No abstract available.
Toes*

No abstract available.
Humerus*

The neurological symptoms of stroke have traditionally provided the foundation for functional mapping of the brain. However, there are many unresolved aspects in our understanding of cerebral activity, especially regarding high-level cognitive functions. This review provides a comprehensive look at the pathophysiology of post-stroke cognitive impairment in light of recent findings from advanced imaging techniques. Combining network neuroscience and clinical neurology, our research focuses on how changes in brain networks correlate with post-stroke cognitive prognosis. More specifically, we first discuss the general consequences of stroke lesions due to damage of canonical resting-state large-scale networks or changes in the composition of the entire brain. We also review emerging methods, such as lesion-network mapping and gradient analysis, used to study the aforementioned events caused by stroke lesions. Lastly, we examine other patient vulnerabilities, such as superimposed amyloid pathology and blood-brain barrier leakage, which potentially lead to different outcomes for the brain network compositions even in the presence of similar stroke lesions. This knowledge will allow a better understanding of the pathophysiology of post-stroke cognitive impairment and provide a theoretical basis for the development of new treatments, such as neuromodulation.

The neurological symptoms of stroke have traditionally provided the foundation for functional mapping of the brain. However, there are many unresolved aspects in our understanding of cerebral activity, especially regarding high-level cognitive functions. This review provides a comprehensive look at the pathophysiology of post-stroke cognitive impairment in light of recent findings from advanced imaging techniques. Combining network neuroscience and clinical neurology, our research focuses on how changes in brain networks correlate with post-stroke cognitive prognosis. More specifically, we first discuss the general consequences of stroke lesions due to damage of canonical resting-state large-scale networks or changes in the composition of the entire brain. We also review emerging methods, such as lesion-network mapping and gradient analysis, used to study the aforementioned events caused by stroke lesions. Lastly, we examine other patient vulnerabilities, such as superimposed amyloid pathology and blood-brain barrier leakage, which potentially lead to different outcomes for the brain network compositions even in the presence of similar stroke lesions. This knowledge will allow a better understanding of the pathophysiology of post-stroke cognitive impairment and provide a theoretical basis for the development of new treatments, such as neuromodulation.

Hansenula anomala is a normal or transient flora of the throat and alimentary tract, and has been reported as an organism causing opportunistic or nosocomial infections in immunocompromised patients, but rarely in immunocompetent hosts. From the review of the literatures, there is no published report on arthritis caused by H. anomala. We experienced a case of H. anomala arthritis in a 59-year old man who had diabetes mellitus and right knee joint swelling with deformity. The findings of magnetic resonance image were consistent with septic arthritis which had bony destruction in distal femur and proximal tibia, abscess formation in joint space, and joint effusion with synovial hypertrophy. A fungus was isolated from a couple of blood cultures and knee joint aspiration fluid, and later identified as H. anomala by yeast biochemical cards. He was successfully treated with extensive debridement and fluconazole for 8 weeks.
Abscess ; Arthritis* ; Arthritis, Infectious ; Congenital Abnormalities ; Cross Infection ; Debridement ; Diabetes Mellitus ; Femur ; Fluconazole ; Fungi ; Humans ; Hypertrophy ; Immunocompromised Host ; Joints ; Knee Joint ; Middle Aged ; Pharynx ; Pichia* ; Tibia ; Yeasts

BACKGROUND: AND PURPOSE: Similar-sized stroke lesions at similar locations can have different prognoses in clinical practice. Lesion-network mapping elucidates network-level effects of lesions that cause specific neurologic symptoms and signs, and also provides a group-level understanding. This study visualized the effects of stroke lesions on the functional brain networks of individual patients. METHODS: We enrolled patients with ischemic stroke who were hospitalized within 1 week of the stroke occurrence. Resting-state functional magnetic resonance imaging was performed 3 months after the index stroke. For image preprocessing, acute stroke lesions were visually delineated based on diffusion-weighted images obtained at admission, and the lesion mask was drawn using MRIcron software. Correlation matrices were calculated from 280 brain regions using the Brainnetome Atlas, and connectograms were visualized using in-house MATLAB code. RESULTS: We found characteristic differences in connectograms between pairs of patients who had comparable splenial, frontal cortical, cerebellar, and thalamocapsular lesions. Two representative patients with bilateral thalamic infarctions showed significant differences in their reconstructed connectograms. The cognitive function had recovered well at 3 months after stroke occurrence in patients with well-maintained interhemispheric and intrahemispheric connectivities. CONCLUSIONS This pilot study has visualized the effects of stroke lesions on the functional brain networks of individual patients. Consideration of the neurobiologic mechanisms underlying the differences between their connectograms has yielded new hypotheses about differences in the effects of stroke lesions.

