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The aim of this study is to estimate eye lens exposure dose when handling radiopharmaceuticals and interacting with patients receiving radiopharmaceuticals, and to verify the usefulness of X-ray protective goggles in mitigating such radiation exposure using phantoms. To evaluate radiation exposure during the handling of radiopharmaceuticals, we employed a fluorescent glass dosimeter to measure the radiation doses associated with 99m Tc, 123 I, 131 I, 111 In, and 18 F at distances of 30 cm and 60 cm, followed by calculation of the 3 mm dose equivalent rate (3DER). We then estimated the dose reduction rates for various scenarios, including the use of syringe shields and X-ray protective goggles with lead equivalences of 0.07, 0.15, 0.75, and 0.88 mmPb, as well as their combined application. X-ray protective goggles with lead equivalence of 0.75 mmPb outperformed those with 0.07 mmPb and 0.15 mmPb, for all radionuclides and at both source distances. X-ray protective goggles with 0.88 mmPb outperformed those with 0.75 mmPb during handling of 131 I and 111 In at a distance of 30 cm. In the remaining scenarios, X-ray protective goggles with 0.88 mmPb resulted in marginal reductions or no discernible additional effects. The overall shielding effect of X-ray protective goggles was less pronounced for 131I and 18F, but the combined use of a syringe shield with X-ray protective goggles with 0.75 or 0.88 mmPb improved the dose reduction rate for all scenarios. In simulating patient care, X-ray protective goggles with 0.88 mmPb demonstrated a dose reduction effect of approximately 50% or more. X-ray protective goggles could reduce the 3DER for the eye lens, and were more effective when combined with a syringe shield. It is valid to use a lead equivalence of 0.88 mmPb to fully harness the protective capabilities of X-ray shielding goggles when dealing with all five types of nuclides in clinical settings., Competing Interests: The authors have no conflicts of interest to disclose., (2024, National Center for Global Health and Medicine.)

A 59-year-old female being treated for multiple myeloma (MM) was referred to the Division of Cardiology due to edema and dyspnea. She developed dyspnea on exertion 2 months previously when carfilzomib, a second-generation selective proteasome inhibitor which was approved for treatment of relapsed and refractory MM, was introduced, and facial edema appeared thereafter. The electrocardiogram showed sinus rhythm with T-wave inversion on extensive leads and the chest X-ray showed cardiomegaly. Although cancer therapeutics-related cardiac dysfunction was assumed to be the complication, echocardiogram revealed no evidence of elevated left ventricular filling pressure whereas elevated tricuspid regurgitation velocity (3.2 m/s) with right ventricular systolic dysfunction suggested pre-capillary pulmonary hypertension (PH). Right heart catheterization demonstrated elevated mean pulmonary artery pressure (33 mmHg) along with high pulmonary vascular resistance (11.54 Wood Units) and normal pulmonary capillary wedge pressure (9 mmHg), confirming the echocardiographic findings. After ruling out other causes, PH associated with carfilzomib was diagnosed. Cessation of carfilzomib along with pulmonary vasodilator therapy led to improvement of symptoms and reduction of right heart size along with reduced estimated pulmonary systolic pressure 2 months later. Although carfilzomib-induced PH is rare, we need to consider its possibility when we find PH in patients receiving carfilzomib., Learning Objective: While adverse cardiovascular events are often found in patients with multiple myeloma (MM) after use of carfilzomib, the occurrence of pulmonary hypertension (PH) is reported to be rare. Because temporal association of echocardiographic findings to carfilzomib therapy plays a key role for the diagnosis of drug-associated PH, serial echocardiographic examinations should be performed when we start carfilzomib therapy in refractory MM patients., Competing Interests: The authors have nothing to be disclosed regarding this case report., (© 2024 Japanese College of Cardiology. Published by Elsevier Ltd.)

