bluuebunny/crossref_metadata_2025_split huggingface dataset:
ROLE OF THROMBOMODULIN IN DETECTION OF ENDOTHELIAL CELL DESTRUCTION AFTER INFECTION WITH FALCIPARUM AND TERTIAN MALARIA
Authors: Mantik Max , Rampengan Tonny , Kilis Mariane , Tuda Josef 
Published: January 2008

INTRODUCTION: Thrombomodulin is an endothelial cell receptor for thrombin. In tropical and tertian malaria, thrombomodulin is secreted after endothelial cell destruction after infections with Plasmodium falciparum or Plasmodium vivax.
OBJECTIVE: Our goal was to investigate whether thrombomodulin levels can be used to detect the endothelial cell destruction after tropical or tertian malaria and whether thrombomodulin is related to the severity of tropical malaria.
METHODS: This was a cross-sectional observational analytical study conducted in 5 hospitals in north Sulawesi, Indonesia, from June to September 2006, in patients aged 2 to 13 years with tropical or tertian malaria. Thrombomodulin levels were determined with an enzyme-linked immunosorbent assay using a thrombomodulin kit (Fujirebio Diagnostics, Inc, Malvern, PA). Data were analyzed by independent t test and Spearman rank correlation coefficient.
RESULTS: For 30 patients with tropical malaria (thrombomodulin level: 0.060–0.180 FU/mL) and 2 patients with tertian malaria (thrombomodulin level: 0.068–0.075 FU/mL), there was a significant difference in t-test results between tropical and tertian malaria (P = .044). For 11 patients with severe malaria (thrombomodulin level: 0.086–0.162 FU/mL), there was also a very significant difference in t-test results for complicated and uncomplicated tropical malaria (P = .009). The Spearman rank test showed significant positive correlation between thrombomodulin and parasitemia levels (rs = 0.686; P = .001).
CONCLUSIONS: Thrombomodulin levels can be used to detect endothelial cell destruction in malaria; the thrombomodulin level in tropical malaria was found to be higher than that of tertian malaria. Thrombomodulin levels were very significantly different in complicated and uncomplicated tropical malaria and also correlated significantly with the degree of parasitemia.
USING NONSTEROIDAL ANTIINFLAMMATORY DRUGS IN VOLUME-DEPLETED CHILDREN CAN PRECIPITATE ACUTE RENAL FAILURE
Authors: John Cheri Mathews , Saroha Vivek , Jones Caroline 
Published: January 2008

INTRODUCTION: Nonsteroidal antiinflammatory drugs (NSAIDs) are ever increasing in popularity in hospital medicine and general practice and are readily available over-the-counter.
OBJECTIVE: Our goal was to illustrate the need to be aware of the effect of NSAIDs on dehydrated patients.
PATHOGENESIS: The risk of renal toxicity is increased in situations in which there is a stimulation of the renin-angiotensin system such as volume depletion. In these conditions, circulating vasoconstrictors are released, maintaining vascular resistance and blood pressure at the potential expense of regional organ blood flow. To maintain renal blood flow, counter-regulatory renal prostaglandins are released that counteract vasoconstrictors and normalize renal blood flow. NSAIDs blunt this counter-regulatory response and intensify the renal vasoconstriction, which leads to acute renal failure. In Table 1 we report 4 children with mild dehydration who developed acute renal failure after the use of therapeutic doses of NSAIDs in a children's hospital.
CONCLUSIONS: We recommend that NSAIDs should be avoided in children with actual or potential intravascular volume depletion. Although we have not proven cause and effect, additional research is needed to define the true risk of the potential renal complications of using NSAIDs in patients who are at risk of dehydration.
NOTE: The cases of the 4 children described in this report have been published elsewhere (John CM, Shukla R, Jones CA. Using NSAID in volume depleted children can precipitate acute renal failure. Arch Dis Child. 2007;92:524–526).
TABLE 1.Acute Renal Failure in 4 Children After Use of NSAIDsPatient No.1234Age, y1371413GenderMaleMaleMaleFemaleUnderlying pathologyCraniopharyngioma diabetes insipidusJuvenile idiopathic arthritis; fasted for surgeryJuvenile idiopathic arthritis with vomitingRelapse of Crohn diseaseNSAIDDiclofenac sodiumIndomethacin diclofenac sodiumDiclofenac sodiumDiclofenac sodiumHighest urea level, mmol urea/L10.712.910.722Highest creatinine level, μmol/L226146376629Normalization, d533Permanent impairment
EFFECT OF BCG VACCINATION ON SPLENIC DENDRITIC CELL DEVELOPMENT IN NEONATAL BALB/C MICE
Authors: Enmei Liu , Chunhua Liu , Yun He , Wei Liu , Xin Li , Liping Jiang , Xiqiang Yang 
Published: January 2008

