Effect of tuftsin on human Kupffer cell

BACKGROUND/AIMS: Kupffer cells are the most important category of reticuloendothelial cells which are critical for host defense in the liver. We investigated the effects of tuftsin (Thr-Lys-Pro-Arg) on human Kupffer cells. METHODOLOGY: Human Kupffer cells were obtained from the livers of patients with colon cancer. Phagocytosis assay was done by microscopic counting of the number of Kupffer cells that engulfed fluorescent particle(s), and the number of the particles engulfed per Kupffer cell when Kupffer cells were incubated with and without tuftsin. Effect of tuftsin on the release of tumor necrosis factor from Kupffer cells was also studied. RESULTS: Phagocytosis was enhanced significantly by tuftsin. The greatest effect on percentage of phagocytic cells was observed at 1.0 microg/ml of tuftsin. The mean number of particles engulfed per Kupffer cell was also increased with tuftsin 1.0 microg/ml. Tumor necrosis factor release was also significantly increased; the greatest effect was observed at 1.0 microg/ml of tuftsin. CONCLUSIONS: Tuftsin enhances phagocytic activity and tumor necrosis factor release of human Kupffer cells, which are advantageous for host defense against invading microorganisms and tumor cells.     

Tests of scaling assumptions and construct validity of the Chinese (HK) version of the SF-36 Health Survey

Few health-related quality of life (HRQOL) survey instruments are available to the Chinese, although many have been developed for Western populations. This article describes the testing of the acceptability, conceptual equivalence, scaling assumptions and construct validity of a Chinese (HK [Hong Kong]) version fo the MOS SF-36 Health Survey. A Chinese (HK) SF-36 survey form was developed by an iterative translation process. It was administered to 236 Chinese subjects who also rated the understanding, difficulty, relevance, and acceptability of each question. The scores were tested against the original scaling assumptions. The SF-36 profile of our subjects was compared to U.S. results for conceptual equivalence. Most subjects did not have any problem in understanding and answering the SF-36. Item means were generally clustered as hypothesized. All but a few items satisfied all scaling assumptions. The shape of the eight-scale SF-36 profile was similar to that of American patients, suggesting conceptual equivalence. We conclude that the Chinese (HK) version of the SF-36 Health Survey has achieved conceptual equivalence and satisfied the psychometric scaling assumptions well enough to warrant further use and testing, using the standard scoring algorithms.     

The use of microsomal in vitro assay to study phase I biotransformation of chlorobornanes (Toxaphene) in marine mammals and birds. Possible consequences of biotransformation for bioaccumulation and genotoxicity

The factors determining the bioaccumulation of lipophilic compounds in wildlife are often poorly understood, partly because it is difficult to do in vivo experiments with animals such as marine mammals and birds. To evaluate the role of phase I biotransformation in the bioaccumulation process of chlorobornanes (toxaphene), this was studied in in vitro assays with hepatic microsomes of animals that could be sampled shortly after death. The capacity of microsomes to metabolise a technical toxaphene mixture decreased in the order Phoca vitulina (harbour seal) > Lagenorhynchus albirostris (whitebeaked dolphin) approximately equal to Diomedea immutabilis (Laysan albatross) > Physeter macrocephalus (sperm whale). Harbour seal microsomes metabolised the chlorobornane (CHB) congeners CHB-32 and CHB-62; whitebeaked dolphin and Laysan albatross microsomes only metabolised CHB-32. Metabolism of CHB-26 and CHB-50 was never observed. The negative chemical ionisation (NCI-) mass spectra of some of the hydroxylated metabolites were obtained. The number of peaks in the toxaphene residues of wildlife extracts decreased in the order of increasing in-vitro biotransformation capacity. Thus, the results of the in vitro assays and residue analysis were in accordance, although assays with microsomes of more individuals of the same species are required for a more general conclusion at the species level. Finally, the effect of in vitro biotransformation was evaluated in terms of the genotoxic potential using the Mutatox assay. Only technical toxaphene and CHB-32 were genotoxic in the direct assay, whereas the addition of rat S9 fraction or microsomes of harbour seal and albatross decreased the genotoxic response. Thus, organisms with a low ability to metabolise chlorobornanes, such as whales, may be most affected by the carcinogenic properties of toxaphene. A hypothetical reaction which fits the experimental results is discussed. Based on these results it is concluded that in vitro assays with microsomes of wildlife animals which died a natural cause can act as a valuable tool to assess the occurrence and effects of phase I metabolism. Some precautions are discussed, that should be taken to reduce the chance of false negative results.     

