bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evolution of the c-kit-Positive Cell Response to Pathological Challenge in the Myocardium
Authors: Fransioli Jenna , Bailey Brandi , Gude Natalie A. , Cottage Christopher T. , Muraski John A. , Emmanuel Gregory , Wu Weitao , Alvarez Roberto , Rubio Marta , Ottolenghi Sergio , Schaefer Erik , Sussman Mark A. 
Published: February 2008

Abstract
Cumulative evidence indicates that myocardium responds to growth or injury by recruitment of stem and/or progenitor cells that participate in repair and regenerative processes. Unequivocal identification of this population has been hampered by lack of reagents or markers specific to the recruited population, leading to controversies regarding the nature of these cells. Use of a transgenic mouse expressing green fluorescent protein driven by the c-kit promoter allows for unambiguous identification of this cell population. Green fluorescent protein (GFP) driven by the c-kit promoter labels a fraction of the c-kit+ cells recognized by antibody labeling for c-kit protein. Expression of GFP by the c-kit promoter and accumulation of GFP-positive cells in the myocardium is relatively high at birth compared with adult and declines between postnatal weeks 1 and 2, which tracks in parallel with expression of c-kit protein and c-kit-positive cells. Acute cardiomyopathic injury by infarction prompts increased expression of both GFP protein and GFP-labeled cells in the region of infarction relative to remote myocardium. Similar increases were observed for c-kit protein and cells with a slightly earlier onset and decline relative to the GFP signal. Cells coexpressing GFP, c-kit, and cardiogenic markers were apparent at 1–2 weeks postinfarction. Cardiac-resident c-kit+ cell cultures derived from the transgenic line express GFP that is diminished in parallel with c-kit by induction of differentiation. The use of genetically engineered mice validates and extends the concept of c-kit+ cells participating in the response to myocardial injury.
Disclosure of potential conflicts of interest is found at the end of this article.
Trends in Perinatal HIV Prevention in New York City, 1994–2003
Authors: Peters Vicki B. , Liu Kai-Lih , Robinson Lisa-Gaye , Dominguez Kenneth L. , Abrams Elaine J. , Gill Balwant S. , Thomas Pauline A. 
Published: February 2008

Objectives. We examined trends in perinatal HIV prevention interventions in New York City implemented during 1994 to 2003 to ascertain the success of the interventions in reducing perinatal transmission. Methods. We used data obtained from infant records at 22 hospitals. We used multiple logistic regression to analyze factors associated with prenatal care and perinatal HIV transmission. Results. We analyzed data for 4729 perinatally HIV-exposed singleton births. Of mothers with prenatal care data, 92% had prenatal care. The overall proportion who received prenatal care and were diagnosed with HIV before delivery was 86% in 1994 to 1996 and 90% in 1997 to 2003. Use of prenatal antiretrovirals among mothers who received prenatal care was 63% in 1994 to 1996 and 82% in 1997 to 2003. From 1994 to 2003, cesarean births among the entire sample increased from 15% to 55%. During 1997 to 2003, the perinatal HIV transmission rate among the entire sample was 7%; 45% of mothers of infected infants had missed opportunities for perinatal HIV prevention. During 1997 to 2003, maternal illicit drug use was significantly associated with lack of prenatal care. Lack of prenatal, intrapartum, and neonatal antiretrovirals; maternal illicit drug use; and low birthweight were significantly associated with perinatal HIV transmission. Conclusions. Interventions for perinatal HIV prevention can successfully decrease HIV transmission rates. Ongoing perinatal HIV surveillance allows for monitoring the implementation of guidelines to prevent mother-to-child transmission of HIV and determining factors that may contribute to perinatal HIV transmission.
County Variation in Children's and Adolescent's Health Status and School District Performance in California
Authors: Stone Susan I. , Jung Sunyoung 
Published: February 2008

Objectives. We examined the association between county-level estimates of children's health status and school district performance in California. Methods. We used 3 data sources: the California Health Interview Survey, district archives from the California Department of Education, and census-based estimates of county demographic characteristics. We used logistic regression to estimate whether a school district's failure to meet adequate yearly progress goals in 2004 to 2005 was a function of child and adolescent's health status. Models included district- and county-level fixed effects and were adjusted for the clustering of districts within counties. Results. County-level changes in children's and adolescent's health status decreased the likelihood that a school district would fail to meet adequate yearly progress goals during the investigation period. Health status did not moderate the relatively poor performance of predominantly minority districts. Conclusions. We found empirical support that area variation in children's and adolescent's health status exerts a contextual effect on school district performance. Future research should explore the specific mechanisms through which area-level child health influences school and district achievement.
Effect of Chlorhexidine Application on Microtensile Bond Strength to Dentin
Authors: Soares C. J. , Pereira C. A. , Pereira J. C. , Santana F. R. , Prado C. J. 
Published: February 2008

