Biomedical subjects

C Y Hsu

Publications and source records attributed to C Y Hsu.

At least 55 records · Page 3Linked to original sources

PubMed2001

Bilateral anomalous origins of the posterior meningeal artery from the ascending pharyngeal arteries.

We present a rare case of angiographically confirmed dural arteriovenous fistula supplied mainly by the posterior meningeal artery with bilateral anomalous origins from the bilateral ascending pharyngeal arteries. The bilaterality of the origins of the posterior meningeal artery is important in the angiographic diagnosis and management of a dural vascular malformation in the posterior fossa or the posterior part of the falx cerebri.

Adult↗

PubMed2001

Surgical treatment for concomitant fractures of the femoral neck and diaphysis: a treatment protocol.

Concomitant ipsilateral femoral shaft and neck fractures are difficult to treat. The standard protocol in our hospital is plates for diaphyseal fractures and lag screws or dynamic hip screws (DHS) fixations for the femoral neck fractures. We treated 21 patients with these complex fractures between 1988 and 1998 with this protocol. All patients were injured from high-energy trauma. There were 15 males and 6 females with an average age of 44 years. The average follow-up period is 50 months. All except one patient united well. During the follow-up period, neither non-union of the femoral neck fracture nor osteonecrosis of the femoral head was noted. There was also no malunion. There were twenty good results and one poor functional result. We conclude that plate on the shaft and sliding hip screws or separate screws in the hip are a reliable method for concomitant ipsilateral femoral neck and shaft fractures.

Adult↗

PubMed2001

Endoscopic optic nerve decompression for the treatment of traumatic optic neuropathy.

Optic nerve decompression has been accomplished by a variety of procedures. Since 1995, endoscopic optic nerve decompression (EOND) has been used to treat traumatic optic neuropathy (TON) patients in our hospital after medical treatment failed. To date, 17 TON patients have received EOND in our hospital and have been followed up for more than half a year. After decompression, vision improved in 9 patients, remained the same in 6, and became worse in 2. The dura was incidentally exposed during the operation in 1 patient. We conclude that it is easier and more precise to perform optic nerve decompression by EOND than by other optic nerve decompression procedures. However, its efficacy still needs further investigation.

Adolescent↗

PubMed2000

iNOS expression inhibits hypoxia-inducible factor-1 activity.

Hypoxia-inducible factor-1 (HIF-1) activates genes important in vascular function such as vascular endothelial growth factor (VEGF), erythropoietin (EPO), and inducible nitric oxide synthase (iNOS). iNOS catalyzes the synthesis of nitric oxide (NO), a free radical gas that mediates a number of cellular processes, including regulation of gene expression, vasodilatation, and neurotransmission. Here we demonstrate that iNOS expression inhibits HIF-1 activity under hypoxia in C6 glioma cells transfected with an iNOS gene and a VEGF promoter-driven luciferase gene. HIF-1 induction of VEGF-luciferase activity in C6 cell is also inhibited by sodium nitroprusside (SNP). Furthermore, pretreatment of C6 cells with N-acetyl-l-cysteine (NAC), an antioxidant, nullified the inhibitory effect of iNOS on HIF-1 binding. These results demonstrate that NO generated by iNOS expression inhibits HIF-1 activity in hypoxic C6 cells and suggest a negative feedback loop in the HIF-1 --> iNOS cascade.

Acetylcysteine↗

PubMed2000

Over-expression of nucleophosmin/B23 decreases the susceptibility of human leukemia HL-60 cells to retinoic acid-induced differentiation and apoptosis.