The origin of the Australasian marsupial fauna and the phylogenetic affinities of the enigmatic monito del monte and marsupial mole

Alternative hypotheses in higher-level marsupial systematics have different implications for marsupial origins, character evolution, and biogeography. Resolving the position of the South American monito del monte (Order Microbiotheria) is of particular importance in that alternate hypotheses posit sister-group relationships between microbiotheres and taxa with disparate temporal and geographic distributions: pediomyids; didelphids; dasyuromorphians; diprotodontians; all other australidelphians; and all other marsupials. Among Australasian marsupials, the placement of bandicoots is critical; competing views associate bandicoots with particular Australasian taxa (diprotodontians, dasyuromorphians) or outside of a clade that includes all other Australasian forms and microbiotheres. Affinities of the marsupial mole are also unclear. The mole is placed in its own order (Notoryctemorphia) and sister-group relationships have been postulated between it and each of the other Australasian orders. We investigated relationships among marsupial orders by using a data set that included mitochondrial and nuclear genes. Phylogenetic analyses provide support for the association of microbiotheres with Australasian marsupials and an association of the marsupial mole with dasyuromorphs. Statistical tests reject the association of diprotodontians and bandicoots together as well as the monophyly of Australasian marsupials. The origin of the paraphyletic Australasian marsupial fauna may be accounted for by (i) multiple entries of australidelphians into Australia or (ii) bidirectional dispersal of australidelphians between Antarctica and Australia.     

Treatment of deep and shallow intrabony defects. A multicenter randomized controlled clinical trial

This prospective multicenter intra-individual randomized controlled clinical trial was designed to compare the efficacy of guided tissue regeneration (GTR) with bioresorbable barrier membranes versus access flap surgery, in intrabony defects. 2 similar defects were selected in each of 23 patients and randomly assigned to 1 of the 2 treatments. Surgery consisted of an identical procedure except for the omission of the barrier membrane in the flap control sites. At 1-year, probing pocket depth reductions were 4.3+/-2.3 mm in GTR treated sites and 3.0+/-1.5 mm in the flap control sites (p=0.02, paired t-test). Clinical attachment level (CAL) gains were 3.0+/-1.7 mm in the GTR sites and 1.6+/-1.8 mm in the control sites (p=0.009, paired t-test). A subset analysis, performed according to the initial depth of the intrabony component of the defects (INFRA), indicated that in shallow defects (INFRA < or =3 mm) treated with the access flap alone, CAL gains were 1+/-1.5 mm, while in deep ones (INFRA > or =4 mm) they were consistently greater (1.9+/-1.9 mm). The % CAL gains, calculated as the % of the baseline intrabony component depth, however, were almost identical in the 2 subpopulations (45.8+/-64.7% in shallow and 43.8+/-37.6% in deep defects). Similarly, in the GTR sites, linear CAL gains were greater in deep (3.7+/-1.7 mm) than in shallow defects (2.2+/-1.3 mm), but no differences were observed in terms of % CAL gains (76.7+/-27.7% and 75.8+/-45%, respectively). The frequency distribution of CAL changes expressed as %s of the baseline INFRA indicates that most of the sites treated with GTR (73% in shallow and 92% in deep defects) gained 50% or more CAL. Furthermore, many defects (64% of shallow and 33% of deep defects) reached 100% of CAL gain. The present study demonstrated that: (i) GTR with bioresorbable barrier membranes resulted in a significant added benefit in comparison with access flap alone; (ii) the linear amounts of CAL gains were greater in deep than in shallow defects; (iii) CAL gains expressed as %s of the baseline depths of the intrabony component, were similar in shallow and deep defects; (iii) the regenerative procedure tested in the present study resulted in CAL gains equal to the depth of the intrabony component of the defect in some, but not in most of the instances.     

Biochemical composition of human peripheral arteries examined with near-infrared Raman spectroscopy

OBJECTIVE: To describe the clinical, serologic, and immunogenetic features of familial idiopathic inflammatory myopathy (IIM) and to compare these with the features of sporadic IIM. METHODS: Clinical signs and symptoms, autoantibodies, HLA-DRB1 and DQA1 alleles, and GM/KM phenotypes were compared among 36 affected and 28 unaffected members of 16 unrelated families in which 2 or more blood relatives developed an IIM. In addition, findings in patients with familial IIM were compared with those in 181 patients with sporadic IIM. The families included 3 pairs of monozygotic twins with juvenile dermatomyositis, 11 families with other siblings or relatives with polymyositis or dermatomyositis, and 2 families with inclusion body myositis. RESULTS: The clinical features of familial IIM were similar to those of sporadic IIM, although the frequency of myositis-specific autoantibodies was lower in familial than in sporadic IIM. DRB1*0301 was a common genetic risk factor for familial and sporadic IIM, but contributed less to the genetic risk of familial IIM (etiologic fraction 0.35 versus 0.51 in sporadic IIM). Homozygosity at the HLA-DQA1 locus was found to be a genetic risk factor unique to familial IIM (57% versus 24% of controls; odds ratio 4.2, corrected P = 0.002). CONCLUSION: These findings emphasize that 1) familial muscle weakness is not always due to inherited metabolic defects or dystrophies, but may be the result of the development of IIM in several members of the same family, and 2) multiple genetic factors are likely important in the etiology and disease expression of familial IIM, as is also the case for sporadic myositis, but DQA1 homozygosity is a distinct risk factor for familial IIM.