Symptom clustering in older Taiwanese children with cancer.

PURPOSE/OBJECTIVES: To derive symptom clusters occurring in a large group of older pediatric patients with cancer in Taiwan and to examine whether each cluster differed based on gender, type of cancer and disease, pain, and functional status. DESIGN: Descriptive, correlational study. SETTING: Pediatric oncology inpatient unit and outpatient clinics in Taiwan. SAMPLE: 144 pediatric patients with cancer, aged 10-18 years. METHODS: Subjects completed the Memorial Symptom Assessment Scale 10-18, the Play Performance Scale for Children, and a demographic questionnaire. Medical records provided disease and treatment data. Cluster analysis techniques were used to identify the symptoms that clustered together by demographic characteristics, as well as disease, pain, and functional status. MAIN RESEARCH VARIABLES: Symptom cluster, pain status, and functional status. FINDINGS: Five clusters were identified from the statistical analysis. The symptoms that clustered together were somewhat surprising, and some can be explained by cultural differences. Patients with pain reported statistically significant higher distress in all five clusters. CONCLUSIONS: Five symptom clusters are identified in older Taiwanese children with cancer. The way and possible rationale of how these symptoms clustered together is discussed. IMPLICATIONS FOR NURSING: This is the first study that used a statistical procedure to derive symptom clusters experienced by pediatric oncology patients. Knowledge from this study can provide a starting point to investigate the stability of symptom clusters with different states of disease, different populations, and over various periods of time.

Cranial repair using BMP-2 gene engineered bone marrow stromal cells.

BACKGROUND: Bone grafts, allografts, and biocompatible artificial bone substitutes all have their shortcomings when used for the repair of cranial bone defects. Tissue engineered bone shows promise as an alternative for the repair of these defects. MATERIALS AND METHODS: Rabbit bone marrow mesenchymal stromal cells (MSCs) were separated from iliac crest aspirates and expanded in a monolayer culture 1 month before implantation. These MSCs were then infected with replication-defective adenovirus-human BMP-2 genes 1 week before implantation. Bilateral critical-size cranial defects were created in the animal with removal of osteoinductive periosteum and dura. MSCs were mixed with alginate UP (ultrapure) to form MSC/polymer construct. MSCs used for the control site were infected with adenovirus beta-galactosidase (beta-gal). After 1 week, 6 weeks, and 3 months, five rabbits from each experimental group were sacrificed and the cranial defect site was examined by histology study. RESULTS: Near-complete repair of the large size cranial defects using the tissue engineered MSC/alginate construct was observed. The H&E stain and von Kossa's staining should better regenerate bone at the experiment site. A statistically significant difference in bone formation was noted by 3D CT imaging at 3 months post-BMP-2 treatment of the cranial defects (0.79 +/- 0.06 versus 0.47 +/- 0.05 cm(2), P < 0.001) but not at 6 weeks (0.36 +/- 0.04 versus 0.33 +/- 0.03 cm(2), P = 0.347). CONCLUSIONS: Near-complete repair of large cranial defects can be achieved using tissue engineered bone. The use of newly developed polymers as well as the integration of the stem cell concept with gene medicine is necessary to attain this goal.

Ex vivo gene therapy in autologous critical-size craniofacial bone regeneration.

In therapeutic bone repairs, autologous bone grafts, conventional or vascularized allografts, and biocompatible artificial bone substitutes all have their shortcomings. The bone formed from peptides [recombinant human bone morphogenetic proteins (BMPs)], demineralized bone powder, or a combination of both is small in size. Tissue engineering may be an alternative for cranial bone repair. In this study, the authors developed an animal model to test the hypothesis that replication-defective, adenovirus-mediated human BMP-2 gene transfer to bone marrow stromal cells enhances the autologous bone formation for repairing a critical-size craniofacial defect. The mesenchymal stromal cells of miniature swine were separated from the iliac crest aspirate and expanded in monolayer culture 1 month before implantation. The cultured mesenchymal stromal cells were infected with recombinant, replication-defective human adenovirus BMP-2, 7 days before implantation. Bilateral 2 x 5-cm2 cranial defects were created, leaving no osteogenic periosteum and dura behind. Mesenchymal stromal cells at 5 x 10(7)/ml were mixed with collagen type I to form mesenchymal stromal cell/polymer constructs. Mesenchymal stromal cells used for the control site were infected with adenovirus beta-Gal under the same conditions. After 6 weeks and 3 months, 10 miniature swine were euthanized and the cranium repair was examined. Near-complete repair of the critical-size cranial defect by tissue-engineered mesenchymal stromal cell/collagen type I construct was observed. The new bone formation area (in square centimeters) measured by three-dimensional computed tomography demonstrated that the improvement from 6 weeks to 3 months was significantly greater on the experimental side than on the control side (2.15 cm2 versus 0.54 cm2, p < 0.001) and significantly greater at 3 months than at 6 weeks (2.13 cm2 versus 0.52 cm2, p < 0.001). The difference between the experimental and control groups was significant at 3 months (mean difference, 2.13 cm2; p < 0.001). The maximal compressive strength of the new bone was similar to that of the normal cranial bone when evaluated by biomechanical testing (cranium bone versus tissue-engineered bone, 88.646 +/- 5.121 MPa versus 80.536 +/- 19.302 MPa; p = 0.227). Adenovirus was absent from all constructs by immunochemical staining at 6 weeks and 3 months after implantation. The successful repair of cranial defects in this experiment demonstrates the efficacy of the integration of the autologous stem cell concept, gene medicine, and polymers in producing tissue-engineered bone.

Primary medulla oblongata germinoma: a case report and review of the literature.