BACKGROUND/AIMS: The apolipoprotein B/A-I ratio (ApoB/A-I) is a powerful clinical indicator of atherosclerosis. Although numerous reports have shown the effect of non-alcoholic fatty liver disease (NAFLD) on cardiovascular disease, few reports have examined the relationship between NAFLD and the ApoB/A-I ratio. The aim of the study was to determine the association between NAFLD and the ApoB/A-I ratio in prediabetic patients. METHODS: This cross-sectional study was performed with data obtained from 701 patients (mean age, 47.9+/-9.6 years) diagnosed with prediabetes. Serum lipid profiles including lipoprotein, apolipoprotein, and calculated ApoB/A-I ratio as well as metabolic syndrome parameters such as fasting glucose and insulin were measured in each subject. RESULTS: Among the 701 patients, 340 (48%) had NAFLD. The number of male patients was 490 (NAFLD+, 276; and NAFLD-, 214). The odds ratios for the prevalence of NAFLD increased according to the quartiles of the ApoB/A-I ratio (1.886, 2.245, and 2.587) (p<0.001). CONCLUSIONS: The prevalence of NAFLD correlated with high ApoB/A-I ratio, suggesting that NAFLD increases the risk for atherosclerosis progression in male prediabetic patients.
Apolipoprotein A-I ; Apolipoproteins ; Atherosclerosis ; Cardiovascular Diseases ; Cross-Sectional Studies ; Fasting ; Fatty Liver ; Glucose ; Humans ; Insulin ; Lipoproteins ; Male ; Odds Ratio ; Prediabetic State ; Prevalence

OBJECTIVE: To compare the incidence and clinical characteristics of tuberculosis (tbc) between patients with systemic lupus erythematosus (SLE) and kidney transplantation (KT) recipients. METHODS: Six hundreds and twenty-two patients who were diagnosed as SLE from 1990 to 2001 in Kang-Nam St. Mary's hospital were reviewed, retrospectively. As a control group, 347 kidney transplant recipients in the same center were evaluated. The extent of tbc was categorized into two groups: (1) limited disease (2) extensive disease. Cumulative steroid dosage and disease activity index including SLEDAI, serum complement levels, and anti-dsDNA titers were compared between the two groups. RESULTS: The cumulative incidence rate of tbc was similar in both groups (37 cases and 5.7% in SLE versus 17 cases and 4.9% in KT). Mean interval from SLE diagnosis or KT to tbc development was not different between the two groups. The most common site of tbc was lung/pleura, and the others included lymph nodes (2 cases), knee joint (1), bone marrow (1), central nervous system (1), kidney (1), colon (1), liver (1), and skin (1) in SLE. In contrast, most of tbc (16/17) developed exclusively in the lung and pleura in KT recipients. Cumulative doses of prednisolone 1 or 6 months before tbc diagnosis were not different between the two groups. Interestingly, extensive disease tended to be more frequent in SLE patients than in KT recipients although immuno-suppressants such as cyclosporine and azathioprine were more frequently administered in KT recipients. There were no differences in disease activity index including SLEDAI, complement levels, and anti-ds DNA titers at the time of tbc diagnosis as well as in the cumulative doses of steroid between extensive and limited diseases of tbc in SLE. CONCLUSION: The cumulative incidence rate of tbc was higher in SLE patients than in general population. The patterns of tbc tended to be more extensive in SLE compared to KT recipients in whom a stronger immuno-suppression was required, suggesting that immune dysfunction implicated by SLE itself may play an important role in determining the incidence and patterns of tbc infection.
Azathioprine ; Bone Marrow ; Central Nervous System ; Colon ; Complement System Proteins ; Cyclosporine ; Diagnosis ; DNA ; Humans ; Incidence ; Kidney ; Kidney Transplantation ; Knee Joint ; Liver ; Lung ; Lupus Erythematosus, Systemic* ; Lymph Nodes ; Pleura ; Prednisolone ; Retrospective Studies* ; Skin ; Transplantation ; Tuberculosis*