Short communication: Detection of mastication speed during rumination in cattle using 3-axis, neck-mounted accelerometers and fast Fourier transfer algorithm.

There have been limited reports on mastication speed during cattle rumination. The objective of this study was to establish a method to detect mastication speed based on data obtained during rumination through the use of a 3-axis accelerometer attached to the neck. A 3-axis accelerometer was attached to 6 dry Holstein cattle. When rumination behavior was observed, the accelerometer and the high-speed camera simultaneously recorded acceleration at the neck and moving image of the head movement. Based on the number of mastication movements recorded on video, mastication speed A was calculated. Data obtained from the 3-axis accelerometer were analyzed with fast Fourier transfer algorithm and identified as mastication speed B. The vibration of the neck recorded in the accelerometer during rumination was considered as mastication movement. Using Bland-Altman plot analysis, the mean difference between mastication speed A and mastication speed B was 0.041 s/bite, and the 95% limits of agreement ranged from -0.080 to 0.161. Since mastication movement occurred periodically, it was possible to detect the movement using spectrum analysis, as mastication speed B. Although there were some differences between calculated speeds and speeds obtained from spectrum analysis, there was clinical compatibility between mastication speed A and B. This study showed the feasibility of establishing a detection method for mastication speed during rumination, which might provide a basic procedure for studying the purpose of mastication and the variable factors involved.

An association of adverse psychosocial factors with diabetes mellitus: a meta-analytic review of longitudinal cohort studies.

AIMS/HYPOTHESIS: There has been substantial interest in the association between psychosocial stress and risk of diabetes mellitus, but no data on the systematic quantification of the causal relationship have been published. This analysis aims to evaluate the association between adverse psychosocial factors and diabetes mellitus. METHODS: We performed a search of Medline, PsycINFO, Web of Science and PubMed up to July 2008. The studies included were prospective cohort studies investigating the association between adverse psychosocial factors and risk of diabetes mellitus. RESULTS: There were 22 relationships between psychosocial factors and disease-related factors (in 14 papers), of which 16 evaluated the associations of adverse psychosocial factors with diabetes control in diabetic populations and six evaluated the associations of adverse psychosocial factors with the incidence of diabetes in populations without any diagnosed diabetes. The overall meta-analysis demonstrated that adverse psychosocial factors were significantly associated with poor diabetes control (combined correlation coefficient, r = 0.096, p = 0.006), whereas adverse psychosocial factors were not associated with incident diabetes mellitus. More notably, sensitivity analyses showed that low social support was more robustly associated with poor diabetes control than stressful events per se or stress-prone personality or coping style, and that adverse psychosocial factors were associated with poor control of type 1 and type 2 diabetes. CONCLUSIONS/INTERPRETATION: The current review revealed a detrimental association of psychosocial factors with the prognosis of both type 1 and type 2 diabetes. However, any aetiological effect of adverse psychosocial factors remains elusive as a result of the small number of individuals enrolled in the cohorts studied.

Walking and primary prevention: a meta-analysis of prospective cohort studies.

OBJECTIVE: To quantify the association between walking and the risk of cardiovascular disease (CVD) and all-cause mortality in healthy men and women. DATA SOURCES: Medline, Cochrane Database of Systematic Reviews, and Web of Science databases were searched to May 2007. STUDY SELECTION: Prospective epidemiological studies of walking and CVD and all-cause mortality. RESULTS: 18 prospective studies were included in the overall analysis, which incorporated 459 833 participants free from CVD at baseline with 19 249 cases at follow-up. From the meta-analysis the pooled hazard ratio of CVD in the highest walking category compared with the lowest was 0.69, (95% CI 0.61 to 0.77, p<0.001), and 0.68 (0.59 to 0.78, p<0.001) for all-cause mortality. These effects were robust among men and women, although there was evidence of publication biases for the associations with CVD risk. Walking pace was a stronger independent predictor of overall risk compared with walking volume (48% versus 26% risk reductions, respectively). There was also evidence of a dose-response relationship across the highest, intermediate, and lowest walking categories in relation to the outcome measures. CONCLUSIONS: The results suggest walking is inversely associated with clinical disease endpoints and largely support the current guidelines for physical activity. The mechanisms that mediate this relationship remain largely unknown and should be the focus of future research.

Carbostyril derivatives having potent beta-adrenergic agonist properties.

