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Biomedical subjects

T Ikenoue

Publications and source records attributed to T Ikenoue.

At least 37 records · Page 2Linked to original sources
PubMed2000

Assessment of gastric carcinoma risk associated with Helicobacter pylori may vary depending on the antigen used: CagA specific enzyme-linked immunoadsorbent assay (ELISA) versus commercially available H. pylori ELISAs.

BACKGROUND: Previous epidemiologic studies produced inconsistent results when examining the relation between Helicobacter pylori infection and the risk of gastric carcinoma by measuring various anti-H. pylori antibodies. This study investigated the increased risk of cancer by examining different antibodies, including the specific anti-CagA antibody and antibodies from two commercially available kits. METHODS: An ELISA for the detection of serum anti-CagA was established using a recombinant CagA protein that the authors previously reported. Serum anti-CagA titer was determined for 80 patients with gastric carcinoma and 80 gender- and age-matched controls. Two anti-H. pylori antibodies from the commercially available kits HEL-p (Amrad, Kew Vic, Australia) and HM-CAP (Enteric Product Inc., Westbury, NY) were also evaluated. RESULTS: Anti-CagA seropositivity differed significantly between gastric carcinoma patients and controls (92.5% vs. 55.0%; P = 0. 0001), showing an odds ratio of 10.4 (95% confidence interval [CI]: 4.23-29.74). The difference was less prominent for the seropositivity of HEL-p (77.5% vs. 58.8%; P = 0.0139; odds ratio: 2. 38; 95% CI: 1.20-4.82) and insignificant for that of HM-CAP (65.0% vs. 57.5%; P = 0.4325; odds ratio: 1.30; 95% CI: 0.68-2.49). CONCLUSIONS: The current study revealed that the antibody assay system used could be one important factor in the assessment of gastric carcinoma risk for patients with H. pylori.

Adult↗
PubMed2000

Differential neurotrophin levels in cerebrospinal fluid and their changes during development in newborn rat.

Cerebrospinal fluid concentration of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) was measured in normal developing rat from birth to postnatal day (PND) 21 by enzyme-linked immunosorbent assay. NGF levels were significantly higher than those of BDNF and NT-3 from PND 1-21. NGF levels decreased from PND 1-3 to PND 9. At PND 15 and 17, NGF levels peaked a second time and rapidly decreased to PND 21. BDNF peaked at PND 13-15, while NT-3 levels peaked at PND 7-9. Each of the three neurotrophins has its own characteristic pattern in changes in cerebrospinal fluid levels.

Aging↗
PubMed2000

Homodimer of two F-box proteins betaTrCP1 or betaTrCP2 binds to IkappaBalpha for signal-dependent ubiquitination.

We found previously that overexpression of an F-box protein betaTrCP1 and the structurally related betaTrCP2 augments ubiquitination of phosphorylated IkappaBalpha (pIkappaBalpha) induced by tumor necrosis factor-alpha (TNF-alpha), but the relationship of the two homologous betaTrCP proteins remains unknown. Herein we reveal that deletion mutants of betaTrCP1 and betaTrCP2 lacking the F-box domain suppressed ubiquitination and destruction of pIkappaBalpha as well as transcriptional activation of NF-kappaB. The ectopically expressed betaTrCP1 and betaTrCP2 formed both homodimer and heterodimer complexes without displaying the trimer complex. Dimerization of betaTrCP1 and/or betaTrCP2 takes place at their conserved NH(2)-terminal regions, termed a "D-domain" (for dimerization domain), located upstream of the F-box domain. The D-domain was necessary and sufficient for the dimer formation. Intriguingly, the betaTrCP homodimer, but not the heterodimer, was selectively recruited to pIkappaBalpha induced by TNF-alpha. These results indicate that not only betaTrCP1 but also betaTrCP2 participates in the ubiquitination-dependent destruction of IkappaBalpha by forming SCF(betaTrCP1-betaTrCP1) and SCF(betaTrCP2-betaTrCP2) ubiquitin-ligase complexes.

Base Sequence↗
PubMed2000

Glial cell line-derived neurotrophic factor protects against ischemia/hypoxia-induced brain injury in neonatal rat.

