PubMed Health⌕ Search

Biomedical subjects

A Sola

Publications and source records attributed to A Sola.

At least 19 recordsLinked to original sources
PubMed2006

Avoiding hyperoxia in infants < or = 1250 g is associated with improved short- and long-term outcomes.

OBJECTIVE: To determine the rate and severity of short- and long-term morbidity in very low birth weight infants treated before and after the implementation of a change in clinical practice designed to avoid hyperoxia. METHODS: Analysis of a prospectively collected database of all infants < or = 1250 g admitted to two Emory University NICU's from January 2000 to December 2004. A change in practice was instituted in January 2003 with the objective of avoiding hyperoxia in preterm infants with target O2 saturation (SpO2) at 93 to 85% (Period II). Before the change in practice, SpO2 high alarms were set at 100% and low alarms at 92% (Period I). Statistical analysis included bivariate analyses and multivariate logistic regression comparing outcomes between the two periods. RESULTS: From January 2000 to December 2004, 502 infants met enrollment criteria and 202 (40%) were born in period II, after change in SpO2 targets. Birth weight, gestational age and survival were similar between both periods. The rates for any retinopathy of prematurity, supplemental oxygen at 36 weeks post-conceptional age and the use of steroids for chronic lung disease were significantly lower in the infants born in Period II. There was no difference in the rates of necrotizing enterocolitis, intraventricular hemorrhage and periventricular leukomalacia. At 18 months corrected age (CA), the infants treated during Period II had a higher Mental Developmental Index (MDI) scores (80.2 +/- 18.3 vs 89.2 +/- 18.5; P 0.02) and similar Psychomotor Developmental Index (PDI) scores (83.9 +/- 18.6 vs 89.4 +/- 17.2; P 0.08) than those treated during Period I. The proportion of infants with an MDI or a PDI less than 70 was similar between the periods. CONCLUSIONS: The change in practice to avoid hyperoxia is associated with a significant decrease in neonatal morbidity and does not have a detrimental effect on developmental outcomes at 18 months CA.

Child Development↗
PubMed2006

Oral sildenafil citrate lacks genotoxicity and cytotoxicity in a primate model: Callithrix jacchus.

OBJECTIVE: To determine sildenafil citrate (SC) genotoxicity and cytotoxicity in the Callithrix jacchus. STUDY DESIGN: Fifteen organisms were assigned to one of three groups as follows: experimental (25 mg/kg of SC); negative control (glucose solution 5%); and positive control (3 mg/kg of cytocine arabinoside). Systemic hemodynamic changes were monitored in each animal before and after each treatment. A drop of blood was obtained before and after the treatment at 24-120 h. Smears were made and the frequency of micronucleated erythrocytes (MNE), micronucleated polychromatic erythrocytes (MNPCE) and polychromatic erythrocytes (PCE) was counted. RESULTS: No significant differences in MNE, MNPCE and PCE were found in the group that received sildenafil and negative control. A significant increase in genotoxicity and cytotoxicity was observed in the positive control group. No changes were observed in systemic hemodynamic changes. CONCLUSION: The macro-dose of SC lacks genotoxic, cytotoxic or systemic hemodynamic changes effects in this species.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2006

Gender differences in long-term beneficial effects of erythropoietin given after neonatal stroke in postnatal day-7 rats.

Recently, we reported that erythropoietin attenuates neonatal brain injury caused by focal cerebral ischemia. The long-term effects of erythropoietin on focal cerebral ischemia-induced injury to the developing brain and the potential gender differences in these long-term effects have not been studied in detail. The current study demonstrated a similarity in the mean infarct volume in both the vehicle-treated male and female rats at 6 and 12 weeks after focal cerebral ischemia. On the other hand, erythropoietin treatment (1000 U/kg x three doses after focal cerebral ischemia) caused a significant reduction in the mean infarct volume in both males and females at 6 weeks after focal cerebral ischemia when compared with the corresponding vehicle-treated animals (males: 141.4+/-48.2 mm3 vs. 194.0+/-59.2 mm3, P<0.05; females: 85.4+/-31.6 mm3 vs. 183.4+/-46.3 mm3, P<0.05). Interestingly, the reduction in the mean infarct volume in the erythropoietin-treated males was significantly less than that in the erythropoietin-treated females at 6 weeks after focal cerebral ischemia (141.4+/-48.2 mm3 vs. 85.4+/-31.6 mm3, P<0.05). At 12 weeks after focal cerebral ischemia, the mean infarct volume in the erythropoietin-treated males significantly increased to 181.0+/-50.4 mm3 (P<0.05). In contrast, the mean infarct volume in the erythropoietin-treated females remained stable (87.0+/-41.7 mm3). Additionally, erythropoietin treatment significantly improved sensorimotor function recovery with a misstep number similar to the sham-operation group at 6 and 12 weeks after focal cerebral ischemia. Moreover, the mean number of missteps in the erythropoietin-treated females was less than that in males at 6 (13.5+/-2.0 vs. 24.5+/-2.5, P<0.05) and 12 (12.5+/-2.0 vs. 20.0+/-2.0, P<0.05) weeks after focal cerebral ischemia. These results indicate that erythropoietin administration after focal cerebral ischemia produces a significant long-term neuroprotective benefit on the developing brain, and that this effect is more beneficial in the female rats.

