Schizophrenia patients have shown altered resting-state functional connectivity (rsFC) of the cingulate cortex; however, it is unknown whether rsFCs of the cingulate subregions are differentially affected in this disorder. We aimed to clarify the issue by comparing rsFCs of each cingulate subregion between healthy controls and schizophrenia patients. A total of 102 healthy controls and 94 schizophrenia patients underwent resting-state functional magnetic resonance imaging with a sensitivity-encoded spiral-in imaging sequence to reduce susceptibility-induced signal loss and distortion. The cingulate cortex was divided into nine subregions, including the subgenual anterior cingulate cortex (ACC), areas 24 and 32 of the pregenual ACC, areas 24 and 32 of the anterior mid-cingulate cortex (aMCC), posterior MCC (pMCC), dorsal (dPCC) and ventral (vPCC) posterior cingulate cortex (PCC) and retrosplenial cortex (RSC). The rsFCs of each cingulate subregion were compared between the two groups and the atrophy effect was considered. Results with and without global signal regression were reported. Most cingulate subregions exhibited decreased rsFCs in schizophrenia after global signal regression (GSR). Without GSR, only increased rsFC was found in schizophrenia, which primarily restricted to the aMCC, PCC and RSC. Some of these increased rsFCs were also significant after GSR. These findings suggest that GSR can greatly affect between-group differences in rsFCs and the consistently increased rsFCs may challenge the functional disconnection hypothesis of schizophrenia.

Acute ischaemic stroke can induce secondary brain injury by activating an inflammatory response that contributes to clinical impairment. As a specific inhibitor of the immunoproteasome subunit low molecular weight polypeptide 7 (LMP7), PR-957 may participate in regulating pathophysiological and inflammatory responses in multiple diseases of the central nervous system (CNS). We investigated the neuroprotective properties of PR-957 in a mouse model of stroke, induced by middle cerebral artery occlusion (MCAO). After MCAO and injections of PR-957 or vehicle, we evaluated mice behaviourally using modified Neurological Severity Scores (mNSS) and sensorimotor tests, including the adhesive-removal test, a foot-fault test and an inclined plane test. Infarct volume was measured 24 and 72 h after MCAO. Infiltration by different lymphocyte subpopulations was evaluated by flow cytometry and immunofluorescent staining of brain tissue from the penumbral area. Quantitative real-time polymerase chain reaction analysis and enzyme-linked immunosorbent assay were used to measure the expression of proinflammatory cytokines: interkeukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-17A, interferon (IFN)-γ, tumour necrosis factor (TNF)-α, granulocyte colony-stimulating factor (GCSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Expression of phosphorylated signal transducer and activator of transcription 3 (pSTAT-3) protein levels in brain was measured by immunoblot. MCAO mice treated with PR-957 showed a significant decrease in infarct volume and had mild neurological deficits compared to vehicle-treated mice. PR-957 administration also significantly decreased IL-1β, IL-6, IL-12, IL-17A and TNF-α. PR-957 provides neuroprotection via inhibiting T lymphocyte infiltration and decreasing T helper type 17 (Th17) cell differentiation in MCAO mice, which may result from the reduced expression of pSTAT-3. The neuroprotective effect of PR-957 indicates its potential utility as anti-inflammatory therapy for ischaemic stroke.

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SummaryIn recent years we have observed that some patients with idiopathic cytopenia of undetermined significance (ICUS) responded well to corticosteroid and high-dose intravenous immunoglobulin treatment, indicating that some cytopenia in ICUS might be mediated by autoantibodies. In this study, we analysed 166 ICUS cases retrospectively, some of which were autoantibodies detected on haemopoietic cells in bone marrow (

STUDY DESIGN: Case report and literature review. OBJECTIVES: Gouty arthritis of the spine is rare. Gout presenting as back pain and quadriplegia may be difficult to distinguish from a spinal tumor. Symptoms vary, and the diagnosis is often delayed. We report an unusual case of thoracic spinal cord compression caused by extradural tophaceous deposits whose initial diagnosis had been lymphoid malignancy. To the best of our knowledge, this is only the second report of using single-photon emission computed tomography (SPECT) to diagnose spinal tophus. METHODS: We retrospectively reviewed the medical records, operative reports and radiographic imaging studies of a single patient. RESULTS: A 26-year-old man with severe tophaceous gout presented with a 4-month history of progressive weakness and dyschesia of both lower extremities. Coronal bone slices evaluated by SPECT indicated increased methylene diphosphonate uptake in the T9 and T10 pedicles. Pathology assessment revealed areas of amorphous substance containing urate crystals surrounded by inflammatory cells. The diagnosis was gouty tophus. CONCLUSION: The position of the spinal tophus may be related to the 'S' type of spinal anatomical structure. Obesity and inactivity may be the two risk factors for spinal tophus. Every effort should be made to lower the serum uric acid level by maximizing the pharmacological regimen. We believe that laminectomy can effectively relieve spinal cord compression. It also improves the longterm prognosis for spinal gouty tophus. SPECT may be a viable method for differentiating spinal gout and a malignant tumor. Spinal Cord Series and Cases INTRODUCTIONWe report a case of gouty arthritis affecting the thoracic spine in a 26-year-old man with thoracic spinal cord compression caused by extradural tophaceous deposits that had initially been diagnosed as lymphoid malignancy.