Induction of Genes Expressed in Endothelial Cells of the Corpus Callosum in the Chronic Cerebral Hypoperfusion Rat Model.

BACKGROUND: Cerebrovascular white matter lesions (WMLs) are associated with cognitive impairment in patients with subcortical vascular dementia. We performed a comprehensive gene expression analysis to elucidate genes associated with WML development in a chronic cerebral hypoperfusion rat model. METHODS: Brains of rats with bilateral carotid ligation (2VO, n = 10) and sham-operated rats (n = 5-10/group) were removed on days 1, 7, or 28 after surgery. Total RNA isolated from the corpus callosum was evaluated by microarray analysis and quantitative reverse transcription-polymerase chain reaction. RESULTS: On days 7 and 28, WMLs exhibited histologic changes. On day 7, 16 genes were differentially expressed between groups. mRNA levels of Ptprb, Kcnj8, Crispld2, Bcl6b, and Gja5 were differentially expressed in 2VO rats on day 7, but then returned to normal, whereas mRNA levels of Vwf and Trappc6a were upregulated after day 7. Immunohistochemistry showed that GJA5 and vWF were detected in endothelial cells, KCNJ8 in endothelial cells and astrocytes, CRISPLD2 in neurons and astrocytes, and TRAPPC6A in neurons. CONCLUSION: Our findings indicate novel genes that may be associated with WML development in the chronic cerebral hypoperfusion rat model, and suggest an important role of neurovascular dysfunction in the pathophysiology.

Effect of white matter lesions on brain perfusion in Alzheimer's disease.

BACKGROUND: This study examined the effect of white matter lesions (WMLs) on regional cerebral blood flow (rCBF) in patients with Alzheimer's disease (AD). METHODS: Ninety-eight patients with AD were included in the study (40 men and 58 women; mean age, 78.1 years). Cognitive function was assessed using the Mini-Mental State Examination. Brain magnetic resonance imaging (MRI) and (99m)Tc ethyl cysteinate dimer single photon emission computed tomography were performed in all subjects. AD patients were divided into two subgroups according to the presence of WMLs on MRI. A voxel-by-voxel group analysis using Statistical Parametric Mapping 8 was used to detect the differences in rCBF between the two groups. RESULTS: Fifty-seven of 98 AD patients (58%) showed mild to moderate WMLs on MRI. The prevalence of hypertension was significantly higher in AD patients with WMLs than in those without WMLs. AD patients with WMLs exhibited a significantly decreased rCBF in the anterior cingulate gyrus and insula, compared to AD patients without WMLs. CONCLUSION: We suggest that WMLs might influence brain regions associated with the limbic system in patients with AD.

Brain perfusion differences in parkinsonian disorders.

We aimed to objectively examine the brain perfusion differences between PD, Parkinson variant of multiple system atrophy, and progressive supranuclear palsy. (99m) Tc ethylcysteinate dimer single-photon emission CT (SPECT) was performed in 28 patients with PD, 12 with Parkinson variant of multiple system atrophy, 19 with progressive supranuclear palsy, and 17 age- and sex-matched control subjects. A voxel-by-voxel group analysis, using statistical parametric mapping 8, was performed to detect the differences of regional cerebral blood flow among three diseases and control groups. Regional cerebral blood flow was measured using the noninvasive Patlak plot method and calculated using a fully automated region of interest technique. Progressive supranuclear palsy showed decreased regional cerebral blood flow in the cingulate gyrus and thalamus, whereas Parkinson variant of multiple system atrophy showed decreased regional cerebral blood flow in the cerebellum, compared with other patients and controls. Regional cerebral blood flow in the thalamus could be used to discriminate progressive supranuclear palsy from other diseases and control subjects with high sensitivity. These findings suggest that parkinsonian disorders, such as PD, Parkinson variant of multiple system atrophy, and progressive supranuclear palsy show a distinct SPECT pattern in the frontal cortex, thalamus, and cerebellum. Moreover, the measurements of regional cerebral blood flow in the thalamus and cerebellum may be helpful in screening for the differential diagnosis of parkinsonian syndrome.

Relationship between thyroid hormone levels and regional cerebral blood flow in Alzheimer disease.

