IV crystalloid fluid for acute alcoholic intoxication prolongs ED length of stay

Objectives

Acute alcohol intoxication is often treated in emergency departments by intravenous crystalloid fluid (IVF), but it is not clear that this shortens the time to achieving sobriety. The study aim was to investigate the association of IVF infusion and length of stay in the ED.

Association of serum hs-CRP and lipids with obesity in school children in a 12-month follow-up study in Japan

Objectives

To investigate the association of serum lipids and high-sensitivity C-reactive protein (hs-CRP) with obesity in school children and to explore whether hs-CRP levels could be used to predict the presence or absence of obesity 12 months later.

Methods

The subjects were school children (6–11 years old) in Japan. Blood sampling and physical measurements were performed in school (2001); low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, and hs-CRP levels were measured. Data from children who could be followed 12 months later were analyzed. Subjects weighing 20 % or more over his/her standard weight were regarded as obese, and the association of obesity with serum parameters was analyzed.

Results

Data from 612 subjects were analyzed (follow-up rate, 75.4 %). The mean of each serum parameter was significantly higher (inverse for HDL-C; lower) in obese than that in non-obese children. Logistic regression analysis for obesity at baseline showed that the odds ratio (OR) of hs-CRP was the highest [OR, 2.15; 95 % confidence interval (CI), 1.65–2.78 for an interquartile rage (IQR) increase]; the association with triglycerides and LDL-C/HDL-C was significant. At the 12-month follow-up, the OR of high hs-CRP remained the highest of all serum parameters (2.09; 95 % CI, 1.63–2.69 for an IQR increase).

Conclusions

High levels of triglycerides, LDL-C/HDL-C, and hs-CRP increased the risk of obesity in school children. Hs-CRP is considered to be a better predictor of obesity 12 months later than is LDL-C/HDL-C.     

Carbon fibre reinforced cellulose-based polymers: intensifying interfacial adhesion between the fibre and the matrix

Interfacial interactions governing the interfacial adhesion between cellulose propionate and carbon fibre surface are placed under scrutiny to pave the way towards the development of green cellulose-based carbon fibre reinforced polymers. A range of molecular entities are deposited on the surface by initially grafting aromatic structures with appropriate functions via diazonium species followed by further derivatization of these entities. Cellulose propionate was also bound covalently to the surface via a tosylated derivative invoking its facile nucleophilic displacement reaction with surface-grafted amino functions. Significant increase in interfacial shear strength was obtained for the cellulose propionate-grafted carbon fibre composite as well as for the 4-(aminomethyl)benzene-functionalized sample, in the latter case possible hydrogen bonding took place with the cellulose propionate matrix. Furthermore, the positive effect of a highly lipophilic and yet compact –CF₃ substituent was also noted. In order to let the grafted structure efficiently penetrate into the matrix, steric factors, lipophilicity and potential secondary interactions should be considered. It needs to be pointed out that we provide the first synthetic strategy to covalently bind cellulose derivatives to a largely graphitic surface and as such, it has relevance to carbonaceous materials being applied in cellulose-based innovative materials in the future.

Interfacial adhesion of a cellulose propionate/carbon fibre composite is tailored providing a synthetic strategy to bind cellulose derivatives to graphitic surfaces.     

Role of apoptosis induction in both peripheral lymph nodes and thymus in progressive loss of CD4+ cells in SHIV-infected macaques

To investigate the role of apoptosis in the progressive loss of CD4+ lymphocytes in HIV infection, we have used macaques infected with SHIV, a hybrid virus of HIV and simian immunodeficiency virus (SIV). In the present study, we sequentially analyzed apoptosis induction in the acute phase of SHIV infection. Four macaques infected with a pathogenic SHIV, SHIV89.6P, and four macaques infected with a nonpathogenic SHIV, NM-3rN, were analyzed during the first 2 or 4 weeks postinfection. In the 89.6P-infected macaques the number of peripheral CD4+ cells sharply decreased at 2 weeks postinfection and was maintained below 50/microl until 4 weeks postinfection, while in the NM-3rN-infected macques the number of the CD4+ cells did not change significantly. Plasma viral loads peaked at 2 and 2-3 weeks postinfection, and the peak values were about 1 x 10(9) and 10(6)-10(7) copies/ml in the 89.6P- and the NM-3rN-infected macaques, respectively. In the 89.6P-infected macaques, Fas antigen expression and the extent of apoptosis in PBMCs and peripheral lymph nodes increased at 1-2 weeks postinfection. A high number of apoptotic cells was also observed in thymus sections 2 and 4 weeks postinfection. On the other hand, apoptosis was scarcely induced in the NM-3rN-infected macaques. These results suggest that the extent of apoptosis induction is closely correlated with the pathogenicity of SHIV and that the apoptosis induction in peripheral lymphoid tissues and thymus, where T cell maturation occurs, may play an important role in the depletion of CD4+ lymphocytes in 89.6P infection.     