Derivatives carrying a substituent in the para position of the phenyl group of 8-hydroxy-5-[2-[(1-phenyl-2-methylprop-2-yl)amino]-1-hydroxyethyl] carbostyril (10) were prepared and their effects on beta-adrenoceptors evaluated in vitro. Unsubstituted compound 10, iodo 11, amino 12, and bromoacetamido 13 derivatives (all racemic) bound to the receptor with 15-100-fold lower dissociation constants than that of (-)-isoproterenol. All the above compounds stimulated adenylate cyclase more potently than (-)-isoproterenol. The intrinsic activities of compounds 10 and 12 were equal to that of (-)-isoproterenol. The intrinsic activities of compounds 11 and 13 were 1.3 and 1.2 times that of (-)-isoproterenol, respectively. Treatment of membrane preparations with bromoacetamido derivative 13 resulted in an irreversible loss of binding sites, and thus, 13 seems to be an alkylating affinity label for beta-adrenoceptors.

Ocular findings in patients with autosomal dominant retinitis pigmentosa and transversion mutation in codon 244 (Asn244Lys) of the peripherin/RDS gene.

OBJECTIVE: To identify phenotypic characteristics of a certain mutation in the peripherin/RDS gene. DESIGN: Case reports with clinical features and results of fluorescein angiography, electroretinography, kinetic visual field testing, dark adaptometry, and DNA analysis. SETTING: University medical center. PATIENTS: We studied the ocular findings in eight members of a Japanese family with autosomal dominant retinitis pigmentosa and cytosine-to-adenine transversion at the third nucleotide in codon 244 of the peripherin/RDS gene. This mutation resulted in a substitution of lysine for asparagine in amino acid 244 of peripherin/RDS, a photoreceptor-specific glycoprotein. RESULTS: Clinical findings of each affected member in this family showed a marked intrafamilial similarity, which may provide the natural course of the phenotype produced by the Asn244Lys mutation. Characteristic features include diffuse pigmentary retinal degeneration in the midperipheral and peripheral fundi associated with macular degeneration in the later stage, starting with bull's-eye maculopathy, and severely deteriorated electroretinographic findings in both rods and cones, even in the early stage. CONCLUSION: The mutation at codon 244 of the peripherin/RDS gene causes both rod and cone degeneration, although the precise mechanism of retinal degeneration is currently unknown.

Autosomal dominant cone-rod dystrophy associated with mutations in codon 244 (Asn244His) and codon 184 (Tyr184Ser) of the peripherin/RDS gene.

OBJECTIVE: To characterize clinical findings associated with mutations in codon 244 (Asn244His) and codon 184 (Tyr184Ser) of the peripherin/RDS gene. DESIGN: Case reports with clinical features and results of fluorescein angiography, electroretinography, kinetic visual field testing, and DNA analysis. SETTING: University medical center. PATIENTS: Four affected members of two Japanese families with autosomal dominant cone-rod dystrophy associated with transversion mutations in codon 244 (Asn244His) and codon (Tyr184Ser) of the peripherin/RDS gene. RESULTS: Characteristic features included the initial symptoms of decreased visual acuity, macular degeneration, central or paracentral scotoma, cone-mediated electroretinographic responses that were more impaired than rod-mediated responses, and pigmentary degeneration in the midperipheral retina in the late stage. These phenotypic features corresponded to cone-rod dystrophy type 2a by the classification of Szlyk and associates. CONCLUSIONS: The Asn244His and Tyr184Ser mutations in the peripherin/RDS gene cause con-rod dystrophy type 2a. These findings imply that a mutation in codon 244 or codon 184 of the peripherin/RDS gene affects the functions and/or structural stability of cones and rods.

Mg2+-dependent unwinding of DNA by nonhistone chromosomal protein HMG(1 + 2) from pig thymus as determined by DNA melting temperature analysis.

