Establishment of standard values for the latency, interval and amplitude parameters of tibial nerve somatosensory evoked potentials (SEPs).

OBJECTIVE: To establish standard values for tibial nerve somatosensory evoked potentials (SEPs). METHODS: We examined SEPs following left tibial nerve stimulation in 65 normal subjects of various ages, and performed multiple regression analysis using height, age, (age-20)(2) and gender as predictor variables. We objectively selected the latency or interval parameters with less intersubject variability as the standard parameters for evaluation. RESULTS: Among 3 cortical bipolar derivations investigated, the Cz'-Cc lead gave a more constant and stable P38 component than the Cz'-Fz or Ci-Cc lead. The latencies of the N8o (N8 onset) of the popliteal potential, P15 (P15 peak) in the contralateral iliac crest-ipsilateral greater trochanter lead, N21, N30 and P38o/P38 in the Cz'-Cc lead, as well as the intervals between these components were selected as standard parameters. P15 was easily identified in all of the subjects and is expected to be a new parameter to evaluate the proximal segment of the tibial nerve. The amplitudes of P15 and the other components were also evaluated. We present nomograms for the normal limit values of each parameter. CONCLUSIONS: We present a thorough set of standard values for tibial SEPs where the subject factors were fully considered, and which is easily applicable to clinical practice.     

In vivo 3D analysis with micro‐computed tomography of rat calvaria bone regeneration using periosteal cell sheets fabricated on temperature‐responsive culture dishes

Transplantable cell sheets containing osteoblasts were fabricated from periostea on temperature‐responsive culture dishes. This study demonstrated the time‐course of bone regeneration in living small animals. This continuous observation of bone regeneration was achieved by micro‐computed tomography (µCT), which assessed the osteogenic capability of periosteal cells without biodegradable scaffolds. Real‐time bone regeneration was non‐invasively monitored in a rat calvarial bone defect model, using µCT. Three‐dimensional (3D) images obtained over time by µCT clearly showed that two different bone regeneration modes, specific to the control and experimental groups, were observed. In the control group, bone was regenerated only from the periphery of the defect edges. In the experimental group, bone regeneration was observed in several small regions within the central portions of the defects that were covered by the transplanted cell sheets. However, bone regeneration observed after periosteal cell sheet transplantation was limited. The results of ALP staining and the time‐course observations concluded that periosteal cell sheets contained a small fraction of cells that could differentiate osteoblasts. Fibroblasts in transplanted cell sheets or from around subcutaneous tissues suppressed bone regeneration. The periosteal cell sheets had a capability to produce ectopic regenerated bones. Therefore, to increase the content of osteogenic cells in harvested cell sheets, the enrichment of cells that could produce osteoblasts was expected by the modification of the initial cell preparation and the culture conditions. With further possible improvements, scaffold‐free periosteal cell sheet fabricated on temperature‐responsive culture dishes will be a valuable method for inducing and accelerating bone regeneration. Copyright © 2010 John Wiley & Sons, Ltd.     

MELAS with diffuse degeneration of the cerebral white matter: Report of an autopsy case

Up to now diffuse white matter demyelination of the cerebrum has been reported in only a few cases of mitochondrial encephalopathy with lactic acidosis and stroke‐like episodes (MELAS). Here we document an autopsy case with this rare neuropathology. Most MELAS cases are diagnosed antemortem by A3243G transition of mitochondrial DNA. While cerebral damage including necrotic foci in the cerebral cortex are common findings in MELAS, prominent white matter involvement best characterizes this MELAS case. There were numerous necrotic foci, varying in size and chronological stage, in the cerebral white matter. In the areas of the white matter without necrotic foci, there was diffuse fibrillary gliosis with the loss of axons and oligodendrocytes. The gliosis was dominant in the deep white matter, sparing the U‐fiber. The cerebral cortex showed diffuse cortical atrophy with few scattered necrotic foci. Distribution of the cerebral lesions does not coincide with the territory of blood supply. The vascular wall presented only slight to mild hyalinosis. We assumed a common pathogenesis to the cortical lesions and the white matter change. The pathogenesis of the present diffuse cerebral lesions may not be just secondary to circulatory disturbance but partly due to metabolic abnormality.     

Comparison of In Vivo with In Vitro Pharmacokinetics of Mercury Between Methylmercury Chloride and Methylmercury Cysteine Using Rats and Caco2 Cells

The in vivo and in vitro pharmacokinetics of mercury (Hg) were compared between methylmercury chloride (MeHg·Cl) and methylmercury cysteine (MeHg-Cys) using rats and Caco2 cells because humans can be exposed to MeHg compounds through dietary fish. The in vivo pharmacokinetics of Hg immediately after the digestion of MeHg compounds are still obscure. In Caco2 cells, membrane uptake and subcellular distribution of MeHg compounds were examined. When rats received it intravenously, MeHg·Cl showed 20-fold greater plasma and 2-fold greater blood concentrations of Hg than MeHg-Cys, indicating that their pharmacokinetic properties are different. One hour later, however, Hg concentrations in plasma and blood became virtually identical between MeHg·Cl and MeHg-Cys, although blood Hg concentrations were?>100-fold greater than those in plasma. When administered into the closed rat’s jejunum loop, MeHg·Cl and MeHg-Cys were rapidly and efficiently taken up by intestinal membranes, and Hg was retained in intestinal membranes for a relatively long time. When administered orally, no difference was observed in plasma and blood Hg concentrations between MeHg·Cl and MeHg-Cys: plasma and blood Hg concentrations increased gradually and reached steady levels at 8?h after administration. In Caco2 cells, uptake of MeHg-Cys was significantly suppressed by l-leucine, although this was not seen with MeHg·Cl. In Caco2 cells, 81?% of Hg was recovered from cytosol fractions and 13?% of Hg from nuclear fractions (including debris) after a 2-h incubation with MeHg-Cys. In conclusion, the mechanism of membrane uptake and volume of distribution in the initial distribution phase were clearly different between MeHg·Cl and MeHg-Cys. However, such pharmacokinetic differences between them disappeared 1?h after intravenous and after oral routes of administration, possibly due to the metabolism in the body.     

