Ischemic stroke is one of the leading causes of adult disability and death. Hyperglycemia is associated with an increased risk of stroke and poor outcomes after brain injury. Dynamin-like protein I (DLP-1) regulates mitochondrial fission and promotes mitochondrial dynamics. Neurodegenerative diseases are associated with mitochondrial dysfunction, and the downregulation of DLP-1 has been previously identified in a stroke animal model. Here, we investigated the changes in DLP-1 protein expression in an animal model of focal cerebral ischemia with induced hyperglycemia. Streptozotocin (40 mg/kg) was intraperitoneally injected into male rats to induce hyperglycemia, and middle cerebral artery occlusion (MCAO) was surgically induced 4 weeks after streptozotocin treatment. Brain tissue was isolated 24 hours after MCAO, and cerebral cortex samples were used for this study. Proteomics revealed a decrease in DLP-1 expression in MCAO animals when compared with controls, and this downregulation was more prominent in MCAO animals with hyperglycemia. Reverse-transcription polymerase chain reaction and Western blot analyses confirmed that DLP-1 was significantly downregulated in MCAO-injured animals with hyperglycemia compared to those without hyperglycemia. The decrease in DLP-1 indicates mitochondrial morphological changes and dysfunction. Together, these results suggest that the severe decrease of DLP-1 seen after brain injury under hyperglycemic conditions may exacerbate the damage to the brain.
Adult ; Animals ; Blotting, Western ; Brain ; Brain Injuries ; Brain Ischemia ; Cerebral Cortex ; Down-Regulation* ; Humans ; Hyperglycemia* ; Infarction, Middle Cerebral Artery ; Male ; Mitochondrial Dynamics ; Models, Animal ; Neurodegenerative Diseases ; Polymerase Chain Reaction ; Proteomics ; Rats ; Streptozocin ; Stroke

Aspergillus tracheobronchitis, an uncommon form of invasive pulmonary aspergillosis, is characterized by the development of a pseudomembrane, ulcers, or an obstruction that is predominantly confined to the tracheobronchial tree. Pseudomembranous Aspergillus tracheobronchitis is the most severe form of Aspergillus tracheobronchitis, and only a few cases have been reported in Korea. We report the characteristic chest CT findings in a patient diagnosed with pseudomembranous Aspergillus tracheobronchitis after bronchoscopy and successfully treated by proper antifungal treatment.

Background: Stroke is caused by disruption of blood supply and results in permanent disabilities as well as death. Chlorogenic acid is a phenolic compound found in various fruits and coffee and exerts antioxidant, anti-inflammatory, and anti-apoptotic effects. Objectives: The purpose of this study was to investigate whether chlorogenic acid regulates the PI3K-Akt-Bad signaling pathway in middle cerebral artery occlusion (MCAO)-induced damage. Methods: Chlorogenic acid (30 mg/kg) or vehicle was administered peritoneally to adult male rats 2 h after MCAO surgery, and animals were sacrificed 24 h after MCAO surgery.Neurobehavioral tests were performed, and brain tissues were isolated. The cerebral cortex was collected for Western blot and immunoprecipitation analyses. Results: MCAO damage caused severe neurobehavioral disorders and chlorogenic acid improved the neurological disorders. Chlorogenic acid alleviated the MCAO-induced histopathological changes and decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. Furthermore, MCAO-induced damage reduced the expression of phospho-PDK1, phospho-Akt, and phospho-Bad, which was alleviated with administration of chlorogenic acid. The interaction between phospho-Bad and 14-3-3 levels was reduced in MCAO animals, which was attenuated by chlorogenic acid treatment. In addition, chlorogenic acid alleviated the increase of cytochrome c and caspase-3 expression caused by MCAO damage. Conclusions The results of the present study showed that chlorogenic acid activates phospho-Akt and phospho-Bad and promotes the interaction between phospho-Bad and 14-3-3 during MCAO damage. In conclusion, chlorogenic acid exerts neuroprotective effects by activating the Akt-Bad signaling pathway and maintaining the interaction between phosphoBad and 14-3-3 in ischemic stroke model.