In the previous studies with endonucleases specific for single-stranded DNA, we have indicated that the nonhistone chromosomal protein HMG(1 + 2) prepared from pig thymus has an activity to unwind DNA partially at low protein-to-DNA weight ratios (Yoshida, M. & Shimura, K. (1984) J. Biochem. 95, 117-124). In the present work, we have pursued the unwinding reaction by HMG(1 + 2) by thermal melting temperature analysis of DNA, and by investigating the effect of Mg2+ on the reaction. The melting temperature of DNA in the presence of HMG(1 + 2) at low protein weight ratios decreased in 2 mM Tris-HCl, pH 7.8, whereas it increased at higher ratios. The depressions of melting temperature by HMG(1 + 2) at low ratios were not observed either in the system of 2 mM Tris-HCl, pH 7.8, containing EDTA or in the system containing samples treated in advance with EDTA. An addition of Mg2+ to the system reproduced the depression of melting temperature at low protein-to-DNA ratios as well as the increase at higher ratios. Analysis by Mg2+-equilibrated gel filtration revealed that HMG(1 + 2) is a Mg2+-binding protein. However, the depression of melting temperature at low protein-to-DNA ratios was not due to removal of Mg2+ from DNA by HMG(1 + 2). From these results, it is concluded that HMG(1 + 2) causes a partial DNA unwinding detectable by thermal melting temperature analysis of DNA, and that Mg2+ is necessary for the unwinding reaction.

Gastric antisecretory effect of FRG-8813, a new histamine H2 receptor antagonist, in rats and dogs.

FRG-8813, a new histamine H2 receptor antagonist, was examined for antisecretory effects and compared with famotidine and cimetidine in rats and dogs. In pylorus-ligated and lumen-perfused rats, FRG-8813 given i.v. reduced basal gastric acid secretion and the acid secretion evoked by histamine, tetragastrin, bethanechol, and 2-deoxy-D-glucose in a dose-dependent manner. The i.v. antisecretory activity of FRG-8813 was equivalent to or slightly less than that of famotidine and the intraduodenal (i.d.) activity was greater than that of cimetidine. The duration of action of FRG-8813 was substantially longer than that of farmotidine and cimetidine for both i.v. and i.d. routes. The i.v. ED40 values for the histamine- and tetragastrin-evoked responses and the i.v. ED30 value for the bethanechol-evoked response were 0.15, 0.09 and 0.43 mg2kg, respectively. In Heidenhain pouch dogs, when the three H2 antagonists were given i.v. or orally, the relative antisecretory potency of the compounds was similar to that in rats. The long-lasting antisecretory effect of FRG-8813 was also observed, and the i.v. ED50 values for histamine-, tetragastrin- and bethanechol-evoked responses were 0.1, 0.24 and 1.0 mg/kg, respectively. Comparison of the parenteral and enteral potencies indicated that FRG-8813 has a lower bioavailability than famotidine and cimetidine in rats and dogs. These data suggest that FRG-8813 has a potent and long-lasting antisecretory effect with a far greater potency than cimetidine and with a slightly lower potency than famotidine.

Coagulation and fibrinolysis in patients with chronic renal failure undergoing conservative treatment.

Eighteen patients with chronic renal failure due to primary glomerular disease undergoing conservative treatment (CRF patients) were studied to evaluate whether coagulation and fibrinolytic activity in plasma are enhanced in the patients. We measured plasma levels of coagulation-fibrinolysis parameters including thrombin-antithrombin III complex (TAT) (an index of thrombin formation), alpha 2-plasmin inhibitor (alpha 2 PI)-plasmin complex (alpha 2 PIC) (an indicator of plasmin production) and cross-linked fibrin degradation products (XL-FDP) (an index of fibrinolysis secondary to coagulation). There was no correlation between plasma levels of TAT, alpha 2PIC and XL-FDP and serum creatinine levels in CRF patients. Both fibrinogen and TAT were found to be significantly higher in CRF patients than in normal controls. TAT was negatively correlated with serum albumin or total protein. Antithrombin III (ATIII) activity was significantly lower in CRF patients than in normal controls. CRF patients showed significantly but slightly higher alpha 2 PIC and XL-FDP when compared to normal controls. These results suggest that TAT, alpha 2PIC and XL-FDP are good indicators of coagulation-fibrinolysis even in patients with decreased renal function. Coagulation activity is significantly increased in CRF patients but fibrinolysis secondary to coagulation is only slightly enhanced.

Plasma von Willebrand factor and thrombomodulin as markers of vascular disorders in patients undergoing regular hemodialysis therapy.