Infective endocarditis (IE) is a highly fatal disease in cases of delayed diagnosis and treatment, although its incidence is low. However, there have been few single-center studies in which the risk of in-hospital death from IE was stratified according to laboratory findings on admission and the organism responsible for IE. In this study, a total of 162 patients who were admitted to our hospital during the period from 2009 to 2021, who were suspected of having IE according to the modified Duke classification, and for whom IE was confirmed by transesophageal echocardiography were retrospectively analyzed. Patients were observed for a mean-period of 43.7 days with the primary endpoint being in-hospital death. The in-hospital death group had a lower level of hemoglobin (Hb), higher white blood cell (WBC) count, lower level of estimated glomerular filtration rate (eGFR), and higher frequency of Staphylococcus being the causative agent than those in the non-in-hospital death group. In overall multivariate analysis, Hb, WBC count, eGFR, and Staphylococcus as the causative agent were identified to be significant prognostic determinants. IE patients with Hb < 10.6 g/dL, WBC count > 1.4 × 10 4 /μL, eGFR < 28.1 mL/minute/1.7 m 2 , and Staphylococcus as the causative agent had significantly and synergistically increased in-hospital death rates compared to those in other IE patients. Low level of Hb, high WBC count, low eGFR, and Staphylococcus as the causative agent of IE were independent predictors of in-hospital mortality, suggesting that these 4 parameters may be combined to additively stratify the risk of in-hospital mortality.

Objective: Perampanel is an oral anti-seizure medication, which is approved in Japan for focal-onset seizures, with/without focal to bilateral tonic-clonic seizures, as monotherapy/adjunctive therapy in patients aged 4 years and older. Treatment for generalized tonic-clonic seizures as adjunctive therapy in patients aged 12 years and older is approved as well. We evaluated the feasibility of intravenous (IV) administration of perampanel as an alternative to oral administration., Methods: Study 240 (NCT03754582) was an uncontrolled, open-label study of IV perampanel, conducted in 21 Japanese patients with epilepsy who received a stable dose of 8-12 mg/day of oral perampanel. Patients received 30-minute IV infusions at equivalent daily doses of oral perampanel for 4 days, then were switched back to oral perampanel. Safety, tolerability, plasma concentration, and maintenance of efficacy throughout the transition between IV and oral dosing of perampanel were assessed. As supportive data, a subgroup analysis was also conducted using data from healthy Japanese subjects (n = 18) who were enrolled in Study 050 (NCT03376997) investigating the pharmacokinetics and safety of IV perampanel in healthy subjects who received an IV infusion (30-, 60-, or 90-minute) of perampanel 12 mg and a single oral administration of perampanel 12-mg tablet., Results: In Study 240, the transition between 30-minute IV and oral perampanel dosing was associated with a ≤1.4-fold increase in the mean change in maximum observed concentration of perampanel. Seizure outcomes demonstrated no considerable changes in efficacy before, during, or after 30-minute IV dosing of perampanel. The safety profiles were similar between IV and oral formulations. In Study 050, the pharmacokinetics of 30- or 60-minute IV infusion of perampanel further support the interchangeability between oral and IV formulations in the Japanese subjects., Significance: These results support that 30-minute IV perampanel may be a potential short-term alternative to oral formulations for patients with epilepsy., (© 2023 The Authors. Epilepsia Open published by Wiley Periodicals LLC on behalf of International League Against Epilepsy.)

Early infantile epileptic encephalopathy with suppression-burst (EIEE), also known as Ohtahara syndrome, is one of the most severe and earliest forms of epilepsy. Using array-based comparative genomic hybridization, we found a de novo 2.0-Mb microdeletion at 9q33.3-q34.11 in a girl with EIEE. Mutation analysis of candidate genes mapped to the deletion revealed that four unrelated individuals with EIEE had heterozygous missense mutations in the gene encoding syntaxin binding protein 1 (STXBP1). STXBP1 (also known as MUNC18-1) is an evolutionally conserved neuronal Sec1/Munc-18 (SM) protein that is essential in synaptic vesicle release in several species. Circular dichroism melting experiments revealed that a mutant form of the protein was significantly thermolabile compared to wild type. Furthermore, binding of the mutant protein to syntaxin was impaired. These findings suggest that haploinsufficiency of STXBP1 causes EIEE.