Stable clones of HL-60 cells in which nucleophosmin/B23 was over-expressed were established. Less percentages (4-20%) of nucleophosmin/B23 over-expressed (pCR3-B23) cells exhibited the morphological characteristic of apoptosis as compared with control vector-transfected (pCR3) cells (6-53%) during the 10 microM RA treatment for 1-4 days. In flow cytometry analysis, a block in the G1 phase was noted in all the pCR3-B23 and pCR3 cells after 2 days of 10 microM RA treatment and continued to be observed at all times measured up to 6 days. Smaller peaks of apoptotic cells with less than G1 DNA content were observed in pCR3-B23 as compared with pCR3 cells after 4-6 days of 10 microM RA treatment. As measured by expressions of differentiation markers and the functional assessment of the ability to reduce nitroblue-tetrazolium, our results further showed that over-expression of nucleophosmin/B23 decreased the response of the cells to RA-induced differentiation. Less cleavage of PARP and in vitro caspase-3 activity were observed in PCR3-B23 cells as compared with pCR3 cells treated with 10 microM RA for 3-4 days. IRF-1 was induced after 6 hr of 10 microM RA treatment in the pCR3-B23 and pCR3 cells. Significantly more nucleophosmin/B23 was co-immunoprecipitated with IRF-1 from pCR3-B23 cells than from pCR3 cells during RA treatment (10 microM; 24 hr, 96 hr). The IRF-1 transcriptional activity was found to be attenuated in pCR3-B23 cells as compared with pCR3 cells during the treatment of cells with RA. Nucleophosmin/B23, through interacting with IRF-1, plays an important role in the control of the susceptibility of cells to RA-induced differentiation and apoptosis.

Apoptosis↗

PubMed2000

Intravenous ancrod for treatment of acute ischemic stroke: the STAT study: a randomized controlled trial. Stroke Treatment with Ancrod Trial.

CONTEXT: Approved treatment options for acute ischemic stroke in the United States and Canada are limited at present to intravenous tissue-type plasminogen activator, but bleeding complications, including intracranial hemorrhage, are a recognized complication. OBJECTIVE: To evaluate the efficacy and safety of the defibrinogenating agent ancrod in patients with acute ischemic stroke. DESIGN: The Stroke Treatment with Ancrod Trial (STAT), a randomized, parallel-group, double-blind, placebo-controlled trial conducted between August 1993 and January 1998. SETTING: Forty-eight centers, primarily community hospitals, in the United States and Canada. PATIENTS: A total of 500 patients with an acute or progressing ischemic neurological deficit were enrolled and included in the intent-to-treat analysis. INTERVENTIONS: Patients were randomly assigned to receive ancrod (n=248) or placebo (n =252) as a continuous 72-hour intravenous infusion beginning within 3 hours of stroke onset, followed by infusions lasting approximately 1 hour at 96 and 120 hours. The ancrod regimen was designed to decrease plasma fibrinogen levels to 1.18 to 2.03 micromol/L. MAIN OUTCOME MEASURES: The primary efficacy end point was functional status, with favorable functional status defined as survival to day 90 with a Barthel Index of 95 or more or at least the prestroke value, compared by treatment group. Primary safety variables included symptomatic intracranial hemorrhage and mortality. RESULTS: Favorable functional status was achieved by more patients in the ancrod group (42.2%) than in the placebo group (34.4%; P=.04) by the prespecified covariate-adjusted analysis. Mortality was not different between treatment groups (at 90 days, 25.4% for the ancrod group and 23% for the placebo group; P=.62), and the proportion of severely disabled patients was less in the ancrod group than in the placebo group (11.8% vs 19.8%; P=.01). The favorable functional status observed with ancrod vs placebo was consistent in all subgroups defined for age, stroke severity, sex, prestroke disability, and time to treatment (< or = 3 or > 3 hours after stroke onset). There was a trend toward more symptomatic intracranial hemorrhages in the ancrod group vs placebo (5.2% vs 2.0%; P=.06), as well as a significant increase in asymptomatic intracranial hemorrhages (19.0% vs 10.7%; P=.01). CONCLUSION: In this study, ancrod had a favorable benefit-risk profile for patients with acute ischemic stroke.

Ancrod↗

PubMed2000

Biphasic effects of dithiocarbamates on the activity of nuclear factor-kappaB.

Dithiocarbamates are well-known antioxidants and nuclear factor-kappaB (NF-kappaB) inhibitors. Recently, they have been characterized as zinc ionophores. Concentration-dependent biphasic effects of dithiocarbamates on NF-kappaB activity have been widely reported. We studied the mechanism of this phenomenon in relation to Zn(2+) influx. Two dithiocarbamates, pyrrolidine dithiocarbamate and diethyldithiocarbamate, showed concentration-dependent biphasic effects in inhibiting NF-kappaB activation in cerebral endothelial cells. These unique effects of dithiocarbamates on NF-kappaB were tightly linked to their ability to elevate intracellular Zn(2+)500 microM), dithiocarbamates started to lose their ability to promote Zn(2+) influx and to inhibit NF-kappaB activation. These results might provide insight into the appropriate use of dithiocarbamates in various disorders.

