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Activated sludge systems are designed and operated globally to remove phosphorus microbiologically, a process called enhanced biological phosphorus removal (EBPR). Yet little is still known about the ecology of EBPR processes, the microbes involved, their functions there and the possible reasons why they often perform unreliably. The application of rRNA-based methods to analyze EBPR community structure has changed dramatically our understanding of the microbial populations responsible for EBPR, but many substantial gaps in our knowledge of the population dynamics of EBPR and its underlying mechanisms remain. This review critically examines what we once thought we knew about the microbial ecology of EBPR, what we think we now know, and what still needs to be elucidated before these processes can be operated and controlled more reliably than is currently possible. It looks at the history of EBPR, the currently available biochemical models, the structure of the microbial communities found in EBPR systems, possible identities of the bacteria responsible, and the evidence why these systems might operate suboptimally. The review stresses the need to extend what have been predominantly laboratory-based studies to full-scale operating plants. It aims to encourage microbiologists and process engineers to collaborate more closely and to bring an interdisciplinary approach to bear on this complex ecosystem.

Experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, can be induced by immunization with a number of myelin antigens. In particular, myelin oligodendrocyte glycoprotein, a central nervous system (CNS)-specific antigen expressed on the myelin surface, is able to induce a paralytic MS-like disease with extensive CNS inflammation and demyelination in several strains of animals. Although not well understood, the egress of immune cells into the CNS in EAE is governed by a complex interplay between pro and antiinflammatory cytokines and chemokines. The hematopoietic growth factor, granulocyte macrophage colony-stimulating factor (GM-CSF), is considered to play a central role in maintaining chronic inflammation. The present study was designed to investigate the previously unexplored role of GM-CSF in autoimmune-mediated demyelination. GM-CSF(-/)- mice are resistant to EAE, display decreased antigen-specific proliferation of splenocytes, and fail to sustain immune cell infiltrates in the CNS, thus revealing key activities for GM-CSF in the development of inflammatory demyelinating lesions and control of migration and/or proliferation of leukocytes within the CNS. These results hold implications for the pathogenesis of inflammatory and demyelinating diseases and may provide the basis for more effective therapies for inflammatory diseases, and more specifically for multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory disorder of the central nervous system (CNS), characterised by focal destruction of myelin. Although it is evident that the immune system contributes to tissue destruction in MS, it is still unclear as to whether this immune response is a cause or a consequence of the disease process. In addition, there is debate over the contribution of axonal damage to clinical progression. We have described a murine model of relapsing-remitting MS (RR-MS), the most common form of the disease, following immunisation with the myelin component, myelin oligodendrocyte glycoprotein (MOG). We showed that a single injection of a MOG peptide (MOG(35-55)) in NOD/Lt mice induces a paralytic relapsing disease with extensive plaque-like demyelination. This model also mimics many of the immunological features associated with RR-MS. To investigate the relationship between clinical episodes, inflammation, and demyelination/remyelination, we analysed lesions during each attack and remission over the course of the disease, using histological, immunocytochemical, and electron microscopy (EM) techniques. We show that morphological features of lesions in our model resemble those observed in MS. Indeed, severe inflammation and demyelination coincide with the peak of clinical episodes while remissions are characterised by quiescent plaques. Furthermore, axonal damage is evident from the earliest stage of the disease and increases in severity with subsequent relapses. These data establish that in the model of MS-like disease, the peak of clinical episodes coincides with severe inflammation and demyelination and that axonal pathology correlates with clinical progression., (Copyright 2001 Wiley-Liss, Inc.)

A 50-year-old female underwent mastectomy for left breast cancer in June, 1991. She received tamoxifen for 36 months and tegafur for 30 months as adjuvant therapy. In November 1997, liver, lung and para-aortic lymph node recurrences were found, and we treated her six times with docetaxel 60 mg. After the chemotherapy, a complete response (CR) of all metastatic lesions was achieved and her serum CA15-3 level was decreased. Adverse reactions were grade 4 neutropenia, grade 2 alopecia, fever, and grade 1 edema. She received medroxyprogesterone acetate after the chemotherapy and has been well without re-growth of any metastases for over eight months.