Ischemic/hypoxic brain damage induced in 7-day-old rats was significantly attenuated in a dose-dependent manner by intracerebral injection of glial cell line-derived neurotrophic factor (GDNF; 2 or 4 microg) within 30 min after the insult. Whereas the great majority of the vehicle-treated animals showed massive infarction involving more than 75% of the affected cerebral hemisphere, GDNF injection resulted in a remarkable reduction in both the incidence and severity of the brain damage (incidence ranging from 76% to 93% in controls to 34% to 64% in the 2.0-microg group and 7% to 29% in 4.0-microg group). The induction of immunoreactive 70-kDa heat shock protein (HSP70) in cerebral cortical neurons was also significantly reduced in GDNF-treated animals as compared to controls. The mechanisms responsible for the neuroprotective effects of GDNF remain unknown, although it has been speculated that these may be endogeneous. The higher expression of GDNF and its mRNA in developing brains may be one of the factors responsible for the relative resistance to ischemia of fetal and neonatal as opposed to adult brains. GDNF may possibly act by protecting against oxidative stress or by scavenging free radicals generated during ischemia. The results of our study strongly suggest that GDNF may prove to be an effective and potent protective agent against perinatal ischemic/hypoxic encephalopathy.

Animals↗
PubMed2000

Primary vaginal adenocarcinoma arising from the metanephric duct remnant.

Primary vaginal adenocarcinoma unrelated to in utero exposure to diethylstilbestrol (DES) is very uncommon. We report a case of 65-year-old Japanese woman who presented with primary adenocarcinoma in the anterior wall of the vagina, where the left ureter-like metanephric duct remnant abnormally terminated. Histological examination in serial sections revealed the direct connection between the carcinoma and the metanephric duct remnant. Moreover, the remnant epithelium showed varying degrees of dysplastic changes, including carcinoma in situ in close proximity to the carcinoma. This patient also had a bicornate uterus and left renal aplasia. To our knowledge, this is the first reported case of a primary vaginal adenocarcinoma arising from the metanephric duct remnant. Although the precise mechanism involved in carcinogenesis in this clinicopathological setting remains unknown, adenocarcinoma should be included in the differential diagnosis of vaginal tumors in patients with renal aplasia and/or an ectopic termination of the ureter or metanephric duct remnant, especially when the tumor is in the anterior wall.

Adenocarcinoma↗
PubMed2000

Important role of 72-kd heat shock protein expression in the endothelial cell in acquisition of hypoxic-ischemic tolerance in the immature rat.

OBJECTIVES: Hypoxic-ischemic tolerance can be induced in neonatal rats through hyperthermic preconditioning. The purposes of this study were to determine the interval between hyperthermic preconditioning and a subsequent hypoxic-ischemic insult that would provide optimal neuroprotection against the insult and to examine the relationship between tolerance induction and heat shock protein expression. STUDY DESIGN: On postnatal day 7 Wistar rat pups were separated into the following 2 groups: a heated group (those exposed to 15 minutes of hyperthermic pretreatment at a brain temperature of 41.5 degrees C-42.0 degrees C) and an unheated control group. At 6, 12, 24, 48, and 72 hours after the hyperthermic stress, rats from both groups were exposed to left carotid artery ligation followed by 2 hours of hypoxia (8% oxygen and 92% nitrogen) at 33 degrees C. Twenty animals from each group were used at each time point. All rats were killed at 1 week after hypoxia-ischemia, at which time the brains were processed and neuronal damage in the cortex and hippocampus was assessed histologically. Another set of 7-day-old rats (n = 30) was studied immunohistochemically at 6, 12, 24, 48, and 72 hours after the same hyperthermic treatment. Expression of 72-kd heat shock protein was measured in neuronal, glial, and vascular endothelial cells. RESULTS: Hyperthermia-induced hypoxic-ischemic tolerance was observed at 6, 12, and 24 hours but not at 48 and 72 hours after hyperthermic preconditioning. Heat shock protein 72 expression in the vascular endothelial cells, rather than in the glial or neuronal cells, was most strongly associated with hypoxic-ischemic tolerance. CONCLUSION: These findings suggest that heat shock protein 72 in endothelial cells plays an important role in the acquisition of hypoxic-ischemic tolerance at postnatal day 7, a time when maximal angiogenesis occurs and the blood-brain barrier is still immature.

Animals↗
PubMed2000

Pena-shokeir type I syndrome with thymic and systemic lymphoid hyperplasia: report of an autopsy case.

