain a problem in the treatment of bladder tumor. In recent trials, bacillus Calmette-Gúerin instillation therapy has been initiated to lower the recurrence rate in superficial tumor and we have had a satisfactory 4-year result.(ABSTRACT TRUNCATED AT 250 WORDS)

Conversion of thyroxine into tri-iodothyronine in zinc deficient rat liver.

Hepatic thyroxine (T4) to tri-iodothyronine (T3) conversion was measured in six animal groups: Group A was fed a severe zinc-deficient diet (1.98 ppm) for 5 weeks; group B was a pair-fed control group for group A; group C was fed a less severe zinc-deficient diet (6.10 ppm) for 5 weeks; group D was a pair-fed control group for group C; group E was fed a zinc-supplemented control diet (90.4 ppm) for 5 weeks; and group F was first fed the severe zinc-deficient diet for 5 weeks and then placed on the zinc-supplemented control diet until a body weight corresponding to the final weight of group E was obtained. Serum T3 and T4 levels and T4 to T3 conversion were significantly reduced in group A. A significant positive correlation was observed between T4 to T3 conversion and alcohol dehydrogenase (zinc-metalloenzyme) activity in liver tissue from the six groups. Thus, it appeared that an appropriate amount of zinc might be one of the factors in thyroxine to tri-iodothyronine conversion in liver tissue normally.

Effects of dietary zinc deficiency on hepatic ornithine carbamoyltransferase and alcohol dehydrogenase activities in rats.

Hepatic ornithine carbamoyltransferase (OCT) and alcohol dehydrogenase (ADH) activities were measured in six groups of rats: (A) fed a severe zinc-(Zn-) deficient diet (1.98 ppm) for 5 weeks; (B) pair-fed control for group (A); (C) fed a less severe Zn-deficient diet (6.10 ppm) for 5 weeks; (D) pair-fed control for group (C); (E) fed a Zn-supplemented control diet (90.4 ppm) for 5 weeks; and (F) first fed the severe Zn-deficient diet for 5 weeks and then replaced on the Zn-supplemented control diet until a body weight corresponding to the final weight of group (E) was obtained. Hepatic OCT was similar in all these six groups. On the contrary, hepatic ADH was significantly reduced in groups (A) and (C) and in each of the corresponding pair-fed groups, (B) and (D). No differences were found between groups (A) and (B) or between groups (C) and (D). In group (F), ADH activity improved to a level equivalent to that in group (E). The changes in ADH activities were accompanied by changes in the hepatic Zn content. Thus, it is clear that: (1) the hepatic Zn content may not be affected by the amount of Zn intake alone, but by the combination of Zn and food intake; and (2) ADH, and not OCT, reflected the hepatic Zn content.