We describe a 62-year-old Japanese woman who exhibited recurrent follicular lichenoid lesions of sarcoidosis. The skin lesions appeared all over the surface of the body without any other organ involvement, and spontaneously regressed within 1 year. Two years later, the lesions recurred on the trunk, especially in the intertriginous areas such as the submammary areas and in fatty folds of the abdomen, and on the thighs and upper arms, with the appearance of uveitis of the right eye. Histological examinations showed that small epithelioid cell granulomas were localized in the perifollicular areas. The present case was characterized by a unique distribution of follicular lichenoid eruptions, which are rare manifestations of sarcoidosis and recurrence of the lesions.

The number of patients treated with interferon (IFN) has increased markedly in Japan since 1992, when the Health and Welfare Ministry approved the use of IFN for treating chronic active hepatitis C. It is important to identify and treat depression, which is one of the psychiatric complications of IFN therapy and often leads to discontinuation of the therapy, in patients with chronic hepatitis C. In this study we prospectively investigated the incidence of depression during IFN therapy in patients with chronic active hepatitis C. The psychiatric status of 85 patients (53 men, 32 women; mean age 49.1 years) with chronic active hepatitis C who began receiving IFN at Showa University Hospital was assessed before and 2, 4, 12 and 24 weeks after the start of IFN therapy, using the major depressive episode diagnostic criteria listed in the DSM-III-R and the Hamilton Depression Scale HDS). All of the patients provided informed consent prior to participation in this study. IFN therapy was discontinued in 5 cases (5.9%) because of physical side effects and in 4 cases (4.7%) because of depression. Two, 11, 14, 25 and 16 patients were diagnosed as having major depressive episodes before and 2, 4, 12 and 24 weeks after the start of IFN therapy, respectively. The number of patients who were asymptomatic before the start of IFN therapy but were diagnosed as having a major depressive episode at least once during IFN therapy was 31 (31/83 = 37.3%). The mean HDS scores at 2, 4, 12 and 24 weeks (5.4, 6.0, 8.8 and 6.6) were significantly higher than that before the start of IFN therapy (3.0). The patients whose first diagnosed major depressive episodes occurred more than 4 weeks after the start of IFN therapy tended to be more severely depressed than those in whom it occurred less than 4 weeks after the start of IFN therapy. Compared to the 47 patients who completed 24 weeks of IFN therapy without experiencing depression, the 31 patients who were diagnosed as experiencing major depressive episodes during IFN therapy had significantly higher neuroticism scores determined using the Eysenck Personality Questionnaire, showed a more severely depressed mood and experienced more severe sleep disturbances before the start of IFN therapy. The latter group of patients also tended to have comorbid chronic physical disorders such as hypertension or diabetes mellitus and the histories of mental disorders before the IFN therapy; however these differences were not statistically significant. There were no differences between the two groups in patient age or sex, the severity of hepatitis before the IFN therapy, the type of IFN used in the therapy or the efficacy of IFN in the treatment of the hepatitis C. Our results indicate that the decision as to whether to treat chronic active hepatitis C with IFN should be made carefully and that early intervention and careful monitoring of depression are required during IFN therapy in the treatment of chronic active hepatitis C.

Seven cases of nonresectable gastric carcinoma with lymph node metastasis were treated with combination chemotherapy [CDDP 75 mg/m2 i.v. day 1 (A method: Ccr > or = 50 ml/min) or 20 mg/m2 i.v. day 1, 2, 4, 5 (B method: Ccr < 50 ml/min), MMC 10 mg/m2 i.v. day 1, etoposide 50 mg/body i.v. day 3, 4, 5, 5'-DFUR 2,100 mg/body po 4 day/week] every 4 weeks as a neoadjuvant chemotherapy. After treatment, the size of the primary tumor was reduced in four of seven cases. The lymph nodes disappeared in one case and were reduced in size in four cases. Metastatic liver tumors were found in four cases. They disappeared in one case and the size was reduced in one of seven cases. One patient with renal dysfunction was treated with B method. However, renal dysfunction did not become worse. Five patients were operated after chemotherapy. Absolute curative resection was performed in three of them. The total rate of curative resection was 43% (3/7). Four patients were alive for 19 months after operation. The main side effects of this therapy were nausea, anorexia and bone marrow suppression, which, were found in all patients. These results suggest that this combination chemotherapy is as effective as neoadjuvant chemotherapy for advanced gastric carcinoma.