The presence of paroxysmal discharges in the epileptic human dentate gyrus provides a physiologic basis for hyperexcitability that may initiate seizure discharges during the development of epilepsy. Although these responses can occur with single orthodromic stimulation, data obtained under conditions that weaken synaptic inhibition (e.g., 1 Hz stimulation or bicuculline disinhibition) suggest that paroxysmal discharges may be a more common feature of tissue from temporal lobe epileptic patients than has been reported previously. Hilar cell loss and weakened synaptic inhibition may provide conditions favorable for the activation of N-methyl-D-aspartate acid (NMDA) receptors that would allow triggering of paroxysmal discharges that normally never are evoked in dentate granule cells in nonepileptic humans. As the dentate gyrus in normal animal tissue is not susceptible to intrinsic bursting behavior and is characterized by a relatively short duration excitatory postsynaptic potential even under pharmacologic disinhibition, paroxysmal discharges in the epileptic human dentate gyrus may provide an important clue to understanding the prerequisite conditions for seizure discharge.

To investigate the influence of maternal antibody to porcine reproductive and respiratory syndrome (PRRS) virus infection, the following examination was done using conventional and SPF pigs. Ten 17-day-old conventional pigs with maternal antibody against PRRS virus and 6 44-day-old SPF pigs seronegative were inoculated intranasally with 10(5.0) TCID50 of PRRS virus. Two conventional and 4 SPF pigs were served as non-inoculated control. In conventional pigs, coughing and febrile response were observed after inoculation, and mean rate of weight gain reduced. One of the inoculated conventional pigs died on post-inoculation-day (PID) 28 and Haemophilus parasuis was isolated from the lung. Although febrile response was also observed in the inoculated SPF pigs, reduction in weight gain rate was not recognized. Virus was isolated from all the sera of inoculated conventional and SPF pigs except one conventional pig between PID 7 and 49, and between PID 7 and 28, respectively. Onset of viremia in the several conventional pigs delayed. Virus was isolated from the tissues of the 5 conventional pigs on PID 65 and from the tissues of the dead pig. On the other hand, virus was not isolated from the tissues of non-inoculated conventional pigs, and inoculated and non-inoculated SPF pigs. At the virus inoculation, antibodies by the indirect fluorescent antibody (IFA) assay against PRRS virus were detected in the sera of conventional pigs with antibody titers of 1:20. Antibody titers gradually decreased after inoculation and rose from PID 21 or 28 and were between 1:160 and 1:640 on PID 63. Virus neutralization (VN) antibody titers were 1:2 or 1:4 at the inoculation and gradually decreased. Apparent rise in VN antibody titer was not observed after the inoculation. In the sera of control pigs, both antibody titers gradually decreased and did not rise. In the sera of the SPF pigs, antibodies by the IFA assay were first detected on PID 7 or 14. The titers of antibodies rose and reached their maximum with 1:320 to 1:2,560 on PID 21 to 35. VN antibodies were first detected in PID 42 to 56 and thereafter, the titers ranged between 1:1 to 1:4. Control SPF pigs were free of antibody throughout the examination. Antigenic variability was not recognized between the inoculated and recovered viruses by the VN test. The prolonged duration of viremia and virus isolation from the tissues on PID 65 in conventional pigs with low maternal antibody might support the present of antibody-dependent enhancement activity of PRRS virus infection.

The reverse transcription polymerase chain reaction (RT-PCR) was applied to detect bovine viral diarrhea virus (BVDV) for the rapid diagnosis. The primers were selected from the p80 region of BVDV gene. The RT-PCR assay detected all of the 17 BVDV strains tested including cytopathogenic and non-cytopathogenic strains, while specific amplification was not observed from 17 bovine viruses other than BVDV. Detection limit of the assay was 10(1.5) TCID50/ml. Sera and organ samples were collected from four field bovine viral diarrhea-mucosal disease (BVD-MD) cases; mucosal disease, abortion, diarrhea and persistent infection. The RT-PCR assay detected BVDV from those samples more than conventional virus isolation method.

