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PubMed2004

Effects of the humic substances of de-inking paper sludge on the antagonism between two compost bacteria and Pythium ultimum.

We investigated the in vitro influence of humic substances (HS) extracted from de-inking paper sludge compost on the inhibition of Pythium ultimum by two compost bacteria, Rhizobium radiobacter (Agrobacterium radiobacter) and Pseudomonas aeruginosa. When low concentrations (5 or 50 mg l(-1)) of HS were added to the culture medium, fungal inhibition by R. radiobacter significantly increased (P<0.01) by 2-3%. In contrast, these low levels of HS had no effect on P. ultimum inhibition by P. aeruginosa. The Fe, chelated by HS, was in part responsible for the decrease of P. ultimum inhibition by the bacteria when increasing amounts of HS were added in the culture medium. The addition of 500 mg l(-1) of humic acids isolated from de-inking paper sludge compost or from fossil origin completely eliminated the inhibition of P. ultimum by R. radiobacter. This Fe effect also stimulated growth of R. radiobacter and reduced its siderophore production in a minimal medium supplemented with HS as sole source of Fe. The results showed that HS influence microbial antagonism when added to a culture medium. However, this effect varies with different factors such as the type of bacteria, concentration of HS, molecular weight and Fe content.

Bacteria↗
PubMedDate not supplied

"Technological" approach versus clamp crushing technique for hepatic parenchymal transection: a comparative study.

We evaluated the feasibility and effectiveness of combining two different electronic devices, the ultrasonic dissector (UD) and the harmonic scalpel (HS), during hepatic resection. One hundred consecutive patients underwent liver resection using UD plus HS between January and December 2004 (UD + HS group). The ultrasonic dissector was used to fracture liver parenchyma and the uncovered vessel was sealed using the HS. Surgical outcomes were compared with 100 consecutive patients who underwent liver resection using the clamp crushing method. Operative variables, postoperative liver function, hospital stay, and type and number of complications were compared. The two groups were equivalent in term of demographic and pathologic variables. The UD + HS group had a decreased blood loss (500 ml versus 700 ml, P = 0.005), number of patients transfused (22 versus 39, P = 0.009), tumor exposure at the transection surface (4 versus 12, P = 00.012), and hospital stay (7 versus 8.5 days, P = 0.020). Postoperative major complications, in particular, fluid collection and biliary fistula, were significantly less frequent in the UD + HS group (2 versus 9, P = 0.030). A longer operative time was recorded in the UD + HS group (385 versus 330 minutes, P = 0.001). The combined use of UD with HS allows liver resection to be safely performed, with the advantage of reducing blood losses and surgery-related complications. The only major disadvantage may be a longer transection time.

Adult↗
PubMedDate not supplied

Retinopathy and hypertension affect serum high-sensitivity C-reactive protein levels in Type 2 diabetic patients.

Several studies suggest that inflammation plays an important role in the pathogenesis of diabetes mellitus, as well as atherosclerosis, and acute-phase reactants have been proposed as monitors for the ongoing process of these diseases. We studied the clinical significance of serum high-sensitivity C-reactive protein (hs-CRP) in relation to chronic diabetic complications using 114 Japanese patients with Type 2 diabetes mellitus. The hs-CRP values were normalized by logarithmic transformation for statistical analysis. Retinopathy and hypertension were extracted as significant modulators for the hs-CRP value in the diabetic patients, in addition to previously known factors, age, and body mass index (BMI), by multivariate analysis. The hs-CRP level in normotensive diabetic patients without retinopathy was not significantly different from that of normal control participants after adjustment for age and BMI. The hs-CRP value was significantly high in the patients with hypertension, despite the existence or absence of diabetes. On the other hand, the hs-CRP level of the diabetic patients complicated with retinopathy was low especially in those with hypertension. The frequency of patients having an hs-CRP value above 1.0 mg/l who are thought to be at risk for cardiovascular diseases was also high in the patients complicated with hypertension and low in the diabetic patients with retinopathy. These results indicate that the presence or absence of hypertension and retinopathy should be taken into consideration for the interpretation of the serum hs-CRP in diabetic patients.