A 65-year-old male diagnosed as an aortic arch aneurysm by computed tomography and angiography was treated surgically with success. He had had cerebral transient ischemic attack, but no symptoms of central nervous system. Cerebral angiography revealed complete occlusion of the right middle cerebral artery. The aneurysm was resected and replaced with Gelseal knitted Dacron prosthesis under the selective cerebral perfusion combining deep hypothermia. During cardiopulmonary bypass cerebral perfusion pressure was maintained over 50 mmHg, and arterial carbon dioxide tension was controlled by alpha-stat method. To our knowledge this is the first case of surgically treated aortic arch aneurysm complicated with middle cerebral artery occlusion. This experience would be valuable to decide about indication for surgical treatment of an aortic arch aneurysm complicated with cerebral vascular disease.

An interview survey was held with the purpose of grasping the problems faced by the home care elderly living in Koga city in Ibaraki prefecture. The subjects of the study were 100 cases who had been registered as elderly requiring home care in the municipality. The main results were as follows: (1) The most frequent underlying disorders that were considered as causes of disabilities in the home care elderly were cerebrovascular diseases, senile dementia and external injuries. In 67 percent of the subjects, one of these three disorders had caused the disabilities. (2) Disabilities in self care activities and in mobility were closely related to each other and the order of the difficulty in performing these activities was similar in many cases. A large number of the subjects sustaining severe disabilities expressed discontent with their daily life. (3) Forty two percent of the subjects were so-called bedridden elderly who got out of bed for less than 3 hours a day. The Barthel index score was 60 or less in all of the bedridden subjects. (4) For most of the bedridden elderly, bed rest was not required and probably exacerbated the disuse syndrome. In order to ameliorate their condition, adequate rehabilitation programs and assistance in their daily activities need to be offered. (5) Seventy eight percent of the care givers complained about the burden of care. Those who had no assistant care giver complained more frequently. Many of the care givers complaining about their burden had their own health problems. (6) The utilization of social welfare services were not always without any problems. The number of the experts who can deal with the psychosocial aspects in the elderly should be increased in order to improve the situation.

A tuberculous aneurysm of the thoracic descending aorta was found in a 60-year-old female with massive hemoptysis. She had had lung tuberculosis one and half years ago. Computed tomography and aortic angiography revealed saccular type aneurysm at left supradiaphragmatic portion of descending aorta. After antituberculous chemotherapy, the aneurysm was resected under the temporary bypass support utilizing Bio-pump and the aorta was grafted with Dacron prosthesis successfully. The microscopic findings of specimens over the aneurysm and surrounding tissues revealed tuberculosis. The patient is doing well one year after the operation.

Bile alcohols in bile, urine, and feces of a patient with cerebrotendinous xanthomatosis have been analyzed by a combination of capillary gas-liquid chromatography and mass spectrometry after fractionation into groups according to mode of conjugation. The presence of at least 18 bile alcohols, which were excreted mainly as glucurono-conjugates in bile and urine, and as unconjugated forms in feces, was demonstrated. The following bile alcohols were identified with certainty by direct comparison with reference compounds: 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol; (23R)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,23-tetrol; 5 alpha- and 5 beta-cholestane-3 alpha,7 alpha,12 alpha,24-tetrols; 5 alpha- and 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25-tetrols; 27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentol; (22R)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,22,25-pentol; (23R)- and (23S)-5 beta-cholestane-3 alpha,7 alpha, 12 alpha,23,25-pentols; 3 alpha,12 alpha,25-trihydroxy-5 beta-cholestane-7-one; (24R)- and (24S)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentols; 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25,26-pentol. Although the bile alcohol profile in urine was quite different from those in bile and feces, the determination of urinary bile alcohols as well as of biliary and fecal bile alcohols could be used for diagnosis of cerebrotendinous xanthomatosis.