Carotid intima-media thickness in Parkinson's disease.

There have been a few studies and inconsistent results regarding the coincidence of Parkinson's disease (PD) and atherosclerotic diseases, such as cerebrovascular disease. Carotid intima-media thickness (IMT) is a known marker for subclinical atherosclerosis. The aim of this study was to investigate the carotid IMT between PD patients and controls. We studied 43 patients with PD and 86 matched controls. The carotid IMT in PD patients was significantly smaller than in controls (0.796 +/- 0.179 mm vs. 0.913 +/- 0.237 mm, P < 0.05). In multivariate analysis, the carotid IMT was inversely associated with the duration of levodopa medication and the severity of PD. These results suggest that PD patients have a lower risk of atherosclerosis.     

Localization of ulnar neuropathy at the elbow using new stimulator for the inching test.

OBJECTIVE: To evaluate the usefulness of the TenElectrodes, a new stimulator for inching test, in the diagnosis and localization of ulnar neuropathy at the elbow (UNE). METHODS: Sixty-two ulnar nerves in 40 control subjects and 24 ulnar nerves in 23 patients with typical symptoms and signs of UNE were studied. The inching test of ulnar motor nerve using TenElectrodes was done along 8 cm across the elbow in the extended position. RESULTS: In the inching test of the control group, the mean segmental latency difference was 0.19+/-0.08 ms. Maximal latency difference over a 1 cm segment did not exceed 0.40 ms in any of the controls but exceeded 0.5 ms or more in all clinical UNE patients. In all UNE patients, the lesion sites were identified by the inching test using TenElectrodes: the retroepicondylar groove (54.2%), the humeroulnar arcade (29.2%), and dual compression (16.6%). CONCLUSIONS: TenElectrodes is a useful stimulator for the inching test in the diagnosis of UNE. The precise localization of compression was possible in all patients with UNE and the most common site was the retroepicondylar groove.     

Antiproliferative Activity Against MCF‐7 Breast Cancer Cells by Diamino‐Triazaspirodiene Antifolates

Two triazaspirodienes, having similar phenoxy propyloxy side chain, were identified as potent mammalian dihydrofolate reductase inhibitors; one having a 6,5‐spiro bicyclic ring system (IC₅₀ = 2.3 nm ) and the other a 6,6‐spiro bicyclic system (IC₅₀ = 6.9 nm ). They also showed more than 50% antiproliferative activity against the MCF‐7 breast cancer cells at 20 μm . This study demonstrated the potential lead of the diamino‐triazaspirodienes in anticancer chemotherapeutical agents’ discovery.     

BKV in Simultaneous Pancreas-Kidney Transplant Recipients: A Leading Cause of Renal Graft Loss in First 2 Years Post-Transplant

With the introduction of more potent immunosuppressive agents, rejection has decreased in simultaneous pancreas/kidney transplant (SPK) recipients. However, as a consequence, opportunistic infections have increased. The purpose of this report is to outline the course of SPK patients who developed polyomavirus-associated nephropathy (PVAN). A retrospective review of 146 consecutive SPK recipients from January 1, 1996 to December 31, 2002 was performed. Immunosuppression, rejection and development of PVAN were reviewed. Nine patients were identified. All received induction with either OKT3 or thymoglobulin. Immunosuppression included tacrolimus/cyclosporine, MMF/azathioprine and sirolimus/prednisone. Two patients were treated for kidney rejection prior to the diagnosis of PVAN. Time to diagnosis was an average of 359.3 days post-transplantation. Immunosuppression was decreased but five ultimately lost function. However, none developed pancreatic abnormalities as demonstrated by normal glucose and amylase. Two underwent renal retransplantation after PVAN diagnosis and both have normal kidney function. PVAN was the leading cause of renal loss in SPK patients in the first 2 years after transplantation and is a serious concern for SPK recipients. The pancreas, however, is spared from evidence of infection, and no pancreatic rejection occurred when immunosuppression was decreased.     

Clinical and laboratory characteristics of cerebral infarction in tuberculous meningitis: a comparative study.

Cerebral infarction as a complication of tubercular (TB) meningitis is not uncommon, but an adequate comparison of patients with and without stroke has not been carried out. This study was performed to evaluate the clinical characteristics of cerebral infarction secondary to TB meningitis, and to investigate predictive factors for cerebral infarction in patients with TB meningitis. Patients with TB meningitis were recruited over a period of 56 months. They were divided into two groups, those with and those without stroke. Demographic features and clinical, laboratory, and neuroradiological findings were compared between the two groups. We classified strokes into subtypes using neuroimaging findings. Of the 38 patients who were diagnosed with TB meningitis, eight also experienced cerebral infarction. The percentage of cerebrospinal fluid leukocytes that were neutrophils was significantly higher in patients with stroke (68%) than in patients without stroke (31%; p=0.0001). Upon initial CT imaging, meningeal enhancement was found in 11 patients, and of these patients, six experienced stroke. There were no significant differences between the groups with respect to other clinical and laboratory features, including demographic features, time between meningitis onset and treatment initiation, peripheral white blood cell count, and cerebrospinal fluid findings. Five of the eight patients who developed stroke had lacunar infarcts. One of the three patients with territorial nonlacunar infarction died due to herniation. When treating patients with TB meningitis, the possibility of cerebral infarction should be considered when patients develop focal neurological signs, meningeal enhancement on a CT scan, and sustained polymorphic cerebrospinal fluid pleocytosis.     

Differential risks of subsequent vascular events for transient ischaemic attack and minor ischaemic stroke.

Using a prospective hospital-based registry, 146 patients with transient ischaemic attack (TIA) were compared with 376 patients with minor first-ever ischaemic stroke with respect to the 3-month risk of subsequent vascular events, in order to clarify the distinctions between the disease entities. All patients were enrolled within 48 h of onset. The risk factor distribution for the two groups was comparable, except that the TIA patients had more previous TIAs. Large artery atherosclerosis (34%) and small vessel occlusion (32%) were the main aetiologies in the TIA group, whereas small vessel occlusion (49%) was the major cause in the stroke group. The 3-month risk of combined endpoints of stroke, myocardial infarction, and vascular death for TIA patients was higher than that for the minor stroke group (15.1% vs. 3.2%; hazard ratio 4.6, 95% confidence interval 2.3-9.3 in multivariate analysis). Large artery atherosclerosis and male sex were the other significant predictors. TIA may demand more urgent management than minor stroke. The fact that aetiology is a predictor, highlights the need for rapid diagnostic tests to establish pathogenesis.