We report a case of Pena-Shokeir type I syndrome in a female neonate who died of respiratory failure shortly after the birth at 32 weeks of gestation. In general appearance, she had apparent ocural hypertelorism, a depressed tip of the nose, low-set malformed ears, and microglossia in the head. There were severe contractures at the ankle, hand, fingers, and toes, and moderate contractures at the hip, shoulder, knee, and elbow. An autopsy analysis showed severe pulmonary hypoplasia and group atrophy of the skeletal muscle tissues. In addition to these findings which are well known characteristics of the infant with this syndrome, the thymus was markedly hyperplastic and lymph nodes were systemically swollen, especially the mesenteric ones which were visible and measured 2-5 mm in diameter. Histologically, the lymph nodes showed massive paracortical hyperplasia without apparent follicular structures, although no atypical lymphocytes were observed in both the thymus and lymph nodes. Immunohistochemically, proliferating lymphocytes seemed to be immature CD4+/CD8+ T cells, suggesting the insufficiency of T-cell negative selection in the thymus. This report is the first case of Pena-Shokeir type I syndrome with T-lymphocytic disorder.

Abnormalities, Multiple↗
PubMed2000

Antepartum evaluation of monochorionic diamniotic (MD) twins; MD-twin score: a new scoring method for perinatal outcome.

OBJECTIVE: Our purpose was to establish a new scoring method to survey monochorionic diamniotic (MD) twins during antepartum periods. STUDY DESIGN: A retrospective study was performed regarding MD twins delivered between January 1992 and July 1996. Maternal and neonatal records were assessed for the following 5 perinatal variables; birth-weight discordance, amniotic-fluid discordance, hydrops fetalis, umbilical-cord insertion, and fetal-heart-rate monitoring. Each variable was coded as normal or abnormal and then assigned an arbitrary weight of 0 if normal and 1 if abnormal, yielding a range of scores from 0 (all normal) to 5 (all abnormal). The relationships between individual variables and their combinations and the outcome of pregnancy was determined. A poor pregnancy outcome consisted of intrauterine death, neonatal death, or neurological sequelae of at least one twin. The 5-variable combination was termed as the MD-twin score. A chi-square test and logistic regression analysis were used to determine statistical significance. RESULTS: There were 59 MD pregnancies, of which 13 pregnancies resulted in a poor outcome. The single variable that most likely contributed to a poor outcome was amniotic-fluid discordance. All 35 pregnancies with an MD-twin score of < or = 2 had a good outcome. There were 14 pregnancies with a score of 3, and 21% of them had a poor outcome. All of the pregnancies with a score of > or = 4 had a poor outcome. When we chose the MD-twin score of 3 as the critical point for a poor outcome, the likelihood ratio statistics became the highest of any single variable or any combination of variables. CONCLUSION: The MD-twin score predicted poor outcomes better than did any single variable or combination of variables.

Amniotic Fluid↗
PubMed2000

[Pharmacological properties of nateglinide, rapid-onset/short-duration insulinotropic agent, in the treatment of type 2 diabetes].

An early defect in Type 2 diabetes is the loss of acute insulin release after food intake, which causes prolonged elevation of postprandial glucose levels. Suppressing postprandial hyperglycemia is considered to be very important for preventing diabetic complications. Sulfonylureas are well-known insulin secretagogues and have been widely used in the treatment of Type 2 diabetes. These agents, however, do not appear to be able to ameliorate impairment of the first phase of insulin secretion and postprandial hyperglycemia. Nateglinide, which is a derivative of D-phenylalanine, is a non-sulfonylurea insulin secretagogue. Although the in vitro insulin-releasing effect of nateglinide is similar to that of sulfonylureas, its hypoglycemic effect is more rapid and short lasting. The in vivo unique pharmacodynamic profile of nateglinide is likely to result from its rapid absorption and elimination. This novel antidiabetic agent has made it possible to compensate for the impaired first phase insulin response and thus suppresses postprandial hyperglycemia. In clinical trials, nateglinide reduced prandial glucose excursion and improved early phase of insulin release dose-dependently after 12 weeks treatment. Nateglinide is a highly physiologic mealtime glucose regulator, which rapidly increases insulin secretion when taken before meals, mimicking early-phase insulin release lost in patients with Type 2 diabetes.

Animals↗
PubMed2000

Fetal cardiovascular function during prolonged magnesium sulfate tocolysis.