Twenty 2nd specific pathogen-free pigs were divided into 4 groups: Group A were infected with porcine reproductive and respiratory syndrome (PRRS) virus at 6 weeks of age and treated with available swine erysipelas and swine fever combined vaccine (vaccinated) at 7 weeks of age; Group B were vaccinated at 7 weeks of age and infected with PRRS virus at 8 weeks of age; Group C were vaccinated at 7 weeks of age: Group D were neither vaccinated nor infected with PRRS virus. All pigs were challenged to Erysipelothrix rhusiopathiae C42 strain at 10 weeks of age. No clinical signs appeared after vaccination of group A and B pigs, thus confirming that the safety of the vaccine was not influenced by infection with PRRS virus. None of the pigs in Groups A and C developed erysipelas after challenge exposure to E. rhusiopathiae. In contrast, fever and/or urticaria appeared transiently in all pigs of Group B after challenge exposure. At the time of challenge exposure to E. rhusiopathiae, the PRRS virus titer was high in sera of Group B, but was low in those from Group A. However, vaccination of pigs with attenuated E. rhusiopathiae was effective in dual infection with PRRS virus and E. rhusiopathiae, because the clinical signs were milder and the E. rhusiopathiae strain was less recovered from these pigs compared to pigs of group D.

Replication of porcine reproductive and respiratory syndrome (PRRS) virus in swine alveolar macrophages (AM) and cell population in broncho-alveolar lavage fluid (BALF) obtained from PRRS virus-infected pigs were investigated. BALF samples were periodically collected from 6 pigs infected with PRRS virus and 3 non-inoculated control pigs by means of fiber-optic bronchoscope between post-inoculation day (PID) 0 and 56. The mean ratio of macrophages in BALF collected from infected group was 92.7 +/- 3.2% before inoculation and gradually decreased from PID 14. On the other hand, the ratio of lymphocytes was 4.8 +/- 3.2% before inoculation and increased from PID 21 and indicated 41.8 +/- 9.1% on PID 28. After that, they decreased gradually and that of macrophages correspondingly increased. The ratio of neutrophils maintained between 0.7% and 5.1%. The ratios of macrophages, lymphocytes and neutrophils collected from control group were almost stable through the examination. Intracellular PRRS virus antigens in AM were detected from PID 2 by indirect immunofluorescence assay (IIFA). PRRS virus was first isolated from BALF samples collected from inoculated group between PID 2 and 49. From serum, virus was isolated between PID 2 and 21. Antibodies in sera measured by IIFA to PRRS virus were first detected on PID 14 and the antibody titer rose to 1:640 or 1:1,280. The results suggested that PRRS virus replicates in swine AM for a relatively long period.

It is unlikely that MF reorganization is the cause of epilepsy, but it may affect the progression of the disease, i.e., the frequency or severity of seizures. We propose that early events, yet undiscovered, lead to an increased likelihood of excitability. This hyperexcitability, which initially may not be manifested in overt seizures, may erode vulnerable hilar neurons that serve an important inhibitory function, as illustrated in Fig. 6-15. As inhibition is lost, hyperexcitability reaches the level of clinically manifested seizures that are severe enough to lead to substantial loss of hilar neurons. When the loss of these cells is sufficiently high, MF reorganization occurs, first to neighboring hilar neurons and later to dendrites of granule cells (Fig. 6-15). Thus, the functional consequence of MF reorganization may provide a compensatory form of inhibition, as well as a circuit for feedback excitation. Although definitive evidence indicating that MF reorganization contributes to the acceleration or progression of epilepsy is missing, the findings to date are consistent with this hypothesis. In the event that reorganization contributes to the epileptic condition, treatments that reduce indicators of neuropathology may lead to a reduction of seizure frequency and severity. Evidence suggests that reorganization in the dentate gyrus may follow the pathways of neuronal processes of hilar neurons that have died. Thus, further study of the events that guide MF reorganization may hold important clues for developing methods for targeting regenerating axons following central nervous system injury.