Animals↗

PubMed2000

Absolute measurements of water content using magnetic resonance imaging: preliminary findings in an in vivo focal ischemic rat model.

Using a magnetic resonance (MR) imaging method, absolute measurements of in vivo brain water content were obtained in 15 male Long Evans rats that underwent a 90-min focal cerebral ischemia. A strong linear relationship (r = 0.80) with a slope of 1 was observed when correlating MR-measured water content to that obtained with the ex vivo wet/dry measurements. This effective spin-density-based method is the first-reported in vivo absolute quantification of brain tissue water content associated with a pathophysiological state and preliminary findings suggest that a noninvasive measurement of brain water content can be obtained with MRI.

Animals↗

PubMed2000

MIB-1 labeling index as a prognostic indicator for survival in patients with FIGO stage IB squamous cell carcinoma of the cervix.

OBJECTIVE: The goal of this study was to assess whether the MIB-1 labeling index (LI) and conventional parameters could distinguish between a good and a poor prognosis in patients with squamous cell cervical carcinoma of the same FIGO stage. METHODS: The study included 97 cases of stage IB squamous cell cervical carcinoma which were treated with radical hysterectomy between 1989 and 1991. The relation of the MIB-1 LI, conventional clinicopathologic parameters, and survival was evaluated. RESULTS: The MIB-1 LI of the entire group of tumors was 57.1 +/- 15.9 (mean +/- SD). The MIB-1 LI was significantly different only in living and dead patients, while it was not related to conventional clinicopathologic prognostic parameters. The 5- and 10-year survival rates of patients with an MIB-1 LI </=55 were 90.0 and 88.6%, respectively, which were significantly better than the survival rates of patients with LI >55, which were 73.1 and 66%, respectively. Multivariate analyses showed that MIB-1 LI >55, lymph node metastasis, and tumor size >/=40 mm were powerful predictors of shorter survival. CONCLUSIONS: Lymph node metastasis, tumor size, and MIB-1 LI were significant prognostic markers in patients with stage IB squamous cell cervical carcinoma.

Adult↗

PubMed2000

Atypical teratoid/rhabdoid tumor of the central nervous system: a comparative study with primitive neuroectodermal tumor/medulloblastoma.

Eleven atypical teratoid/rhabdoid tumors (AT/RT) and 121 primitive neuroectodermal tumors/medulloblastomas (PNET/MB) were included in this study for evaluation of the histopathological features of AT/RT and comparison between AT/RT and PNET/MB. Histopathological studies of AT/RT showed that in addition to the commonly recognized components, i.e., rhabdoid cells, small (PNET/MB) cells, spindle cells and epithelial components, there was a previously unrecognized component, sickle-shaped embracing cells, which were present in all cases and could be useful as a histological marker of this tumor. Immunohistochemical studies showed divergent differentiation of the tumor cells and among the 16 antibodies studied, vimentin, neuron-specific enolase, epithelial membrane antigen and glial fibrillary acidic protein were most commonly reactive. The frequency of AT/RT expressed as a ratio of AT/RT to PNET/MB was 1:11 in general and increased to 1:3.8 among patients younger than 3 years old. The AT/RT patients were younger than those with PNET/MB and had a female predominance. The MIB-1 labeling index of AT/RT was significantly higher than that of PNET/MB (mean 63.9 vs 40.1), which correlated with a shorter survival in patients with AT/RT than those with PNET/MB (median survival time 15.4 months vs 156.4 months).

Antigens, Nuclear↗

PubMed2000

What animal models have taught us about the treatment of acute stroke and brain protection.

Stroke research has progressed in leaps and bounds in the past decades. A driving force is the increasing availability of new research tools in this field (eg, animal stroke models). Animal stroke models have been extensively applied to advance our understanding of the mechanisms of ischemic brain injury and to develop novel therapeutic strategies for reducing brain damage after a stroke. Animal stroke models have been useful in characterizing the molecular cascades of injury processes. These "injury pathways" are also the targets of therapeutic interventions. The major achievements made in the past 2 decades applying animal stroke models include 1) the identification of the mediator role of excitotoxin and oxygen free radicals in ischemic brain injury; 2) the confirmation of apoptosis as a major mechanism of ischemic cell death; 3) the characterization of postischemic gene expression; 4) the delineation of postischemic inflammatory reaction; 5) the application of transgenic mice to confirm the roles of purported mediators in ischemic brain injury; 6) development of novel magnetic resonance imaging sequences for early noninvasive detection of ischemic brain lesions; and, 7) the development of novel therapeutic strategies based on preclinical findings derived from animal stroke models.

