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Biomedical subjects

H Hu

Publications and source records attributed to H Hu.

At least 19 recordsLinked to original sources
PubMed2006

Transcatheter closure of patent ductus arteriosus with severe pulmonary arterial hypertension in adults.

BACKGROUND: Surgical closure of patent ductus arteriosus (PDA) with severe pulmonary arterial hypertension in adults carries higher risk than in children. OBJECTIVES: To investigate the application of self-expandable occluders for transcatheter closure of PDA associated with severe pulmonary arterial hypertension in adults, and the assessment of immediate and short-term results. METHODS: 29 adult patients (6 men, 23 women) underwent attempted transcatheter closure of PDA at a mean (standard deviation (SD)) age of 31.1 (11.4) years (range 18-58 years) and a mean (SD) weight of 54.1 (7.1) kg (range 42-71 kg). On the basis of haemodynamic and clinical data obtained before and after trial occlusion, the final duct occlusion was determined and carried out. Radiographs of the chest, electrocardiograms and echocardiograms were used for follow-up evaluation of the treatment within 1 day, 1 month and 3-6 months after successful closure. RESULTS: 20 of the 29 patients had successful occlusion (group 1), and 9 patients failed (named group 2). In group 1, in which occlusion was successful, mean (SD) pulmonary arterial pressures decreased markedly after trial occlusion: 78 (19.3) mm Hg (range 50-125 mm Hg) before occlusion and 41 (13.8) mm Hg (range 23-77 mm Hg) after occlusion. Systemic arterial oxygen saturation was found to be >90% in 19 patients and <90% in the remaining patient before inhalation of oxygen, and >95% during inhalation of oxygen or after occlusion in all 20 patients. In group 2, the occlusion was not successful, because in two patients the device was not available; another two patients showed worsening of symptoms. The other five patients showed increased pulmonary arterial pressures after trial closure; their mean (SD) pulmonary arterial pressures increased by 10.3 (6) mm Hg (4-16 mm Hg) after trial occlusion, and systemic arterial oxygen saturation was 85.5% (2.6%) (range 82.6-88%) before inhalation of oxygen and 94.7% (1.7%) (range 90.7-99.1%) during inhalation of oxygen. In group 1, the dimensions of the left atrium, left ventricle and pulmonary artery increased considerably in 3-6-months of follow-up compared with those of preocclusion. CONCLUSIONS: Transcatheter closure is an effective treatment for adults with PDA associated with reversible severe pulmonary arterial hypertension. Further research is needed for the evaluation of long-term results.

Adolescent↗
PubMed2006

Kv7/KCNQ/M-channels in rat glutamatergic hippocampal axons and their role in regulation of excitability and transmitter release.

M-current (I(M)) plays a key role in regulating neuronal excitability. Mutations in Kv7/KCNQ subunits, the molecular correlates of I(M), are associated with a familial human epilepsy syndrome. Kv7/KCNQ subunits are widely expressed, and I(M) has been recorded in somata of several types of neurons, but the subcellular distribution of M-channels remains elusive. By combining field-potential, whole-cell and intracellular recordings from area CA1 in rat hippocampal slices, and computational modelling, we provide evidence for functional M-channels in unmyelinated axons in the brain. Our data indicate that presynaptic M-channels can regulate axonal excitability and synaptic transmission, provided the axons are depolarized into the I(M) activation range (beyond approximately -65 mV). Here, such depolarization was achieved by increasing the extracellular K(+) concentration ([K(+)](o)). Extracellular recordings in the presence of moderately elevated [K(+)](o) (7-11 mm), showed that the specific M-channel blocker XE991 reduced the amplitude of the presynaptic fibre volley and the field EPSP in a [K(+)](o)-dependent manner, both in stratum radiatum and in stratum lacknosum moleculare. The M-channel opener, retigabine, had opposite effects. The higher the [K(+)](o), the greater the effects of XE991 and retigabine. Similar pharmacological modulation of EPSPs recorded intracellularly from CA1 pyramidal neurons, while blocking postsynaptic K(+) channels with intracellular Cs(+), confirmed that active M-channels are located presynaptically. Computational analysis with an axon model showed that presynaptic I(M) can control Na(+) channel inactivation and thereby affect the presynaptic action potential amplitude and Ca(2+) influx, provided the axonal membrane potential is sufficiently depolarized. Finally, we compared the effects of blocking I(M) on the spike after-depolarization and bursting in CA3 pyramidal neuron somata versus their axons. In standard [K(+)](o) (2.5 mm), XE991 increased the ADP and promoted burst firing at the soma, but not in the axons. However, I(M) contributed to the refractory period in the axons when spikes were broadened by a low dose 4-aminopyridine (200 microm). Our results indicate that functional Kv7/KCNQ/M-channels are present in unmyelinated axons in the brain, and that these channels may have contrasting effects on excitability depending on their subcellular localization.