INTRODUCTION: As an immunoregulator, Mycobacterium BCG has the potential to be applied in allergic disease such as asthma prevention in clinic. Previous studies showed that neonatal BCG vaccination promoted mouse splenic T helper 1 development.
OBJECTIVE: The objective of this study was to investigate further the impact of BCG vaccination on dendritic cell (DC) development in neonatal mice.
METHODS: Neonatal and adult BALB/C mice were divided into 2 groups: the control group and the BCG-treated group in which BALB/C mice were inoculated with 1 × 105 colony-forming units of BCG intraperitoneally. After 4 weeks, splenic cells were isolated and co-stimulatory molecules and major histocompatibility complex molecules were analyzed by flow cytometry on CD11c-positive cells.
RESULTS: CD11c+CD8α+ and CD11c+CD8α− DCs were found in spleen cells of BALB/C mice. In comparison with the control group, the percentage of CD8α− DCs was significantly decreased (45.00 ± 14.14 vs 67.00 ± 8.27) and that of CD8α+ DCs was strikingly increased (55.00 ± 14.14 vs 33.00 ± 8.27) in BCG-treated neonatal mice. In contrast, the percentage of CD8α− DCs markedly increased from 57% to 70% and that of CD8α+ DCs noticeably decreased from 43% to 30% in adult mice that were vaccinated. BCG vaccination upregulated the expression of co-stimulatory molecules on DC in adult and neonatal mice.
CONCLUSIONS: Our results indicate that development of T cells was induced by BCG vaccination through an effect on DC differentiation and maturation in BALB/C mice, possibly not only by DC phenotype but also by cytokines.
EXPRESSION CHANGE OF AQUAPORIN 1 IN HYPEROXIC LUNG INJURY
Authors: Xu Feng , Hao Jie , Tan Liping 
Published: January 2008

INTRODUCTION: Bronchopulmonary dysplasia (BPD) is a disease that is caused by prolonged high-concentration oxygen therapy, and its typical pathologic character is edema of pulmonary alveolus. Aquaporins play an important role in the fluid transition.
OBJECTIVE: The objective of this study was to examine the expression change of aquaporin 1 (AQP1) in hyperoxia-induced lung injury and the mechanism of action in lung edema.
METHODS: Thirty-two juvenile Wistar rats were randomly divided into breathing room air (n = 8) and hyperoxia exposure (O2 &gt; 95%; n = 8 at 3, 7, and 14 days, respectively). The distribution of AQP1 in the lung tissues and its mRNA expressions were detected by immunohistochemistry and reverse-transcription polymerase chain reaction.
RESULTS: Light microscopic findings in the hyperoxia group included edema, hemorrhage, and extensive inflammatory cells. The lung wet/dry ratio, the protein content in bronchoalveolar lavage fluid, and the lung leak index in the hyperoxia group were significantly higher than those in room air group. The expression of AQP1 mRNA in the lungs was significantly decreased at 3 days of hyperoxia exposure, minimized at 7 days, and increased from 14 days. Immunohistochemistry for AQP1 was seen primarily in microvascular endothelia cells around bronchus and alveolus and interstitial cells; the positive regions were similar between the room air group and the hyperoxia group, AQP1 protein expression in the lungs was significantly decreased at 3 days of hyperoxia exposure, minimized at 7 days, but increased at 14 days. The dynamic changes of AQP1 protein level coincided with the changes of AQP1 mRNA expression.
CONCLUSIONS: Hyperoxic lung injury may induce regulative imbalance of aquaporin expression. It may be 1 of the reasons for lung edema caused by hyperoxic lung injury.
SERUM LEVELS OF MYCN AMPLIFICATION IN NEUROBLASTOMA WITH TUMOR-RELEASED DNA BY REAL-TIME QUANTITATIVE POLYMERASE CHAIN REACTION
Authors: Sugimoto Tohru , Gotoh Takahiro , Iehara Tomoko , Tsuchiya Kunihiko , Ohira Miki , Nakagawara Akira , Hosoi Hajime 
Published: January 2008