Subclinical thyroid disease and even variations in thyroid function within the normal range is associated with cognitive function and a risk of Alzheimer disease (AD). Several studies reported the effect of thyroid hormones on cerebral blood flow. The aim of this study was to objectively evaluate regional cerebral blood flow (rCBF) in association with thyroid hormone levels within the normal range in patients with AD. Serum thyroid-stimulating hormone (TSH), free T3, and free T4 levels were measured in 62 patients with AD (23 men and 39 women; age 56 to 91 y; mean age 77.3 y) and 27 control subjects (9 men and 18 women; age 61 to 93 y; mean age 75.8 y). The 99mTc ethylcysteinate dimer single photon emission computed tomography was performed in all subjects. The rCBF in the region of interest was measured by the noninvasive Patlak plot method and calculated using FineSRT, which is a fully automated region of interest technique. No significant correlation was found between thyroid hormone levels and Mini-Mental State Examination scores or global CBF values. Serum levels of TSH, but not free T3 or free T4, were significantly inversely correlated with rCBF in the middle and inferior temporal regions of right cerebral hemisphere in patients with AD. Control subjects showed no significant correlation between thyroid hormone levels and rCBF. Although these findings of a regional relationship must be considers preliminary, this study proposed the hypothesis that altered TSH levels within the normal range may be related to brain perfusion in right temporal region.

CD203c expression on human basophils is associated with asthma exacerbation.

BACKGROUND: CD203c is a basophil cell surface marker used to diagnose and monitor various allergic diseases, but its relationship to asthma is not clear. OBJECTIVE: We determined whether CD203c expression levels are associated with stable and exacerbated asthma. METHODS: We used flow cytometry to compare spontaneous expression levels of surface markers on basophils from patients with stable or exacerbated asthma and from healthy subjects. Longitudinal changes in these expression levels were measured after basophil stimulation by IgE-dependent or IgE-independent mechanisms and compared with patients' asthma status. RESULTS: Spontaneous expression levels of CD203c were significantly higher on basophils from patients with asthma exacerbation than patients with stable asthma or healthy subjects. In contrast, no differences in spontaneous expression levels of CD63 or CD69 were observed among the 3 groups. Anti-IgE-induced expression of CD203c significantly increased in basophils during asthma exacerbation (P = .005). Low concentrations of Dermatophagoides pteronyssinus or IL-3 induced higher expression levels of CD203c during asthma exacerbation than during clinical improvement; induction of CD203c expression by these antigens therefore correlates with asthma control. In the patients with clinical improvement, there was a correlation between spontaneous CD203c expression levels and the percent predicted values of FEV(1) (r = -0.761; P = .022). CONCLUSION: Asthma exacerbation was accompanied by increased expression of CD203c on basophils that decreased significantly during remission. Basophil expression levels of CD203c might therefore be used to monitor asthma in patients.

Increase in salivary cysteinyl-leukotriene concentration in patients with aspirin-intolerant asthma.

BACKGROUND: Cysteinyl-leukotrienes (CysLTs; LTC4, LTD4, and LTE4) play a considerable role in the pathophysiology of aspirin-intolerant asthma (AIA). Saliva has recently been validated as novel, simple, and noninvasive method for investigating inflammation in patients with asthma. The aim of this study is to clarify the molecular species of CysLT in saliva and to evaluate the CysLT and LTB4 concentrations in saliva in AIA patients. We also examined how the CysLT concentration in saliva reflects that of their corresponding urinary metabolite. METHODS: We preformed an analytical cross-sectional study. CysLT and LTB4 concentrations in saliva were quantified by enzyme immunoassay (EIA) following purification by high-performance liquid chromatography (HPLC). RESULTS: 1. When analyzed by EIA in combination with HPLC, saliva was found to consist of LTC4, LTD4 and LTE4 in similar amounts. 2. In saliva analysis among the three groups (AIA patients, aspirin-tolerant asthma [ATA] patients, and healthy subjects), both the concentrations of CysLTs and LTB4 were significantly higher in AIA patients than in ATA patients and healthy subjects. 3. We found significant correlations between CysLT concentration and LTB4 concentration in saliva in each group. 4. No significant correlation was found between the concentration of LTE4 in urine and that of CysLTs in saliva. CONCLUSIONS: In this study, we found higher concentrations of CysLTs and LTB4 in saliva from AIA patients than in saliva from ATA patients, suggesting that the quantification of CysLT and LTB4 concentrations in saliva may be another diagnostic strategy for AIA.

[A case of limbic encephalitis repeated aphasic status epilepticus with periodic lateralized epileptiform discharges].

