Human body mass estimation: a comparison of "morphometric" and "mechanical" methods.

In the past, body mass was reconstructed from hominin skeletal remains using both "mechanical" methods which rely on the support of body mass by weight-bearing skeletal elements, and "morphometric" methods which reconstruct body mass through direct assessment of body size and shape. A previous comparison of two such techniques, using femoral head breadth (mechanical) and stature and bi-iliac breadth (morphometric), indicated a good general correspondence between them (Ruff et al. [1997] Nature 387:173-176).

[Cross-linked hyaluronic acid in the treatment of osteoarthritis of the knee--results of a prospective randomized trial].

Purpose: The objective of this trial was to compare the effectiveness of intraarticular injection of highly cross-linked hyaluronic acid (HA) with intraarticular injection of gaseous oxygen (O 2 ) in patients with clinical symptoms of cartilage damage in the knee.

Methods: Based on arthroscopically verified diagnosis, 111 patients were randomised and treated prospectively either with HA or O 2. The treatment was completed with an exercise program.

Evolving dissatisfaction among primary care physicians.

Objective: To examine trends in career satisfaction among physicians working with managed care plans.

Study Design: Cross-sectional surveys conducted in 1996 and 1999.

Participants And Methods: We surveyed primary care physicians (PCPs) affiliated with 5 large health plans in Massachusetts and assessed physicians' ratings of overall satisfaction with their current practice situation and with managed care.

Identification of an IL-6 response element in the human LCAT promoter.

LCAT is a key enzyme of reverse cholesterol transport that is essential to maintain HDL-mediated lipid transport and cholesterol homeostasis. Alterations in LCAT expression have a profound effect on plasma HDL cholesterol concentrations. Previously LCAT mRNA and activity were shown to be regulated by several inflammatory cytokines, including the pleiotrophic cytokine interleukin-6 (IL-6).

Reverse cholesterol transport and future pharmacological approaches to the treatment of atherosclerosis.

The apparent protective effect of high density lipoprotein cholesterol (HDL) with respect to coronary heart disease (CHD) is generally thought to reside in its ability to transport cholesterol from peripheral cells to the liver for excretion from the body. Knozon as reverse cholesterol transport (RCT), this process involves many key steps and lipoprotein interconversions, and there is no consensus as to which step is most suitable for possible drug intervention. The membrane proteins, scavenger receptor class B, type 1 (SR-B1) and the ATP-binding cassette 1 (ABC1), have been strongly implicated as being important in cholesterol efflux; the former as a bona fide receptor for HDL and the latter as a lipid transporter.

The combined effect of inhibiting both ACAT and HMG-CoA reductase may directly induce atherosclerotic lesion regression.

We hypothesized that coadministration of avasimibe and simvastatin would limit size, composition and extent of atherosclerotic lesions and potentially promote lesion regression, since bioavailable ACAT inhibitors decrease monocyte-macrophage enrichment and HMG-CoA reductase inhibitors limit smooth muscle cell migration and proliferation. Male New Zealand white rabbits were sequentially fed a 0.5% cholesterol, 3% peanut oil, 3% coconut oil diet for 9 weeks and a chow-fat diet for 6 weeks prior to drug administration.

Lipoprotein lipase greatly enhances the retention of lipoprotein(a) to endothelial cell-matrix.

The trapping of apolipoprotein (apo)B containing lipoproteins within the arterial subendothelial matrix (ECM) is an early event in atherosclerosis. When lipoprotein lipase, a constituent of the ECM, is prebound to ECM both LDL and oxidized LDL binding is greatly enhanced. In this study we compared the binding of lipoprotein(a) (Lp(a)), a lipoprotein correlated with atherosclerosis and restenosis, to ECM in the presence of varying concentrations of LPL.

Dose-response to a two-component acellular pertussis vaccine in infants and comparison with whole-cell vaccine.

In an effort to determine the optimal dose of pertussis toxoid (PT) and filamentous haemagglutinin (FHA) for use in acellular pertussis vaccines we compared the immunogenicity and safety of acellular pertussis vaccine combined with diphtheria and tetanus toxoids containing 12.5 microg (DTaP-12.5) or 25 microg (DTaP-25) each of PT and FHA with a whole cell pertussis vaccine in infants immunized at 2, 4 and 6 months of age.