Biomarkers↗
PubMed2005

Effects of estrogen, raloxifene, and hormone replacement therapy on serum C-reactive protein and homocysteine levels.

OBJECTIVES: To investigate the effects of conjugated equine estrogen (CEE), CEE plus medroxyprogesterone acetate (MPA), CEE plus Nomegestrol acetate (NA), and raloxifene on serum high sensitivity C-reactive protein (hs-CRP) and homocysteine (Hcy) levels in healthy postmenopausal women. MATERIALS: One hundred seven healthy postmenopausal women were recruited in a prospective, randomized, and placebo-controlled 6 months study. Of these, 18 were hysterectomized and received daily oral 0.625 mg CEE. Eighty nine non-hysterectomized women were randomly allocated to one of four groups: a group (22 patients) treated with CEE, 0.625 mg/daily plus MPA 2.5 mg/daily; a group (22 patients) treated with CEE, 0.625 mg/daily plus NA 5 mg/daily; a group (23 patients) treated with raloxifene hydrochloride, 60 mg once daily; and a placebo group (22 patients). Hcy and hs-CRP were measured at baseline and at 3 and 6 months. RESULTS: CEE (20%, P=0.03) and CEE+MPA (59%, P=0.006) increased serum hs-CRP levels significantly, whereas CEE+NA decreased serum hs-CRP by 25% (P=0.01). Raloxifene had no significant effect on serum hs-CRP levels during and after the treatment. In all active treatment groups serum Hcy levels decreased significantly compared to baseline and placebo. CONCLUSIONS: Conjugated equine estrogen, hormone replacement therapies, and raloxifene lower serum Hcy levels to a comparable extent in postmenopausal women. Hs-CRP, as a cardiovascular risk factor, is not influenced by raloxifene, whereas CEE and CEE plus MPA significantly increase hs-CRP levels. Treatment with CEE plus NA reduces serum hs-CRP levels.

Adult↗
PubMed2026

Glycoinformatic Profiling of Label-Free Intact Heparan Sulfate Oligosaccharides.

Heparan sulfates (HSs) are a group of heterogenous linear, sulfated polysaccharides that play a role in health and many diseases, including cancer, cardiovascular, and kidney diseases. The structural variety of HS has greatly challenged the development and utility of HS analytics, particularly for native (nondepolymerized) structures, leaving a significant gap in HS technologies for clinical application. Mass spectrometry-based profiling with bioinformatics offers an approach that can retain variety in large datasets. Using healthy human plasmas, we developed a mass spectrometry glycoprofiling approach for native HS oligosaccharides, which retains the structural complexity of each individual HS chain and generates an HS "index" (or Heparan-ome) for each patient. As a proof of concept, analysis of 53 plasma samples ranging from four groups of kidney disease patients revealed a new subset cluster (21%, 4/19) of membranous glomerulopathy patients with distinct HS profiles, highlighting the potential of HS glycoprofiling as a powerful new approach to clinical practice, which warrants future development into quantitative oligosaccharide glycosaminoglycanomics and clinical diagnostics of kidney and other diseases.

Humans↗
PubMed2004

Adiponectin, insulin resistance, and C-reactive protein in postpubertal Asian Indian adolescents.

