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Biomedical subjects

Daniel C Lu

Publications and source records attributed to Daniel C Lu.

6 recordsLinked to original sources
PubMed2007

Corpectomy followed by the placement of instrumentation with titanium cages and recombinant human bone morphogenetic protein-2 for vertebral osteomyelitis.

OBJECT: The treatment of vertebral osteomyelitis includes antibiotics with or without surgical intervention. The decision to place instrumentation into an infected spinal column remains controversial. The use of recombinant human bone morphogenetic protein-2 (rhBMP-2) in patients with osteomyelitis is also extremely controversial. The authors review their experience in performing corpectomy and fusion with titanium cages and rhBMP-2 in patients with vertebral instability and/or neurological compromise due to vertebral osteomyelitis. METHODS: Data obtained in 15 patients treated between 2001 and 2005 were included in this analysis. Nine patients presented primarily with axial pain and six with radiculopathy or myelopathy. Seven patients had an associated epidural abscess. The cervical spine was affected in six patients, the thoracic spine in five, and the lumbar spine in four. All patients underwent corpectomy of the involved vertebral bodies; the authors then performed spinal reconstruction, placing a titanium cage-plate system with morcellized allograft/autograft and rhBMP-2. In 10 patients, supplemental posterolateral screw-rod fixation was conducted. A one-level corpectomy was performed in one patient, a two-level corpectomy in 13, and a six-level corpectomy in one. A morcellized allograft and rhBMP-2-filled titanium cage was used in 10 patients, and an autograft and rhBMP-2-filled cage in five patients. The most common pathogen was Staphylococcus aureus. All patients received intravenous antibiotics for at least 6 weeks postoperatively, and life-long antibiotic therapy was required in three patients with coccidiomycoses, candida, and tuberculosis osteomyelitis, respectively. There were no recurrent infections. Radiography demonstrated evidence of fusion in all patients at the last follow-up examination. The mean follow-up period was 20 months. CONCLUSIONS: Corpectomy followed by titanium cage-plate reconstruction and the placement of rhBMP-2 may be a safe and effective treatment for selected patients with vertebral osteomyelitis. This surgical therapy does not appear, at least based on preliminary results, to lead to recurrent hardware infections. Based on the results obtained in this limited series, the authors found that rhBMP-2 can be used in the setting of active infection with excellent fusion rates and without complication. The morbidity associated with the autograft donor site is avoided when using cages. Antibiotic therapy tailored to the specific organism should be continued for at least 6 weeks after surgery, and life-long therapy is required in cases of fungal or tuberculosis infections.

Adult↗
PubMed2006

Multimodality treatment of trigeminal neuralgia: impact of radiosurgery and high resolution magnetic resonance imaging.

This study was conducted to evaluate the two main surgical modalities, microvascular decompression (MVD) and gamma-knife radiosurgery (GK), the treatment of trigeminal neuralgia (TN) and outline for an algorithm for the selection of these procedures. The authors have identified distinct differences in the two treatment groups and formulated a scale that predicts the outcome and satisfaction of patients who underwent the procedures. This series included 34 TN patients treated in 2000 and 2001 with MVD (19) and GK (15). Patients with TN associated with tumor or multiple sclerosis were excluded. Each patient's age, past medical history, clinical features of pain or pre-operative pain grade, duration of TN, medications, and prior surgical procedures were recorded. Long-term results were assessed by a structured interview by telephone. Clinical outcome was classified as excellent (complete relief without medications and numbness), good (complete relief without medications), fair (> 50% relief or with substantial numbness and weakness), or poor (< 50% relief or treatment failure). Patient self-rated satisfaction score was rated on a scale of 1 (unsatisfied) to 10 (completely satisfied). Statistical analysis was performed by paired t-tests and anova with post-hoc analysis by the Tukey-Kramer method. The median follow-up was 17 months (18 months for MVD and 16 months for GK). The average age of MVD patients was 61 years compared to 74 years for GK patients (p = 0.0005). In both groups there was a female majority (68% for MVD and 60% for GK). The latency between first symptom of TN and treatment procedure was 3.0 years for MVD and 3.9 years for GK (p > 0.05). There was no significant difference in pain grade between the two groups. The average TN complexity grade was significantly different between the two groups (3.0 for MVD and 5.8 for GK) (p < 0.001). Average response to procedure for MVD was 3.4 (good) and 2.4 (fair) for GK (p = 0.017). The satisfaction outcome for MVD was 8.7 compared to 6.4 for GK (p = 0.02). There was a significant correlation (r = -0.818, p < 0.001) between TN complexity grade and response. Additionally, a significant correlation between TN complexity grade and patient satisfaction was found (r = -0.763, p < 0.0001). The data here support the treatment algorithm employed by the senior author (JFA) of this study. The TN complexity grade accurately correlates with the patient's response and satisfaction to the surgical procedure. This complexity grade may be useful for patient counseling when choosing between treatment options.

