bluuebunny/crossref_metadata_2025_split huggingface dataset:
17β-Estradiol and Tamoxifen Prevent Gastric Cancer by Modulating Leukocyte Recruitment and Oncogenic Pathways in Helicobacter Pylori–Infected INS-GAS Male Mice
Authors: Sheh Alexander , Ge Zhongming , Parry Nicola M.A. , Muthupalani Sureshkumar , Rager Julia E. , Raczynski Arkadiusz R. , Mobley Melissa W. , McCabe Amanda F. , Fry Rebecca C. , Wang Timothy C. , Fox James G. 
Published: June 2011

Abstract
Helicobacter pylori infection promotes male predominant gastric adenocarcinoma in humans. Estrogens reduce gastric cancer risk and previous studies showed that prophylactic 17β-estradiol (E2) in INS-GAS mice decreases H. pylori–induced carcinogenesis. We examined the effect of E2 and tamoxifen (TAM) on H. pylori–induced gastric cancer in male and female INS-GAS mice. After confirming robust gastric pathology at 16 weeks postinfection (WPI), mice were implanted with E2, TAM, both E2 and TAM, or placebo pellets for 12 weeks. At 28 WPI, gastric histopathology, gene expression, and immune cell infiltration were evaluated and serum inflammatory cytokines measured. After treatment, no gastric cancer was observed in H. pylori–infected males receiving E2 and/or TAM, whereas 40% of infected untreated males developed gastric cancer. E2, TAM, and their combination significantly reduced gastric precancerous lesions in infected males compared with infected untreated males (P &lt; 0.001, 0.01, and 0.01, respectively). However, TAM did not alter female pathology regardless of infection status. Differentially expressed genes from males treated with E2 or TAM (n = 363 and n = 144, Q &lt; 0.05) associated highly with cancer and cellular movement, indicating overlapping pathways in the reduction of gastric lesions. E2 or TAM deregulated genes associated with metastasis (PLAUR and MMP10) and Wnt inhibition (FZD6 and SFRP2). Compared with controls, E2 decreased gastric mRNA (Q &lt; 0.05) and serum levels (P &lt; 0.05) of CXCL1, a neutrophil chemokine, leading to decreased neutrophil infiltration (P &lt; 0.01). Prevention of H. pylori–induced gastric cancer by E2 and TAM may be mediated by estrogen signaling and is associated with decreased CXCL1, decreased neutrophil counts, and downregulation of oncogenic pathways. Cancer Prev Res; 4(9); 1426–35. ©2011 AACR.
Massive Cerebral Infarction with Severe Brain Swelling: A CLINICOPATHOLOGICAL STUDY
Authors: NG LARRY K. Y. , NIMMANNITYA JESADA 
Published: June 2011

All cases of acute supratentorial cerebral infarction which came to postmortem examination over the past 10 years at the Philadelphia General Hospital were reviewed. Of a total of 353 such cases, 45 showed severe brain swelling.
Seventy-eight percent of these 45 patients died within seven days of the acute infarction. The rapidly fatal outcome appeared to be directly related to the acute brain swelling with transtentorial herniation and brain-stem edema or hemorrhage.
In those patients who survived longer than one week following onset of the ictus (22%), clinical and anatomic findings suggested that increased intracranial pressure probably did not develop until later in the course of the illness. A second massive infarct was probably superimposed upon an earlier one and produced the acute brain swelling noted at the time of postmortem examination. Complicating visceral diseases were more common in this group and seemed to contribute to death in the majority of these patients.
Although it has been established that a large cerebral infarct may produce sufficient brain swelling and simulate an acutely expanding lesion, this is not widely recognized as playing an important part in determining the patient's clinical outcome.
The role of increased intracranial pressure resulting from acute brain swelling should not be overlooked in the management of patients with severe strokes.
Delayed Arterial Spasm and Thrombosis as a Cause of Post-Traumatic Hemiplegia (Spate Thrombosis)
Authors: JACKSON FREDERICK E. , BACK JAMES B. 
Published: June 2011

