ABSTRACT
PURPOSE: Thoracolumbar spine injury is frequently seen with high-energy trauma but dislocation fractures are relatively rare in spinal trauma, which is often neurologically severe and requires urgent treatment. Therefore, it is essential to understand other concomitant injuries when treating dislocation fractures. The purpose of this study is to determine the differences in clinical features between thoracolumbar spine injury without dislocation and thoracolumbar dislocation fracture. METHODS: We conducted an observational study using the Japan Trauma Data Bank (2004-2019). A total of 734 dislocation fractures (Type C) and 32,382 thoracolumbar spine injuries without dislocation (Non-type C) were included in the study. The patient background, injury mechanism, and major complications in both groups were compared. In addition, multivariate analysis of predictors of the diagnosis of dislocation fracture using logistic regression analysis were performed. RESULTS: Items significantly more frequent in Type C than in Non-type C were males, hypotension, bradycardia, percentage of complete paralysis, falling objects, pincer pressure, accidents during sports, and thoracic artery injury (P < 0.001); items significantly more frequent in Non-type C than in Type C were falls and traffic accidents, head injury, and pelvic trauma (P < 0.001). Logistic regression analysis showed that younger age, male, complete paralysis, bradycardia, and hypotension were associated with dislocation fracture. CONCLUSION: Five associated factors were identified in the development of thoracolumbar dislocation fractures. LEVEL OF EVIDENCE: III.
Subject(s)
Fracture Dislocation , Joint Dislocations , Spinal Fractures , Spinal Injuries , Humans , Male , Female , Spinal Fractures/diagnostic imaging , Bradycardia , Thoracic Vertebrae/diagnostic imaging , Thoracic Vertebrae/injuries , Lumbar Vertebrae/diagnostic imaging , Lumbar Vertebrae/injuries , Spinal Injuries/diagnosis , Joint Dislocations/diagnostic imaging , ParalysisABSTRACT
We report the construction of diagnostics for ultrafast surface plasmon polariton (SPP) pulses that evolve spatiotemporally in femtosecond and nanometer scales. We constructed two types of scanning near-field optical microscopes (SNOMs) and verified that the temporal waveform of ultrafast SPP pulses can be measured by combining spectral interferometry (SI). In the illumination-collection (I-C) mode SNOM, which uses a single fiber probe to excite samples and collect optical responses, a lock-in detection scheme using a lock-in camera detects SI fringes even for extremely weak signal light pulses. With this I-C SI-SNOM scheme, we measured the complex plasmon response functions of gold (Au) nanorods on Ge2Sb2Te5 thin film, both in the crystal and amorphous phases. For a dual-probe SNOM (DSNOM), a dual-band modulation technique was introduced to independently control the probe-sample and probe-probe distances. With the DSNOM and by employing femtosecond SPP pulse excitation, we successfully measured the temporal waveform of an ultrafast SPP pulse that is propagating on an Au thin layer.
ABSTRACT
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a selective loss of dopaminergic neurons in the substantia nigra (SN), and oxidative stress is thought to contribute to the pathogenesis. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway, which is a cellular defense system against oxidative stress, is a promising target for therapeutics aimed at reducing neuronal death in PD. Previously, we have isolated 2',3'-dihydroxy-4',6'-dimethoxychalcone (DDC) from green perilla leaves as an activator of the Nrf2-ARE pathway. The present study showed the protective effect of DDC on PD models in vivo and in vitro. In a 6-hydroxydopamine (6-OHDA)-induced hemiparkinson's disease mouse model, intracerebral administration of DDC suppressed the dopaminergic neuronal loss and behavioral dysfunction. DDC upregulated the expression of heme oxygenase-1 (HO-1), one of the ARE-driven antioxidant enzymes, in astrocytes and microglia of the SN. In primary mesencephalic cultures, treatment with DDC also increased the HO-1 expression in astrocytes and microglia. DDC showed a protective effect against 6-OHDA-induced dopaminergic neuronal death, and the effect was suppressed by an HO-1 inhibitor. These results suggest that DDC prevents dopaminergic neurons from oxidative stress by upregulation of glial expression of HO-1.