Animals↗
PubMed2006

Actin cytoskeleton derangement induces apoptosis in renal ischemia/reperfusion.

UNLABELLED: This study evaluated whether cytoskeletal alterations during the ischemic conditions associated with kidney preservation could determine apoptosis. Cytoskeletal alterations are among the main effects of ischemia and may induce apoptosis. Rat kidneys were preserved in University of Wisconsin (UW) solution for 24 h. Some groups of animals underwent 45 min of warm ischemia (WI) to evaluate its effect on both the actin cytoskeleton and apoptosis (assessed by caspase-3 activity and TUNEL staining). Swinholide A (SwinA) and Latrunculin B (LB), two actin cytoskeleton-targeted agents, were administered to assess the effect of direct actin disruption on apoptosis. Jasplakinolide (JP), a compound that stabilizes actin filaments, was administered to evaluate the effect of actin stabilization. Apoptosis was evaluated at 3 h of ex vivo reperfusion using the isolated perfused rat kidney (IPK) model. RESULTS: Apoptosis increased during reperfusion with WI or administration of actin disruptor agents. Administration of stabilizing agents reversed apoptosis in kidneys that had previously undergone WI or had received an actin disruptor agent. CONCLUSION: The disruption of the actin cytoskeleton during ischemic conditions associated with kidney preservation induces apoptosis upon reperfusion through caspase-3 activation.

Actin Cytoskeleton↗
PubMed2006

Postprandial glycaemia: a plea for the frequent use of delta postprandial glycaemia in the treatment of diabetic patients.

Postprandial hyperglycaemia is a phenomenon often neglected by patients as well as doctors. While patients only voluntarily measure morning and preprandial capillary glycaemia, physicians do not encourage the measurement of anything further. The specific role of postprandial hyperglycaemia in the determination of late diabetes complications, such as micro- and macroangiopathy, remains controversial. It is however undeniable that the postprandial glycaemic excursion plays an important role in total hyperglycaemia reflected by an increase in glycated haemoglobin. The postprandial glycaemia measurement or, more appropriately, the postprandial glycaemic excursion (the difference between postprandial and preprandial glycaemia, also called the postprandial delta glycaemia), is important to measure and there are specific tools to correct it when abnormal. Postprandial delta glycaemia should lie between 30 and 50 mg/dl. It is thus suggested to measure it not necessarily on a daily basis, but when it is expected that the glycaemic couple, or "pre-postprandial couple", is high. The specific tools for treatment of postprandial hyperglycaemia can be dietetic (carbohydrate quantity reduction or ingestion of fiber-rich and/or low glycaemic index foods) or medicinal. Among the specific medicinal treatments are the alpha-glucosidase-inhibitors (which can be used for both type 1 and type 2 diabetic patients), glinides and fast-acting insulins. Rather than first treating fasting and interprandial hyperglycaemia, as has been commonly done by physicians, the authors recommend the simultaneous treatment of pre-, inter- and postprandial hyperglycaemia. The optimal time at which to evaluate postprandial glycaemia is approximately 1 h and 15 minutes for type 1 and type 2 diabetic patients.

Blood Glucose↗
PubMed2006

Mitochondrial NOS upregulation during renal I/R causes apoptosis in a peroxynitrite-dependent manner.

In the last decade, various groups have found evidence of nitric oxide production by mitochondrial nitric oxide synthase (mNOS) in a range of experimental models. However, little is known about the role of mNOS in renal ischemia-reperfusion (I/R) injury and its possible involvement in the apoptotic pathway. We analyzed the role of mNOS in apoptosis promotion in rat kidney I/R and its direct implication through experiments in which isolated kidney mitochondria were subjected to hypoxia/reoxygenation. Results showed that neuronal NOS located in the inner mitochondrial membrane is upregulated during renal I/R and that this upregulation, together with the increase in nitric oxide production, is involved in the generation of intramitochondrial peroxynitrite, which in turn leads to cytochrome c release and apoptosis induction in renal I/R.

