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Endocrine dysfunction can considerably impact the nervous system. Various nonspecific neurological symptoms can manifest, including headache, muscle weakness, involuntary movements, and impaired consciousness. Because of their lack of specificity, endocrine abnormalities underlying neurological symptoms may not be recognized and making the diagnosis may be challenging. It is essential that clinicians not overlook endocrine disorders when diagnosing neurological symptoms, as prompt and appropriate treatment, such as hormone replacement therapy, can improve a patient's general condition and neurological symptoms.

A quinquagenarian woman visited our hospital due to experiencing headache around the right upper eyelid for the previous 2 months. T 2 -weighted MRI of the head showed multiple high-signal-intensity lesions in the corpus callosum and bilateral corona radiata. She was thought to have an autoimmune disease and was treated with steroid pulse therapy, but the light reflex of the right eye diminished and the patient developed inferior horizontal hemianopsia. T 2 -weighted orbital MRI showed an enlarged right optic nerve, a high-intensity signal in the superior half of the optic nerve, and an enhancing effect. She also tested positive for anti-aquaporin 4 antibodies, so she was diagnosed with neuromyelitis optica spectrum disorder (NMOSD). This case shows that headache can be an initial symptom of NMOSD and that clinicians should consider NMOSD when attempting to diagnose patients presenting with headaches.

Reactive oxygen species (ROS) derived from mitochondria play an essential role in stroke as well as in neurodegenerative disorders. Although hyperglycemia associated with diabetes mellitus is well known to enhance ROS production in vascular endothelial cells, the effects of either acute or chronic high glucose environments on neurons and glial cells remain unclear. Astroglia play a pivotal role in glucose metabolism. Thus, the astroglial metabolic response to high glucose environments is an interesting subject. In particular, the glutathione/pentose phosphate pathway (PPP) system, which is a major defense mechanism against ROS in the brain, contributes to glucose metabolism and is more active in astroglia. We propose that high glucose environments activate PPP through an increased flux to the hexosamine biosynthetic pathway (HBP). HBP is known to induce endoplasmic reticulum (ER) stress under hyperglycemia, resulting in the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nrf2), a master regulator of phase 2 detoxifying enzymes including glucose-6-phosphate dehydrogenase that regulates PPP activity, as Nrf2 is reported to be a direct substrate of protein kinase RNA (PKR)-like ER kinase (PERK), a transducer of ER stress. Therefore, the phosphorylation of Nrf2 by hyperglycemia-induced ER stress facilitates Nrf2 translocation through PERK, thus activating the PPP. If acute or chronic hyperglycemia induces PPP activation in astroglia to reduce ROS, reducing the glucose concentration may be accompanied by a risk, which may explain the lack of evidence that strict glycemic control during the acute phase of stroke conveys no beneficial effect.

This article analyses the Draft of Guidelines for Human Body Dissection for Clinical Anatomy Education and Research drawn by the Study Group for Future Training Systems of Surgical Skills and Procedures established by the Fiscal Year 2010 research program of the Ministry of Health, Labor and Welfare. The purpose of the Draft of Guidelines is: First, to lay out the required basic guidelines for human cadaver usage to allow medical and dental faculty to conduct clinical education and research in accordance with existing regulations. Second, the guidelines are expected to give physicians a regulatory framework to carry out cadaver training in accordance with the current legal framework. This article explains the Draft of Guidelines in detail, outlines the future of cadaver training, and describes issues which must still be solved.

This article analyses the Draft of Guidelines for Human Body Dissection for Clinical Anatomy Education and Research drawn by the Study Group for Future Training Systems of Surgical Skills and Procedures established by the Fiscal Year 2010 research program of the Ministry of Health, Labor and Welfare. The purpose of the Draft of Guidelines is: First, to lay out the required basic guidelines for human cadaver usage to allow medical and dental faculty to conduct clinical education and research in accordance with existing regulations. Second, the guidelines are expected to give physicians a regulatory framework to carry out cadaver training in accordance with the current legal framework. This article explains the Draft of Guidelines in detail, outlines the future of cadaver training, and describes issues which must still be solved.

Behçet's disease patients who visited the eye clinic of Tokyo University Hospital during the past 20 years were surveyed retrospectively, and their epidemiological features and visual prognosis were demonstrated. We evaluated the number of patients, sex ratio, age of onset, ratio of complete type to incomplete type, and ratio of major symptoms other than the ocular manifestation. The results showed a tendency similar to the results of the nationwide hospital survey in Japan. We also evaluated the visual prognosis of Behçet's disease patients in our clinic by the least square method. In the groups of patients whose visual acuity at the initial visit was over 0.4, the visual prognosis of those who visited from 1984 till 1993 was significantly better than that of those who visited from 1974 till 1983. The use of cyclosporine was presumed to be one of the most important factors in the improved visual prognosis of Behçet's disease patients in our clinic.