Animals↗

PubMed2000

Diabetes, hemoglobin A(1c), cholesterol, and the risk of moderate chronic renal insufficiency in an ambulatory population.

Moderate chronic renal insufficiency is common, with 12.5 million individuals in the United States estimated to have a creatinine clearance less than 50 mL/min/1.73 m(2). Little is known about the risk factors for moderate chronic renal insufficiency. We studied 1, 428 subjects with Cockcroft-Gault-estimated creatinine clearances greater than 70 mL/min in a hospital-based ambulatory population. Over a mean of 5.7 +/- 1.3 years, 86 subjects developed moderate chronic renal insufficiency, defined as a decrease in creatinine clearance to less than 60 mL/min (1.1 case/100 person-years). Risk factors for moderate chronic renal insufficiency were identified using a proportional hazards model controlling for age, sex, race, systolic blood pressure, and angiotensin-converting enzyme (ACE) inhibitor use. The risk for developing moderate chronic renal insufficiency was associated with diabetes mellitus (relative risk, 2.1; 95% confidence interval [CI], 1.3 to 3.3) and elevated hemoglobin A(1c) levels. Compared with subjects with normoglycemia (hemoglobin A(1c) </= 5.7%), the relative risk for moderate chronic renal insufficiency for patients in the upper quartile of hemoglobin A(1c) (>9.0%) was 2.7 (95% CI, 1.4 to 5.1). The development of moderate chronic renal insufficiency was also independently predicted by elevated maximum serum cholesterol level. Compared with subjects with maximum cholesterol levels of 250 mg/dL or less, the relative risk for those with maximum cholesterol levels greater than 350 mg/dL was 2.4 (95% CI, 1.1 to 5.2). Similar relative risks were obtained when moderate chronic renal insufficiency was defined by the development of an increase in serum creatinine level. Hypercholesterolemia was also associated with moderate chronic renal insufficiency among persons without diabetes. In conclusion, the risk for developing moderate chronic renal insufficiency is increased by diabetes and elevated hemoglobin A(1c) and serum cholesterol levels. Modification of these risk factors may decrease the incidence of moderate chronic renal insufficiency.

Cholesterol↗

PubMed2000

Chronic renal confusion: insufficiency, failure, dysfunction, or disease.

The terms routinely used to describe states of reduced glomerular filtration rate (GFR) not requiring renal replacement therapy are poorly defined. With increasing interest in the epidemiology of chronic renal insufficiency and the timing of initiation of dialysis, terms such as "pre-ESRD" and "pre-dialysis" have been popularized, again without clear definition. Unambiguous terminology should be adopted. The authors favor using the term chronic renal insufficiency to describe states of reduced GFR not severe enough to require dialysis or transplantation. The authors propose classifying patients with GFR of 60 to 41 mL/min, 40 to 21 mL/min, and 20 mL/min or below as having mild, moderate, and advanced degrees of chronic renal insufficiency, respectively. The use of this terminology will facilitate communication among nephrologists and other physicians and provide a framework for comparison of populations across cohort studies and clinical trials.

Glomerular Filtration Rate↗

PubMed2000

An absolute measurement of brain water content using magnetic resonance imaging in two focal cerebral ischemic rat models.

Magnetic resonance imaging (MRI) was utilized to obtain absolute estimates of regional brain water content (W), and results were compared with those obtained with conventional wet/dry measurements. In total, 31 male Long-Evans rats were studied and divided into two groups based on the surgical procedures used to induce cerebral focal ischemia: suture (n = 18) and three-vessel ligation (TVL: n = 13) groups. Both relative spin density and T1 were extracted from the acquired MR images. After correcting for radiofrequency field inhomogeneities, T2* signal decay, and temperature effects, in vivo regional brain water content, in absolute terms, was obtained by normalizing the measured relative brain spin density of animals to that of a water phantom. A highly linear relationship between MR-estimated brain water content based on the normalized spin density and wet/dry measurements was obtained with slopes of 0.989 and 0.986 for the suture (r = 0.79) and TVL (r = 0.83) groups, respectively. Except for the normal subcortex of the TVL group (P < 0.02) and the normal hemisphere of the suture group (P < 0.003), no significant differences were observed between MR-estimated and wet/dry measurements of brain water content. In addition, a highly linear relationship between MR-measured R1 (= 1/T1) and 1/W of wet/dry measurements was obtained. However, slopes of the linear regression lines in the two groups were significantly different (P < 0.02), indicating that different R1 values were associated with the same water content depending on the model. These results show that an absolute measurement of in vivo regional brain water content can be obtained with MRI and potentially serves as a noninvasive means to monitor different therapeutic interventions for the management of brain edema subsequent to stroke and head trauma.