Animals↗
PubMed2005

Blood glucose changes and adjustments of diet and insulin doses in type 1 diabetic patients during scuba diving (for a change in French regulations).

OBJECTIVE: In France, diabetic subjects were not allowed to dive. The principal risk is hypoglycemia during immersion. However scuba diving is allowed in many countries. To follow blood glucose changes, food intake and insulin adjustments in type 1 diabetic patients when diving, and to propose specific guidelines for such patients willing to practice recreational scuba diving. METHODS: Fifteen well-controlled (mean HbA1c: 7.2%) type 1 diabetic patients without complications were volunteer to dive under strict medical monitoring. They dove 8 times in 4 days in autumn at a depth of 20 meters, in 12 degrees C to 16 degrees C water. A strict protocol based on blood glucose was implemented to prevent hypoglycaemia. RESULTS: No case of hypoglycemia was observed and no faintness was reported underwater. Mean blood glucose before diving was 200 mg/dl (11 mmol/l). There was a mean fall in blood glucose of 40 mg/dl (2.2 mmol/l) during dives, a mean decrease in daily insulin doses by 19.3% on the last day. Daily energy intake was 3,225 Kcal in average. A continuous glucose monitoring (CGMS) was performed in one patient and showed a rather stable glycemia during immersion but a decrease within the 8 hours after. CONCLUSION: When respecting a strict protocol to prevent hypoglycaemia, the risk of hypoglycaemia appears quite low. We recommend an ideal glycemic goal of 200-250 mg/dl (11-13.75 mmol/l) before immersion, a higher reduction of insulin doses (-30%) and taking carbohydrates on board in any case. The present data have recently led the French diving federation (FESSM) to allow type 1 diabetic patients to dive with some restrictive qualification requirements: dives within the "safety curve" (no decompression curve), in above 14 degrees C water, depth limited to the median space range (6 to 20 meters), plus mandatory guidance by a diving instructor.

Blood Glucose↗
PubMed2004

Intestinal ischemic preconditioning: less xanthine accumulation relates with less apoptosis.

Ischemic preconditioning has shown to reduce apoptosis in the intestinal mucosa during ischemia/reperfusion. This study evaluated if the decrease of apoptotic events found during preconditioning could be related with a reduction of the substrate (i.e., xanthine/hypoxanthine) available for xanthine oxidase (XO). Animals were randomly assigned to the following study groups: C, control; I/R, ischemia/reperfusion; P+I/R, ischemic preconditioning; P+I/R+H/X, ischemic preconditioning plus hypoxanthine/xanthine, and P+I/R+H/X+Allo, ischemic preconditioning plus hypoxanthine/xanthine plus allopurinol. Caspase-3 activity, DNA fragmentation and TUNEL staining increased in the I/R group compared to control. Ischemic preconditioning (P+I/R group) was able to reverse these apoptotic variables to a level similar to that of control rats. The addition of hypoxanthine/xanthine to rats subjected to ischemic preconditioning (P+I/R+H/X group) showed the highest apoptotic activity; however, further addition of allopurinol (P+I/R+H/X+Allo group) decreased significantly apoptotic activity and events. In conclusion, intestinal ischemic preconditioning is able to reduce apoptosis during the following sustained ischemia/reperfusion event because of a reduced accumulation of xanthine/hypoxanthine nucleotide.

Allopurinol↗
PubMed2003

Minimally invasive silicon probe for electrical impedance measurements in small animals.

It is commonly accepted that electrical impedance provides relevant information about the physiological condition of living tissues. Currently, impedance measurements are performed with relatively large electrodes not suitable for studies in small animals due to their poor spatial resolution and to the damage that they cause to the tissue. A minimally invasive needle shaped probe for electrical impedance measurements of living tissues is presented in this paper. This micro-probe consists of four square platinum electrodes (300 microm x 300 microm) on a silicon substrate (9 mm x 0.6 mm x 0.5 mm) and has been fabricated by using standard Si microelectronic techniques. The electrodes are not equally spaced in order to optimise the signal strength and the spatial resolution. Characterisation data obtained indicate that these probes provide high spatial resolution (measurement radius <4 mm) with a useful wide frequency band going from 100 Hz to 100 kHz. A series of in vivo experiments in rat kidneys subjected to ischemia was performed to demonstrate the feasibility of the probes and the measurement system. The impedance modulus and phase were measured at 1 kHz since this frequency is sufficiently low to permit the study of the extracellular medium. The extracellular pH and K+ were also simultaneously measured by using commercial miniaturised Ion Selective Electrodes. The induced ischemia period (45 min) resulted in significant changes of all measured parameters (Delta/Z/ approximately 65%; DeltapH approximately 0.8; DeltaK+ approximately 30 mM).