High-sensitivity C-reactive protein (hs-CRP) levels are closely associated with adiposity and predict coronary heart disease and type 2 diabetes mellitus. However, relationships of CRP to adiponectin and other markers of insulin resistance have been inadequately researched in children. We measured fasting serum levels of adiponectin, insulin, hs-CRP, and lipoproteins, and recorded the anthropometric profile and percentage of body fat (%BF; bioimpedance method) in 62 (36 normal weight, 26 overweight) healthy, urban, postpubertal Asian Indian males (aged 14 to 18 years). Serum levels of adiponectin were lower (P = not significant [NS]), whereas those of fasting insulin (P = .01) and hs-CRP (P = .02) were higher in overweight subjects. Adiponectin levels inversely correlated with body mass index (BMI; r = -0.26, P < .05), %BF (r = -0.24, P < .05), fasting insulin (r = -0.32, P < .05) and insulin resistance measured by the homeostasis model of assessment (HOMA-IR; r = -0.31, P < .05), but not with hs-CRP levels. Fasting insulin and hs-CRP levels correlated significantly with BMI, %BF, waist circumference (WC), waist-to-hip circumference ratio (W-HR), and triceps and subscapular skinfold thickness. The correlation of adiponectin with insulin sensitivity was independent of abdominal obesity, but became nonsignificant after controlling for BMI and %BF. Further, BMI was an independent predictor of adiponectin levels and the ratio of adiponectin and %BF was an independent predictor of fasting insulin levels. Although adiponectin levels did not correlate with hs-CRP levels, we observed dichotomous relationships of adiponectin and hs-CRP levels with generalized and abdominal obesity, respectively. We conclude that generalized obesity affects the adiponectin-insulin relationship in postpubertal Asian Indian males; however, the relationship of adiponectin with hs-CRP needs further evaluation.

Adiponectin↗
PubMed2006

Case reports and literature review: the association between reactivation of human herpes virus-6 and peripheral white blood cell count in patients with carbamazepine-induced hypersensitivity syndrome.

Eruptions induced by anticonvulsants can often be experienced clinically, and the clinical diagnosis of "drug induced hypersensitivity syndrome (HS)" was proposed to characterize these drug eruptions. Reactivation of human herpes virus-6 seems to be an integral component of HS. Previously, we experienced two cases of carbamazepine (an anticonvulsant) induced HS and both cases did not show a reactivation of human herpes virus-6 infection (no elevation of anti-human herpes virus-6 IgG titres). The features of these two cases were compared with other reported cases that presented HS with the reactivation of human herpes virus-6. In the early phase of HS, a change in peripheral white blood cell count seems to be important and could be used as an indicator to predict whether late phase HS with reactivation of human herpes virus-6 will occur, since the increase in white blood cell count is seen before the increase in anti-human herpes virus-6 titres. Reactivation of human herpes virus-6 may cause severe clinical symptoms such as encephalitis. When an increase in white blood cells are observed in HS cases at onset, immediate discontinuation of cause drug and intensive care are necessary to avoid the more severe symptoms of HS.

Adult↗
PubMed2005

A protein canyon in the FGF-FGF receptor dimer selects from an à la carte menu of heparan sulfate motifs.

Heparan sulfate (HS) is an essential and dynamic regulator of fibroblast growth factor (FGF) signaling. Two fundamentally different crystallographic models have been proposed to explain, at the molecular level, how HS/heparin enables FGF and FGF receptor (FGFR) to assemble into a functional dimer on the cell surface. In the symmetric 'two-end' model, the heparin-binding sites of FGF and FGFR merge to form a basic canyon that recruits two HS for binding. Within this canyon, the HS molecules primarily act to orchestrate and fortify multivalent and cooperative protein-protein contacts within the dimer that are the foundations of dimerization. In contrast, in the asymmetric model, which mechanistically resembles the previously proposed trans FGF dimer model, a single heparin molecule facilitates dimerization by cross-linking two FGFs into a trans dimer that brings together the two FGFRs. Interestingly, the crystal structure upon which the asymmetric model is based contains a symmetric dimer reminiscent of the symmetric two-end model, suggesting that a different interpretation of the crystal structure has led to the postulation of the asymmetric model. Importantly, the symmetric two-end model provides an intriguing solution to the problem of how HS selectivity is achieved in FGF signaling. The model reveals that, within the canyon, FGF and FGFR no longer adhere to their individual HS binding specificities, but instead act in unison to search for a unique HS motif from a plethora of HS epitopes that are expressed in a tissue-specific and developmentally regulated fashion. Primary sequence differences within the heparin-binding sites of FGFs and FGFRs, together with ligand-induced changes in FGFR conformation, lead to the formation of distinct canyons with unique HS specificity for individual FGF-FGFR complexes.

Animals↗
PubMed2006

Hypertonic saline resuscitation improves intestinal microcirculation in a rat model of hemorrhagic shock.