4-Aminopyridine↗
PubMed2006

Delta-aminolevulinic acid dehydratase polymorphism and the relation between low level lead exposure and the Mini-Mental Status Examination in older men: the Normative Aging Study.

OBJECTIVE: To determine whether a polymorphism the in delta-aminolevulinic acid dehydratase (ALAD) gene modifies the neurotoxicity of lead in older adults. METHODS: The authors studied men participating in the Department of Veterans Affairs' Normative Aging Study, assessing their recent exposure to lead by measuring blood lead (n = 915) at each triennial clinic visit, and, beginning in 1991, assessing their cumulative exposure by measuring lead levels in tibia (n = 722) and patella (n = 720), using K-shell x ray fluorescence. Starting in 1993 and again at each triennial visit, the authors administered the Mini-Mental State Examination (MMSE) to assess their cognitive functioning. The relation of the lead biomarkers to MMSE score was evaluated and this association was compared among men who carried the variant allele, ALAD-2, versus men without the allele. RESULTS: Sixteen per cent of men carried the ALAD-2 allele. Median tibia and patella lead levels (first-third quartile) were 19 (13-28) and 27 (18-39) microg/g. Blood lead levels were consistent with non-occupational exposure: only 6% of men had levels > or =10 microg/dl. In multivariable adjusted analyses, higher levels of blood lead were associated with poorer performance on the MMSE. This association was most pronounced among ALAD-2 carriers, among whom a 3 microg/dl increment in blood lead (the interquartile range) was associated with a 0.26 point lower mean MMSE score (95% CI -0.54 to 0.01), compared with a 0.04 point lower score (95% CI -0.16 to 0.07) among non-carriers. The modest 0.22 point difference in these associations did not attain statistical significance, however (p(interaction) = 0.13). The associations between bone lead levels and MMSE score did not vary by ALAD-2 status. CONCLUSIONS: Although not statistically significant, these findings suggest that ALAD genotype may modify blood lead's adverse association with cognition among older men who had community exposures to lead. However, despite a relatively large sample size and the use of sensitive methods for measuring lead burden, the evidence overall was fairly weak.

Adult↗
PubMed2006

Prevention of murine experimental autoimmune encephalomyelitis by in vivo expression of a novel recombinant immunotoxin DT390-RANTES.

Experimental autoimmune encephalomyelitis (EAE) is a T-cell-mediated autoimmune disease. Chemokine receptor CCR5 has been shown to be essential for the T-cell recruitment to the inflammatory site in EAE. In this study, we assumed that an immunotoxin directed at CCR5+ cells would be able to reduce the disease activity of EAE. A recombinant immunotoxin, DT390-RANTES-SRalpha, was constructed in an eukaryotic cell expression plasmid consisting of regulated on activation normal T cells expressed and secreted (RANTES) as the targeting moiety and DT390 as the toxic moiety. DT390-RANTES was expressed in vitro and was highly toxic to activated mouse T cells with the inhibitory concentration 50 at 0.18 ng/ml. To evaluate whether DT390-RANTES was effective in preventing EAE, C57BL/6 mice were immunized with myelin basic protein, emulsified with complete Freund's adjuvant and were treated by injecting cationic liposome-embedded plasmid DNA into the muscle of hind limbs. Mice treated with DT390-RANTES-SRalpha developed a much milder EAE compared to mice treated with phosphate-buffered saline or the empty plasmid DNA. Much less CCR5+-infiltrating cells were found in the central nervous system in DT390-RANTES-SRalpha-treated mice than in the control mice. This study indicates that recombinant immunotoxin can be expressed in vivo, and targeting CCR5 can attenuate the disease activity of EAE in mice.