Animals↗
PubMed2003

Exogenous adenosine enhances caspase-3 activity in warm renal ischaemia.

Renal injury due to ischaemia/reperfusion (I/R) leads to impaired renal function. One of the essential pathological changes thereby is cell death due to apoptosis. This study investigated the effect of adenosine administration on caspase-3 (C3) activity and expression during warm renal ischaemia in rat kidney and the role of nitric oxide (NO) as a mediator of the adenosine-induced effect. The following experimental groups were studied: control, ischaemia, ischaemia with adenosine administration, ischaemia with adenosine and N-nitro- l-arginine methyl ester (L-NAME) treatment and ischaemia with NO donor administration. C3 activity was measured and its protein expression determined by Western blot analysis. Supplementation of adenosine or NO during ischaemia increased C3 activity and protein expression but the effect of adenosine was reversed in rats treated with L-NAME. We conclude that adenosine increases C3 activity through an NO-dependent mechanism.

Adenosine↗
PubMed2003

Knee arthrodesis with the Wichita fusion nail.

We reviewed 32 patients who all had knee arthrodesis performed after failed knee replacement. The minimum clinical follow-up was 1 year. The arthrodesis was performed by means of the Wichita fusion nail in 11, by external fixation in 15 cases, by plating in three and by intramedullary nailing in three. The mean patient age was 68.6 years. When the Wichita nail was used, fusion was achieved in ten out of 11 cases after a mean period of 4.5 (3-7) months. Of the remaining 21 patients, fusion was only achieved in 11 cases after a mean period of 6.5 (4.5-10) months.

Aged↗
PubMed2003

Multiparametric monitoring of ischemia-reperfusion in rat kidney: effect of ischemic preconditioning.

BACKGROUND: Microelectrode technology is a promising tool for monitoring kidney ischemia and the changes induced by its therapeutic management. Ischemic preconditioning, that is, brief ischemic periods before sustained ischemia, has been shown to protect several organs, including the kidney, from ischemia-reperfusion injury. We tested whether the effect of preconditioning could be appraised by real-time measurement of parameters representative of tissue hypoxia. METHODS: In a sample of pentobarbital-anesthetized and mechanically ventilated rats, we studied the effect of renal ischemic preconditioning (10-min ischemia and 10-min reflow interval) on subsequent ischemia-reperfusion (45 min and 60 min). Renal tissue electrical impedance, extracellular pH, and potassium concentration [K+] were measured continuously by implanted microelectrodes. RESULTS: Ischemia induced an early, rapid rise in extracellular potassium and impedance module, followed by a phase of slower increase, whereas pH decreased rapidly, reaching a plateau. Preconditioning treatment did not cause significant changes in interstitial pH and [K+] but increased ischemic tissue impedance. During reperfusion, the three variables recovered progressively; however, after a decline, electrical impedance showed a clear postischemic increase. This rise was suppressed by preconditioning. CONCLUSIONS: Real-time measurement of any of the three parameters showed capability for early detection of ischemia. In contrast with findings in myocardial tissue, preconditioning in the kidney did not increase potassium cell loss during ischemia or improve ischemic acidosis or tissue impedance. Electrical impedance increased for a second time during reperfusion, indicating the presence of a postischemic cellular edema; concealing this episode was the most noticeable effect of the preconditioning treatment.

Acidosis↗
PubMed2003

Role of nitric oxide in apoptosis and cell necrosis for intestinal transplantation.

INTRODUCTION: Nitric oxide (NO) is an important mediator of both physiological and pathological responses. Its dual role in the ischemia-reperfusion syndrome is still a matter of controversy. The aim of this study was to analyze the effect of NO on apoptosis and cell necrosis associated with heterotopic small bowel transplant. METHODS: Sprague-Dawley rats underwent heterotopic small bowel transplants with 3 hours of cold ischemia and 5 hours of reperfusion. Animals were assigned to the following study groups: Sham; bowel transplant (Trp); bowel transplant + NO donor (Trp + NONOS); bowel transplant + NO synthesis inhibitor (Trp + L-NAME). We studied histological changes and bacterial translocation in mesenteric nodes, liver and spleen as parameters of cell necrosis and caspase-3 activity as a parameter of apoptosis. RESULTS: Histological changes and bacterial translocation showed that exogenous administration of NO protected the transplant. Simple bowel transplant, with or without inhibition of NO synthesis, did not display this protective effect. Significantly greater levels of apoptosis were observe in grafts among the group administered NO at pharmacological doses. CONCLUSIONS: In experimental bowel transplantation rats administered exogenous NO show less necrosis but at the same time stimulation of apoptosis.

Animals↗