Delayed stenosis of the treated artery following mechanical thrombectomy is known to occur in approximately 10% of the patients after the procedure. It is usually asymptomatic, and was frequently found within 1 year after the procedure. Here we report a 58-year-old stroke patient who suffered from recurrent transient ischemic attacks due to a delayed stenosis of the middle cerebral artery 2 years after the mechanical thrombectomy for an abrupt embolic occlusion of the vessel.

Background: Cognitive impairment is the second most common clinical manifestation in cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). However, understanding of cognitive impairment in CADASIL has been hampered by lack of consensus on diagnosis of vascular cognitive impairment (VCI). We used vascular impairment of cognition classification consensus study principles (VICCCS-1) and protocols (VICCCS-2) to assess the cognitive impairment in CADASIL. We also evaluated the impact of MRI markers on major and mild VCI in CADASIL. Methods: We prospectively recruited 64 patients who underwent standardized brain MRI and detailed neuropsychological test. MRI analysis included number of lacunes, number of cerebral microbleeds (CMB), normalized volume of white-matter hyperintensities (nWMH), and brain parenchymal fraction (BPF). BPF has been used to measure brain atrophy. The patients were divided into three groups: those with normal cognition (CADASIL-NC, n=14), those with mild VCI (CADASIL-mild VCI, n=38), and those with major VCI (CADASIL-major VCI, n=11). Results: The three groups differed according to age, with the major VCI group being older. The major VCI group had more lacunes, more CMB, more extensive white matter lesions and lower BPF than NC group. There were no significant differences between NC and mild VCI groups in BPF. BPF and age were the independent predictors of major VCI. There was a tendency that women were at higher risk for mild VCI, though it did not reach statistical significance. Women were older than men, but had lower number of lacunes in mild VCI. Conclusions These findings suggest that brain atrophy and age are the main predictors of major VCI in CADASIL.

It is uncommon for Fabry's disease (FD) patient to present with an isolated ischemic stroke without other typical symptoms or signs of FD. A 48-year-old woman presented with recurrent limb weakness and her brain magnetic resonance imaging revealed multiple ischemic brain lesions. Ten years ago, the patient had been diagnosed with heterozygote FD by the genetic test, but she had not shown any typical symptoms or sign of FD so far. Isolated organ involvement could occur in heterozygote FD.
Brain ; Brain Ischemia ; Extremities ; Fabry Disease ; Female ; Heterozygote ; Humans ; Magnetic Resonance Imaging ; Middle Aged ; Stroke

Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 µg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.
Adult ; Animals ; Astrocytes ; Body Weight ; Cerebral Cortex ; Cytokines ; Glial Fibrillary Acidic Protein ; Humans ; Injections, Intraperitoneal ; Male ; Mice ; Microglia ; Necrosis ; Neuroglia ; NF-kappa B ; Oxidative Stress ; Reactive Oxygen Species

Hyperglycemia is one of the major risk factors for stroke. Hyperglycemia can lead to a more extensive infarct volume, aggravate neuronal damage after cerebral ischemia. α-Synuclein is especially abundant in neuronal tissue, where it underlies the etiopathology of several neurodegenerative diseases. This study investigated whether hyperglycemic conditions regulate the expression of α-synuclein in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury. Male Sprague-Dawley rats were treated with streptozotocin (40 mg/kg) via intraperitoneal injection to induce hyperglycemic conditions. MCAO were performed four weeks after streptozotocin injection to induce focal cerebral ischemia, and cerebral cortex tissues were obtained 24 hours after MCAO. We confirmed that MCAO induced neurological functional deficits and cerebral infarction, and these changes were more extensive in diabetic animals compared to non-diabetic animals. Moreover, we identified a decrease in α-synuclein after MCAO injury. Diabetic animals showed a more serious decrease in α-synuclein than non-diabetic animals. Western blot and reverse-transcription PCR analyses confirmed more extensive decreases in α-synuclein expression in MCAO-injured animals with diabetic condition than these of non-diabetic animals. It is accepted that α-synuclein modulates neuronal cell death and exerts a neuroprotective effect. Thus, the results of this study suggest that hyperglycemic conditions cause more serious brain damage in ischemic brain injuries by decreasing α-synuclein expression.
alpha-Synuclein* ; Animals ; Blotting, Western ; Brain ; Brain Injuries ; Brain Ischemia ; Cell Death ; Cerebral Cortex ; Cerebral Infarction ; Humans ; Hyperglycemia* ; Infarction, Middle Cerebral Artery* ; Injections, Intraperitoneal ; Male ; Middle Cerebral Artery* ; Neurodegenerative Diseases ; Neurons ; Neuroprotective Agents ; Polymerase Chain Reaction ; Rats, Sprague-Dawley ; Risk Factors ; Streptozocin ; Stroke