3T3 Cells↗
PubMed2006

ERK2 activation in arteriolar and venular murine thrombosis: platelet receptor GPIb vs. P2X.

The functional significance of extracellular signal-regulated kinase 2 (ERK2) activation was investigated during shear induced human platelet aggregation (SIPA) in vitro and during shear controlled thrombosis in vivo in intestinal arterioles and venules of wild type (WT) and transgenic (TG) mice with platelet-specific overexpression of human P2X(1) (TG). In SIPA, ERK2 was rapidly phosphorylated during GPIb stimulation, its activation contributing to SIPA for 50%, independently of P2X(1) regulation. Thrombotic occlusion of injured arterioles occurred considerably faster in TG (4.3 +/- 2.3 min) than in WT (38 +/- 8 min) arterioles, but occlusion times in TG (19 +/- 12) and WT (48 +/- 4.5 min) venules differed less. Both the alphabeta-meATP triggered desensitization of platelet P2X(1), as well as P2X(1) antagonism by NF279 or NF449 prolonged mean occlusion to about 75 min in WT and 65 min in TG arterioles, but venular occlusion times were less affected. Preventing ERK2 activation by U0126 prolonged occlusion times in TG (41 +/- 10 min) and WT (51 +/- 17) arterioles more than in TG (46 +/- 5 min) and WT (56 +/- 6 min) venules, uncovering a role for ERK2 in shear controlled thrombosis. Antagonism of GPIb by a recombinant murine von Willebrand factor (VWF)-A1 fragment prolonged occlusion times to comparable values, ranging from 55 to 58 min, both in TG and WT arterioles and venules. Further inhibition strategies, combining VWF-A1, U0126 and NF449 in WT and TG mice and resulting in occlusion in various time windows, identified that inhibition by VWF-A1 largely abrogated the ERK2 contribution to thrombosis. In conclusion, P2X(1) and ERK2 both participate in shear stress controlled thrombosis, but ERK2 activation is initiated predominantly via GPIb-VWF interactions.

Animals↗
PubMed2005

Rice SERK1 gene positively regulates somatic embryogenesis of cultured cell and host defense response against fungal infection.

Here we report on the isolation and characterization of a somatic embryogenesis receptor-like kinase (OsSERK1) gene in rice (Oryza sativa). The OsSERK1 gene belongs to a small subfamily of receptor-like kinase genes in rice and shares a highly conserved gene structure and extensive sequence homology with previously reported plant SERK genes. Though it has a basal level of expression in various rice organs/tissues, as high expression level was detected in rice callus during somatic embryogenesis. Suppression of OsSERK1 expression in transgenic calli by RNA interference resulted in a significant reduction of shoot regeneration rate (from 72% to 14% in the japonica rice Zhonghua11). Overexpression of OsSERK1, however, increased the shoot regeneration rate (from 72% to 86%). Interestingly, OsSERK1 is significantly activated by the rice blast fungus, particularly during the incompatible interaction, and is associated with host cell death in Sekigushi lesion mimic mutants. This gene is also inducible by defense signaling molecules such as salicylic acid, jasmonic acid, and abscisic acid. Furthermore, constitutive overexpression of OsSERK1 in two rice cultivars led to an increase in host resistance to the blast fungus. Our data suggest that OsSERK1 may partially mediate defense signal transduction in addition to its basic role in somatic embryogenesis.

Amino Acid Sequence↗
PubMed2005

A study of neonatal swimming (water therapy) applied in clinical obstetrics.