The serological property and replication in swine alveolar macrophages (SAM) and MARC-145 cell cultures of 35 porcine reproductive and respiratory syndrome (PRRS) viruses isolated in SAM were investigated. All the isolates were reacted almost equally with antisera against three Japanese isolates including EDRD-1 strain (American type) in immunoperoxidase monolayer assay (IPMA), but weakly or did not react with antiserum against Lelystad virus (European type) indicating that the Japanese isolates are more closely related to an American type virus. Twenty two of 35 isolates replicated with CPE both in SAM and MARC-145 cells, whereas remaining 13 isolates did not show CPE in MARC-145 cells. The antigenicity of the isolates did not relate to the virus origin and the replication in the cell cultures.

An abnormal electrophysiological response in brain slices of the dentate gyrus from biopsy material from patients surgically treated for intractable epilepsy (46/57), exhibited characteristics similar to the physiological hallmark of epilepsy, the paroxysmal discharge, a prolonged (30-600 ms) and often large amplitude field potential. The most striking feature of the prolonged response to a single perforant path stimulus was a predominantly biphasic field potential (23/46 cases). The biphasic response was characterized by a negative field potential of substantial duration exceeding 180 ms which followed an initial shorter duration positive field potential. Multiple population spikes occurred during both phases of the response. During a 1 Hz stimulus train applied to the perforant path, the magnitude and duration of the negative component of the field response was significantly increased. Approximately half of the cases (Group 1; 30/57) exhibited potentiation of the biphasic response, while the remaining cases (Group 2; 27/57) exhibited no negative field component during 1 Hz stimulation trains. This repetitive stimulation, in general, increased the area of the field response in a large majority of cases (44/57) regardless of the sign of the field potential. The number of population spikes following 1 Hz stimulation increased significantly for cases in both groups, although the increase was greater for those in Group 1 than in Group 2. Paired pulse depression (20 ms ISI) was reduced in cases that exhibited potentiated biphasic responses during 1 Hz stimulation (Group 1) in comparison to cases that exhibited no negative field potentials (Group 2). Paired pulse depression at a 200 ms ISI was not significantly different between the groups. During a single stimulus, bicuculline disinhibition (20 microM) resulted in either a prolonged positive or biphasic field potential. Intracellularly recorded responses to single perforant path stimuli also exhibited prolonged and large depolarizations that were comparable in time course to the duration of field potentials recorded in the same area whether generated in the absence or presence of bicuculline. The prolonged field potential after bicuculline was reduced by APV (20 microM). We suggest that the prolonged field response, whether biphasic or monophasic when generated by either 1 Hz stimulation or bicuculline disinhibition, may be due directly or indirectly to an increase in membrane depolarization mediated by activation of the NMDA receptor.