INTRODUCTION: MYCN amplification (MNA) indicates a poor prognosis in neuroblastoma and is routinely assayed for therapy stratification.
OBJECTIVE: We aimed to develop a diagnostic tool to predict MYCN status by using serum DNA, which, in patients with cancer, predominantly originates from tumor-released DNA.
METHODS: Using DNA-based real-time quantitative polymerase chain reaction, we simultaneously quantified MYCN (2p24) and a reference gene, NAGK (2p12), and evaluated MYCN copy number as a MYCN/NAGK ratio in 87 patients with neuroblastoma whose MYCN status had been determined by Southern blotting. Of these patients, 17 had MYCN-amplified neuroblastoma, and 70 had nonamplified neuroblastoma.
RESULTS: The serum MYCN/NAGK ratio in the MNA group (median: 199.32; range: 17.1–901.6 [99% confidence interval: 107.0–528.7]) was significantly (P &lt; .001) higher than that in the non-MNA group (median: 0.87; range: 0.25–4.6 [99% confidence interval: 0.82–1.26], Mann-Whitney U test). The sensitivity and specificity of the serum MYCN/NAGK ratio as a diagnostic test were both 100% when the serum MYCN/NAGK ratio cutoff was set at 10.0. Among 6 patients in the MNA group whose clinical courses were followed, the serum ratios decreased to within the normal range in the patients in remission (n = 3), but they rose to high levels in the patients who had a relapse (n = 2) or failed to achieve remission (n = 1). The serum MYCN/NAGK ratio in the MNA group is likely to be the more sensitive tumor marker than conventional urinary vanillylmandelic and homovanillic acid markers and neuron-specific enolase markers to predict patients' clinical course.
CONCLUSIONS: Measurement of the serum MYCN/NAGK ratio seems to be a promising method for accurately assessing MYCN status in neuroblastoma.
APOPTOSIS OF ALVEOLAR TYPE II CELL AND C-JUN N-TERMINAL KINASE SIGNAL TRANSDUCTION INDUCED BY OXIDATIVE STRESS
Authors: Zhonhyi Lu , Yueqiang Fu 
Published: January 2008

INTRODUCTION: Alveolar epithelial apoptosis has been described in the early stages of bronchopulmonary dysplasia. The production of reactive oxygen species during hyperoxia is thought to contribute to alveolar epithelial apoptosis, but the molecular mechanisms of oxidative stress–induced alveolar epithelial cell death is unclear.
OBJECTIVE: The objective of this study was to explore the role of the c-Jun N-terminal protein kinase (JNK) pathway in the apoptosis of alveolar epithelial cells that is induced by oxidative stress.
METHODS: Primary cultured rat alveolar type cells were treated with 500 μM hydrogen peroxide (H2O2) at various time intervals (0, 1, 3, 6, and 9 hours), whereas some cells were pretreated with a specific JNK inhibitor (SP600125). Mitochondrial membrane potential (MMP) change, cell survival, and apoptotic ratios were measured by fluorescence microscopy, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and flow cytometry analysis, respectively. The expression of phosphorylated JNK and Bax was detected by Western blot.
RESULTS: H2O2 treatment resulted in cell apoptosis and a decrease of MMP and cell viability in a time-dependent manner. Meanwhile, the JNK was activated and peaked at 30 minutes, and the Bax expression level was increased. Pretreated SP600125 enhanced cell viability and decreased apoptotic ratios after H2O2 treatment. The expression of Bax declined after using SP600125 compared with cells that were treated with H2O2 only.
CONCLUSIONS: High levels of oxidative stress induced cell apoptosis in a time-dependent manner. The mechanisms of oxidative stress–induced cell apoptosis involves JNK activation, Bax upregulation, and MMP decrease. JNK activation could improve the expression of Bax and play a proapoptotic role in the regulation of apoptosis that is induced by oxidative stress.
Assessment of mitochondrial impairment in traumatic brain injury using high-resolution proton magnetic resonance spectroscopy
Authors: Signoretti Stefano , Marmarou Anthony , Aygok Gunes A. , Fatouros Panos P. , Portella Gina , Bullock Ross M. 
Published: January 2008