The case of a Marine in whom a vertex epidural hematoma developed, depressing the superior sagittal sinus as a result of a fracture of the vertex of the skull, is presented. The hematoma was removed, and the patient did well until signs of progressive right hemiparesis suddenly developed two days after the hematoma removal. Serial carotid angiography demonstrated the interval development of spaism of the left internal carotid, anterior cerebral and middle cerebral arteries, and occlusion of the posterior parietal branch of the left middle cerebral artery. Prior to the development of the arterial spasm an earlier angiogram had shown these vessels to be of normal diameter.
This delayed or "spate" spasm and thrombosis of major intracranial vessels is a rare but serious complication of head injuries.
In addition to the usual causes of post-traumatic hemiplegias, this vascular spasm or thrombosis should be suspected in patients in whom progressive neurological signs develop after head injuries.
The Effect of Electrocautery, Atmospheric Exposure, and Surgica Retraction on the Permeability of the Blood-Brain-Barrier
Authors: HUDGINS W. R. , GARCIA JULIO H. 
Published: June 2011

Alterations in the permeability to Evans-blue dye of the blood-brain-barrier were encountered in a group of squirrel monkeys that were being readied for surgical occlusion of the middle cerebral artery. Extravasation of the dye and grossly visible hemispheric cerebral swelling took place before the artery was clipped. These permeability modifications are felt to be directly related to any of the following factors: (1) use of unipolar electrocautery on the scalp and underlying muscles, (2) exertion of mechanical pressure (i.e., retraction) on the surface of the cerebrum, and (3) exposure of the arachnoid membrane and underlying cerebral cortex to atmospheric conditions for periods of up to five hours.
Previously reported experiments involving alterations in the permeability of cerebral vessels should be reevaluated in the light of the findings herein reported. Methods are described to avoid the previously mentioned artefacts on the function of the blood-brain-barrier.
Cerebral Apoplexy (Stroke): Pathogenesis, Pathophysiology and Therapy as Illustrated by Regional Blood Flow Measurements in the Brain
Authors: PAULSON OLAF B. 
Published: June 2011

Pathophysiological and pathogenetic concepts, particularly in occlusive cerebrovascular disease, are reviewed and discussed with emphasis on the results of current research. Therapy is discussed in the context of these concepts.
When focal ischemia, with or without cerebral infarction, is not associated with definable arterial occlusion, studies of regional cerebral blood flow strongly support the thromboembolic theory; the arterial defect is relatively transient and is caused by an embolus or thrombus which rapidly disappears (fragments or is lysed). The treatment of transient ischemic attacks by the administration of anticoagulant or surgical reconstruction of the appropriate artery is discussed.
When cerebral infarction is caused by arterial occlusion there is vasomotor paralysis (loss of autoregulation and of reactivity to carbon dioxide). In some instances hypercapnia apparently causes only the vessels in nonaffected brain to dilate so that an increased amount of blood streams to these parts while blood pressure falls in collaterals leading to the focus and blood flow to the infarct is decreased (steal syndrome). If blood flow is decreased to nonaffected brain, by vasoconstriction caused by hyperventilation, increased amounts of blood may be shunted into the infarct (reverse steal) where autoregulation is lost. Vasoconstriction, as a treatment, might be beneficial. However, in patients with severe cerebral infarction no convincing favorable affect has been noted. The potential therapeutic action of hyperventilation in patients with mild cerebral infarction has not been studied.
Extensive (global) changes in the cerebral blood flow in cerebral infarction, certain aspects of intracerebral hemorrhage, and the role of hypertension in cerebrovascular disease are also dealt with.
Effects of Freezing on Major Arteries
Authors: COOPER IRVING S. , SAMRA KHAIRY , WISNIEWSKA KRYSTYNA 
Published: June 2011

Thirty experiments were performed in dogs to assess the effects of freezing on carotid and femoral arteries. These vessels withstood freezing and thawing without rupture. Blood within the vessels did not clot and was lysed during thawing.
Histological changes of vessel walls consisted of early degeneration followed by a reparative process. Occasional secondary thrombosis occurred close to bifurcation of ligated branches and was related to extent and frequency of freezing and thawing.
Epidemiological characteristics of lacunar infarcts in a population.
Authors: Sacco S E , Whisnant J P , Broderick J P , Phillips S J , O'Fallon W M 
Published: June 2011