OBJECTIVE: To study the significance of some clinical parameters related to neonatal 'swimming' (water therapy) during hospitalization. METHODS: Normal newborns were randomly divided into two groups to observe their birth weight, weight before discharge,time of first defecation and meconium turning yellow. Group one was the swimming (study) group, comprising a total of 223 newborns including 127 babies delivered after spontaneous vaginal delivery and 96 babies after Cesarean section. Group two was the bathing (control) group, comprising 154 newborns including 109 babies delivered after spontaneous vaginal delivery and 45 babies after Cesarean section. RESULTS: There was no significant difference in birth weight between the two groups (p > 0.05). However, the mean weight before discharge of the babies in the study group was 3.29 + 0.35 and 3.51 + 0.40 kg, spontaneous vaginal delivery vs. Cesarean section, compared with 3.09 + 0.38 and 3.17 + 0.48 kg, respectively, in the control group (p < 0.01). The corresponding mean times of meconium turning yellow were 39.15 + 15.88 and 39.02 + 13.60 h in the study group compared with 48.01 + 19.42 and 55.67 + 25.05 h in the control group. This difference was significant (p < 0.01), as was the difference between the time of first defecation (p < 0.05). CONCLUSION: Neonatal swimming can accelerate babies' growth in the early stage.

Baths↗
PubMed2005

Lead exposure as a risk factor for amyotrophic lateral sclerosis.

BACKGROUND: The etiology of amyotrophic lateral sclerosis (ALS) likely involves an environmental component. We qualitatively assessed literature on ALS and lead exposure. Problems of study design make case reports and studies of lead in blood or tissues difficult to interpret. Most previous case-control studies found an association of ALS with self-reported occupational exposure to lead, with increased risks of 2- to >4-fold. However, these results may have been affected by recall bias. OBJECTIVE: To address inconsistencies among published reports, we used both lead biomarkers and interview data to assess lead exposure, and we evaluated the role of genetic susceptibility to lead. METHODS: We conducted a case-control study in New England in 1993-1996 with 109 ALS cases and 256 population-based controls. We measured blood and bone lead levels, the latter using X-ray fluorescence, and interviewed participants regarding sources of lead exposure. RESULTS: In our study, ALS was associated with self-reported occupational lead exposure, with a dose response for cumulative days of exposure. ALS was also associated with blood and bone lead levels, with a 1.9-fold increase in risk for each mug/dl increment in blood lead and a 2.3- to 3.6-fold increase for each doubling of bone lead. A polymorphism in the delta-aminolevulinic acid dehydratase gene was associated with a 1.9-fold increase in ALS risk. CONCLUSION: These results, together with previous studies, suggest that lead exposure plays a role in the etiology of ALS. An increase in mobilization of lead from bone into blood may play a role in the acute onset of disease.

Amyotrophic Lateral Sclerosis↗
PubMed2005

Muscle and plasma coenzyme Q10 concentration, aerobic power and exercise economy of healthy men in response to four weeks of supplementation.

AIM: To investigate whether 4 weeks of oral supplementation with coenzyme Q10 (CoQ10) would increase its concentration in skeletal muscle, and affect aerobic power (VO2max) and oxygen consumption during submaximal exercise in healthy, physically active men. METHODS: Six volunteers with an average (+/-SD) age of 29.7+/-7.2 years and VO2max of 39.4+/-8.5 mL.kg-1.min-1, participated in a single-blind trial. The experiment consisted of 4 2-week phases, in the order of placebo run-in, CoQ10 supplementation (150 mg daily), CoQ10 (150 mg) plus vitamin E (1,000 IU daily), and placebo wash-out. A three-stage cycle economy test (4 minutes at each of 50, 100, and 150 watts), followed by a VO2max test (25 watts increment every minute till exhaustion), were performed prior to the supplementation and at the end of each phase. Blood samples were taken pre and post each VO2max test, and biopsy samples were obtained from the vastus lateralis muscle pre and post the 4 weeks of CoQ10 supplementation. RESULTS: The plasma CoQ10 concentration was significantly elevated by the supplementation (P<0.05), however, it did not vary significantly pre and post each exercise test (P>0.05). The muscle CoQ10 concentration, VO2max ventilatory threshold, exercise economy and oxygen deficit showed no significant changes in response to the supplementation. CONCLUSION: It was speculated that the non-significant effects of supplementation in healthy, non CoQ10-deficient men could be due to either that the mitochondrial membrane is normally saturated with CoQ10, or that the selected exercise testing protocol and variables were not sensitive enough to detect the effects.