Increased plasma levels of von Willebrand factor antigen (vWF:Ag) are regarded as reflecting the release reaction by vascular endothelial cells and/or endothelial cell injury, and increased levels of thrombomodulin (TM) antigen as reflecting damage to endothelial cells. We investigated changes in plasma vWF:Ag and TM antigen levels during the course of regular hemodialysis treatment (RDT) in 14 patients undergoing RDT in order to evaluate the effect of hemodialysis (HD) on endothelial cells. vWF:Ag and TM were both measured by the sandwich EIA method. Predialysis levels of vWF:Ag and TM in RDT patients were both significantly higher than normal control values. Neither patient age nor blood pressure was not correlated with predialysis vWF:Ag and TM levels. Both vWF:Ag and TM levels significantly increased during a single HD session. There was a positive correlation between predialysis TM levels and duration of HD and an inverse correlation between the amount of vWF:Ag released during HD and duration of HD. It appears that HD procedures induce stimulation and damage of endothelial cells and that long-term, recurrent HD treatment may predispose to vascular disorders.

X linked ocular albinism in Japanese patients.

Thirteen affected Japanese male patients and 13 female carriers with X linked ocular albinism from seven families were examined to assess their clinical findings and to compare them with those of white and black patients. Affected Japanese patients had poor visual acuity, horizontal nystagmus, macular hypoplasia, and loss of stereopsis. Some affected patients had non-albinotic fundus with moderate pigmentation. The amount of pigment in the fundus varied among affected patients and appeared to be between that of the white and black patients. All affected patients had brown irides that show no translucency. Interestingly, two affected patients had megalocornea and a third affected patient had posterior embryotoxon. All female carriers exhibited good visual acuity, normal eye position, stereopsis, brown irides without translucency, and the typical mosaic pattern in the fundus. The pigmented iris and fundus made the correct diagnosis of these affected patients difficult. Nine affected patients (70%) had been diagnosed initially as having congenital nystagmus, with or without macular hypoplasia, until they were reviewed for this study.

The effect of hemodialysis on lymphocyte subsets during dialysis.

To clarify the effect of hemodialysis on immune response of dialysis patients, peripheral lymphocyte subsets were measured using monoclonal antibodies, OKT3, OKT4, OKT8, OKIal and Leu7. The absolute numbers of OKT3+, OKT4+, OKT8+ and OKIal+ cells were significantly lower in dialysis patients than controls. During dialysis, the relative proportions of OKT3+ and OKT4+ cells increased, and the absolute numbers of OKIal+ and OKT8+ cells decreased, 30 minutes after initiation of dialysis. At the end of the dialysis, the absolute numbers of OKT3+ and OKT4+ cells increased. The absolute number of Leu7+ cells showed low values during dialysis. These changes of lymphocyte subsets during dialysis may have influence on the immune response of dialysis patients.

Enhanced fibrinolytic activity during the course of hemodialysis.

In order to clarify the effect of hemodialysis (HD) on the fibrinolytic system, fibrinolytic activity was evaluated in 27 patients undergoing regular hemodialysis treatment (RDT) using new parameters including plasma alpha 2-plasmin inhibitor (alpha 2 PI), alpha 2-plasmin inhibitor-plasmin complex (alpha 2 PIC), cross-linked fibrin degradation products (XL-FDP), tissue plasminogen activator (t-PA) activity, t-PA antigen and plasminogen activator inhibitor-1 (PAI-1) antigen. Predialysis baseline levels of plasminogen and alpha 2PI activity in RDT patients were significantly lower and those of alpha 2PIC were significantly higher than normal control values. During a single HD session, alpha 2PIC exhibited a continuous, significant increase reaching about 180% of initial values by the end of HD. alpha 2PI activity was significantly decreased at the end of the HD, though there were no significant changes in plasminogen activity during HD. Predialysis baseline levels of XL-FDP in RDT patients were significantly higher than normal control values. No significant changes in XL-FDP were observed during HD. Both t-PA activity and t-PA antigen significantly increased during HD, and PAI-1 antigen significantly decreased during HD. Von Willebrand factor (vWF) antigen in plasma, which is regarded as reflecting a release reaction by vascular endothelial cells to certain stimuli, also significantly increased during HD. However, neither vWF antigen nor t-PA antigen was increased by heparin administration alone. The changes in alpha 2PI and alpha 2PIC levels suggest that fibrinolytic activity is slightly higher in RDT patients and is even higher during HD.(ABSTRACT TRUNCATED AT 250 WORDS)

Activation of platelets in patients with chronic proliferative glomerulonephritis and the nephrotic syndrome.

