Taurine reverses neurological and neurovascular deficits in Zucker diabetic fatty rats

Increased oxidative stress is implicated in the pathogenesis of diabetic peripheral neuropathy (DPN). However, the efficacy of antioxidant therapy on DPN complicating type 2 diabetes remains unexplored. We therefore determined the ability of the antioxidant taurine to reverse deficits of hind limb sciatic motor and digital sensory nerve conduction velocity (NCV), nerve blood flow (NBF), and sensory thresholds in hyperglycemic Zucker diabetic fatty (ZDF) rats. Experimental groups comprised lean nondiabetic (ND), ND treated with taurine (ND + T), untreated ZDF diabetic (D), and D rats treated with taurine (D + T). Compared to ND rats, 23%, 15% and 56% deficits of motor NCV, sensory NCV and NBF, respectively as well as thermal and mechanical hyperalgesia were reversed by taurine. An 84% deficit of dorsal root ganglion neuron calcitonin gene-related peptide in D rats was prevented by taurine. In summary, the antioxidant taurine reverses neurological and neurovascular deficits in experimental type 2 diabetes.     

Differential glutamate dehydrogenase (GDH) activity profile in patients with temporal lobe epilepsy

PURPOSE: Pathophysiologic mechanisms underlying temporal lobe epilepsy (TLE) are still poorly understood. One major hypothesis links alterations in energy metabolism to glutamate excitotoxicity associated with seizures in TLE. The purpose of this study was to determine whether changes in the activities of enzymes critical in energy and neurotransmitter metabolism contributed to the alterations in metabolic status leading to the excitotoxic effects of glutamate. METHODS: Activities of four key enzymes involved in energy metabolism and glutamate cycling in the brain [aspartate aminotransferase (AAT), citrate synthase (CS), glutamate dehydrogenase (GDH), and lactate dehydrogenase (LDH)] were measured in anterolateral temporal neocortical and hippocampal tissues obtained from three different groups of medically intractable epilepsy patients having either mesial, paradoxical, or mass lesion-associated temporal lobe epilepsy (MTLE, PTLE, MaTLE), respectively. RESULTS: We found that GDH activity was significantly decreased in the temporal cortex mainly in the MTLE group. A similar trend was recognized in the hippocampus of the MTLE. In all three patient groups, GDH activity was considerably lower, and AAT and LDH activities were higher in cortex of MTLE as compared with the corresponding activities in hippocampus (p<0.05). In the MTLE cortex and hippocampus, GDH activities were negatively correlated with the duration since the first intractable seizure. CONCLUSIONS: Our results support the hypothesis suggesting major alteration in GDH activity mainly in the MTLE group. It is proposed that significant alterations in the enzyme activities may be contributing to decreased metabolism of glutamate, leading to its accumulation.     

Neuropsychological correlates of error negativity and positivity in schizophrenia patients

The purpose of the present paper was to determine error-monitoring ability and its relationship with executive function in patients with schizophrenia. In order to evaluate error-monitoring ability, the error negativity (Ne) and error positivity (Pe) were measured using the Stroop task. The correct-related negativity (CRN) and positivity (Pc) were also measured. In addition, neuropsychological tests were administered in order to evaluate executive function. The patients with schizophrenia had significantly reduced Ne and augmented CRN amplitudes, but the Pe and Pc amplitudes of the patients were comparable to those of the controls. In addition, the Ne amplitude, measured at Fcz was positively correlated with the Trail Making Test (TMT), part B response time, and the categories achieved on the Wisconsin Card Sorting Test (WCST) in patients with schizophrenia. No significant correlations were found between Ne amplitude and performance on the neuropsychological tests in the controls. And no associations were detected between CRN, Pe, Pc amplitudes and neuropsychological performance, in either the patients with schizophrenia or the controls. Reduced Ne amplitudes and augmented CRN amplitudes in patients with schizophrenia suggest the dysfunctional behavior-monitoring system in these patients. The functional significances of Ne and Pe are discussed.     

A proton MRSI study of brain N-acetylaspartate level after 12 weeks of citalopram treatment in drug-naive patients with obsessive-compulsive disorder

OBJECTIVE: Reductions in the level of N-acetylaspartate within subcortical structures of patients with obsessive-compulsive disorder (OCD) have been reported in several studies. However, there have been, as yet, no reports regarding N-acetylaspartate levels in the prefrontal cortex of adult drug-naive OCD patients. The authors used proton magnetic resonance spectroscopic imaging ((1)H-MRSI) to investigate regional N-acetylaspartate level abnormalities and changes after 12 weeks of pharmacotherapy with citalopram in drug-naive OCD patients. METHOD: Thirteen drug-naive OCD patients and 13 age- and sex-matched healthy comparison subjects were included in this study. N-acetylaspartate levels (obtained from ratios of N-acetylaspartate with creatine, choline, and creatine plus choline) in the prefrontal cortex, parietal cortex, anterior cingulate, posterior cingulate, frontal white matter, and parietal white matter were measured by (1)H-MRSI. In OCD patients, measurements were taken before and after 12 weeks of citalopram treatment. Correlations between N-acetylaspartate concentrations in regions of interest and clinical measures were also assessed. RESULTS: Drug-naive OCD patients exhibited significantly lower N-acetylaspartate levels in the prefrontal cortex, frontal white matter, and anterior cingulate at baseline than did comparison subjects. Significant increases in N-acetylaspartate level were detected in the prefrontal cortex and frontal white matter in OCD patients after 12 weeks of citalopram treatment. CONCLUSIONS: These data suggest that reductions in neuronal viability occur in the frontal region of OCD patients and that these reductions may be partly reversible.     