Clinical Relevance
Based on the results of this study, the application of chlorhexidine solution at a concentration of 0.12 and 2% before, after or associated with phosphoric acid etching, presented similar behavior with no adverse effect on 24-hour bond strength.
Class I Gap-formation in Highly-viscous Glass-ionomer Restorations: Delayed vs Immediate Polishing
Authors: Irie M. , Maruo Y. , Nishgawa G. , Suzuki K. , Watts D. C. 
Published: February 2008

Clinical RelevanceDelaying polishing for one day resulted in improved gap-formation for Class I restoration of highly-viscous conventional and conventional glass-ionomer cements
Chemical, Physical, and Genetic Factors Interfering with DNA Repair-a Review
Authors: Bernheim Naomi Jean , Falk Hans 
Published: February 2008

Because of its function as transmitter of genetic information, DNA is the most important macromolecule in need of protection from attack by chemical and physical agents, but mechanisms have evolved for repairing such damage to DNA. The presence of the adaptive response and other cellular repair systems (excision, post-replication, SOS, etc.) diminishes the toxicologic effects of low doses of toxic or muta-genic substances. Whether or not these genotoxic effects can be reduced to undetectable levels is not certain. Nonetheless, this repair-mediated diminution of damage due to chemicals constitutes one of the arguments in favor of existence of “safe” threshold levels of chemical exposure (Schendel, 1981). In turn, the repair process itself may be affected by chemical and physical agents. To determine the mode of action of a specific compound on the process of DNA repair becomes complex when all factors are taken into consideration. There are agents which interfere with DNA repair but they are also as active or more active in suppressing replicative DNA synthesis, as well as RNA and protein synthesis. The interference with repair may arise from other major processes such as alteration of energy metabolism and effects on precursor pathways and/or enzymatic cofactors. Whether or not an agent can specifically inhibit DNA repair enzymes has not been answered. The point must be made, however, that this type of interference with essential protective mechanisms is taking place and it may change anticipated outcomes of chemical or physical exposures. The magnitude of this effect due to the exposure of people to so many chemicals should be recognized and studied for their degree of interference with all the processes of DNA repair.
Chasing A Receding Zero: Impact of the Zero Threshold Concept on Actions of Regulatory Officials
Authors: Jukes Thomas H. 
Published: February 2008

The principle of toxicological threshold was stated in 1564 by Paracelsus as “All things are poisonous, yet nothing is poisonous. Dosage alone determines poisoning.” This principle remains valid, even with consideration of today's public concern with low-dosage effects of compounds that are categorized as carcinogens, mutagens and teratogens. Modern laboratory methods enable detection of increasingly small traces of such compounds in foods. The search for these has been termed “Chasing a receding zero, ” and this quest has been stimulated by statements that no one knows how small an amount of a carcinogen, taken for how short a time, can induce cancer, and that even one molecule of a carcinogen, acting on a single cell, can transform a normal cell into a cancer cell. This latter proposal is a stochastic impossibility. Every cell contains millions of carcinogenic molecules. Examples are arsenic, cadmium and chromium. In addition, there are estrogens and other steroid hormones present in each cell and needed for normal bodily functions. These substances are regarded as carcinogens because of their effect at high levels on increasing the cancer rate in experimental animals. Obviously, there must be a threshold for this effect. An estimate has been made by Dingman that “a threshold for biological activity exists within a cell at 10, 000 atoms.” It is also obvious that there is a threshold for deficiencies that induce cancer, such as that of iodine. Iodine deficiency is mimicked by administration of goitrogens, and these are present naturally at low to moderate levels in many common foods. The threshold principle is stated by Claus and Bolander to be a law of nature, valid in many circumstances, and governing the fact that a causative agent must be present in a quantity exceeding a definite minimum in order to produce the effect.
Dietary and other Modulators of Carcinogenesis
Authors: Rogers Adrianne E. 
Published: February 2008