Object
The goal of this study was to demonstrate the posttraumatic neurochemical damage in normal-appearing brain and to assess mitochondrial dysfunction by measuring N-acetylaspartate (NAA) levels in patients with severe head injuries, using proton (1H) magnetic resonance (MR) spectroscopy.

Methods
Semiquantitative analysis of NAA relative to creatine-containing compounds (Cr) and choline (Cho) was carried out from proton spectra obtained by means of chemical shift (CS) imaging and single-voxel (SV) methods in 25 patients with severe traumatic brain injuries (TBIs) (Glasgow Coma Scale scores ≤ 8) using a 1.5-tesla MR unit. Proton MR spectroscopy was also performed in 5 healthy volunteers (controls).

Results
The SV studies in patients with diffuse TBI showed partial reduction of NAA/Cho and NAA/Cr ratios within the first 10 days after injury (means ± standard deviations 1.59 ± 0.46 and 1.44 ± 0.21, respectively, in the patients compared with 2.08 ± 0.26 and 2.04 ± 0.31, respectively, in the controls; nonsignificant difference). The ratios gradually declined in all patients as time from injury increased (mean minimum values NAA/Cho 1.05 ± 0.44 and NAA/Cr 1.05 ± 0.30, p < 0.03 and p < 0.02, respectively). This reduction was greater in patients with less favorable outcomes. In patients with focal injuries, the periphery of the lesions revealed identical trends of NAA/Cho and NAA/Cr decrease. These reductions correlated with outcome at 6 months (p < 0.01). Assessment with multivoxel methods (CS imaging) demonstrated that, in diffuse injury, NAA levels declined uniformly throughout the brain. At 40 days postinjury, initially low NAA/Cho levels had recovered to near baseline in patients who had good outcomes, whereas no recovery was evident in patients with poor outcomes (p < 0.01).

Conclusions
Using 1H-MR spectroscopy, it is possible to detect the posttraumatic neurochemical damage of the injured brain when conventional neuroimaging techniques reveal no abnormality. Reduction of NAA levels is a dynamic process, evolving over time, decreasing and remaining low throughout the involved tissue in patients with poor outcomes. Recovery of NAA levels in patients with favorable outcomes suggests marginal mitochondrial impairment and possible resynthesis from vital neurons.
En bloc petrosectomy for malignant tumors involving the external auditory canal and middle ear: surgical methods and long-term outcome
Authors: Okada Takeshi , Saito Kiyoshi , Takahashi Masakatsu , Hasegawa Yasuhisa , Fujimoto Yasushi , Terada Akihiro , Kamei Yuzuru , Yoshida Jun 
Published: January 2008

Object
The aim of this study was to describe a method for resecting malignant tumors originating in the external auditory canal or middle ear and requiring en bloc resection of the petrous bone.