This study evaluated the characteristics and natural history of patients with lacunar (small, deep) cerebral infarcts in a defined population for comparison of these characteristics to those in patients with nonlacunar infarcts.
This is a population-based study in Rochester, Minnesota, from 1960 to 1984, that used the medical record-linkage system to identify and characterize patients with cerebral infarction.
The age- and sex-adjusted average annual incidence rate of lacunar cerebral infarction was 13.4/100,000 persons, accounting for 12% of all first cerebral infarcts. Temporal trends in incidence rates, stroke recurrence rates, prevalence of diabetes mellitus, and causes of death (given survival for 30 days) for cases of lacunar infarction were not significantly different from those for cases of nonlacunar infarction. Hypertension was found in 81% of patients who had a lacunar infarct and in 70% of patients who had a nonlacunar infarct (p = 0.05). A potential cardiac source of embolism was found in 12% of patients who had a lacunar infarct and in 28% of patients who had a nonlacunar infarct (p = 0.002). Survival was significantly better after a lacunar infarct than after a nonlacunar infarct.
Small, deep cerebral infarcts had many of the epidemiological characteristics of other cerebral infarcts but there was a slightly higher frequency of hypertension, significantly lower frequency of a cardiac embolic source, and significantly better survival in patients with lacunar infarction than in those with nonlacunar infarction.
Lacunar infarcts. Pathogenesis and validity of the clinical syndromes.
Authors: Boiten J , Lodder J 
Published: June 2011

In this study, we investigated the lacunar hypothesis to answer three questions: 1) Is the lacunar syndrome valid for diagnosing lacunar infarction? 2) What is the frequency of potential cardiac versus carotid sources of embolism in patients with lacunar versus cortical infarct? 3) What is the frequency of vascular risk factors in these two groups of patients?
The study was performed in a well-defined prospective series of 103 patients with a first-ever lacunar infarct and 144 other patients with a first-ever infarct involving the cortex.
Sensitivity and specificity of the lacunar syndromes in diagnosing lacunar infarction were 95% and 93%, respectively. Positive and negative predictive values of diagnosing lacunar infarction in patients with lacunar syndromes were 90% and 97%, respectively. Risk factor analysis showed no differences for either group of cerebral infarction. A cardiac source of embolism was significantly less frequent in patients with lacunar infarction (odds ratio = 0.32, 95% confidence interval = 0.17-0.61, p less than 0.001). Significant carotid stenosis (diameter reduction greater than or equal to 50%) was also less frequent in patients with lacunar infarction (odds ratio = 0.35, 95% confidence interval = 0.16-0.76, p less than 0.001).
These findings show that the lacunar syndrome is an excellent clinical test for diagnosing lacunar infarction and that cardiac and carotid embolism are unlikely causes of lacunar infarction, supporting the hypothesis that lacunar infarcts are usually caused by small vessel disease.
Early computed tomographic findings for thrombolytic therapy in patients with acute brain embolism.
Authors: Okada Y , Sadoshima S , Nakane H , Utsunomiya H , Fujishima M 
Published: June 2011

The benefits and safety of thrombolytic therapy was studied in patients with acute brain embolism.
We intravenously administered recombinant tissue plasminogen activator (20-30 MU for 1 hour) to 10 patients with acute (less than 6 hours) brain embolism and examined the neurological outcomes in relation to the findings on computed tomography and angiography.
The symptoms ameliorated in four patients within 24 hours after onset, and reopening of the occluded arteries occurred in two of the patients immediately after recombinant tissue plasminogen activator infusion. On the initial computed tomographic scan (less than 3 hours), four patients had already demonstrated early indications of brain ischemia, that is, an obscure margin of the lentiform nuclei, reduced tissue attenuation, or effacement of cortical sulci. These patients failed to demonstrate reopening of the occluded arteries, and one developed a massive brain hemorrhage with clinical deterioration. Of the remaining six patients, two obtained clinical improvement with recanalization soon after the therapy and demonstrated little to slight hemorrhagic complications. The outcomes at 1 month were favorable in five patients and poor in three; death occurred in two.
Thrombolytic therapy with recombinant tissue plasminogen activator may be safe and effective when there are no early computed tomographic findings within 3 hours from the onset of embolic stroke.
A model of acute focal ischemia in the territory of the anterior cerebral artery in baboons.
Authors: Liu X G , Branston N M , Kawauchi M , Symon L 
Published: June 2011