Platelet count, volume and aggregation and plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) were measured in 54 patients with chronic glomerulonephritis (CGN). Platelet count and platelet aggregation induced by ADP, adrenaline and collagen were significantly higher in the patients than in normal subjects, and platelet aggregation was markedly increased in the cases with progressive glomerular lesions. Plasma levels of beta-TG and PF-4 were significantly higher in the patients than in the normal subjects. There was a significant inverse correlation between plasma beta-TG and creatinine clearance. Nephrotic patients showed significantly smaller platelet volume and markedly elevated plasma beta-TG levels when compared to the controls. Plasma beta-TG decreased remarkably in 3 out of 4 patients with markedly increased beta-TG levels when they were given antiplatelet drugs. The results suggest that platelet aggregation and the release reaction were increased in patients with CGN. Activated platelets may be an important factor in the genesis of the thrombotic tendency in the nephrotic syndrome.

Association of beta-fibrinogen and factor VII polymorphism with plasma fibrinogen and factor VII levels, and no association of PAI-1 polymorphism with plasma PAI-1 levels in hemodialysis patients.

AIMS: Recent studies have stressed the roles of genetic factors on the plasma levels of hemostatic markers and on cardiovascular complications. We investigated the association of DNA polymorphisms for beta-fibrinogen, factor VII, and PAI-1 with plasma levels of these factors and with ischemic heart disease (IHD) and cerebral infarction (CI) in patients undergoing hemodialysis (HD). METHODS: beta-fibrinogen G/A-455, factor VII R353Q and PAI-1 4G/5G polymorphisms were determined by PCR-RFLP in 149 HD patients and in 100 controls. The plasma levels of fibrinogen, factor VII and PAI-1 were also measured. RESULTS: The allele frequencies and the genotype frequencies of these 3 polymorphisms were not different between HD patients and controls. In HD patients, plasma fibrinogen levels were significantly lower in the GG genotype than in the GA genotype, and plasma factor VII activity was significantly higher in the RR genotype than in the RQ genotype. Multiple regression analysis disclosed that CRP and beta-fibrinogen polymorphism were the significant determinants of fibrinogen levels. Plasma PAI-1 levels were not different among the 3 genotypes. The frequency of the A-455 allele was significantly higher in HD patients with CI than in those without CI, and the genotype distribution for beta-fibrinogen differed significantly between the 2 groups. Between the same 2 groups, however, significant differences were found neither in the frequency of the 353Q or 4G allele nor in the genotype distribution for factor VII and PAI-1. No significant differences in the frequency of the G-455, 353Q or 4G alleles, or in the genotype distribution for beta-fibrinogen, factor VII and PAI-1 were observed between patients with IHD and those without IHD. Multiple logistic regression analysis demonstrated that neither polymorphism was associated with CI or IHD. CONCLUSIONS: In HD patients, beta-fibrinogen and factor VII polymorphisms affected plasma levels of fibrinogen and factor VII, respectively. Beta-fibrinogen polymorphism was not an independent but a possible risk factor for CI in HD patients. Further study will be needed to confirm the precise role of 5-fibrinogen polymorphisms in the pathogenesis of CI in HD patients.

Long-term effects of steroid treatment on nephrotic syndrome associated with Kimura's disease and a review of the literature.

A 68-year-old Japanese male (Case 1) and a 59-year-old Japanese male immigrant to Brazil (Case 2) who suffered from subcutaneous eosinophilic lymphoid granuloma (Kimura's disease) of several years duration, developed nephrotic syndrome. Renal biopsy demonstrated membranous nephropathy in Case 1 and minimal-change lesion in Case 2. Both patients were treated with prednisolone for several months. There was complete remission of nephrotic syndrome in eight years in Case 1 and in three months in Case 2. Proteinuria did not reappear after remission of nephrotic syndrome in either case. In contrast subcutaneous tumors subsided in both cases during steroid treatment but again became active immediately following discontinuation of the drug. These clinical observations suggest that, though some common factor(s) might mediate the development of both skin and renal lesions, the mechanism of action on these two target organs may differ, perhaps serving only as a "trigger" for the initiating mechanism of renal disease.

One amino Acid change in cucumber mosaic virus RNA polymerase determines virulent/avirulent phenotypes on cowpea.