Nutritional or dietary status and interactions between carcinogens and nutrient absorption, storage or metabolism influence carcinogenesis in many experimental animal models and probably in people. Use of dose-response data to indicate a threshold exposure for carcinogenesis must include consideration of dietary and nutritional factors that may alter the dose response. Two models in rats in which there is clear evidence of dietary or nutritional modulation of chemical carcinogenesis are mammary tumors induced by 7, 12-dimethylbenzanthracene (DMBA) or N-nitrosomethyl-urea (NMU) and hepatocarcinomas induced by many compounds. Mammary tumorigenesis is increased by increasing dietary content of some, but not all, fats. The time in tumor development at which fats act varies. Their mechanisms of action are not known but appear to include effects on the hormonal mileu and possibly mammary gland cell turnover and response to hormones. Hepatocarcinogenesis by chemicals is increased by dietary deficiency of the lipotropes methionine, choline and folate, possibly through alteration of carcinogen metabolism and increased hepatocyte DNA synthesis. The same deficiency induces cirrhosis. In humans, cirrhosis induced by alcoholism, viral hepatitis or unknown factors increases the risk for hepatocarcinoma. Alcohol-induced folate or other deficiency can be a contributory factor in the alcoholics. Infection with hepatitis B virus is increased in alcoholics and in patients with hepatocarcinoma and may be an initiating or modulating factor for tumors.
Influence of cocaine on ruptured intracranial aneurysms: a case control study of poor prognostic indicators
Authors: Vannemreddy Prasad , Caldito Gloria , Willis Brian , Nanda Anil 
Published: February 2008

Object
The purpose of this study was to determine whether cocaine use is a significant prognostic factor for outcome measures such as Hunt and Hess grade and Glasgow Outcome Scale (GOS) score among patients presenting with ruptured intracranial aneurysms (IAs).

Methods
The authors performed a MEDLINE/PubMed search for cases of ruptured IAs associated with cocaine use. Fourteen cases from the authors' experience were combined with 50 from a literature review, for a total of 64 cases associated with cocaine use. These 64 cases were compared with 65 cases without cocaine use (controls), which had been obtained from an aneurysm database. Logistic regression analysis was performed to determine significant prognostic factors for a poor Hunt and Hess grade and a poor GOS score, and a general linear model was applied to identify significant factors for these measures among cocaine users.

Results
There were 40 women in each group. The mean age was 32.3 ± 8.1 years in the cocaine group and 49.7 ± 10.6 years in the control group; thus, patients in the cocaine group were significantly younger (p < 0.01). Cocaine was snorted in 21% of cases, smoked in 55%, and intravenously injected or taken in through a combination of routes in 24%. Fifty-one percent of cocaine users and 7.7% of nonusers presented with a poor GOS score (p < 0.01). Fifty-six percent had ictus during cocaine abuse. At the end of a 30-day follow-up, 51% of the patients in the cocaine group had a good GOS score compared with 92% in the control group (p < 0.01). Controlling for the effects of other significant factors, cocaine use had a significant effect on Hunt and Hess grade (p < 0.03) and GOS score (p < 0.01). The odds of having a poor Hunt and Hess grade among cocaine users were 4.2 times greater than those in nonusers, and the odds of having a poor GOS score among cocaine users were 38.8 times greater.

Conclusions
Aneurysms were significantly smaller and ruptured at a younger age among cocaine users compared with nonusers. Although the poor clinical grade was not significantly different between the 2 groups, outcome was significantly worse in cocaine users.
Preoperative visualization of neurovascular anatomy in trigeminal neuralgia
Authors: Miller Jonathan , Acar Feridun , Hamilton Bronwyn , Burchiel Kim 
Published: February 2008

Object
The authors report on a novel technique to identify neurovascular compression in trigeminal neuralgia (TN). Using 3D reconstructed high-resolution balanced fast-field echo (BFFE) images fused with 3D time-of-flight (TOF) magnetic resonance (MR) angiography and Gd-enhanced 3D spoiled gradient recalled sequence, it is possible to objectively visualize the trigeminal nerve and nearby arteries and veins.

Methods
Magnetic resonance imaging was performed in 18 patients with unilateral TN using 3 sequences: BFFE, 3D TOF angiography, and 3D Gd-enhanced imaging. The images were imported into OsiriX imaging software; after their fusion, a 3D false-color reconstruction was produced using surface rendering. The reconstructed images objectively differentiate nerves and vessels and can be viewed from any angle, including the anticipated surgical approach.

Results
Fifteen patients were predicted to have neurovascular compression on the symptomatic side (9 arterial and 6 venous compressions). All patients had a vascular structure that was identical in location and configuration to that predicted on preoperative analysis. The 3 patients without predicted compression underwent surgical exploration because they manifested the classic symptoms. As expected, exploration in 2 of these patients revealed no offending vessel. The third patient had a small vein embedded in the trigeminal nerve that was beyond the resolution of the 3D Gd-enhanced study.