Influence of lipoprotein(a) plasma concentration on neointimal growth in a monkey model of vascular injury.

Lipoprotein(a) [Lp(a)] has been proposed as a risk factor for both restenosis and coronary heart disease. Recently, we identified Lp(a) in the arterial wall during the initial rapid neointimal growth phase that occurs after balloon injury in cynomolgus monkeys. The purpose of this study was to determine the relationship between circulating Lp(a) levels and the extent of early neointimal formation.

A novel compound that elevates high density lipoprotein and activates the peroxisome proliferator activated receptor.

In the current studies we describe the effects of PD 72953 and related compounds on lipoprotein levels in chow-fed male rats. After 2 weeks, 10 mg/kg of PD 72953 daily was as effective as 100 mg/kg gemfibrozil for elevating HDL-cholesterol. At 100 mg/kg, PD 72953 further elevated HDL-cholesterol to 232% of control levels, and was associated with increased HDL size and plasma apoE (169% of control), despite no change in hepatic apoE mRNA.

Attenuation of plasma low density lipoprotein cholesterol by select 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in mice devoid of low density lipoprotein receptors.

Low density lipoprotein (LDL) reduction independent of LDL receptor regulation was investigated using HMG-CoA reductase inhibitors in LDL receptor-deficient mice. In males, LDL cholesterol dose-dependently decreased with atorvastatin treatment after 1 week. As untreated mice grew older, their LDL cholesterol progressively rose above basal levels, but was quelled with atorvastatin treatment.

Measures to overcome HAMA interferences in immunoassays.

The incidence of human anti-mouse antibodies (HAMA) in different patient sera panels may be debatable, the interference of HAMA, if present, in immunochemically based assays is, however, a fact. This interference can lead to falsely elevated or depressed results depending on the nature of the HAMAs involved and the particular assay format chosen. For several reasons, assays for serum tumor markers may be especially prone to HAMA interference.

Mouse peritoneal macrophages contain abundant omega-6 lipoxygenase activity that is independent of interleukin-4.

The action of an omega-6 lipoxygenase (LO) has been implicated in the development of atherosclerosis through a mechanism involving oxidation of LDL, and its regulation in macrophages may have important implications for the disease process. Human monocyte-derived macrophages (HMDMs) showed no demonstrable LO protein or activity unless they were incubated with interleukin-4 (IL-4). In contrast, mouse peritoneal macrophages (MPMs) possessed significant basal levels of LO activity and protein that were augmented by IL-4 treatment.

Opposite effects of bezafibrate and gemfibrozil in both normal and hypertriglyceridemic rats.

Chow and sucrose-fed rats were used as animal models to study the dose-responses of bezafibrate and gemfibrozil in normolipidemic and hypertriglyceridemic states, respectively. Although both drugs lowered plasma triglycerides (TG) to about the same extent in chow-fed rats, gemfibrozil lowered liver TG as well as plasma total and LDL-cholesterol (LDL-C), but elevated HDL-cholesterol (HDL-C) and plasma apo E concentrations. Bezafibrate produced opposite effects, namely, decreased HDL-C, apo E and liver TG, and tended to increase LDL-C.

Soluble CD56 (NCAM): a new differential-diagnostic and prognostic marker in multiple myeloma.

A retrospective study was carried out to determine the diagnostic and prognostic value of the soluble form of the embryonal neural cell adhesion molecule NCAM (CD56) in paraproteinemia. NCAM, beta 2-microglobulin, and interleukin-6 levels were measured in the sera of 170 patients with paraproteinemia. Of these, 125 had multiple myeloma, 20 Waldenström's disease, and 25 monoclonal gammopathy of unknown significance.

The neural cell adhesion molecule NCAM in multiple myeloma.

The Neural Cell Adhesion Molecule NCAM is a membrane glycoprotein and belongs to the immunoglobulin superfamily. It is expressed on neural cells as well as on various neuroendocrine tumors and can be detected in sera of patients with small cell lung cancer. Its role is attributed to tumor invasion and formation of metastases.