Obesity, physical activity and the risk of pancreatic cancer in a large Japanese cohort

It is unclear whether body mass index (BMI) and physical activity are associated with the risk of pancreatic cancer in Asian populations. We examined these associations in the Japanese Collaborative Cohort Study for Evaluation of Cancer Risk. Our cohort study included 110,792 Japanese men and women at enrollment (1988-1990). Data on height, body weight (at baseline and at age 20 years) and physical activity were obtained from a questionnaire. Cox proportional hazards models were used to estimate the relative risks of pancreatic cancer mortality. We observed a total of 402 pancreatic cancer deaths during the follow-up period. Men with a BMI of 30 or more at age 20 years had a 3.5-fold greater risk compared with men with a normal BMI. Women with a BMI of 27.5-29.9 at baseline had approximately 60% increased risk compared with women with a BMI of 20.0-22.4. In men, weight loss of 5 kg or more between 20 years of age and baseline age was associated with an increased risk of pancreatic cancer death. In contrast, women with weight loss of 5 kg or more over the same period had a decreased risk. Physical activity was not associated with pancreatic cancer risk in either men or women. Obesity in young adulthood may be associated with an increased risk of death from pancreatic cancer in Japanese men. The risk of pancreatic cancer in relation to BMI seems to differ according to sex and the period over which BMI was measured.     

Protective effect of dexamethasone against hypoxia-induced disruption of barrier function in human corneal epithelial cells

The corneal epithelium functions as a barrier to protect the cornea from external agents such as infectious organisms and toxins and thereby contributes to corneal homeostasis. The barrier function of epithelia is dependent on the formation of tight and adherens junctions between adjacent epithelial cells. We have previously shown that hypoxia disrupts the barrier function of cultured human corneal epithelial (HCE) cells by affecting tight junctions. We have now examined the effect of dexamethasone on this barrier disruption induced by hypoxia in HCE cells. Measurement of transepithelial electrical resistance revealed that the hypoxia-induced decrease in the barrier function of HCE cells was inhibited by dexamethasone in a concentration-dependent manner. The hypoxia-induced loss of the tight junction protein ZO-1 from the borders of adjacent HCE cells (as revealed by immunofluorescence analysis) as well as the hypoxia-induced down-regulation of ZO-1 expression (as revealed by immunoblot analysis) were also inhibited by dexamethasone, whereas this drug had no effect on the expression or distribution of the tight junction protein occludin or of the adherens junction proteins E-cadherin and β-catenin. Moreover, dexamethasone attenuated the reorganization of the actin cytoskeleton, the formation of focal adhesions, and the up-regulation of myosin light chain kinase expression induced by hypoxia in HCE cells. Our results thus suggest that dexamethasone protects corneal epithelial cells from the hypoxia-induced disruption of barrier function by maintaining the distribution and expression of ZO-1 as well as the organization of the actin cytoskeleton.     

Deep sylvian meningioma without dural attachment: a case report

A 34-year-old female presented with an 8-year history of temporal lobe epilepsy. Magnetic resonance imaging showed a multilobular, well-demarcated and homogeneous tumorous lesion of 5 cm in diameter deep in the left sylvian fissure. Intraoperative findings revealed that the tumor was mainly in the left insular region without dural attachment and strongly adhered to the left middle cerebral artery and its perforators. The histopathological diagnosis was transitional meningioma without malignancy. There are few reported cases of deep sylvian meningioma without dural attachment. We review the literature and summarize the clinicopathological characteristics of this condition.     

Dual-isotope myocardial SPECT in patients with redefined myocardial infarction

BACKGROUND: According to the redefinition of myocardial infarction (MI) by the ESC/ACC Committee, patients with unstable angina (UA) without significant elevation of creatine kinase (CK) but with elevation of troponin T should be diagnosed as MI. METHODS: One hundred and forty-six consecutive patients formerly diagnosed as UA, with peak CK levels0.10 ng/ml). Dual SPECT findings were analyzed qualitatively and quantitatively in blinded manner. RESULTS: Forty-seven patients (32%) were redefined as MI and 99 patients (68%) were redefined as UA. On admission, there were small but statistically significant elevations in laboratory parameters such as white blood cell count, C-reactive protein, CK and CK-MB in the redefined MI group compared with the redefined UA group. The proportion of patients with perfusion and metabolic abnormalities was significantly higher in the redefined MI group (Tl defect 36% vs. 4%, odds ratio: 13.5, p<0.001; BMIPP defect 64% vs. 23%, odds ratio: 5.8, p<0.001). Semi-quantitative evaluation revealed that the total Tl and BMIPP scores were significantly higher in the redefined MI patients (p<0.001). CONCLUSIONS: In the redefined MI patients, perfusion and metabolic abnormalities occurred frequently and more extensively. However, Tl/BMIPP dual SPECT had limited ability to detect minor myocardial infarcts classified as redefined MI. A more sensitive stratification combined with troponin T directed assignment should be established to incorporate the ongoing minor infarcts which could not be assessed by serial dual-scintigraphic evaluations.