The purpose of this study was to evaluate the fetal cardiovascular function during prolonged magnesium sulfate tocolysis. We performed a fetal ultrasonographic examination in 15 patients (Mg group) during magnesium sulfate tocolysis for the treatment of preterm labor. The maternal serum magnesium concentration was 5.7 +/- 0.5 mg/dl at the time of the examination. Sixteen fetuses in normal pregnancies at similar gestational ages were used as the control group. The fetal heart rate and the middle cerebral artery pulsatility index in the Mg group were lower than in the control group (p < 0.01). Fractional shortening (FS) of the right ventricle in the Mg group was lower (p < 0.01), while FS of the left ventricle was higher (p < 0.01) than in the controls. The calculated blood flow through the tricuspid orifice in the Mg group was lower than in the control group (p < 0.01). In contrast, the blood flow through the mitral orifice in the Mg group was higher than in the control group (p < 0.01). In conclusion, in spite of the fact that the right ventricular function is depressed, the fetus maintains its cardiac output during prolonged hypermagnesemia by increasing its left ventricular function. These results indicate the different fetal intracardiac and peripheral circulation, especially in the brain, from normal fetuses.

Adult↗
PubMed2000

Effects of shear stress on articular chondrocyte metabolism.

The articular cartilage of diarthrodial joints experiences a variety of stresses, strains and pressures that result from normal activities of daily living. In normal cartilage, the extracellular matrix exists as a highly organized composite of specialized macromolecules that distributes loads at the bony ends. The chondrocyte response to mechanical loading is recognized as an integral component in the maintenance of articular cartilage matrix homeostasis. With inappropriate mechanical loading of the joint, as occurs with traumatic injury, ligament instability, bony malalignment or excessive weight bearing, the cartilage exhibits manifestations characteristic of osteoarthritis. Breakdown of cartilage in osteoarthritis involves degradation of the extracellular matrix macromolecules and decreased expression of chondrocyte proteins necessary for normal joint function. Osteoarthritic cartilage often exhibits increased amounts of type I collagen and synthesis of proteoglycans characteristic of immature cartilage. The shift in cartilage phenotype in response to altered load yields a matrix that fails to support normal joint function. Mathematical modeling and experimental studies in animal models confirm an association between altered loading of diarthrotic joints and arthritic changes. Both types of studies implicate shear forces as a critical component in the destructive profile. The severity of cartilage destruction in response to altered loads appears linked to expression of biological factors influencing matrix integrity and cellular metabolism. Determining how shear stress alters chondrocyte metabolism is fundamental to understanding how to limit matrix destruction and stimulate cartilage repair and regeneration. At present, the precise biochemical and molecular mechanisms by which shear forces alter chondrocyte metabolism from a normal to a degenerative phenotype remain unclear. The results presented here address the hypothesis that articular chondrocyte metabolism is modulated by direct effects of shear forces that act on the cell through mechanotransduction processes. The purpose of this work is to develop critical knowledge regarding the basic mechanisms by which mechanical loading modulates cartilage metabolism in health and disease. This presentation will describe the effects of using fluid induced shear stress as a model system for stimulation of articular chondrocytes in vitro. The fluid induced shear stress was applied using a cone viscometer system to stimulate all the cells uniformly under conditions of minimal turbulence. The experiments were carried using high-density primary monolayer cultures of normal and osteoarthritic human and normal bovine articular chondrocytes. The analysis of the cellular response included quantification of cytokine release, matrix metalloproteinase expression and activation of intracellular signaling pathways. The data presented here show that articular chondrocytes exhibit a dose- and time-dependent response to shear stress that results in the release of soluble mediators and extracellular matrix macromolecules. The data suggest that the chondrocyte response to mechanical stimulation contributes to the maintenance of articular cartilage homeostasis in vivo.

Adult↗
PubMed2000

Antithrombin therapy for severe preeclampsia: results of a double-blind, randomized, placebo-controlled trial. BI51.017 Study Group.

