Pulmonary spread of laryngeal papillomatosis: radiological findings

Laryngeal papillomatosis is a rare benign disease seen in children and young adults. The spread of laryngeal papillomas throughout the respiratory tract occurs rarely; and involvement of the distal bronchi, bronchioles, and lung parenchyma is very rare. We report a case of pulmonary spread of laryngeal papillomatosis in a 34-year-old man, focusing on the radiological evidence. Chest radiographs showed pulmonary nodules, but computed tomography scans more clearly demonstrated multiple small nodules showing cavitations and distributed centrilobularly. Pulmonary nodules and cavitations progressed gradually through the 6-year follow-up. The combination of clinical and characteristic radiological features suggests a diagnosis of pulmonary spread of laryngeal papillomatosis.     

Evaluation of setup error and adequate setup margins in patients with prostate cancer treated by IMRT and fixed in the prone position using a set of immobilization devices

PURPOSE: Positional reproducibility in patients with prostate cancer fixed in the prone position with a set of immobilization devices for external-beam intensity-modulated radiation therapy (IMRT) was evaluated. In addition, the adequacy of our positional error reduction strategy and current planning target volume (PTV) margins was also evaluated. RESULTS: Systematic error was corrected by the positional correction that we executed at the first stage of irradiation. The setup margin that we had calculated was 1.1 mm in the L-R direction, 1.3 mm in the A-P direction, and 2.7 mm in the C-C direction. CONCLUSION: We determined that the effectiveness of the method of correcting the error margin and the setup accuracy of the fixed method were well maintained.     

Transcranial photo-inactivation of neural activities in the mouse auditory cortex

Flavoprotein fluorescence in the brain is intimately coupled with neuronal aerobic energy metabolism. If flavoproteins are photobleached, neural activities may be affected owing to dysfunction in aerobic energy metabolism in mitochondria. We tested this possibility in cortical slices from mice, and found that exposure to blue light (λ = 475 nm) derived from a 20 mW diode laser for 50 min suppresses trans-synaptic components of field potentials. This finding formed the basis of a transcranial photo-inactivation technique, that was used to investigate auditory signal transmission between the anterior auditory field (AAF) and the primary auditory cortex (AI) in anesthetized mice. Cortical responses in AAF and AI, elicited by 5 kHz tonal stimuli, were visualized using transcranial flavoprotein fluorescence imaging. After determining responsive areas in AAF and AI, the auditory cortex was exposed to the blue diode laser via the intact skull, while either AAF or AI was protected with a piece of carbon paper. Although the photo-inactivation of AI had no significant effect on the fluorescence responses in AAF, the photo-inactivation of AAF significantly reduced the fluorescence responses in AI, indicating the presence of auditory signal transmission from AAF to AI.     

A case of recurrent breast cancer with multiple lung metastases responding to anastrozole monotherapy

A 51-year-old postmenopausal woman was referred to our hospital for treatment of ER-positive recurrent breast cancer. The patient had lung and pleural metastases with pleural effusion from breast cancer. She was treated with anastrozole, a 3rd-generation aromatiase inhibitor. The efficacy of the treatment was definite: the multiple metastatic lung lesions showed a partial response after 5 months' treatment, and reached a complete response after 14 months' treatment. The patient experienced no adverse effects with this therapy. Anastrozole therapy is a useful treatment for postmenopausal woman with ER-positive recurrent breast cancer.     

Amyotrophic lateral sclerosis models and human neuropathology: similarities and differences

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that primarily involves the motor neuron system. The author initially summarizes the principal features of human ALS neuropathology, and subsequently describes in detail ALS animal models mainly from the viewpoint of pathological similarities and differences. ALS animal models in this review include strains of rodents that are transgenic for superoxide dismutase 1 (SOD1), ALS2 knockout mice, and mice that are transgenic for cytoskeletal abnormalities. Although the neuropathological results obtained from human ALS autopsy cases are valuable and important, almost all of such cases represent only the terminal stage. This makes it difficult to clarify how and why ALS motor neurons are impaired at each clinical stage from disease onset to death, and as a consequence, human autopsy cases alone yield little insight into potential therapies for ALS. Although ALS animal models cannot replicate human ALS, in order to compensate for the shortcomings of studies using human ALS autopsy samples, researchers must inevitably rely on ALS animal models that can yield very important information for clarifying the pathogenesis of ALS in humans and for the establishment of reliable therapy. Of course, human ALS and all ALS animal models share one most important similarity in that both exhibit motor neuron degeneration/death. This important point of similarity has shed much light on the pathomechanisms of the motor neuron degeneration/death at the cellular and molecular levels that would not have been appreciated if only human ALS autopsy samples had been available. On the basis of the aspects covered in this review, it can be concluded that ALS animal models can yield very important information for clarifying the pathogenesis of ALS in humans and for the establishment of reliable therapy only in combination with detailed neuropathological data obtained from human ALS autopsy cases.     

Autosomal dominant Parkinson's disease

Over the past two decades the understanding and classification of Parkinson's disease (PD) has been revolutionized by genetic research. Currently, sixteen PARK loci have been identified with autosomal dominant genes such as SNCA, and LRRK2, and autosomal recessive genes such as PRKN, DJ-1, and PINK1. Among these genes, LRRK2 is the most prevalent. Additionally, susceptibility variants located on some of these genes are widely recognized as risk factors for PD in certain ethnic populations. Alpha synuclein Lewy body (LB) pathology, the hallmark of sporadic PD, is predominantly seen in carriers of SNCA and LRRK2. Recently two new autosomal dominant PD genes have been discovered, eukaryotic translation initiation factor 4-gamma (EIF4G1) and vacuolar protein sorting 35 (VPS35). EIF4G1 is associated with LB pathology; however, only limited data currently exists on pathology of the VPS35. Thus, it remains to be seen if LB pathology can be identified on autopsy examination of carriers of VPS35 gene. The mechanism behind the cause of PD has yet to be elucidated; however, genetic studies on autosomal dominant PD have provided novel insights into the potential etiology of PD. Thus, paving the way for future targeted therapies aimed at disease prevention and cure.