We report a case of limbic encephalitis repeated aphasic status epilepticus with periodic lateralized epileptiform discharges (PLEDs). A 51-year-old man developed convulsions, psychiatric symptoms such as anxiety, phobia and ease of anger, and Wernicke's aphasia. Analysis of the cerebrospinal fluid (CSF) showed increase of leukocyte count (148/microl, mononuclear cells). Brain magnetic resonance imaging (MRI) showed hyperintensity lesions in the left medial temporal area and basal frontal area on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images. The electroencephalography (EEG) showed PLEDs over the left hemisphere, occurring at intervals of 0.5-1 Hz. Although his limbic symptoms improved, Wernicke's aphasia occurred periodically with PLEDs appearance. After the administration of antiepileptic drugs, his language performance improved, and PLEDs were completely disappeared. We diagnosed him limbic encephalitis with non-convulsive repeated aphasic status epilepticus with periodic lateralized epileptiform discharges. Aphasic status epilepticus should be considered in the patients with limbic encephalitis, and careful evaluation of aphasia and EEG should be necessary to diagnose of aphasic status epilepticus.

[A case of neurosarcoidosis with swelling and gadolinium enhancement of spinal nerve roots on magnetic resonance imaging].

An 80-year-old woman was admitted to our hospital because of developed sense of constriction in the trunk and gradually progressive numbness and muscle weakness in the upper and lower extremities. Cerebrospinal fluid analysis showed increased cell count and protein level. Gadolinium enhanced magnetic resonance imaging (MRI) of spine showed the enhancement and swelling of bilateral nerve root in the cervical and lumbar segments. Although chest computed tomography showed neither bilateral hilar lymphoadenopathy nor lung lesions and serum angiotensin converting enzyme and lysozyme (ACE) were normal, tuberculin skin test was negative and cell count and CD4/CD8 elevated in bronchoalveolar lavage fluid. Biopsy specimen of scalene lymph node showed noncaseating granuloma. The patient was treated with oral predonisolone, which improved her symptoms and abnormalities on MRI. It is important to consider neurosarcoidosis in the differential diagnosis of polyradiculopathy with swelling and gadolinium enhancement of spinal nerve roots.

Induction of GNE in myofibers after muscle injury.

OBJECTIVE: The aim of the present study was to clarify the expression of uridine diphospho-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) protein and mRNA in damaged or regenerating myofibers. METHODS: We investigated the muscle expression pattern of GNE protein by immunohistochemistry using a murine model involving intramuscular injection of cardiotoxin (CTX), and the expression level of GNE mRNA by quantitative real-time polymerase chain reaction analysis of damaged or regenerating myofibers that had been collected directly from tissue sections using laser-capture microdissection. RESULTS: The expression of GNE protein was increased in severely damaged myofibers as well as in regenerating myofibers with central nuclei, both of which also showed an increase in the expression of GNE mRNA. In regenerating myofibers, immunoreactivity for GNE protein in nuclei relative to that in the cytoplasm was higher at 7 days than at 4 days after CTX injection. CONCLUSION: Our findings suggest that GNE expression is induced when myofibers are damaged or regenerating, and that GNE plays a role in muscle regeneration.

Osteopontin levels are elevated in patients with eosinophilic pneumonia.

BACKGROUND AND OBJECTIVE: Osteopontin is a key cytokine involved in pro-inflammatory T helper type 1 (Th1)-associated immune responses, which has recently been implicated in allergic diseases. We investigated the pathogenic role of osteopontin in eosinophilic pneumonia. METHODS: The concentrations of osteopontin and Th1- or Th2-associated cytokines were measured in BAL fluid (BALF) from 41 patients with eosinophilic pneumonia, including those with acute (AEP, n = 12), chronic (CEP, n = 16), or drug-induced eosinophilic pneumonia (DEP, n = 13). The results were compared with those from patients with other interstitial lung diseases. Immunocytochemistry and double immunofluorescence labelling were performed to determine the cellular source of osteopontin. RESULTS: Osteopontin was significantly elevated in BALF from patients with eosinophilic pneumonia as compared with BALF from patients with drug-induced interstitial pneumonia, hypersensitivity pneumonitis, idiopathic interstitial pneumonia, or sarcoidosis, and also compared with BALF from healthy volunteers. Osteopontin concentrations elevated at the time of exacerbation decreased during clinical improvement, either spontaneously or as a result of corticosteroid therapy. Elevated concentrations of CXCL10, CCL17 and IL-10 were also detected in BALF from patients with eosinophilic pneumonia. Osteopontin concentrations in BALF of AEP patients were correlated with IL-5, as well as IL-10, CCL11, CCL17 and CXCL10 concentrations. In AEP and DEP patients, serum osteopontin concentrations were also elevated. Double immunofluorescence labelling showed that in patients with eosinophilic pneumonia, osteopontin was expressed in lung eosinophils. CONCLUSIONS: Osteopontin is likely to contribute to the development of inflammation in patients with eosinophilic pneumonia.