Adult↗
PubMed2004

Cerebellar ataxia and Purkinje cell dysfunction caused by Ca2+-activated K+ channel deficiency.

Malfunctions of potassium channels are increasingly implicated as causes of neurological disorders. However, the functional roles of the large-conductance voltage- and Ca(2+)-activated K(+) channel (BK channel), a unique calcium, and voltage-activated potassium channel type have remained elusive. Here we report that mice lacking BK channels (BK(-/-)) show cerebellar dysfunction in the form of abnormal conditioned eye-blink reflex, abnormal locomotion and pronounced deficiency in motor coordination, which are likely consequences of cerebellar learning deficiency. At the cellular level, the BK(-/-) mice showed a dramatic reduction in spontaneous activity of the BK(-/-) cerebellar Purkinje neurons, which generate the sole output of the cerebellar cortex and, in addition, enhanced short-term depression at the only output synapses of the cerebellar cortex, in the deep cerebellar nuclei. The impairing cellular effects caused by the lack of postsynaptic BK channels were found to be due to depolarization-induced inactivation of the action potential mechanism. These results identify previously unknown roles of potassium channels in mammalian cerebellar function and motor control. In addition, they provide a previously undescribed animal model of cerebellar ataxia.

Animals↗
PubMed2004

Exercise-induced platelet and leucocyte activation is not enhanced in well-controlled Type 1 diabetes, despite increased activity at rest.

AIMS/HYPOTHESIS: Stress can evoke a prothrombotic state with activated platelets and leucocytes, and increased platelet activation at rest has been reported for diabetic subjects. Thus, prothrombotic responses to stress may be enhanced in diabetes mellitus. We therefore evaluated platelet and leucocyte responses to exercise in Type 1 diabetic patients. METHODS: Type 1 diabetes mellitus patients with good metabolic control and healthy subjects matched for age and body mass index ( n=15 for both) performed a maximal exercise test. Platelet and leucocyte activation and their heterotypic aggregation were monitored by whole blood flow cytometry. RESULTS: Diabetic platelets did not show higher basal levels of P-selectin expression, but were more reactive to ADP and thrombin stimulation. Diabetic patients had increased lymphocyte and monocyte CD11b expression, and increased circulating platelet-monocyte aggregates. Exercise evoked thrombocytosis, increased circulating platelet P-selectin expression, enhanced platelet sensitivity to ADP and thrombin, and elevated plasma levels of soluble P-selectin to a similar degree in diabetic patients and healthy subjects. Exercise induced marked leucocytosis and elevated plasma elastase, but only slightly increased leucocyte CD11b expression and leucocyte reactivity to stimulation by N-formyl-methionyl-leucyl-phenylalanine. In all of these there was no difference between diabetic patients and healthy subjects. The numbers, but not percentages of circulating platelet-leucocyte aggregates were markedly increased by exercise, but the increase was less prominent among diabetic patients. CONCLUSIONS/INTERPRETATION: Strenuous exercise evokes platelet and leucocyte activation in Type 1 diabetic patients and healthy subjects. Platelet and monocyte hyperactivity were found at rest, but responses to stress were not augmented in metabolically well-controlled Type 1 diabetes mellitus patients.

Adenosine Diphosphate↗
PubMed2004

Enhanced P-selectin expression and increased soluble CD40 Ligand in patients with Type 1 diabetes mellitus and microangiopathy: evidence for platelet hyperactivity and chronic inflammation.