BACKGROUND: Conventional resuscitation (CR) from hemorrhagic shock (HS) often restores and maintains hemodynamics but fails to restore intestinal perfusion. Post-CR intestinal ischemia has been implicated in the initiation of a gut-derived exaggerated systemic inflammatory response and in the progressive organ failure following HS. We propose that intestinal ischemia can be prevented with hypertonic saline resuscitation (HTSR). METHODS: Anesthetized male Sprague-Dawley rats (200 to 215 g) were hemorrhaged to 50% of mean arterial pressure (MAP) for 60 minutes and randomly assigned to 1 of the resuscitation groups (n = 7 each): Group I: sham operation and no HS; Group II: HS + CR with the return of the shed blood + 2 volumes of normal saline (NS); Group III: HS + return of the shed blood + hypertonic saline (HTS); (7.5 % NaCl, 4 ml/kg); Group IV: HS + HTS, then return of the shed blood after 60 minutes; Group V: HS + HTS, then 1 volume of NS after 60 minutes. Microvascular diameters of inflow (A1) and proximal and distal premucosal arterioles (A3) in terminal ileum and flow in A1 were measured using in vivo videomicroscopy and optical Doppler velocimetry. Hematocrit, plasma osmolarity, and electrolytes were measured in Groups II and III. RESULTS: HS caused a selective vasoconstriction in A1 arterioles that was not seen in the premucosal arterioles. CR restored and maintained MAP and caused generalized, progressive vasoconstriction at all intestinal arteriolar levels that is associated with hypoperfusion. HTSR failed to restore or maintain MAP or intestinal A1 arteriolar blood flow until the shed blood was returned. However, HTSR prevented the post-resuscitation, premucosal vasoconstriction and produced an insidious selective vasodilation in the A3 arterioles, which was most significant with early blood return (Group III). This selective arteriolar vasoactivity was associated with a significant improvement of endothelial cell function. Plasma hyperosmolality and hypernatremia persisted during the entire 2 hours post-resuscitation with HTS. CONCLUSIONS: Small-volume HTSR can be used as a resuscitation regimen at the trauma scene and for selective clinical conditions where hypotensive resuscitation is indicated. HTSR improves intestinal perfusion by selective vasodilation of the precapillary arterioles even at MAP close to shock levels.

Animals↗
PubMed2003

High-sensitivity C-reactive protein and cardiovascular risk: rationale for screening and primary prevention.

Inflammation is a major factor in atherothrombotic disease. Levels of high-sensitivity C-reactive protein (hs-CRP), a marker of systemic inflammation and a mediator of atherothrombotic disease, have been shown to correlate with cardiovascular disease risk. Recent findings in 27,939 healthy women in the Women's Health Study indicate that hs-CRP (1) is a stronger predictor of risk than low-density lipoprotein (LDL) cholesterol, (2) predicts elevated risk in subjects without overt hyperlipidemia, and (3) adds prognostic information to risk scoring and LDL cholesterol categories. Other data from this cohort show that hs-CRP level adds prognostic information to the diagnosis of the metabolic syndrome. Taken together with other data in men on the association of hs-CRP with vascular risk, a strong argument is provided for screening in the primary prevention population. With regard to potential treatment, statins have been found to reduce hs-CRP levels, and data from statin treatment trials raise the possibility that subjects with elevated hs-CRP levels may derive greater benefit from treatment than do patients without elevated hs-CRP. The Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial is planned to examine the effects of rosuvastatin treatment in preventing cardiovascular events in 15,000 healthy subjects with elevated hs-CRP levels in the absence of overt hyperlipidemia.

Aged↗
PubMed1997

Heparan sulfate modifies the effects of basic fibroblast growth factor on glial reactivity.