Latamoxef (LMOX) (50 mg/kg) was administrated intravenously to burned patients over 1 hour period. Burn blister fluid and serum were taken during 8 hours after injection, and concentrations of LMOX in burn blister fluid and serum were determined by bioassay using E. coli as a test organism. The serum concentrations of LMOX were 170.8 +/- 30.6 micrograms/ml at 30 minutes, 227.0 +/- 19.8 micrograms/ml at 1 hour, 90.3 +/- 21.4 micrograms/ml at 2 hours, 52.9 +/- 14.6 micrograms/ml at 3 hours, 38.7 +/- 13.3 micrograms/ml at 4 hours, 25.1 +/- 8.1 micrograms/ml at 5 hours, 20.5 +/- 8.1 micrograms/ml at 6 hours, 13.0 +/- 5.5 micrograms/ml (mean +/- S.D., n = 5) at 8 hours after the injection. The LMOX concentrations in burn blister fluid were 36.9 +/- 32.8 micrograms/ml at 30 minutes, 77.5 +/- 42.2 micrograms/ml at 1 hour, 85.4 +/- 19.6 micrograms/ml at 2 hours, 76.4 +/- 18.5 micrograms/ml at 3 hours, 63.5 +/- 17.8 micrograms/ml at 4 hours, 54.9 +/- 17.1 micrograms/ml at 5 hours, 34.8 +/- 10.3 micrograms/ml at 6 hours, 25.2 +/- 4.8 micrograms/ml (mean +/- S.D., n = 7) at 8 hours after the injection. The data obtained were analysed pharmacokinetically. The serum levels were analysed by two-compartment model, and the LMOX levels in burn blister fluid were analysed by the model, in which blister was considered as a small part of the peripheral compartment. In results, Tmax and Cmax of LMOX levels in burn blister fluid were calculated as 1.81 hours and 90.6 micrograms/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Transfer of sulbactam/cefoperazone (SBT/CPZ) into the burn blister fluid was studied in 10 burn patients after one shot intravenous injection of 50 mg/kg SBT/CPZ (CPZ 25 mg/kg, SBT 25 mg/kg). CPZ and SBT concentrations in serum and burn blister fluid were determined using bioassay and high performance liquid chromatography (HPLC). The concentration of CPZ in serum reached 109.5 +/- 9.2 micrograms/ml (mean +/- S.E.) at 0.25 hour after injection, and decreased to 6.8 +/- 2.3 micrograms/ml after 8 hours. The concentration of CPZ in burn blister fluid peaked at 4 hours and reached 28.2 +/- 8.0 micrograms/ml. The concentration of SBT in serum reached 75.7 +/- 8.3 micrograms/ml at 0.25 hour after injection, and decreased to 2.3 +/- 0.7 micrograms/ml after 8 hours. The peak concentration of SBT in burn blister fluid was 13.5 +/- 1.8 micrograms/ml at 3 hours. The data obtained were analysed pharmacokinetically. Cmax of CPZ and SBT levels in burn blister fluid were calculated to be 30.4 micrograms/ml and 13.6 micrograms/ml, respectively. The AUC0-8 hrs. (area under the burn blister fluid concentration of drug-time curve between 0 and 8 hours after injection), absorption rate constant (ka) and therapeutic AUC (AUC where drug concentrations were above minimum effective concentration) of CPZ were calculated to be 194.0 micrograms.hr/ml, 1.52 hr-1 and 97.1 micrograms.hr/ml (0.3-11.1 hours), respectively. The AUC0-8 hrs. and ka of SBT were also calculated as 68.3 micrograms.hr/ml and 0.62 hr-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Transfer of cefmenoxime (CMX) into the burn blister fluids was studied in 10 burned patients with 2 administrated doses (25, 50 mg/kg). CMX concentrations in serum and burn blister fluid after 1 hour intravenous drip infusion were measured using Proteus mirabilis ATCC 21100 as the test organism grown in the DST agar medium. In the case of CMX 25 mg/kg dose, the peak serum concentration was observed 61.5 micrograms/ml at 1 hour, while the peak burn blister fluid concentration was observed 15.2 micrograms/ml at 2 hours. Pharmacokinetic parameters of serum concentration calculated were 1.02 hours as half-life (beta) and 0.42 L/kg as distribution volume, respectively. In the case of CMX 50 mg/kg dose, the peak serum concentration was observed 122.0 micrograms/ml at 1 hour and the peak burn blister fluid concentration was observed 40.8 micrograms/ml at 2 hours. Pharmacokinetic parameters of serum concentration calculated were 1.27 hours as half-life (beta) and 0.55 L/kg as distribution volume. From this study, the dose dependency between 25 mg/kg dose and 50 mg/kg dose in serum and in burn blister fluid is recognized.

Fosfomycin (FOM) (50 mg/kg) was administered to burned patients by intravenous bolus injection. Burn blister fluid and serum were taken during 8 hours after injection, and concentrations of FOM in burn blister fluid and serum were determined by bioassay using Proteus sp. (MB-838) as the test organism. The serum concentrations of FOM were 257 +/- 34.6 micrograms/ml at 15 minutes, 222 +/- 34.8 micrograms/ml at 30 minutes, 166 +/- 34.6 micrograms/ml at 1 hour, 114 +/- 43.9 micrograms/ml at 2 hours, 79.5 +/- 34.9 micrograms/ml at 3 hours, 63 +/- 36.4 micrograms/ml at 4 hours, 44.3 +/- 27.6 micrograms/ml at 5 hours, 29.6 +/- 20.9 micrograms/ml at 6 hours and 17.9 +/- 12.8 micrograms/ml at 8 hours after the injection. FOM concentrations in burn blister fluid were 64.4 +/- 18.1 micrograms/ml at 30 minutes, 77 +/- 26.0 micrograms/ml at 1 hour, 71.6 +/- 24.7 micrograms/ml at 2 hours, 64.8 +/- 23.6 micrograms/ml at 3 hours, 43.2 +/- 8.8 micrograms/ml at 4 hours, 24.8 +/- 7.9 micrograms/ml at 6 hours and 17.9 +/- 10.5 micrograms/ml at 8 hours after the injection. The obtained data were analysed pharmacokinetically. The serum levels were analysed by a two-compartment model, and the transfer of FOM into burn blister was analysed by a modified deconvolution method. In results, Tmax and Cmax of FOM levels in burn blister fluid were calculated as 1.3 hours and 80.9 micrograms/ml, respectively. The transfer rate constant of FOM from serum to burn blister fluid (K1) and that from burn blister fluid to serum (K2) were calculated as 0.612 hr-1 and 1.10 hr-1, respectively.