Baicalin is a natural flavonoid that exerts a variety of pharmaceutical effects such as anti-inflammatory and antioxidant. Lipopolysaccharide (LPS) is an endotoxin that releases inflammatory cytokines and induces inflammatory response. This study was investigated the anti-inflammatory mechanism of baicalin against LPS-induced inflammatory response in the hippocampus. Adult mice were randomly grouped into control, LPS-treated, and LPS and baicalin co-treated animals. LPS (250 μg/kg/day) and baicalin (10 mg/kg/day) were administered intraperitoneally for 7 consecutive days. We measured neuroglia cells activation and inflammatory factors activation using Western blot analysis and immunofluorescence staining techniques. Ionized calcium binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) are widely used as microglia and astrocyte markers, respectively. LPS treatment increased Iba-1 and GFAP expression, while baicalin co-treatment attenuated this overexpression. Nuclear factor-kappa B (NF-κB) is a key mediator of inflammation. Baicalin co-treatment alleviated LPS-induced increase of NF-κB in the hippocampus. In addition, LPS treatment upregulated pro-inflammatory cytokines including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). However, baicalin co-treatment prevented LPS-induced increases of IL-1β and TNF-α in the hippocampus. Results from the present study showed that baicalin suppresses LPS-induced neuroinflammation by regulating microglia and astrocyte activation and modulating inflammatory factors in the hippocampus. Thus, these results demonstrate that baicalin has neuroprotective effect by alleviates microglia and astrocyte activation and modulates inflammatory response by suppressing NF-κB expression in hippocampus with neuroinflammation caused by LPS.

PURPOSE: To evaluate the results of iliac artery angioplasty and stent placement as an option for the treatment of aortoiliac occlusive disease. METHOD: The records of 30 patients (mean age, 65.5 years) who underwent iliac artery angioplasty and/or stent placement were reviewed retrospectively. Presenting symptoms included asymptomatic (6.7%), claudication (73.3%), rest pain (10%), ulceration/tissue loss (3.3%), and blue toe syndrome (6.7%). Follow-up included angioplasty, Doppler ultrasound, and clinical examination. Mean follow-up time was 32 months. RESULT: Forty iliac lesions were treated. Thirty-seven percent of patients had hypertension, 33% had diabetes mellitus, 23% had coronary arterial disease, 6.6% had cerebrovascular disease, 3.3% had hyperlipidemia and 3.3% had renal insufficiency. TASC (Trans Atlantic Inter-Society Consensus) A, B, C and D disease types were 11 (36.7%) patients, 5 (16.7%), 10 (33.3%) and 4 (13.3%). Ipsilateral superficial femoral artery occlusion was present in 6 (20%) patients. Concomitant femoral artery bypass surgery was performed in 10 (33.3%) patients. The cumulative primary patency rates were 83.4%, 71.9% and 64.7% at 1, 2, and 3 years, respectively. CONCLUSION: Iliac artery angioplasty and stent placement is a technically safe and effective treatment modality in patients without ipsilateral superficial femoral artery occlusion.
Angioplasty* ; Blue Toe Syndrome ; Diabetes Mellitus ; Femoral Artery ; Follow-Up Studies ; Humans ; Hyperlipidemias ; Hypertension ; Iliac Artery ; Renal Insufficiency ; Retrospective Studies ; Stents* ; Ultrasonography