Our previous studies have shown that injection of basic fibroblast growth factor (bFGF) into a brain wound enhances astrocyte hypertrophy and macrophage-microglia proliferation in areas adjacent to the lesion. In the present study, designed to test the effects of co-administration of bFGF and heparan sulfate (HS), rats received injections of 200 ng bFGF, 200 ng bFGF with 50 microg HS, or 50 microg HS into a brain wound. Glial proliferation and astrocyte hypertrophy were evaluated in seven non-overlapping subfields in the mid-cortex including the wound edge. Our results show that bFGF-HS, compared to bFGF or HS alone, enhanced the total area of GFAP staining in all subfields except the one nearest to the wound edge. The combination of bFGF and HS did not increase total glial or astrocyte proliferation. We propose that the observed effects resulted from a greater diffusion of bFGF-HS complex into the brain parenchyma, where it bypassed low-affinity binding sites that would otherwise sequester free bFGF. Our results suggest that bFGF-HS complex, compared to bFGF alone, may gain entry into the brain more readily, reach higher concentrations and be more effective as a neurotrophic agent.

Animals↗
PubMed2003

COX-2: an in vivo evidence of its participation in heat stress-induced myocardial preconditioning.

OBJECTIVE: Heat stress (HS) is known to induce delayed protection against myocardial infarction. We have previously shown that inducible nitric oxide synthase (iNOS), was involved in mediating this form of preconditioning. Since iNOS and cyclooxygenase-2 (COX-2) are co-induced in various cell types, the goal of this study was to investigate whether COX-2 could also participate to the HS-induced cardioprotection. METHODS AND RESULTS: A total of 78 male Wistar rats, subjected to either heat stress (42 degrees C for 15 min) or sham anaesthesia were used for this study. Twenty-four hours later, they were treated or not with a selective COX-2 inhibitor, either celecoxib (3 mg kg(-1), i.p.) or NS-398 (5 mg kg(-1), i.p.), 30 min before being subjected to a 30-min occlusion of the left coronary artery followed by a 120-min reperfusion, in vivo. HS resulted in a marked increase in myocardial COX-2 protein expression at 24 h, associated with a significant protection against infarction (46.0+/-1.4% in sham vs. 26.8+/-3.8% in HS group) (P<or=0.05). Administration of selective COX-2 inhibitor 24 h after HS, completely abrogated this delayed cardioprotection (46.4+/-3.6 and 48.0+/-2.8%, respectively, in HS+celecoxib and HS+NS-398 groups). CONCLUSION: This study provides the first evidence of an implication of COX-2 as a mediator of HS-induced cardioprotection. This suggests that prostaglandins are involved in this type of cardioprotective preconditioning.

Animals↗
PubMed1996

Passive immune cross-protection in mice produced by rabbit antisera against different serotypes of Pasteurella multocida.

Haemorrhagic septicaemia (HS) and fowl cholera (FC) are specific diseases caused by certain serotypes of Pasteurella multocida. Strains that usually cause HS in cattle and water buffalo do not produce FC in avian species, and strains that cause FC do not produce HS in cattle and water buffalo. A variety of P. multocida serotypes, including unusual strains which can cause HS in wild ruminants, were evaluated in passive immune protection studies to determine the immunological relationship between strains associated with HS and FC. Various degrees of cross-protection were seen among the strains. Antiserum against a serotype B:3,4 strain protected against strains capable of causing HS (serotypes B:1, B:2, B:3,4, B:4 and E:2) and FC (serotypes A:1, A:3 and A:5). Antiserum against an FC strain (serotype A:5) similarly protected against strains capable of causing HS and FC. Antigenic analyses indicated that cross-protection was not necessarily induced by serotype-specific capsular (beta) or somatic (gamma) antigens or major porin protein. SDS-PAGE and immunoblots of whole cell lysates of the different HS and FC strains showed many protein-staining bands with similar mobilities and antigenic activity. These cross-reactive antigenic bands occurred in the 20- to 120-kDa range. Adsorption of antiserum with a heterologous serotype removed its reactivity with most of these bands, as well as its ability to cross-protect.

Animals↗
PubMed2003

Biosorption of humic and fulvic acids to live activated sludge biomass.