Effect of splenic artery embolization for splenic artery steal syndrome in liver transplant recipients: estimation at computed tomography based on changes in caliber of related arteries

Purpose

To estimate the effect of splenic artery embolization (SAE) on blood flow in orthotopic liver transplantation (OLT) recipients with splenic artery steal syndrome (SASS) based on changes in caliber of related arteries upon serial computed tomography (CT) scans.

Methods

Between 2004 and 2007, nine OLT recipients with SASS underwent SAE. They had CT scans before and after SAE: short-, mid-, and long-term, ie, approximately 1 week, 1 month, and 1 year, respectively. The diameters of the celiac axis (CA), common hepatic artery (CHA), and splenic artery (SA) were measured with arterial phase of each CT scan and the ratios of SA to CHA diameter (SA/CHA) calculated to analyze their changes during the follow-up period.

Results

The diameters of celiac axis, CHA, and SA and SA/CHA changed most rapidly during the short-term period. The CHA diameter significantly increased short-term post-SAE by CT and slightly decreased thereafter. However, the mid-term and long-term post-SAE CT values were still significantly greater than those on the pre-SAE CT. The SA diameter steadily decreased throughout the follow-up. The SA/CHA decreased until the mid-term. The SA diameter and SA/CHA were significantly smaller upon mid-term and long-term post-SAE CT compared with those at pre-SAE CT.

Conclusions

The effect of SAE to improve hepatic arterial flow in OLT recipients with SASS might be expected for at least approximately one year. The effect maximally occurred during the short-term after SAE on the basis of changes in the caliber of related arteries upon CT.     

Effect of posterior tibial slope on knee biomechanics during functional activity

Treatment of medial compartment knee osteoarthritis with high tibial osteotomy can produce an unintended change in the slope of the tibial plateau in the sagittal plane. The effect of changing posterior tibial slope (PTS) on cruciate ligament forces has not been quantified for knee loading in activities of daily living. The purpose of this study was to determine how changes in PTS affect tibial shear force, anterior tibial translation (ATT), and knee‐ligament loading during daily physical activity. We hypothesized that tibial shear force, ATT, and ACL force all increase as PTS increases. A previously validated computer model was used to calculate ATT, tibial shear force, and cruciate‐ligament forces for the normal knee during three common load‐bearing tasks: standing, squatting, and walking. The model calculations were repeated with PTS altered in 1° increments up to a maximum change in tibial slope of 10°. Tibial shear force and ATT increased as PTS was increased. For standing and walking, ACL force increased as tibial slope was increased; for squatting, PCL force decreased as tibial slope was increased. The effect of changing PTS on ACL force was greatest for walking. The true effect of changing tibial slope on knee‐joint biomechanics may only be evident under physiologic loading conditions which include muscle forces. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:223–231, 2011     

Sustained delivery of transforming growth factor beta three enhances tendon‐to‐bone healing in a rat model

Despite advances in surgical technique, rotator cuff repairs are plagued by a high rate of failure. This failure rate is in part due to poor tendon‐to‐bone healing; rather than regeneration of a fibrocartilaginous attachment, the repair is filled with disorganized fibrovascular (scar) tissue. Transforming growth factor beta 3 (TGF‐β3) has been implicated in fetal development and scarless fetal healing and, thus, exogenous addition of TGF‐β3 may enhance tendon‐to‐bone healing. We hypothesized that: TGF‐β3 could be released in a controlled manner using a heparin/fibrin‐based delivery system (HBDS); and delivery of TGF‐β3 at the healing tendon‐to‐bone insertion would lead to improvements in biomechanical properties compared to untreated controls. After demonstrating that the release kinetics of TGF‐β3 could be controlled using a HBDS in vitro, matrices were incorporated at the repaired supraspinatus tendon‐to‐bone insertions of rats. Animals were sacrificed at 14–56 days. Repaired insertions were assessed using histology (for inflammation, vascularity, and cell proliferation) and biomechanics (for structural and mechanical properties). TGF‐β3 treatment in vivo accelerated the healing process, with increases in inflammation, cellularity, vascularity, and cell proliferation at the early timepoints. Moreover, sustained delivery of TGF‐β3 to the healing tendon‐to‐bone insertion led to significant improvements in structural properties at 28 days and in material properties at 56 days compared to controls. We concluded that TGF‐β3 delivered at a sustained rate using a HBDS enhanced tendon‐to‐bone healing in a rat model. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29: 1099–1105, 2011     

Selective posterior decompression of the cervical spine

Posterior decompression of the cervical spine is an accepted treatment for patients with cervical canal disease, but some patients experience postoperative axial pain and C5 or C6 palsy that affect their quality of life. Here we describe selective posterior decompression using a spinous process-splitting approach to prevent these complications performed in 17 patients with myelopathy treated at median 2.4 levels by selective posterior decompression via the transspinous approach. Clinical symptoms, axial pain, and C5 or C6 palsy were compared before and after treatment. The range of motion of the cervical spine and shift of the cervical cord were studied at the C5 level. All patients experienced symptom improvement and none suffered deterioration or required reoperation. The Japanese Orthopaedic Association score improved from 10.9 to 14.4 points and none of the patients reported C5 or C6 palsy or axial pain at the last follow-up visit. There was no statistically significant change in pre- and postoperative cervical alignment and range of motion. The posterior shift of the spinal cord at the C5 level was 1.7 mm. None of our 17 patients experienced significant postoperative axial pain after selective posterior decompression via the transspinous approach. Minimal spinal cord shift at the C5 level may have contributed to the reduced incidence of postoperative C5 or C6 palsy in our series. Selective posterior decompression is less invasive and effective in some patients with cervical canal disease.