AIMS/HYPOTHESIS: Platelet activation, endothelial dysfunction and inflammation may be involved in early stages of diabetic microangiopathy. We therefore investigated patients with Type 1 diabetes mellitus, without ( n=19) and with ( n=20) microangiopathy, matched for glycaemic control and duration of disease, and matched with healthy control subjects ( n=27). METHODS: Platelet activation was measured as platelet P-selectin expression using whole blood flow cytometry and as soluble P-selectin by immunoassay. Von Willebrand factor antigen in plasma, serum soluble E-selectin, CD40 ligand (sCD40L) and C-reactive protein (CRP) served as markers for endothelial function and inflammation. RESULTS: Thrombin-induced platelet P-selectin expression was enhanced, and soluble P-selectin and sCD40L concentrations were increased in patients with microangiopathy compared with the control subjects ( p<0.01 for both) and with patients without microangiopathy ( p<0.05 for P-selectin expression and sP-selectin), whereas all three parameters were similar in patients without microangiopathy and in the control subjects. CRP and soluble E-selectin were increased in patients with microangiopathy, compared with the control subjects ( p<0.01 and p<0.05), whereas von Willebrand factor did not differ between the groups. CONCLUSIONS/INTERPRETATION: Microangiopathy in Type 1 diabetes is associated with platelet hyperactivity, endothelial dysfunction and low-grade inflammation, indicating an increased risk for cardiovascular disease.

Adult↗
PubMed2004

The steroidal aromatase inhibitor exemestane prevents bone loss in ovariectomized rats.

The irreversible steroidal aromatase inhibitor exemestane (EXE) is one of three third generation aromatase inhibitors currently prescribed for advanced breast cancer in postmenopausal women. Its principal mechanism of action is to reduce estrogen by inhibiting its synthesis. In addition to its efficacy against breast cancer, its effects on other organs are important, especially when given to women with good-prognosis breast cancer or potentially to healthy women at increased risk of developing breast cancer. The purpose of this study was to evaluate the effects of EXE on bone and lipid metabolism in ovariectomized (OVX) rats. Ten-month-old Sprague-Dawley female rats were sorted into intact controls, intact + EXE, OVX controls, and OVX + EXE groups, and treated by weekly intramuscular injection with vehicle or 100 mg/kg EXE for 16 weeks. The bone mineral density (BMD), mechanical testing, histomorphometry, bone resorption marker-serum pyridinoline (PYD), and bone formation marker-serum osteocalcin (OC) were used to determine the effects of treatment on bone. In addition, total serum cholesterol, triglyceride, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) were determined. BMD of the lumbar spine and femur were 11% and 7%, respectively, higher in OVX animals given EXE than in OVX controls (all Ps<0.001). Significant increases in the bending strength and toughness of the femora as well as the compressive strength and elastic modulus of the vertebrae were observed in OVX rats given EXE (all Ps<0.02 vs. OVX controls). Trabecular bone volume (BV) was significantly higher in OVX rats treated with EXE than in OVX controls (P<0.0001). In OVX animals, EXE reduced the OVX-induced increase of serum PYD by 96% (P<0.0001), and the OVX-induced increase of serum OC was completely prevented by treatment with EXE. In OVX animals, EXE resulted in a 28% reduction of serum cholesterol (P<0.0001) and reduced LDL by 64% compared with OVX controls (P<0.0001). The positive results of EXE on bone and lipid metabolism in the OVX rat model merit further investigation of the effects of EXE in postmenopausal women.

Androstadienes↗
PubMed2004

Prothrombotic responses to exercise are little influenced by clopidogrel treatment.

AIMS: Adenosine diphosphate (ADP) is involved in shear-induced platelet activation, which may be important for platelet responses to stress. We therefore tested the hypothesis that ADP receptor antagonism by clopidogrel treatment would attenuate exercise-induced platelet activation. METHODS AND RESULTS: Fifteen healthy volunteers performed exhaustive exercise without and with clopidogrel pretreatment (75 mg/day; 7 days) in a randomised crossover study. Filtragometry readings (reflecting platelet aggregability in vivo) and 11-dehydro-thromboxane B(2) (TxM) in plasma were determined before and after exercise. Platelet and leukocyte activity, platelet-platelet (PPA), and platelet-leukocyte aggregates (PLAs) in vivo and their responsiveness to agonist stimulation in vitro were assessed by flow cytometry. Clopidogrel treatment inhibited ADP-induced platelet P-selectin expression by 72% (54-85%). Exercise increased platelet aggregation (filtragometry and PPAs), elevated plasma TxM, increased single platelet P-selectin expression, elevated circulating PLAs, and enhanced ADP and thrombin-stimulated P-selectin expression. Clopidogrel prolonged filtragometry readings and attenuated agonist stimulated P-selectin expression at rest, but did not influence TxM in plasma or urine or attenuate platelet or leukocyte responses to exercise. Clopidogrel treatment did not influence plasma CD40L (ligand) at rest or after exercise. CONCLUSION: Clopidogrel treatment attenuates platelet activity in vivo at rest, but exercise counteracts the platelet stabilizing effects of clopidogrel. The hypothesis that ADP is involved in stress-induced platelet activation was not supported.