Biosorption of high molecular weight humic substances (HS) to activated sludge (AS) biomass may be considered as a preliminary step previous to enzymatic hydrolysis breakdown and biological uptake. Two standard HS, Suwannee River humic and fulvic acids, were biosorbed onto live AS biomass collected from full-scale wastewater treatment plants. Biosorption isotherms were corrected for interference from organic matter desorbed from AS biomass. The effect of pH, calcium and ionic strength on biosorption was tested. HS biosorption to live AS biomass obeyed the Freundlich isotherm equation. Biosorption increased with decreasing pH, increasing calcium and ionic strength concentration. Higher biosorption at low pH may be attributed to hydrophobic interactions between HS and AS biomass extracellular polymers (EPS). Hydrophobic and cationic bridging effects between HS and AS EPS were the mechanisms responsible for biosorption under the presence of divalent cations; however, the former was most significant at low pH, whereas the latter was predominant near neutral pH. The effect of ionic strength on HS biosorption followed the colloidal chemistry theory as the electric double layer became compressed when the ionic strength increased, resulting in closer approach of HS and AS biomass. The humic acid fraction of Suwannee River was removed more efficiently than its fulvic acid fraction because the humic acid was more hydrophobic. These results showed that pH, divalent cation concentration and ionic strength play an important role in the fate and removal of influent wastewater HS in full-scale treatment plants.

Absorption↗
PubMed2001

Influence of proteasome and redox state on heat shock-induced activation of stress kinases, AP-1 and HSF.

We studied the pattern of activation of stress kinases and of transcription factors activator protein-1 (AP-1) and heat shock factor (HSF) in FAO cells by combining two treatments, i.e. heating (42 degrees C for 1 h) and proteasome inhibition, each known to cause cellular heat shock response. The co-treatment heat shock (HS) and proteasome inhibitor (a peptidyl aldehyde or lactacystin) showed cumulative effects on the intensity and duration of activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) at the end of the HS period and during recovery. Similarly, the thiol-reducing agents N-(2-mercaptoethyl)-1,3-diaminopropane and dithiothreitol strongly activated both JNK and p38 MAPK in cells undergoing HS. AP-1 DNA binding activity in response to proteasome inhibitors was so strong that it shadowed the stimulatory effect of HS in the combined treatment, but lactacystin, which is the most potent and specific proteasome inhibitor, decreased the binding late during recovery from HS. Thiol-reducing agents prevented AP-1 DNA binding induced by HS. The combined HS/proteasome inhibitors or HS/thiol-reducing agents treatments cooperatively activated HSF DNA binding. Expression of collagenase I and hsp 70 mRNAs reflects the different behavior of AP-1 and HSF transcription factors in cells exposed to HS and proteasome inhibition. The data seem to indicate that JNK and p38 MAPK activations are not necessarily coupled to DNA binding of AP-1, which can be either increased or inhibited when these kinases are activated. AP-1 and HSF show opposite patterns of response to HS in the presence of proteasome inhibitors or reducing agents.

Animals↗
PubMed2004

Interstitial heparan sulfate in granulomatous inflammatory skin diseases.

BACKGROUND: Heparan sulfate (HS) is a glycosaminoglycan that is anchored to the outside of cell membranes. Under ordinary circumstances, it is not present in the interstitium, but under certain circumstances, mainly in the setting of inflammation and tissue repair, HS can be shed from the cell surface into the interstitium in a regulated fashion. Under these circumstances, interstitial HS seems to have an immunomodulatory function because of its binding of many cytokines. However, it is not known which cell types present at an inflammatory site are responsible for this shedding. OBJECTIVE: We have investigated the presence of interstitial HS by immunohistochemistry in various inflammatory skin diseases characterized by different compositions of the inflammatory infiltrate. RESULTS: Strong interstitial HS immunoreactivity was present only in diseases with a predominantly histiocytic infiltrate but not in diseases with a predominantly lymphocytic or neutrophilic infiltrate. CONCLUSIONS: This indicates that histiocytes have a direct or indirect role in the HS shedding process. In the well-formed granulomas of sarcoidosis, interstitial HS immunoreactivity was spatially associated with the fibrotic ring at the periphery of the granulomas, but not with the center harboring the histiocytes. This suggests that histiocytes can stimulate fibroblasts to shed HS into the interstitium.