Methods
Between 1995 and 2005, the authors performed en bloc petrosectomy for 18 malignant tumors in 9 male and 9 female patients, ranging in age from 15 to 74 years. Fourteen tumors originated in the external ear, 2 in the middle ear, and 2 in the parotid gland. The pathological entities included 15 squamous cell carcinomas, 2 adenoid cystic carcinomas, and 1 rhabdomyosarcoma. Through an L-shaped temporosuboccipital craniotomy, a medial osteotomy was created through the inner ear for tumors without extension into the inner ear (14 cases) and through the tip of the petrous bone for tumors reaching the inner ear (4 cases). Temporal dura mater in 3 patients and the base of the temporal lobe in 2 patients were included in the en bloc resection.

Results
Surgical complications occurred in 5 patients (28%) with no deaths. During a mean follow-up period of 45 months, 3 patients died of tumor recurrence. Overall, 2- and 5-year survival rates were 86 and 78%, respectively. Two of three patients with dural extension and 1 of 2 with brain invasion remain alive. Two of four patients with tumor extension into the inner ear died.

Conclusions
En bloc petrosectomy is recommended for malignant tumors of the ear. It is safe and effective for lesions limited to the middle ear and may be the procedure of choice for tumors reaching the inner ear and those with dural or brain invasion.
Length of tumor–cochlear nerve contact and hearing outcome after surgery for vestibular schwannoma
Authors: Yong Raymund L. , Westerberg Brian D. , Dong Charles , Akagami Ryojo 
Published: January 2008

Object
Tumor size is likely to be a major determinant of hearing preservation after surgery for vestibular schwannoma. Findings in some large case series have not supported this concept, possibly due to variation in the technique used for tumor measurement. The authors sought to determine if the length of tumor–cochlear nerve contact was predictive of hearing outcome in adults undergoing resection of a vestibular schwannoma.

Methods
Patients who underwent a hearing-preserving approach for resection of a vestibular schwannoma at one institution by a neurosurgeon/neurotologist team between 2001 and 2005 were screened. Patients with American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS) Class A or B hearing preoperatively were included. Magnetic resonance images were reviewed and used to calculate the length of tumor–cochlear nerve contact. Tumors were also measured according to AAO-HNS guidelines.

Results
Thirty-one patients were included, 8 (26%) of whom had hearing preservation. Univariate analysis revealed that extracanalicular length of tumor–cochlear nerve contact (p = 0.0365), preoperative hearing class (p = 0.028), I–V interpeak latency of the brainstem auditory evoked potential (p = 0.021), and the interaural I–V interpeak latency difference (p = 0.018) were predictive of hearing outcome. Multivariate analysis confirmed the predictive value of extra-canalicular length of contact and preoperative hearing class (p = 0.041 and p = 0.0235, respectively).

Conclusions
Vestibular schwannomas with greater lengths of tumor–cochlear nerve contact increase a patient's risk for hearing loss after surgery with attempted hearing preservation. Involvement of the internal auditory canal produces a constant risk of hearing loss. Data from the experience of a single surgical team can be used to estimate the probability of good hearing outcome for any given patient with serviceable hearing and a vestibular schwannoma.
Gamma Knife thalamotomy for essential tremor
Authors: Kondziolka Douglas , Ong Joseph G. , Lee John Y. K. , Moore Robert Y. , Flickinger John C. , Lunsford L. Dade 
Published: January 2008

Object
The purpose of this study was to evaluate the results following Gamma Knife thalamotomy (GKT) for medically refractory essential tremor in a series of patients in whom open surgical techniques were not desirable.

Methods
Thirty-one patients underwent GKT for disabling essential tremor after medical therapy had failed. Their mean age was 77 years. Most patients were elderly or had concomitant medical illnesses. A single 4-mm isocenter was used to target a maximum dose of 130 or 140 Gy to the nucleus ventralis intermedius. Items from the Fahn-Tolosa-Marin clinical tremor rating scale were used to grade tremor and handwriting before and after radiosurgery.

Results
The median follow-up was 36 months. In the group of 26 evaluable patients, the mean tremor score (± standard deviation) was 3.7 ± 0.1 preoperatively and 1.7 ± 0.3 after radiosurgery (p < 0.000015). The mean handwriting score was 2.8 ± 0.2 before GKT and 1.7 ± 0.2 afterward (p < 0.0002). After radiosurgery, 18 patients (69%) showed improvement in both action tremor and writing scores, 6 (23%) only in action tremor scores, and 3 (12%) in neither tremor nor writing. Permanent mild right hemiparesis and speech impairment developed in 1 patient 6 months after radiosurgery. Another patient had transient mild right hemiparesis and dysphagia.