We developed a model of acute focal ischemia in the territory of the anterior cerebral artery in baboons to study the ischemic pattern following occlusion and changes in regional cerebral blood flow.
In nine anesthetized animals, a Scoville clip was placed on the proximal segment of the common anterior cerebral artery via a unilateral transorbital approach. Regional cerebral blood flow was measured by hydrogen clearance in the cortex and corpus callosum. Postexperimentally, arteries were selectively injected.
The resulting ischemia involved both hemispheres symmetrically and the corpus callosum. Cortical flows were significantly reduced within a region 15 mm from the midline on each side (p less than 0.01). A gradient of cortical flow reduction was produced between 10 and 25 mm from the midline. This area defines the boundary region between the territories of the anterior and middle cerebral arteries, and is identified as the "penumbra" of the ischemic core, which itself lies within 10 mm of the midline. Blood flows in the corpus callosum decreased from an average of 21.0 to 6.7 ml/100 g/min in the body (p less than 0.01) and from 22.5 to 10.7 ml/100 g/min in the genu (p less than 0.05).
This ischemic model has close physiological and morphological relevance to stroke-related clinical circumstances, in particular the acute conditions of focal cerebral ischemia associated with vascular surgery. It also provides a new framework for experimental investigation of the ischemic penumbra.
Reduction in ischemic brain injury in rabbits by the anion transport inhibitor L-644,711.
Authors: Kohut J J , Bednar M M , Kimelberg H K , McAuliffe T L , Gross C E 
Published: June 2011

We studied the anion transport inhibitor L-644,711, which is known to reduce astrocyte swelling and excitotoxin release in primary astrocyte culture, in two models of thromboembolic stroke to assess its capacity to influence ischemic brain injury.
New Zealand White rabbits were used in this study. The two models include autologous clot embolized to the brain via the carotid artery, with one model using a transient period of systemic hypotension. Cerebral blood flow was determined by the hydrogen clearance method, intracranial pressure was measured with a fiberoptic transducer, and infarct size was assessed with triphenyltetrazolium chloride staining of the coronally sectioned brain. Both models received a 2-hour infusion of L-644,711 (total dose, 12 mg/kg) beginning 20 minutes before embolization.
In both the normotensive (p less than 0.01) and the hypotensive (p less than 0.05) model, treatment with L-644,711 resulted in a significant reduction in infarct size and a significant improvement in regional cerebral blood flow (p less than 0.03, normotensive model, and p less than 0.05, hypotensive model). Raised intracranial pressure, unique to the hypotensive model, was abolished by the administration of L-644,711 (p less than 0.05). A hyperglycemic response associated with embolization, also unique to the hypotensive model, was significantly reduced by the administration of L-644,711 (p less than 0.05).
The ability of L-644,711 to limit brain injury in two related models of thromboembolic stroke suggests a potential therapeutic role for anion channel blockers in cerebral ischemia.
Assessment of intracranial hemodynamics in sleep apnea syndrome.
Authors: Klingelhöfer J , Hajak G , Sander D , Schulz-Varszegi M , Rüther E , Conrad B 
Published: June 2011