Paired-pulse field responses were recorded from the granule cell layer of the dentate gyrus in brain slices from temporal lobe epileptic patients. Paired-pulse depression (PPD) was examined using perforant path stimulation of low to moderate intensity at an inter-stimulus interval (ISI) of 20 ms. The paired-pulse ratio (PS2/PS1) was expressed as the population spike amplitude of the second response (PS2) relative to that of the first response (PS1). Representative tissue response from each patient biopsy were divided into two groups that were significantly different based on the magnitude of the highest paired-pulse ratio recorded for each biopsy specimen: the strong paired-pulse depression group (PS2/PS1 = 0.12 +/- 0.03; n = 15) and the weak paired-pulse depression group (PS2/PS1 = 0.68 +/- 0.06; n = 13). Paired-pulse ratios from the strong PPD group were relatively independent of stimulus intensity, whereas, PPD was dependent on stimulus intensity in the weak PPD group; i.e., PPD was greatest at the lowest intensity and reached a plateau at higher intensities. Bicuculline (20 microM) and low concentrations of baclofen (0.1-0.2 microM) reduced paired-pulse depression in the strong PPD group, but did not significantly change the paired-pulse ratio in the weak PPD group. Paired-pulse facilitation was observed in some cases after inhibition was blocked pharmacologically. The number of population spikes was increased in the presence of bicuculline but was unchanged by baclofen. In the strong PPD group, baclofen significantly altered the EPSP-population spike (E-S) relationship by increasing the slope of the relationship for the second response, without having an effect on the slope of the first response. Baclofen had no effect on the E-S relationship of either response in the weak PPD group. The data are consistent with (1) less inhibition in the weak PPD group compared to the strong PPD group, (2) reduction of feedback inhibition in the strong PPD group by bicuculline and by low concentrations of baclofen, and (3) the occurrence of paired-pulse facilitation when inhibition was pharmacologically reduced in the dentate gyrus of temporal lobe epileptic patients. The results are also consistent with the presence of GABAB receptors on human inhibitory interneurons that, when activated by baclofen, result in disinhibition of granule cells through feedback circuits. Although inhibition may be compromised in some epileptic human biopsy specimens, the presence of strong inhibition in other patients' biopsy material suggest the re-evaluation of the role of inhibition in epilepsy.

The number of orthodromically evoked population spikes was used to classify brain slice tissue from the dentate gyrus of temporal lobe epileptic patients as "more excitable" (multiple population spikes) or "less excitable" (a single population spike). During orthodromic stimulation, "more excitable" tissue exhibited less paired-pulse depression in comparison to "less excitable" tissue. During antidromic stimulation, both multiple population spikes and paired-pulse depression were observed in "more excitable" tissue. "Less excitable" tissue exhibited a single antidromic spike and often no antidromically evoked paired-pulse depression. The strength of antidromic paired-pulse depression was correlated positively with the number of antidromic spikes and was correlated negatively with orthodromic paired-pulse depression. Although orthodromic and antidromic paired-pulse depression were correlated to the number of orthodromically evoked population spikes, this correlation was not as strong as that between orthodromic paired-pulse depression, antidromic paired-pulse depression, and number of antidromically evoked population spikes. The antidromic paired-pulse depression observed in tissue exhibiting antidromically evoked multiple population spikes was enhanced rather than blocked by bicuculline. In addition, the blockade of the antidromic paired-pulse depression by CNQX indicated that this inhibition is mediated by an AMPA-type glutamatergic synapse. We suggest that alterations in circuitry occur in the dentate gyrus of some temporal lobe epileptic patients and were manifested by both a loss of inhibitory input as well as an increase of inhibition, which was dependent on the pathway of stimulation. The results of pairing antidromic and orthodromic stimuli were consistent with these conclusions.

In vitro and in vivo replication of Aujeszky's disease virus (ADV) in swine alveolar macrophages (AM) was studied using two virulent strains and a vaccine strain with deletions in the thymidine kinase and gIII genes. In vitro, AM were highly permissive to virulent ADV infection. Virus progeny titers of virulent strains in the cell phase and in the fluid phase were higher than 10(7.3) TCID50/ml at 84 hr post-inoculation (PI). For vaccine strain infection, AM were less permissive, yielding virus titers of 10(2.3) TCID50/ml at 84 hr PI. To study in vivo replication of ADV in AM, virus isolations were made from AM collected at intervals from pigs inoculated intranasally with both the virulent and vaccine strains. Virus was isolated from AM samples collected from all pigs infected with the virulent strain from days 2 to 22 PI. On the contrary, no virus was detected in AM samples collected from pigs infected with the vaccine strain. The results presented suggested that in vivo virulent ADV replicates for a relatively long period in swine alveolar macrophages.