Conclusions
Combining BFFE with MR angiography and Gd-enhanced MR images capitalizes on the advantages of both techniques, enabling MR angiography and contrast-enhanced MR imaging discrimination of vascular structures at BFFE resolution. This results in an unambiguous 3D image that can be used to identify the neurovascular compression and plan the surgical approach.
Anatomical study of the trigeminal and facial cranial nerves with the aid of 3.0-tesla magnetic resonance imaging
Authors: Kakizawa Yukinari , Seguchi Tatsuya , Kodama Kunihiko , Ogiwara Toshihiro , Sasaki Tetsuo , Goto Tetsuya , Hongo Kazuhiro 
Published: February 2008

Object
Neuroimages often reveal that the trigeminal or facial nerve comes in contact with vessels but does not produce symptoms of trigeminal neuralgia (TN) or hemifacial spasm (HFS). The authors conducted this study to determine how often the trigeminal and facial nerves came in contact with vessels in individuals not suffering from TN or HFS. They also investigated the correlation between aging and the anatomical measurements of the trigeminal and facial nerves.

Methods
Between November 2005 and August 2006, 220 nerves in 110 individuals (60 women and 50 men; mean age 55.1 years, range 19–85 years) who had undergone brain magnetic resonance (MR) imaging for other reasons were studied. The lengths, angles, ratio, and contact points were measured in each individual. A correlation between each parameter and age was statistically analyzed.

Results
The mean (± standard deviation) length of the trigeminal nerve was 9.66 ± 1.71 mm, the mean distance between the bilateral trigeminal nerves was 31.97 ± 1.82 mm, and the mean angle between the trigeminal nerve and the midline was 9.71 ± 5.83°. The trigeminal nerve was significantly longer in older patients. Of 220 trigeminal nerves, 108 (49.0%; 51 women and 57 men) came in contact with vasculature. There was 1 contact point in 99 nerves (45%) and 2 contact points in 9 nerves (4.1%). Contact without deviation of the nerve was seen in 91 individuals (43 women and 48 men), and mild deviation was noted in 17 individuals (8 women and 9 men). There was no moderate or severe deviation in any individual in this series. The mean length of the facial nerve was 29.78 ± 2.31 mm, the mean distance between the bilateral facial nerves was 28.65 ± 2.22 mm, the angle between the nerve and midline was 69.68 ± 5.84°, and the vertical ratio at the porus acusticus was 0.467 ± 0.169. Of all facial nerves, 173 (78.6%; 101 in women and 72 in men) came in contact with some vasculature. Contact without deviation was seen on 64 sides (in 37 women and 27 men), mild deviation on 98 sides (in 57 women and 41 men), and moderate deviation on 11 sides (in 7 women and 4 men). There was no severe deviation of the facial nerve in this series. The proximal length of the facial nerve, interval, angle, and ratio against the age were significantly shorter or smaller in the older individuals.

Conclusions
The findings in asymptomatic individuals in this study will help in deciding which findings observed on MR images may cause symptoms. In addition, the authors describe the variations of normal anatomy in older individuals. Knowledge of the normal anatomy helps to hone the diagnostic practices for microvascular decompression, which may increase the feasible results on such surgery.
A stereotactic device for rabbits based on mandibular and cranial landmarks
Authors: Kockro Ralf A. , Giacomelli Rainer , Scheihing Martin , Aschoff Alfred , Hampl Juergen A. 
Published: February 2008

✓ The authors have developed a stereotactic device for use in rabbits that uses the plane at the base of the mandible combined with cranial sutures as an anatomical reference. The device was developed for a study designed to evaluate catheters for infection prophylaxis, and this required the implantation of silicone catheters along a reproducible trajectory through the lateral ventricle. Cadaver and atlas studies demonstrated consistent spatial relationships between intracranial structures and the surface plane on which the animals were resting during the surgery. This plane is formed by the 2 mandibular angles and the mandibular tip. The authors developed a stainless steel stereotactic device that uses this mandibular plane as well as the coronal and sagittal sutures as spatial references.
Operations were performed in 60 animals using the stereotactic device, and postmortem dissections of the animals' brains demonstrated 78.6% accuracy of the trajectory within a tolerance of deviation of 5°, and 94.6% accuracy within a tolerance of 10°. The accuracy of the trajectory of the last 18 consecutively operated animals was constantly within a tolerance of 5°. The device can be autoclaved and, since it is relatively simple and inexpensive to build, the authors manufactured 3 identical frames and used them alternately to operate under sterile conditions. The fast and pain-free head fixation minimized anesthesia-related risks. The authors' experiences suggest that the device is suitable for ventricular punctures and, dependant on the individual requirements of accuracy, other procedures that require “approximate” stereotactic guidance especially when a series of animals need to undergo operations quickly.
Pathophysiology and treatment of focal cerebral ischemia
Authors: Siesjö Bo K. 
Published: February 2008

✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk,” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K+/Ca++ transients, and inhibition of protein synthesis.
Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca++, Na+, and Cl−, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH.
In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca++) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca++.
A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca++ is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca++.