Adult↗
PubMed2004

Management of pilocytic astrocytoma with diffuse leptomeningeal spread: two cases and review of the literature.

INTRODUCTION: Leptomeningeal dissemination of juvenile pilocytic astrocytoma (JPA) is a rare event. We report two children with disseminated JPAs treated with a chemotherapeutic agent, temozolomide, after progression of the disease despite surgery, traditional chemotherapy, and/or radiation therapy. CASE REPORTS: Patient 1 presented with hydrocephalus and progressive lower extremity weakness, and was found to have a suprasellar mass as well as extensive spinal disease. Ventriculoperitoneal shunting, decompressive laminectomy with spinal tumor debulking, and chemotherapy with carboplatin and vincristine were initially employed. However, disease progressed and craniospinal irradiation and temozolomide were used. Patient 1 remains in a fair condition today, 2 years later. Patient 2 presented at 8 months of age with failure to thrive. Imaging revealed a cystic lesion in the hypothalamic region with extensive subarachnoid metastatic disease to the spine. Biopsy was performed followed by chemotherapy with vincristine, cyclohexylchloroethylnitrosourea (CCNU), 6-TG, and procarbazine. Due to the continued progression of the disease, cytoreductive surgery was performed and her chemotherapeutic regimen was switched to temozolomide. Two years after initial presentation patient 2 is clinically much improved with stable residual disease. DISCUSSION: We review the literature and discuss treatment strategies for this challenging disease.

Antineoplastic Agents, Alkylating↗
PubMed2003

Amyloid beta protein toxicity mediated by the formation of amyloid-beta protein precursor complexes.

The amyloid-beta protein precursor, a type 1 transmembrane protein, gives rise to the amyloid beta-protein, a neurotoxic peptide postulated to be involved in the pathogenesis of Alzheimer's disease. Here, we show that soluble amyloid beta protein accelerates amyloid precursor protein complex formation, a process that contributes to neuronal cell death. The mechanism of cell death involves the recruitment of caspase-8 to the complex, followed by intracytoplasmic caspase cleavage of amyloid precursor protein. In vivo, the levels of soluble amyloid beta protein correlated with caspase-cleaved fragments of the amyloid precursor protein in brains of Alzheimer's disease subjects. These findings suggest that soluble amyloid beta protein-induced multimerization of the amyloid precursor protein may be another mechanism by which amyloid beta protein contributes to synapse loss and neuronal cell death seen in Alzheimer's disease.

Amyloid beta-Peptides↗
PubMed2003

Caspase cleavage of the amyloid precursor protein modulates amyloid beta-protein toxicity.

The amyloid beta-protein precursor (APP) is proteolytically cleaved to generate the amyloid beta-protein (Abeta), the principal constituent of senile plaques found in Alzheimer's disease (AD). In addition, Abeta in its oligomeric and fibrillar forms have been hypothesized to induce neuronal toxicity. We and others have previously shown that APP can be cleaved by caspases at the C-terminus to generate a potentially cytotoxic peptide termed C31. Furthermore, this cleavage event and caspase activation were increased in the brains of AD, but not control, cases. In this study, we show that in cultured cells, Abeta induces caspase cleavage of APP in the C-terminus and that the subsequent generation of C31 contributes to the apoptotic cell death associated with Abeta. Interestingly, both Abeta toxicity and C31 pathway are dependent on the presence of APP. Both APP-dependent Abeta toxicity and C31-induced apoptotic cell death involve apical or initiator caspases-8 and -9. Our results suggest that Abeta-mediated toxicity initiates a cascade of events that includes caspase activation and APP cleavage. These findings link C31 generation and its potential cell death activity to Abeta cytotoxicity, the leading mechanism proposed for neuronal death in AD.

Amino Acid Substitution↗