Significance of serum vascular endothelial growth factor level in patients with idiopathic pulmonary fibrosis.

Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis, which has been implicated in the pathogenesis of fibrotic lung diseases, including idiopathic pulmonary fibrosis (IPF). The aim of this study was to examine the clinical significance of the serum VEGF level for evaluating disease severity and progression. The levels of VEGF in serum were measured in 41 patients with IPF, 14 patients with lung cancer, and 43 healthy volunteers. We measured the serum levels of CRP, LDH, KL-6, SP-D, and the parameters obtained from arterial blood gas analysis and pulmonary function tests. High-resolution computed tomography (HRCT) was performed to determine the extent of the interstitial and the alveolar opacities. The ability of each biomarker to predict disease severity was estimated by measuring the area under the receiver operating characteristic curve (AUC). The VEGF levels of IPF patients with high alveolar-arterial difference of oxygen (AaDO(2)) levels were significantly elevated than those with low AaDO(2) levels and those of healthy volunteers. When examined within the IPF group, a significant positive correlation was found between the VEGF levels and the HRCT interstitial score (p = 0.027) and the KL-6 levels (p = 0.037). Among several serum biomarkers, VEGF showed the largest AUC for predicting disease severity as defined by a high AaDO(2) value. There was an inverse correlation between the baseline VEGF level and the monthly change in percent predicted vital capacity. The serum VEGF level may reflect the severity of IPF and offer clinical benefits to predict the disease's progression.

[Case of Parkinson disease with heat retention due to sweating dysfunction].

A 71-year-old man was diagnosed as Parkinson disease at age 59, and levodopa therapy was started. Eleven years after the beginning of treatment, he noticed high fever (38.0 degrees C-39.0 degrees C) in July, but hyperthermia spontaneously disappeared three months later. In early July of the following year, he was re-admitted to our hospital because of continuous high fever, despite no any inflammation. Neurological examination revealed flexion posture of trunk and limbs and short step gait. He also presented limb rigidity, akinesia, and resting tremor during off period. Routine laboratory examinations and radiological examinations showed no remarkable findings. Autonomic testing revealed orthostatic hypotension and anhidrosis below trunk and lower limbs. By controlling the room temperature at 26 degrees C, hyperthermia showed a marked decline. In despite of no reports found associations between heat retention and Parkinson disease, in this case we speculate hyperthermia was caused by heat retention.

Low podoplanin expression of tumor cells predicts poor prognosis in pathological stage IB squamous cell carcinoma of the lung, tissue microarray analysis of 136 patients using 24 antibodies.

The aim of this study was to identify clinicopathological and biological prognostic markers for patients who had undergone complete resection of pathological stage IB squamous cell carcinoma (SqCC) of the lung. A total of 136 consecutive stage IB SqCC patients fulfilled eligibility criteria, and their clinicopathological factors were evaluated. Tissue microarrays were also constracted, and immunohistochemical staining with 24 antibodies was performed. Correlations between clinicopathological factors, antibody immunohistochemical reactions, the patients' overall survival (OS) and relapse-free survival (RFS) were evaluated. The univariate analysis showed that 70-year-old and over elderly group had a shorter OS time and RFS time than the younger group (p=0.0086 and p=0.0091, respectively). The univariate analysis for immunohistochemical staining showed that the podoplanin-negative group had a shorter OS time and RFS time than the podoplanin-positive group (p=0.0106 and p=0.0308, respectively). Multivariate analysis revealed a significant correlation between both the 70-year-old and over elderly group and the podoplanin-negative group and poor outcome (OS, p=0.007 and p=0.008, respectively; RFS, p=0.008 and p=0.024, respectively). The results showed that patient age and a novel biological prognostic marker, podoplanin, are useful for predicting a poor outcome of patients after complete resection of stage IB SqCC of the lung.

Elevated concentrations of liver-expressed chemokine/CC chemokine ligand 16 in bronchoalveolar lavage fluid from patients with eosinophilic pneumonia.