ABSTRACT The elicitation of the hypersensitive response (HR) is known to depend on the interaction between a resistance gene of a host plant and a corresponding avirulence gene of a pathogen. The cv. Kurodane-Sanjaku of cowpea (Vigna unguiculata) has the Cry locus that confers resistance against cucumber mosaic virus strain Y (CMV-Y). The resistance is overcome by infection with a legume strain of CMV (CMV-L). RNA 2, which codes for the 2a protein, a subunit of the viral replicase components, has been known to control virulent/avirulent phenotypes. We generated chimeric constructs of full-length cDNA clones of RNA 2 of both strains and inoculated infectious transcripts to delimit the domain controlling symptoms. A 243-base pair fragment containing a coding region for the GDD RNA-dependent RNA polymerase core sequence was shown to be responsible for the phenotypic differences. From sequence alignment analysis, two amino acids (Phe631 and Ala641) of the HR-type 2a protein encoded in this fragment were specifically exchanged to Tyr and Ser, respectively, in the 2a proteins of resistance-breaking strains. Point mutations introduced into RNA 2 backgrounds of both strains that were designed to change the amino acid at position 631 resulted in a change of symptoms, indicating that a single nucleotide change determines the reactions elicited by both strains. Analysis for one additional mutant RNA 2 showed that symptom determination may be correlated with the nature of the lateral chain of amino acid 631.

A correlation between computer-predicted changes in secondary structure and the phenotype of retinal degeneration associated with mutations in peripherin/RDS.

PURPOSE: To investigate a molecular understanding of how mutations can lead to different phenotypes, we analyzed the relationship between altered secondary structures predicted by missense mutations in the peripherin/RDS and clinical severity of autosomal-dominant retinal degeneration. METHODS: We analyzed thirteen different kinds of missense mutations in the second intradiscal loop of peripherin/RDS, previously reported in peer review journals. Alteration of the secondary structure of peripherin/RDS was predicted by computer-assisted protein structure analysis. The number of amino acid residues that would be involved in the secondary structural change produced by a given missense mutation was scored as a grade of molecular change. Clinical severity was estimated by the impairment based on electroretinographic recordings of rods and cones, and was scored according to the severity of their recordings. Regression analysis was carried out between both scores of molecular change and clinical severity. Effects of patients' ages on clinical severity was also analyzed. RESULTS: Significant correlation was found between scores of molecular change and those of clinical severity (rods, r = 0.89, p < 0.001; cones, r = 0.76, p < 0.005) by regression analysis. There was no correlation between clinical severity and patients' ages. CONCLUSION: . These findings indicate that the degree of change in the secondary structure of peripherin/RDS can explain in part the correlation between genotype and phenotype in autosomal-dominant retinal degeneration associated with missense mutations in the peripherin/RDS gene.

Long-term use of low molecular weight heparin ameliorates hyperlipidemia in patients on hemodialysis.

Hyperlipidemia is one of the major risk factors for cardiovascular death in long-term hemodialysis (HD) patients. To clarify whether unfractionated heparin (UFH) contributes to the pathogenesis of hyperlipidemia, nine Type IIb, seven Type IV, and 10 normolipidemic patients, who had been dialyzed with 80.7 IU/Kg heparin, were dialyzed with 40 anti-Xa U/kg of low molecular weight heparin (LMWH) (Logiparin, Novo-Nordisk, Gentfe, Denmark) for 6 months. Seven normolipidemic patients were also dialyzed with heparin as controls. Decreases in triglyceride (TG) during HD with LMWH were significantly less than those with heparin. However, lipoprotein lipase activities (LPL) during HD with LMWH and heparin, and those before and after 6 months on LMWH, were no different. During the 6 months on LMWH, serum total cholesterol, TG, and alpha lipoprotein significantly decreased in Type IIb patients but did not change in Type IV. In contrast, beta lipoprotein slightly increased in Types IIb, IV, and normolipidemic patients who were dialyzed with LMWH but was unchanged in the controls. These observations suggest that UFH aggravates hyperlipidemia in patients, but these effects cannot be attributed to depletion of endothelial LPL liberated by UFH.

Laterality of theta waves recorded from the bilateral hippocampi in freely moving male rats.

The correlation of rhythmic slow activity (RSA, "theta rhythm") of the rat hippocampus with voluntary movement is well known. However, it is not clear whether there is any difference between the right and left hippocampal function, and profiles of each electroencephalogram (EEG) in the rat. We fixed two paired chronically indwelling electrodes in the bilateral hippocampi, bilaterally enclosing the dorso-ventral structure. It was demonstrated that the distribution of the EEG frequency from the right ventral hippocampus was not the same as that on the other side when the rats were walking in an open area as a novelty environment. Morphological investigation suggested that there was no symmetry in structure between the right and left hippocampi in the rat. In the present investigation, bilateral hippocampal EEGs were also not identical. It is assumed that the left and right hippocampi have different functions in the rat.