Conclusions
Gamma Knife thalamotomy is a safe and effective therapy for medically refractory essential tremor. Its use is especially valuable for patients ineligible for radiofrequency thalamotomy or deep brain stimulation. Patients must be counseled on potential complications, including the low probability of a delayed neurological deficit.
The regulation of adult rodent hippocampal neurogenesis by deep brain stimulation
Authors: Toda Hiroki , Hamani Clement , Fawcett Adrian P. , Hutchison William D. , Lozano Andres M. 
Published: January 2008

Object
To examine the influence of deep brain stimulation on hippocampal neurogenesis in an adult rodent model.

Methods
Rats were anesthetized and treated for 1 hour with electrical stimulation of the anterior nucleus of the thalamus (AN) or sham surgery. The animals were injected with 5′-bromo-2′-deoxyuridine (BrdU) 1–7 days after surgery and killed 24 hours or 28 days later. The authors counted the BrdU-positive cells in the dentate gyrus (DG) of the hippocampus. To investigate the fate of these cells, they also stained sections for doublecortin, NeuN, and GFAP and analyzed the results with confocal microscopy. In a second set of experiments they assessed the number of DG BrdU-positive cells in animals treated with corticosterone (a known suppressor of hippocampal neurogenesis) and sham surgery, corticosterone and AN stimulation, or vehicle and sham surgery.

Results
Animals receiving AN high-frequency stimulation (2.5 V, 90 μsec, 130 Hz) had a 2- to 3-fold increase in the number of DG BrdU-positive cells compared with nonstimulated controls. This increase was not seen with stimulation at 10 Hz. Most BrdU-positive cells assumed a neuronal cell fate. As expected, treatment with corticosterone significantly reduced the number of DG BrdU-positive cells. This steroid-induced reduction of neurogenesis was reversed by AN stimulation.

Conclusions
High-frequency stimulation of the AN increases the hippocampal neurogenesis and restores experimentally suppressed neurogenesis. Interventions that increase hippocampal neurogenesis have been associated with enhanced behavioral performance. In this context, it may be possible to use electrical stimulation to treat conditions associated with impairment of hippocampal function.
Comparison of the therapeutic potential of adult and embryonic neural precursor cells in a rat model of Parkinson disease
Authors: Muraoka Kenichiro , Shingo Tetsuro , Yasuhara Takao , Kameda Masahiro , Yuen Wen Ji , Uozumi Takashi , Matsui Toshihiro , Miyoshi Yasuyuki , Date Isao 
Published: January 2008

Object
The therapeutic effects of adult and embryonic neural precursor cells (NPCs) were evaluated and their therapeutic potential compared in a rat model of Parkinson disease.

Methods
Adult NPCs were obtained from the subventricular zone and embryonic NPCs were taken from the ganglionic eminence of 14-day-old embryos. Each NPC type was cultured with epidermal growth factor. The in vitro neuronal differentiation rate of adult NPCs was approximately equivalent to that of embryonic NPCs after two passages. Next, the NPCs were transfected with either green fluorescent protein or glial cell line–derived neurotrophic factor (GDNF) by adenoviral infection and transplanted into the striata in a rat model of Parkinson disease (PD) induced by unilateral intrastriatal injection of 6-hydroxydopamine. An amphetamine-induced rotation test was used to evaluate rat behavioral improvement, and immunohistochemical analysis was performed to compare grafted cell survival, differentiation, and host tissue changes.

Results
The rats with GDNF-transfected NPCs had significantly fewer amphetamine-induced rotations and less histological damage. Except for the proportion of surviving grafted cells, there were no significant differences between adult and embryonic NPCs.

Conclusions
Adult and embryonic NPCs have a comparable therapeutic potential in a rat model of PD.