Oxidation of low density lipoproteins greatly enhances their association with lipoprotein lipase anchored to endothelial cell matrix.

Native and oxidized low density lipoprotein retention within arterial wall endothelial cell matrix (ECM) is an early event in the pathogenesis of atherosclerosis. Previously we showed lipoprotein lipase (LPL) addition to ECM enhanced the retention of apoB-containing lipoproteins. In the present studies we examined whether the oxidation of low density lipoprotein (LDL) increases its retention by LPL-containing ECM.

Serum neural cell adhesion molecule in multiple myeloma and other plasma cell disorders.

Serum embryonic neural cell adhesion molecule (eNCAM) levels were measured at diagnosis in 92 patients with plasma cell disorders. Significantly elevated levels of serum eNCAM were detected in patients with multiple myeloma when compared to both normal controls and patients with monoclonal gammopathy of uncertain significance (MGUS). Very high levels of serum eNCAM were seen in patients with high tumour burdens.

Hypolipidemic activity of select fibrates correlates to changes in hepatic apolipoprotein C-III expression: a potential physiologic basis for their mode of action.

For the last 30 years fibrates have been widely prescribed to treat human dyslipidemia. However, the primary mechanism by which they lower plasma lipid levels is still unknown. Studies with transgenic mice have suggested that changes in apoC-III expression levels have a dramatic influence on plasma triglyceride levels.

Apolipoprotein B and E basic amino acid clusters influence low-density lipoprotein association with lipoprotein lipase anchored to the subendothelial matrix.

Lipoprotein accumulation in the subendothelial matrix is an important step in atherogenesis. We have previously shown that addition of lipoprotein lipase (LPL) markedly increased binding of apolipoprotein B (apoB)-containing lipoproteins to an endothelial cell-derived matrix, and this enhanced lipoprotein binding was inhibited by apoE. In the present studies we examined the role of various regions of apoB in the binding of LDL to LPL-containing endothelial cell matrix and the ability of various apoE domains to decrease lipoprotein retention.

Comparative effects of HMG-CoA reductase inhibitors on apo B production in the casein-fed rabbit: atorvastatin versus lovastatin.

Rabbits fed a diet enriched in casein develop an endogenous hypercholesterolemia (EH) due both to an increased low density lipoprotein (LDL) synthetic rate and decreased LDL receptor activity. Pre-established EH in this model was used to assess the ability and mechanism by which atorvastatin lowers total plasma cholesterol (TPC) compared to the reference agent lovastatin. Rabbits were fed a casein diet for 6 weeks, obtaining average TPC levels above 200 mg/dl.

Characterization of tumor-associated neural cell adhesion molecule in human serum.

In human serum, at least two molecular species of the neural cell adhesion molecule (NCAM) with molecular weights of 110,000-130,000 and 150,000-180,000, respectively, can be identified by Western blotting. Both are characterized by the absence of epitopes for monoclonal antibodies KD11 and MG5, which specifically recognize intracellular domains of the human NCAM transmembrane isoforms, NCAM-140 and NCAM-180. In contrast to the M(r) 110,000-130,000 molecule also detectable in serum samples from healthy blood donors, the M(r) 150,000-180,000 molecule appears to be tumor associated.

ACAT inhibition decreases LDL cholesterol in rabbits fed a cholesterol-free diet. Marked changes in LDL cholesterol without changes in LDL receptor mRNA abundance.

Rabbits fed low-fat, cholesterol-free diets containing casein as the sole protein source develop endogenous hypercholesterolemia (EH). To test the hypothesis that lipoprotein cholesteryl esters in EH rabbits are acyl coenzyme A:cholesterol acyltransferase (ACAT) derived, we treated EH rabbits with CI-976, a potent and selective ACAT inhibitor. In addition, since cholesterol and bile acid synthesis as well as low-density lipoprotein (LDL) receptor activity are reduced in EH rabbits, we determined whether changes in gene expression for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, 7 alpha-hydroxylase, and the LDL receptor might be associated with the efficacy due to ACAT inhibition.