Animals↗

PubMed2000

Induction of angiopoietin and Tie receptor mRNA expression after cerebral ischemia-reperfusion.

The angiopoietin/Tie receptor system may contribute to angiogenesis and vascular remodeling by mediating interactions of endothelial cells with smooth muscle cells and pericytes. The temporal expression of angiopoietin-1 (Angpo-1), angiopoietin-2 (Angpo-2), Tie-1, and Tie-2 mRNA was studied in a focal cerebral ischemia model in rats. The cDNA fragments obtained from reverse transcription polymerase chain reaction amplification were cloned and used as a probe to detect individual genes. Northern blot analysis showed a delayed increase of a 4.4-kb Angpo-1 transcript for up to 2 weeks after ischemia, eightfold higher than the values of the sham-operated controls. A biphasic expression of a 2.4-kb Angpo-2 transcript was noted, peaking at 24 hours (6.4-fold) and 2 weeks (4.6-fold) after ischemia. The expression of Tie-2 mRNA (4.3 kb), a receptor for Angpo-1, and Tie-1 mRNA (4.3 kb) also increased starting 24 hours after reperfusion and remained elevated for up to 2 weeks after ischemia. The temporal profiles of the expression of these genes were different from those of other angiogenic genes such as basic fibrobast growth factor/fibroblast growth factor receptor and vascular endothelial growth factor/vascular endothelial growth factor receptor and proteolytic enzymes (tissue-type plasminogen activator and urokinase plasminogen activator) and their inhibitors (plasminogen activator inhibitor-1). The expression patterns of these genes could be related to progressive tissue liquefaction and neovascularization after ischemia in this stroke model. Differential expression of these angiogenesis genes suggests the involvement of complex regulatory mechanisms that remain to be characterized.

Angiopoietin-1↗

PubMed2000

Effects of lipopolysaccharide priming on acute ischemic brain injury.

BACKGROUND AND PURPOSE: Infection has been implicated as a stroke risk factor. Activation and infiltration of polymorphonuclear neutrophils (PMNs) after cerebral ischemia may contribute to ischemic brain injury. This study was conducted to investigate how enhanced postischemic PMN infiltration by lipopolysaccharide (LPS) altered the acute ischemic outcomes. METHODS: LPS (0.05 mg/kg SC) or vehicle was given to Long-Evans male rats 24 hours before ischemia. Focal cerebral ischemia was induced by temporary ligation of the right middle cerebral artery and both common carotid arteries for 45 minutes. Animals were killed 6 and 24 hours after reperfusion to determine the extent of PMN infiltration (myeloperoxidase assay), brain edema (wet-dry weight method), and vascular injury (fluorescein isothiocyanate-conjugated dextran extravasation). The infarct volumes were measured on the basis of TTC stain 24 hours after ischemia. RESULTS: LPS had little effect on body temperature or peripheral white count but substantially enhanced PMN infiltration into the ischemic right middle cerebral artery cortex on the basis of myeloperoxidase activity (6 hours: control, 0 U/g; LPS, 0.186+/-0. 025 U/g; 24 hours: control, 0.185+/-0.025 U/g; LPS, 0.290+/-0.040 U/g; P<0.001) and morphological studies. The extent of vascular injury defined by the extravasation of fluorescein isothiocyanate-conjugated dextran into the ischemic tissue (6 hours: control, 3.11+/-0.41 microliter/mg protein; LPS, 0.48+/-0.16 microliter/mg protein; 24 hours: control, 1.77+/-0.23 microliter/mg protein; LPS, 0. 90+/-0.19 microliter/mg protein; P<0.001) and brain edema determined by the brain water content (6 hours: control, 84.77+/-1.63%; LPS, 82. 09+/-1.25%; 24 hours: control, 89.40+/-0.43%; LPS, 87.88+/-0.58%; P<0.01) were paradoxically reduced by LPS priming. LPS-primed rats also had smaller infarct volumes (control, 135+/-5 mm(3); LPS, 108+/-12 mm(3); P<0.05). CONCLUSIONS: Enhanced postischemic PMN infiltration is anticipated to facilitate ischemic brain injury. Contrary to this expectation, results from the present study suggest that an increase in postischemic PMN infiltration after LPS priming was not detrimental. These findings challenge the notion that postischemic PMN infiltration is uniformly deleterious.