Sleep apnea syndrome may lead to changes in cerebral hemodynamics due to altered alveolar ventilation. We investigated the dynamics of CO2- and blood pressure-regulated alterations of cerebral blood flow velocities during apneic episodes and evaluated CO2 reactivity during different sleep stages.
A computer-assisted pulsed Doppler system (2 MHz) was used for continuous overnight recordings of middle cerebral artery flow patterns together with simultaneous polysomnography, continuous blood pressure recordings, and measurements of end-expiratory CO2 in six patients with sleep apnea syndrome.
Increases in mean flow velocity of 19-219% and in blood pressure of 12.5-83.1% could be observed during the apneic episodes, with maximum increases during rapid eye movement (REM) sleep. CO2 reactivity was in the normal range (4.4 +/- 1.2%) in the waking state and was markedly increased during sleep stages 1 and 2 (p less than 0.005 compared with awake). The greatest increase was found during REM sleep, with a rise of up to three times the waking value (p less than 0.0001 compared with sleep stage 2).
The changes of mean flow velocity could be interpreted as reactive adaptation processes because of CO2 and blood pressure increases corresponding to apnea. The increased CO2 reactivity during sleep may indicate a "hypersensitivity" of intracranial vascular CO2 or pH receptors and a disturbance of central catecholaminergic and cholinergic systems. The pronounced velocity changes during apneic episodes and the concomitant alterations of vessel wall tension might lead to microangiopathies and macroangiopathies due to chronic strain on the brain vessels.
Leukoaraiosis in relation to prognosis for patients with lacunar infarction.
Authors: Miyao S , Takano A , Teramoto J , Takahashi A 
Published: June 2011

Close relations between leukoaraiosis detected by computed tomography or magnetic resonance imaging and stroke, particularly lacunar infarction, have been reported. We studied whether leukoaraiosis is related to long-term prognosis for patients with lacunar infarction.
We examined monthly 215 patients with lacunar infarction after their first stroke. They comprised 95 patients with leukoaraiosis disclosed by computed tomography on admission (58 men and 37 women; mean age, 71.3 +/- 9.0 years) and 120 patients without leukoaraiosis (81 men and 39 women; mean age, 65.5 +/- 8.9 years). These patients had no previous history of either stroke or obvious dementia before their index stroke. We compared the prognosis with and without leukoaraiosis based on analysis of recurrent stroke, survival, and the prevalence of dementia and rate of dependence in activities of daily living.
Life table analysis revealed that the recurrent stroke rate was significantly higher in the patients with leukoaraiosis than in those without it (p = 0.004). The prevalence of dementia and rate of dependence in activities of daily living both 1 month after the index stroke and at the end of the follow-up period were significantly higher in the patients with leukoaraiosis (all parameters, P less than 0.001). Their survival rate was significantly lower than in those not suffering from leukoaraiosis (p = 0.012). Significant differences in these comparisons were also observed after matching for age and sex.
The presence of leukoaraiosis as identified by computed tomography indicates a poor prognosis for patients with lacunar infarction.
Secular trends in stroke incidence and mortality. The Framingham Study.
Authors: Wolf P A , D'Agostino R B , O'Neal M A , Sytkowski P , Kase C S , Belanger A J , Kannel W B 
Published: June 2011

The reduction in US stroke mortality has been attributed to declining stroke incidence. However, evidence is accumulating of a trend in declining stroke severity.
We examined secular trends in stroke incidence, prevalence, and fatality in Framingham Study subjects aged 55-64 years in three successive decades beginning in 1953, 1963, and 1973.
No significant decline in overall stroke and transient ischemic attack incidence or prevalence occurred. In women, but not men, incidence of completed ischemic stroke declined significantly. Stroke severity, however, decreased significantly over time. Stroke with severe neurological deficit decreased in later decades, with a fall in rates of severe stroke cases in which patients were unconscious on admission to the hospital. There was no substantial change in the case mix of infarcts and hemorrhages and no decline in hemorrhage to account for the decline in severity. The proportion of isolated transient ischemic attacks increased significantly over the 30 years studied, yielding an apparent and significant decline in case-fatality rates in men only.
Secular trends in stroke incidence and fatality did not follow a clear or definite pattern of decline. While a significant decline in stroke severity occurred over three decades, incidence of infarction fell only in women. The decline in total case fatality rates occurred only in men and resulted largely from an increased incidence of isolated transient ischemic attacks. The severity of completed stroke was significantly lower in the later decades under study.