Effect of low dosage of interferon on natural killer activity in patients with HBsAg-positive chronic active hepatitis

The effect of human leukocyte interferon (IFN) on natural killer (NK) activity in 7 patients with HBsAg-positive chronic active hepatitis was investigated. Human leukocyte IFN was intramuscularly given once a week for 4 consecutive weeks (10 X 10(5), 5 X 10(5), 2 X 10(5) and 1 X 10(5) U). 1 week after the initial injection, NK activity showed a significant rise compared with the preinjection levels (p less than 0.001) and remained elevated during the 1-month treatment, while it fell after the cessation of IFN therapy. 4 of 5 patients showed a marked decrease in Dane particle-associated DNA-polymerase activity. Serum HBeAg disappeared in 3 of 6 patients and serum transaminase levels markedly improved in all patients. Only a transient reduction in HBsAg was observed in 2 patients after the treatment period. The findings indicate that a low dosage of human leukocyte IFN such as 18 X 10(5) U, administered in decreasing doses, enhances NK activity in patients with HBsAg-positive chronic active hepatitis, and that the effect of IFN is involved in the immune mechanisms associated with natural cytotoxicity.     

Endothelial Progenitor Cells Dysfunction and Senescence: Contribution to Oxidative Stress

The identification of endothelial progenitor cells (EPCs) has led to a significant paradigm in the field of vascular biology and opened a door to the development of new therapeutic approaches. Based on the current evidence, it appears that EPCs may make both direct contribution to neovascularization and indirectly promote the angiogenic function of local endothelial cells via secretion of angiogenic factors. This concept of arterial wall repair mediated by bone marrow (BM)-derived EPCs provided an alternative to the local “response to injury hypothesis” for development of atherosclerotic inflammation. Increased oxidant stress has been proposed as a molecular mechanism for endothelial dysfunction, in part by reducing nitric oxide (NO) bioavailability. EPCs function may also be highly dependent on a well-controlled oxidant stress because EPCs NO bioavailability (which is highly sensitive to oxidant stress) is critical for their in vivo function. The critical question is whether oxidant damage directly leads to an impairment in EPCs function. It was revealed that activation of angiotensin II (Ang II) type 1 receptor stimulates nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase in the vascular endothelium and leads to production of reactive oxygen species. We observed that Ang II accelerates both BM- and peripheral blood (PB)-derived EPCs senescence by a gp91phox-mediated increase of oxidative stress, resulting in EPCs dysfunction. Consistently, both Ang II receptor 1 blockers (ARBs) and angiotensin converting enzyme (ACE) inhibitors have been reported to increase the number of EPCs in patients with cardiovascular disease. In this review, we describe current understanding of the contributions of oxidative stress in cardiovascular disease, focusing on the potential mechanisms of EPCs senescence.Key Words: Endothelial progenitor cell, oxidative stress, senescence, angiotensin II, telomerase, nitric oxide.     

Rare somatic inactivation of the multiple endocrine neoplasia type 1 gene in secondary hyperparathyroidism of uremia

The molecular pathway of autonomous growth of the parathyroid glands in uremic patients is poorly understood. Loss of heterozygosity at the recently identified multiple endocrine neoplasia type 1 (MEN1) gene locus on chromosome 11q13 has been found in a subset of parathyroid glands from patients with refractory hyperparathyroidism. To clarify the role of the MEN1 gene in parathyroid tumorigenesis, we analyzed 81 parathyroid glands from 22 Japanese uremic patients for allelic loss on chromosomal arm 11q13 DNA using 3 flanking markers (PYGM, D11S4946, and D11S449) and for mutations of the MEN1-coding exons by PCR-based single strand conformation polymorphism analysis and sequencing. Allelic loss on 11q13 was observed in 6 glands (7%), and 1 of 6 demonstrated a previously unrecognized somatic frameshift deletion (331delG) of the MEN1 gene. This mutation would probably result in a nonfunctional menin protein, consistent with a tumor suppressor mechanism. Clinical and pathological characteristics of hyperparathyroidism were unrelated to the presence or absence of loss of heterozygosity on 11q13 and MEN1 gene mutations. These observations indicate that somatic inactivation of the MEN1 gene contributes to the pathogenesis of uremia-associated parathyroid tumors, but its role in this disease appears to be very limited.     

Grades of 43 fish species in Japan based on IgE-binding activity.

BACKGROUND: Hypersensitivity reactions to fish are a common food allergy, but IgE-binding activity to fish species have not been fully elucidated. The aim of this study was to identify fish with high binding activity to IgE in sera from Japanese fish-hypersensitive individuals. METHODS: 38 children with a history of at least one episode of hypersensitivity after ingestion of fish were enrolled and 34 children with no history of reactions and negative IgE results for at least five kinds of fish antigen were included as controls. Using a radioallergosorbent test, we examined IgE-binding to each fish species using sera from fish-hypersensitive subjects. Fish were then graded according to IgE-binding activity. RESULTS: Many fish species, including red salmon, silver salmon, yellowfin tuna, big eyed tuna, Atlantic tuna, saurel, skipper, yellowtail, Japanese sardine, bonita and mackerel had high IgE-binding activity. All of these fish are abundantly consumed in Japan. The hypersensitivity reactions experienced by many subjects occurred after ingestion of species with high IgE-binding activity. Only halibut (Osteichthyes) and sharks (Chondrichthyes) had low IgE-binding activity. CONCLUSIONS: A correlation was observed between IgE levels and expression of symptoms after fish ingestion. High consumption of salmon, tuna, scad (including saurel), skipper, yellowtail, sardine, bonita and mackerel in Japan might be the cause of the high IgE-binding activity of these species. The grades of fish species consumed widely in Japan are likely to be useful for nutritional instruction of fish-allergic patients.