A double-blind, randomized, placebo-controlled trial was conducted to evaluate whether treatment with Antithrombin (AT) concentrates improved the clinical and perinatal outcome in patients with severe preeclampsia. Severe preeclamptic patients (24 to 35 weeks of gestation. Gestosis Index (GI) > or = 6 points) were randomized into two groups: 66 received AT and 67 received placebo. There were no statistical differences in the clinical profiles of the two groups. Study drugs were given intravenously once daily for 7 consecutive days. Maternal symptoms were evaluated from the difference of GI between before and after treatment, and fetal findings were evaluated from the changes of the biophysical profile score and the estimated fetal weight gain. Improvement was significantly greater in the AT group for both the GI (p = 0.020) and the estimated fetal weight gain (p = 0.029). The improvement of coagulation parameters was also evaluated. The D-dimer levels increased significantly in the placebo group (p = 0.026), but did not change in the AT group. Gestation was significantly prolonged (p = 0.007), and the number of low-birth weight infants was significantly smaller (p = 0.011) in the AT group. No adverse events related to AT were observed. It is revealed that AT concentrate therapy for preeclampsia is effective and safe, leading to an improved perinatal outcome.

Acute Disease↗
PubMed1999

Inhibitory effects of activin-A on osteoblast differentiation during cultures of fetal rat calvarial cells.

Activin-A is a member of the transforming growth factor-beta (TGF-beta) superfamily and is expressed by osteoblasts. However, the role of activin-A on osteoblasts is not clearly understood. We examined the effects of activin-A on osteoblast proliferation or differentiation, and mineralization by the osteoblasts in the first subcultures of fetal rat osteoblasts obtained from calvarial bones. Exogenous activin-A led to impaired formation of bone nodules in a dose-dependent manner, although it did not influence cell proliferation using an MTT assay. This inhibitory effect depended upon the time at which activin-A was added to the culture media, and the effect was most significant when addition took place at the early phase of the culture. In addition, exogenous activin-A inhibited gene expression of type I procollagen, alkaline phosphatase, osteonectin, and osteopontin in the cultured cells using Northern blot analysis. The peak of osteocalcin mRNA was delayed. Gene expression for TGF-beta was not influenced by exogenous activin-A. The betaA subunit (activin-A) mRNA was detected during the early phase of this culture. These results indicate that activin-A inhibited early differentiation of the fetal rat calvarial cells, or osteoblasts.

Activins↗
PubMed1999

Hyperthermic preconditioning prevents blood-brain barrier disruption produced by hypoxia-ischemia in newborn rat.

Effect of hyperthermic preconditioning on disruption of blood-brain barrier induced by hypoxic-ischemic insult was examined. Seven-day-old Wistar rats were separated into (1) pre-heated (15 min of hyperthermia at 41.5-42.0 degrees C) or (2) non-heated group (33 degrees C). Twenty-four hours after conditioning, all rats were subjected to 2 h hypoxia-ischemia (8% oxygen/92% nitrogen, at 33 degrees C), then 24 h later all brains were examined for immunohistological staining of endogenous macromolecule, IgG extravasation and staining of microtubule-associated protein 2 (MAP2) with MAP2 loss being an early marker of neuronal damage. Significant reduction in the area of IgG staining and loss of MAP2 staining was observed in the pre-heated group as compared to that in non-heated group. There was a close relationship between IgG staining and MAP2 staining loss, with the former area always found in the latter, suggesting that extravasation associates neuronal injury. Serum cortisol concentration in pre-heated group was significantly higher than that in non-heated group 24 h after hyperthermic treatment (14.8+/-0.6 vs. 12.5+/-0.3 ng/ml, p<0.01). These data indicate that hyperthermic preconditioning prevents disruption of blood-brain barrier, resulting in amelioration of hypoxic-ischemic neuronal damage in newborn rat.

Animals↗
PubMed1999

IkappaBalpha ubiquitination is catalyzed by an SCF-like complex containing Skp1, cullin-1, and two F-box/WD40-repeat proteins, betaTrCP1 and betaTrCP2.

Destruction of the transcriptional inhibitor IkappaB by the ubiquitin (Ub) system is required for signal-dependent activation of the multifunctional transcriptional factor NF-kappaB, but details of this ubiquitination are largely unknown. We report here that the IkappaBalpha-ubiquitin ligase (IkappaBalpha-E3) is an SCF-like complex containing Skp1, cullin-1, and two homologous F-box/WD40-repeat proteins, betaTrCP1 and betaTrCP2. Intriguingly, all these components are cooperatively recruited to bind to a phosphorylated IkappaBalpha (pIkappaBalpha) produced by tumor necrosis factor-alpha (TNF-alpha) stimulation. IkappaBalpha-E3 bound to pIkappaBalpha catalyzed in vitro ubiquitination of pIkappaBalpha in the presence of ATP, Ub, and E1-activating and E2-conjugating enzymes. Forced expression of betaTrCP1 and betaTrCP2 resulted in dramatic augmentation of the in vitro polyubiquitination activity of IkappaBalpha-E3. These results indicate that the long-sought IkappaBalpha-E3 is an SCF-like complex consisting of multiple proteins which are coordinately assembled during phosphorylation of IkappaBalpha in response to external signals.