A hemagglutination-inhibition (HI) test was applied to distinguish virulent Aujeszky's disease virus infected pigs from those immunized with a glycoprotein gIII deletion vaccine. The vaccine strain, dlg92/dltk, did not have hemagglutination activity with mouse erythrocytes and the pigs vaccinated five times with the dlg92/dltk strain failed to develop HI antibody, although they developed neutralizing antibody with 128 to 512 titers to Aujeszky's disease virus. On the other hand, these pigs produced HI antibody 1 to 2 weeks after virulent virus inoculation. Thus the animals infected with virulent strain were easily differentiated from the animals immunized with the gIII deletion vaccine.

Field recordings from the dentate granule cell layer of in vitro brain slices of temporal lobe epileptic patients were evoked by antidromic stimulation. Tissue from the same specimen was stained by the Timm-sulfide method to assess the pattern and degree of mossy fiber reorganization into the supragranular layer. A wide range of physiological responses and Timm staining patterns was present across patients. A significant correlation was observed between the abnormality of antidromic responses, reflected by multiple secondary population spikes, and the degree of Timm staining of the supragranular layer. This relationship lends support to the hypothesis that mossy fiber synapses located in the supragranular layer may have functional implications for granule cell excitability in human epileptic tissue.

The effects of phospholipase blockers on tetanus-induced long-term potentiation (LTP) and of diacylglycerol (DG) and arachidonic acid (AA) on synaptic transmission were studied in CA1 neurons of guinea pig hippocampal slices to evaluate the role of protein kinase C (PKC) and AA on the maintenance of LTP. Tetanus-induced LTP was suppressed by perfusion with neomycin (1 mM) or 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (NCDC, 0.1 mM), blockers of phospholipase. 1-Oleoyl-2-acetyl-glycerol (OAG, 100 micrograms/ml) and AA (100 microM) produced a temporal increase in both the amplitude of the population spike (PS) and the slope of the field excitatory postsynaptic potentials (EPSPs) but failed to produce LTP. Application of OAG or AA in low-Mg2+ (0.1 mM) solution induced LTP. OAG- and AA-induced LTP was blocked by DL-2-amino-phosphopentanoic acid (AP5; 50 microM). The administration of a potent activator of PKC, phorbol-12,13-dibutyrate (PDBu), in low-Mg2+ (0.1 mM) solution enhanced the PS and EPSPs for 2 or 3 h but this enhancement did not persist. These results suggest that PKC activation is not as important as AA for the maintenance of LTP and that OAG and AA play important roles in the maintenance of LTP in synergy with the influx of Ca2+ through NMDA receptor-coupled channels.

Serum vitamin E and cholesterol levels were determined for the residents in rural regions of Yamagata Prefecture, Japan. The average serum vitamin E were 0.99 +/- 0.25 mg/100ml in 166 men, and 1.06 +/- 0.26 mg/100ml in 178 women. Only 0.6% of the subjects were below 0.5 mg/100 ml. There was a significant difference between the serum vitamin E levels of men and women. However there were no statistically significant differences among serum vitamin E of various age groups. The best correlation for serum vitamin E was found with serum cholesterol.

The distribution of vitamin E in human serum lipoprotein fraction was investigated by measuring the amount of vitamin E in various protein fractions prepared by ultracentrifugation, gel filtration and electrophoresis. The larger part of the total serum vitamin E (up to 44%) was present in the alpha1-lipoproteins, while the beta-lipoproteins contained smaller concentrations (up to 26%).

The serum levels of vitamin E, cholesterol and lipoproteins, alpha1-lipoproteins and beta-lipoproteins in pregnant women were investigated. It was found that serum vitamin E, cholesterol and the lipoproteins had a tendency to increase throughout gestation. The mean serum alpha1-lipoprotein concentration was higher in pregnant women than in healthy control women. The ratios of the vitamin E concentration to the sum of alpha1-lipoproteins and beta-lipoproteins concentration in sera was constant. Furthermore, it was found that serum vitamin E was correlated closely to the lipoprotein content (r = 0.814, p less than 0.001), except in a few subjects with abnormally high vitamin E levels.