68 research outputs found
Antiangiogenic activity of zoledronic acid: inhibition of the VEGF-VEGFR-2 autocrine loop in the endothelial cells of patients with multiple myeloma
No full textBody mass index, metabolic syndrome and carotid atherosclerosis.
No full textOBJECTIVE: Body fatness and fat distribution are widely accepted as coronary
heart disease risk factors. In this study, we have evaluated the contribution of
generalized adiposity, assessed by body mass index (BMI), to carotid
atherosclerosis, in participants with or without metabolic syndrome (MetS).
METHODS: We have analysed 840 female and 1002 male participants in a regional
Cardiovascular Disease Prevention Campaign. Blood glucose and lipids were
analysed by standard methods. According to BMI, calculated as weight (in
kilograms)/height (in square metres), participants were divided into normal
weight (BMI <25 kg/m2), overweight (BMI between 25 and 29.9 kg/m2) and obese
(BMI>29.9 kg/m2). Carotid atherosclerosis was evaluated by echo Doppler.
RESULTS: Blood pressure, waist circumference, triglycerides and glucose were
significantly higher, and high-density lipoprotein was lower, in overweight and
obese participants, compared with normal weight. MetS was more frequent among
obese and overweight than normal-weight participants (51.7 vs. 21.5 vs. 9.8%,
respectively). The prevalence of carotid atherosclerosis was 45.29% in
participants with MetS, significantly higher than in participants without MetS
(33.04%, P<0.0001), but it was similar across the three weight categories.
Furthermore, in multiple regression analyses BMI was not significantly associated
with carotid atherosclerosis.
CONCLUSION: The present findings suggest that increasing body weight favours the
clustering of coronary heart disease risk factors. Overweight and obesity,
however, do not independently associate with carotid atherosclerosis
The influence of PON1 192 polymorphism on endothelial function in diabetic subjects with or without hypertension.
No full textHypertension and type 2 diabetes mellitus (T2DM) cause endothelial dysfunction
probably through increased oxidant stress. Paraoxonase (PON1) is an high-density
lipoprotein (HDL)-linked anti-oxidant enzyme whose capacity is influenced by a
genetic polymorphism at codon 192. In the present study we have investigated the
role of PON1 polymorphism on endothelial function in subjects with T2DM with or
without hypertension. Three groups of male subjects were enrolled: 65 healthy
control subjects without T2DM or hypertension (CON), 51 with only T2DM (DM), and
67 with both hypertension and T2DM (HYP+DM). The PON1 Gln192Arg polymorphism was
determined by polymerase chain reaction (PCR) amplification and restriction
analysis. Endothelial function was evaluated as flow-mediated vasodilatation
(FMD) of the brachial artery after forearm ischemia. Data were analyzed according
to the presence or absence of the Arg allele. Subjects with T2DM had markedly
impaired FMD, compared with those of the CON group. In the CON and HYP+DM groups
no difference was observed in FMD between subjects homozygous for the Gln allele
and those carrying the Arg allele. In the DM group FMD was lower among those
carrying the Arg allele compared with Gln/Gln homozygotes (2.1+/-2.4% vs.
6.2+/-5.2%, p=0.002). In conclusion, the present findings demonstrated that FMD
was less impaired in normotensive diabetic subjects homozygous for the Gln
allele, consistent with the notion that this isoform has a more effective
antioxidant action that serves to protect circulating low-density lipoprotein
(LDL). Hypertension seems to abolish the protective effect of the Gln isoform.
These findings, however, warrant further investigation to clarify their clinical
import
Lymphatics at crossroads of angiogenesis and lymphangiogenesis
No full textThe lymphatic system is implicated in interstitial fluid balance regulation, immune cell trafficking, oedema and cancer metastasis. However, the sequence of events that initiate and coordinate lymphatic vessel development (lymphangiogenesis) remains obscure. In effect, the understanding of physiological regulation of lymphatic vasculature has been overshadowed by the greater emphasis focused on angiogenesis, and delayed by a lack of specific markers, thereby limiting this field to no more than a descriptive characterization. Recently, new insights into lymphangiogenesis research have been due to the discovery of lymphatic-specific markers and growth factors of vascular endothelial growth factor (VEGF) family, such as VEGF-C and VEGF-D. Studies using transgenic mice overexpressing VEGF-C and VEGF-D have demonstrated a crucial role for these factors in tumour lymphangiogenesis. Knowledge of lymphatic development has now been redefined at the molecular level, providing an interesting target for innovative therapies. This review highlights the recent insights and advances into the field of lymphatic vascular research, outlining the most important aspects of the embryo development, structure, specific markers and methods applied for studying lymphangiogenesis. Finally, molecular mechanisms involved in the regulation of lymphangiogenesis are described. © Anatomical Society of Great Britain and Ireland 2004
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