BACKGROUND: Eosinophilic pneumonia is characterized by the prominent accumulation of eosinophils and lymphocytes in the lung parenchyma. Liver-expressed chemokine (LEC)/CC chemokine ligand 16 (CCL16) is a novel functional ligand for H4 which is expressed on eosinophils and also an affinity ligand for CCR1, CCR2, CCR5 and CCR8 which are expressed on T lymphocytes and monocytes. The purpose of this study is to clarify the role of LEC/CCL16 in eosinophilic pneumonia. METHODS: The LEC/CCL16 level was measured using an enzyme-linked immunosorbent assay in the bronchoalveolar lavage fluid (BALF) of 33 patients with eosinophilic pneumonia, 26 patients with sarcoidosis and 10 healthy volunteers. The cell sources of LEC/CCL16 in BALF were evaluated by immunocytochemistry. RESULTS: The LEC/CCL16 levels in BALF from patients with eosinophilic pneumonia were significantly higher than those from patients with sarcoidosis and healthy volunteers. The BALF LEC/CCL16 levels correlated with the numbers of BALF eosinophils and lymphocytes, respectively. The BALF LEC/CCL16 levels were significantly decreased after remission in eosinophilic pneumonia. In immunocytochemistry, the LEC/CCL16 expression was clearly observed in CD1a-positive dendritic cells as well as in CD68-positive macrophages harvested from patients with eosinophilic pneumonia, but not from the controls. CONCLUSIONS: These results suggest that LEC/CCL16 produced by dendritic cells as well as by alveolar macrophages contributes to the accumulation of eosinophils and lymphocytes into the inflamed lungs of patients with eosinophilic pneumonia.

Increase in inflammatory mediator concentrations in exhaled breath condensate after allergen inhalation.

BACKGROUND: Although a number of studies have been carried out to examine the baseline concentrations of inflammatory mediators in asthmatic patients, the clinical utility of exhaled breath condensate (EBC) in allergen-induced bronchoconstriction has not yet been clarified. OBJECTIVE: We examined whether the release of inflammatory mediators can be detected in EBC after allergen-induced bronchoconstriction in asthmatic patients. METHODS: We quantified mast cell-associated mediators in EBC and their corresponding urinary metabolites before and after allergen inhalation. RESULTS: Early asthmatic responses (EARs) caused significant increases in the concentrations of cysteinyl leukotrienes (CysLTs; median, 10.4 vs 99.0 pg/mL; P < .0001) and prostaglandin D(2) (PGD(2); median, 2.26 vs 8.72 pg/mL; P = .0077), but not that of histamine, from baseline concentrations. Significant increases in the concentrations of urinary leukotriene E(4) and 9alpha, 11beta-prostaglandin F(2) were detected in patients with EARs. However, the percentage increases in the concentrations of CysLTs and PGD(2) in EBC did not correlate with those of their corresponding urinary metabolites. The increases in concentrations of CysLTs and PGD(2) in EBC in patients with EARs correlated with each other and correlated with the extent of decrease in FEV(1). An insignificant difference in tyrosine concentration before and after the inhalation test demonstrated that errors caused by dilution of inflammatory mediators are negligibly small in EBC collected over a short period. CONCLUSION: In patients with allergen-induced EARs, pulmonary generation of mast cell-associated mediators can be evaluated by quantifying CysLTs and PGD(2) in EBC, suggesting that the quantification of EBC mediators might be useful in monitoring acute asthmatic airway inflammation.

[Case of Vogt-Koyanagi-Harada disease associated with non-herpetic acute limbic encephalitis with autoantibodies against glutamate receptor epsilon2 in the cerebrospinal fluid].

We report a case of Vogt-Koyanagi-Harada (VKH) disease associated with non-herpetic acute limbic encephalitis with autoantibodies against glutamate receptor epsilon2 in the cerebrospinal fluid. A 42-year-old woman developed a complaint of visual distortion, visual disturbance, headache and mild psychiatric symptoms, such as anxiety and depression. She was diagnosed as VKH through the fidings of fluorescein fundus angiography, which revealed patchy hypofluorescence associated with delayed choroidal filling at early fluorescein angiographic phase, and spotted choroidal hyperfluorescence and pooling of dye at late phase. Analysis of the cerebrospinal fluid (CSF) showed slight increase of leukocyte count (49/microl, mononuclear cells) and immunoglobulin (Ig) G index. An anti-GluRepsilon2 IgM antibody was positive in CSF. Brain magnetic resonance imaging (MRI) showed a monofocal hyperintensity lesion in the left parahippocampal gyrus on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images. We diagnosed her VKH disease associated with non-herpetic acute limbic encephalitis. She was treated with oral prednisone, 70 mg day and her symptoms have gradually improved. To our knowledge, meningoencephalitis in VKH disease is extremely rare and the analysis of anti-GluRepsilon2 IgM antibody in CSF has not been reported. We speculate that a certain immunologic mechanism, including the anti-GluRepsilon2 IgM antibody, contributes to the pathogenesis of the VKH disease with non-herpetic acute limbic encephalitis.