Cell Communication↗
PubMed2000

Effects of increased oxygen breathing in a volume controlled hemorrhagic shock outcome model in rats.

It is believed that victims of traumatic hemorrhagic shock (HS) benefit from breathing 100% O(2). Supplying bottled O(2) for military and civilian first aid is difficult and expensive. We tested the hypothesis that increased FiO(2) both during severe volume-controlled HS and after resuscitation in rats would: (1) increase blood pressure; (2) mitigate visceral dysoxia and thereby prevent post-shock multiple organ failure; and (3) increase survival time and rate. Thirty rats, under light anesthesia with halothane (0. 5% throughout), with spontaneous breathing of air, underwent blood withdrawal of 3 ml/100 g over 15 min. After HS phase I of 60 min, resuscitation phase II of 180 min with normotensive intravenous fluid resuscitation (shed blood plus lactated Ringer's solution), was followed by an observation phase III to 72 h and necropsy. Rats were randomly divided into three groups of ten rats each: group 1 with FiO(2) 0.21 (air) throughout; group 2 with FiO(2) 0.5; and group 3 with FiO(2) 1.0, from HS 15 min to the end of phase II. Visceral dysoxia was monitored during phases I and II in terms of liver and gut surface PCO(2) increase. The main outcome variables were survival time and rate. PaO(2) values at the end of HS averaged 88 mmHg with FiO(2) 0.21; 217 with FiO(2) 0.5; and 348 with FiO(2) 1. 0 (P<0.001). During HS phase I, FiO(2) 0.5 increased mean arterial pressure (MAP) (NS) and kept arterial lactate lower (P<0.05), compared with FiO(2) 0.21 or 1.0. During phase II, FiO(2) 0.5 and 1. 0 increased MAP compared with FiO(2) 0.21 (P<0.01). Heart rate was transiently slower during phases I and II in oxygen groups 2 and 3, compared with air group 1 (P<0.05). During HS, FiO(2) 0.5 and 1.0 mitigated visceral dysoxia (tissue PCO(2) rise) transiently, compared with FiO(2) 0.21 (P<0.05). Survival time (by life table analysis) was longer after FiO(2) 0.5 than after FiO(2) 0.21 (P<0. 05) or 1.0 (NS), without a significant difference between FiO(2) 0. 21 and 1.0. Survival rate to 72 h was achieved by two of ten rats in FiO(2) 0.21 group 1, by four of ten rats in FiO(2) 0.5 group 2 (NS); and by four of ten rats of FiO(2) 1.0 group 3 (NS). In late deaths macroscopic necroses of the small intestine were less frequent in FiO(2) 0.5 group 2. We conclude that in rats, in the absence of hypoxemia, increasing FiO(2) from 0.21 to 0.5 or 1.0 does not increase the chance to achieve long-term survival. Breathing FiO(2) 0.5, however, might increase survival time in untreated HS, as it can mitigate hypotension, lactacidemia and visceral dysoxia.

Animals↗
PubMed2002

Role of heparan sulfate-2-O-sulfotransferase in the mouse.

Heparan sulfate (HS) is a long unbranched polysaccharide found covalently attached to various proteins at the cell surface and in the extracellular matrix. It plays a central role in embryonic development and cellular function by modulating the activities of an extensive range of growth factors and morphogens. HS 2-O-sulfotransferase (Hs2st) occupies a critical position in the succession of enzymes responsible for the biosynthesis of HS, catalysing the transfer of sulfate to the C2-position of selected hexuronic acid residues within the nascent HS chain. Previous studies have concluded that 2-O-sulfation of HS is essential for it to cooperate in many growth factor/receptor interactions. Surprisingly therefore, embryos lacking functional Hs2st survive until birth, but die perinatally, suffering complete failure to form kidneys. However, this rather late lethality belies a more intricate involvement of 2-O-sulfated HS during development. The purpose of this review is to summarise the requirements for 2-O-sulfated HS during mouse development, at the morphological and molecular level. The implications that altered HS structure may have on growth factor/receptor signalling in vivo will be discussed.

Animals↗