Amino Acid Sequence↗
PubMed1999

Heat shock protein 70 and heat shock cognate protein 70 messenger ribonucleic acid induction in the brains, hearts, and livers of neonatal rats after hypoxic stress.

OBJECTIVE: The aim of this study was to examine the production of 2 types of heat shock protein 70 in the organs of neonatal rats during an episode of mild hypoxic stress that was insufficient to produce histologic changes. STUDY DESIGN: Seven-day-old rats were subjected to hypoxia (inspired gas of 8% oxygen and 92% nitrogen) at 33 C for 2 hours (n = 5), 3 hours (n = 5), and 4 hours (n = 5). Control rats (n = 5) inspired room air for 4 hours. The brains, hearts, and livers were removed after 4 hours of recovery. The levels of heat shock protein 70 and heat shock cognate protein 70 messenger ribonucleic acid were measured by Northern blot analysis. Arterial pH, Pao 2, PACO 2, and brain temperature were measured before, during, and at 4 hours of hypoxia in another 16 animals. Histologic examinations were carried out in these 16 animals 7 days after hypoxic stress. RESULTS: PaO 2, PACO 2, and brain temperature decreased during the hypoxic stress and returned to prehypoxic values at recovery time. Arterial pH did not change. No histologic changes were observed in any areas of the brain. Heat shock cognate protein 70 messenger ribonucleic acid was normally expressed in the brain, heart, and liver and was further induced after hypoxia in the brain and the heart. There was, however, no additional increase of heat shock cognate protein 70 messenger ribonucleic acid in the liver. there were no increments of the stress-induced form of heat shock protein 70 messenger ribonucleic acid in these organs. CONCLUSION: Mild hypoxia selectively induced messenger ribonucleic acid of heat shock cognate protein 70, which may play an important role in protecting the brain and the heart against stress.

Animals↗
PubMed1999

Pretreatment with magnesium sulfate protects against hypoxic-ischemic brain injury but postasphyxial treatment worsens brain damage in seven-day-old rats.

OBJECTIVE: Our purpose was to study the neuroprotective effect of magnesium sulfate on hypoxicischemic brain damage and how the timing of magnesium administration changes its effect in the newborn rat. STUDY DESIGN: Seven-day-old rats (n = 91) were exposed to unilateral carotid artery ligation followed by 2 hours of hypoxia (8% oxygen in 92% nitrogen). Magnesium sulfate (270 mg/kg) was intraperitoneally administered 30 minutes before (pretreatment) or 30 minutes after (posttreatment) the 2 hours of hypoxia. In each experiment equivalent amounts of saline solution were administered as controls. Seven days after the injury the rats were killed and the brains were removed for histologic study with hematoxylin and eosin staining. The severity of brain atrophy and neuronal damage was evaluated in the cerebral cortex and hippocampus and compared by chi2 test between the magnesium group and the controls. RESULTS: Ionized magnesium concentrations were significantly increased from 0.52 +/- 0.02 mmol/L to 1.38 +/- 0.07 mmol/L at 0.5 hour after injection and thereafter gradually decreased to 0.73 +/- 0.07 mmol/L at 3.5 hours. Magnesium significantly reduced the incidence of weight loss (0% in magnesium vs 29% in controls) and protected the cerebral cortex from neuronal loss (the incidence of normal, mild, moderate, and severe neuronal loss was 48%, 29%, 5%, and 19% in magnesium and 30%, 5%, 25%, and 40% in controls, respectively) in the pretreatment group. In the posttreatment group magnesium caused increased neuronal damage compared with the controls. CONCLUSION: Magnesium sulfate has neuroprotective effects against hypoxia-ischemia. This effect is restricted to the pretreatment group in which magnesium sulfate is administered before the insult.

Animals↗