Adenosine Diphosphate↗
PubMed2004

Statistics of Poincaré recurrences for maps with integrable and ergodic components.

Recurrence gives powerful tools to investigate the statistical properties of dynamical systems. We present in this paper some applications of the statistics of first return times to characterize the mixed behavior of dynamical systems in which chaotic and regular motion coexist. Our analysis is local: we take a neighborhood A of a point x and consider the conditional distribution of the points leaving A and for which the first return to A, suitably normalized, is bigger than t. When the measure of A shrinks to zero the distribution converges to the exponential e(-t) for almost any point x, if the system is mixing and the set A is a ball or a cylinder. We consider instead a system, a skew integrable map of the cylinder, which is not ergodic and has zero entropy. This map describes a shear flow and has a local mixing property. We rigorously prove that the statistics of first return is of polynomial type around the fixed points and we generalize around other points with numerical computations. The result could be extended to quasi-integrable area preserving maps such as the standard map for small coupling. We then analyze the distribution of return times in a region which is composed by two invariants subdomains: one with a mixing dynamics and the other with an integrable dynamics given by our shear flow. We show that the statistics of first return in this mixed region is asymptotically given by the exponential law, but this limit is attained by an intermediate regime where exponential and polynomial laws are linearly superposed and weighted by some factors which are proportional to the relative sizes of the chaotic and regular regions. The result on the statistics of first return times for mixed regions in the phase space can provide a basis to analyze such a property for area preserving maps in mixed regions even when a rigorous result is not available. To this end we present numerical investigations on the standard map which confirm the results of the model.

Algorithms↗
PubMed2004

Enhanced leukocyte-platelet cross-talk in Type 1 diabetes mellitus: relationship to microangiopathy.

BACKGROUND: Platelets and leukocytes may influence each others' function, i.e. platelet-leukocyte cross-talk. Diabetes mellitus (DM) is associated with platelet and leukocyte dysfunction. OBJECTIVE: To evaluate platelet-leukocyte cross-talk, and if this might contribute to platelet and leukocyte dysfunction and microangiopathy in DM patients. PATIENTS AND METHODS: We evaluated platelet and leukocyte function, and cross-talk between these cells in Type 1 DM patients without (n = 19) and with (n = 20) microangiopathy, and healthy subjects (n = 27), using whole blood flow cytometry. Platelet-leukocyte cross-talk was studied in hirudinized whole blood incubated at 37 degrees C with stirring. RESULTS: Basal single platelet P-selectin and leukocyte CD11b expression were similar in DM patients and healthy subjects, whilst circulating platelet-leukocyte aggregates and plasma elastase levels were elevated in DM patients. The thromboxane A2 analog U46619 (3 x 10(-7) m) induced more marked increases of platelet P-selectin expression and platelet-leukocyte aggregation in DM patients than in healthy subjects. The leukocyte-specific agonist N-formyl-methionyl-leucyl-phenylalanine (fMLP) (10(-7) m) induced more marked CD11b expression in DM patients with microangiopathy, compared with healthy subjects. Platelet-leukocyte cross-talk induced by U46619 (10(-6) m) showed no difference between DM patients and healthy subjects. fMLP (10(-6) m) evoked marked leukocyte activation, which subsequently caused mild platelet P-selectin expression. This leukocyte-platelet cross-talk was more pronounced in DM patients than in healthy subjects. Furthermore, enhanced leukocyte-platelet cross-talk was correlated to platelet hyperreactivity among DM patients with microangiopathy only. CONCLUSIONS: Type 1 DM is associated with platelet and leukocyte hyperactivity, and enhanced leukocyte-platelet cross-talk, which may contribute to platelet hyperactivity and the microvascular complications seen in Type 1 DM.

Adult↗