[A case of pulmonary sarcoidosis demonstrating panlobular ground-glass opacity with mosaic distribution].

A 68-year-old woman presenting dyspnea on exertion was admitted. Hypoxemia and a considerably elevated level of serum KL-6 were noted. Chest high-resolution computed tomography (HRCT) scans demonstrated panlobular ground-glass opacities with a mosaic distribution and hilar and mediastinal lymphadenopathy. Bronchoalveolar lavage revealed an increased percentage of lymphocytes and an elevated CD4/CD8 ratio, implicating a diagnosis of sarcoidosis. However, as we could not exclude other diffuse lung diseases because of unusual HRCT pattern in sarcoidosis, video-assisted thoracoscopic lung biopsy was performed. The histology of epithelioid cell granulomas in the specimens of the lung and the lymph nodes confirmed a diagnosis of sarcoidosis. The lung specimens corresponding to areas of increased opacity demonstrated diffuse alveolitis with minimal fibrosis between individual granulomas. Immunohistochemistry for KL-6 provided positive results on alveolar lining cells in areas of alveolitis but not on granulomas. After steroid treatment, the ground-glass opacities disappeared and the serum KL-6 level normalized. We discuss this rare case of pulmonary sarcoidosis presenting panlobular ground-glass opacities with mosaic distribution.

Asthma and sinusitis: association and implication.

BACKGROUND: Sinusitis occurs frequently in asthmatic patients. Epidemiologic data on sinusitis and lower airway disease must be evaluated with caution because they are based mostly on symptoms and do not include nasal endoscopic or computed tomography (CT) findings. Clinical support and evidence for this association are lacking. We evaluated the impact of sinusitis on lower airway disease in patients with well-characterized asthma. METHODS: Subjects (n = 188) completed a questionnaire designed to provide information about their signs and symptoms related to asthma, allergic rhinitis (AR) and sinus disease. Patients (n = 104) were divided into four groups based on the presence or absence of sinusitis and/or AR. Clinical findings were compared in asthma patients with and without diagnosed sinusitis, by an otorhinolaryngologist or based on sinus CT findings. RESULTS: The prevalence of sinusitis in patients with asthma was 36.7%. Sinus CT scan abnormalities were detected in 66.3% of patients with asthma. The scans revealed abnormal opacity in 17.9% of asthmatic patients without a history of sinusitis. There was a significant correlation between the rate of asthma severity and sinus morphologic abnormalities in patients with and without sinusitis. In adult-onset asthma (>or=16 years old), sinusitis frequently preceded asthma, whereas in non-adult-onset asthma (<16 years old) it preceded sinusitis. The complication rate of sinusitis in asthmatic patients was significantly higher in adult-onset asthma than in non-adult-onset asthma. CONCLUSIONS: Our findings suggest that bronchial asthma is closely related to sinusitis and the onset age of asthma is important when considering allergic disease frequency. Whether sinus disease directly affects the intensity of bronchial inflammation remains to be elucidated.

Corticobasal degeneration presenting with progressive conduction aphasia.

We report the case of a woman with primary progressive aphasia (PPA) presenting with conduction aphasia. Neurological findings showed bilateral finger tremor and signe de poignet figé in her right hand. Memory, orientation, and activities of daily living were well preserved. Linguistic examination showed severe impairment in repetition, fluent spontaneous speech with phonemic paraphasia, and relatively well preserved comprehension. Limb-kinetic apraxia and parkinsonism were not observed during the course of her illness. T1-weighted magnetic resonance imaging revealed severe atrophy of the left temporal lobe and dilatation of the left Sylvian fissure. Neuropathological findings demonstrated the most severe atrophy in the left superior temporal gyrus and Gallyas-Braak-positive or phosphorylated tau-immunoreactive cytoskeletal structures, which were consistent with corticobasal degeneration (CBD). We speculate that the progressive conduction aphasia of our patient might have been caused by left temporal lobe impairment. We suggest that progressive conduction aphasia may be a feature of CBD presenting with PPA.