Animals↗

PubMed2000

Differences in vulnerability to permanent focal cerebral ischemia among 3 common mouse strains.

BACKGROUND AND PURPOSE: Genetically engineered mice are used to study the role of single genes in cerebral ischemia, but inherent, strain-dependent differences in neuronal vulnerability may affect experimental end points. To examine this possibility, tissue injury resulting from focal ischemia and its relationship to cerebral hemodynamics were determined in 3 common mutant mouse strains. METHODS: Permanent middle cerebral artery ligation was performed in male C57BL/6J, Balb/C, and 129X1/SvJ mice. Mean arterial blood pressure, blood gases, basal and postischemic cortical blood flow ([(14)C]iodoantipyrine autoradiography and laser-Doppler flowmetry), posterior communicating artery patency, and infarct size were determined. RESULTS: Basal cortical blood flow did not differ among strains. Ten minutes after middle cerebral artery ligation, relative red cell flow in the ischemic cortex was 6% to 7% of preischemic flow in every strain. Despite similar hemodynamics, cortical infarcts in Balb/C mice were 3-fold larger than those in 129X1/SvJ and C57BL/6J mice; infarct size in the latter 2 strains was not significantly different. The posterior communicating artery was either poorly developed or absent in >90% of the Balb/C and C57BL/6J but in <50% of the 129X1/SvJ mice. CONCLUSIONS: The extent of ischemic injury differed markedly between the 3 strains. The presence and patency of posterior communicating arteries, although variable among strains, did not affect preischemic or postischemic cortical blood flow or bear any relationship to ischemic injury. Therefore, intrinsic factors, other than hemodynamic variability, may contribute to the differences in ischemic vulnerability among strains. These findings underscore the importance of selecting genetically matched wild-type controls.

Animals↗

PubMed2000

Transient and permanent resolution of ischemic lesions on diffusion-weighted imaging after brief periods of focal ischemia in rats : correlation with histopathology.

BACKGROUND AND PURPOSE: The early ischemic lesions demonstrated by diffusion-weighted imaging (DWI) are potentially reversible. The purposes of this study were to determine whether resolution of initial DWI lesions is transient or permanent after different brief periods of focal brain ischemia and to evaluate histological outcomes. METHODS: Sixteen rats were subjected to 10 minutes (n=7) or 30 minutes (n=7) of temporary middle cerebral artery occlusion or sham operation (n=2). DWI, perfusion-weighted imaging (PWI), and T(2)-weighted imaging (T(2)WI) were performed during occlusion; immediately after reperfusion; and at 0.5, 1.0, 1.5, 12, 24, 48, and 72 hours after reperfusion. After the last MRI study, the brains were fixed, sectioned, stained with hematoxylin and eosin, and evaluated for neuronal necrosis. RESULTS: No MRI or histological abnormalities were observed in the sham-operated rats. In both the 10-minute and 30-minute groups, the perfusion deficits and DWI hyperintensities that occurred during occlusion disappeared shortly after reperfusion. The DWI, PWI, and T(2)WI results remained normal thereafter in the 10-minute group, whereas secondary DWI hyperintensity and T(2)WI abnormalities developed at the 12-hour observation point in the 30-minute group. Histological examinations demonstrated neuronal necrosis in both groups, but the number of necrotic neurons was significantly higher in the 30-minute group (95+/-4%) than in the 10-minute group (17+/-10%, P<0.0001). CONCLUSIONS: Transient or permanent resolution of initial DWI lesions depends on the duration of ischemia. Transient resolution of DWI lesions is associated with widespread neuronal necrosis; moreover, permanent resolution of DWI lesions does not necessarily indicate complete salvage of brain tissue from ischemic injury.

Animals↗