We describe a case of primary intracranial medulla oblongata germinoma in a 16-year-old girl who presented with progressive headache and blurred vision. Magnetic resonance imaging demonstrated a heterogeneous exophytic mass arising from dorsal aspect of medulla oblongata with extension into fourth ventricle. The differential diagnosis for this patient had included ependymoma, exophytic glioma, medulloblastoma and choroid plexus papilloma. After surgical resection and radiation therapy, she remains alive and recurrence-free for 7 years.

Sleep deprivation inhibits expression of NADPH-d and NOS while activating microglia and astroglia in the rat hippocampus.

This study investigated the expression of nitric oxide (NO)-synthesizing enzymes and the glial reaction in the rat hippocampal formation following sleep deprivation for 5 days. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity was markedly reduced in the hippocampal CA1, CA2 and CA3 sectors as well as in the dentate gyrus, suggesting a suppression of NO production in these areas. Microglial cells were hypertrophic and showed an up-regulation of complement type 3 receptors as determined by antibody OX-42. However, expression of major histocompatibility complex class I and II antigens, and antigen of monocyte/macrophage lineage marked by OX-18, OX-6 and ED1, respectively, was undetected. Astrocytes also displayed hypertrophied processes with enhanced glial fibrillary acidic protein (GFAP) immunoreactivity. Western blots of hippocampal tissues corroborated the above-mentioned morphological findings in that expression of NO-synthase (NOS) was decreased while that of OX-42 and GFAP was increased in the sleep-deprived rats. Since NO is thought to be involved in memory consolidation processes in the hippocampus during sleep, the inhibition of NADPH-d and NOS reactivities may account for the memory decline after long-term sleep deprivation. The concomitant reactions in microglia and astrocytes suggest the involvement of these cells in the deleterious effect of prolonged sleep deprivation.

Synaptic remodeling in the dorsal motor nucleus of the vagus nerve following vagal-hypoglossal nerve anastomosis in the cat.

Horseradish peroxidase (HRP) retrograde tracing techniques and morphometric analyses were performed to investigate synaptic remodeling associated with neuronal and glial changes in the dorsal motor nucleus of the vagus (DMV) of cats after vagal-hypoglossal nerve anastomosis (VHA). At 25 days postoperation (dpo), in the early target-reinnervation stage, there were 50% fewer presynaptic boutons containing round vesicles (R) or round and large dense-cored synaptic vesicles (R+D) contacting HRP-labeled DMV motoneurons. The loss of R boutons was maintained throughout the remaining postoperative intervals up to 500 dpo, whereas R+D boutons were further reduced at 123 dpo but were restored at 315 dpo, so that, by 500 dpo, 71.4% of them had gained access to the DMV motoneurons. Boutons containing pleomorphic synaptic vesicles (P) were completely disconnected from the DMV motoneurons at 25 dpo and did not reappear even in the long-term reinnervation stage. Loss and recovery of presynaptic boutons occurred in parallel with changes in astroglial ensheathment of the DMV motoneurons. It is suggested that synaptic remodeling associated with astroglial ensheathment in the DMV may be influenced by some retrogradely transported factors/signals derived from the newly acquired target organ, viz. tongue skeletal musculature. Our results further suggest that the observed changes in boutonal configurations may be attributable to modified functions of the DMV motoneurons induced by VHA.

Pituitary apoplexy due to prolactinoma in a Taiwanese boy: patient report and review of the literature.

We report a Taiwanese boy who presented with apoplexy of a prolactinoma. A 12 9/12 year-old boy presented to our clinic with headache and visual deficit of bitemporal hemianopsia. Skull X-ray showed an enlarged sella. Magnetic resonance imaging (MRI) of the sella turcica showed a 4 x 2.5 x 2.5 cm mass, located at the sella turcica and extending upward to compress the optic chiasm. Preoperative laboratory data showed hyperprolactinemia, hypothyroidism and hypocortisonism. After a stress dose of i.v. hydrocortisone was given, he underwent transsphenoid surgery to remove the tumor. Immunohistochemical stains were positive for PRL in the tumor cells. After surgery, he suffered from neurogenic diabetes insipidus, hypopituitarism and hyperprolactinemia, with serum PRL level of 491 ng/ml. Visual field examination was normal 4 months later. In conclusion, pituitary apoplexy is rare in children but should be considered if a patient suffers from headache, vomiting, and visual deficit. Brain MRI is preferred for diagnosis. Dopaminergic agonists should be given if residual tumor or recurrence of prolactinoma is found after transsphenoidal surgery.

Minimally invasive procedure for ventriculoatrial shunt-combining a percutaneous approach with real-time transesophageal echocardiogram monitoring: report of six cases.

To make the ventriculo atrial (VA) shunt procedure less invasive and avoid atrial catheter malpositioning, we combined a percutaneous approach with transesophageal echocardiogram (TEE) to monitor the atrial catheter tip. From July 1995 to October 1996, we performed 6 VA shunt procedures by combining these 2 techniques. Except for one patient who had a concomitant Port-A catheter, which obscured the detection of TEE in the procedure, all other atrial catheters achieved ideal positioning and good function. The mean operation time was shorter, and the complications were fewer than those using the conventional procedure in our hospital. In addition to this particular aspect, by combining these 2 techniques, the VA shunt procedure can be performed much less invasively, but more accurately, quickly, and safely.

Spontaneous intracranial hemorrhage caused by pheochromocytoma in a child.

We report a 6-year-old boy who presented with left occipital spontaneous lobar hematoma and hypertension. Cerebral angiography failed to demonstrate a vascular malformation. Subsequently, a left adrenal tumor was found that proved to be a pheochromocytoma. This is the first report in the literature of a lobar hematoma in a child caused by a concomitant pheochromocytoma. In children with hypertension and resulting intracerebral hematoma, a pheochromocytoma should be considered in the differential diagnosis.