Recent epidemiological studies have shown that vascular risk factors may be involved in Alzheimer's disease (AD) as well as dementia in general. To investigate the relation between a vascular disorder and AD pathology, current criteria are defective because most depend on exclusion of a cerebrovascular disorder. Epidemiological studies have indicated the possibilities that arteriosclerosis, abnormal blood pressure, diabetes mellitus and smoking may be related to the pathogenesis of AD. As for the mechanism that vascular disorders influence AD, it is presumed that amyloid deposition may be caused by a vascular disorder. Alternatively, a vascular event may cause progression of subclinical AD to a clinical stage. Insulin resistance and apolipoprotein E may also be involved in these mechanisms. Our studies show that ischemia-induced the Alzheimer-associated gene presenilin 1 (PS1) and endoplasmic reticulum-stress, generated from a vascular disorder, may unmask clinical AD symptoms caused by presenilin mutation, suggesting that a vascular factor might be involved in the onset of familial AD.

Alzheimer Disease↗

PubMedDate not supplied

Inactivation of Escherichia coli DnaA protein by DNA polymerase III and negative regulations for initiation of chromosomal replication.

Genetic and biochemical evidence indicates that initiation of chromosomal replication in Escherichia coli occurs in a nucleoprotein complex at the replication origin (oriC) formed with DnaA protein. The frequency of initiation at oriC is tightly regulated to only once per chromosome per cell cycle. To prevent untimely, extra initiations, negative control for initiation is indispensable. Recently, we found that the function of the initiator protein, DnaA, is controlled by DNA polymerase III holoenzyme, the replicase of the chromosome. The ATP-bound form of DnaA protein, an active form for initiation, is efficiently converted to the ADP bound form, an inactive form, since a subunit of the polymerase loaded on DNA (beta subunit sliding clamp) stimulates hydrolysis of ATP bound to DnaA protein. Comparison of this system, RIDA (regulatory inactivation of DnaA), with other systems for negative regulation of initiation is included in this review, and the roles of these systems for concerted control for initiation during the cell cycle are discussed.

Adenosine Diphosphate↗

PubMedDate not supplied

Hydroxylation of beta-carotene on micro-cel C.

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Adsorption↗

PubMedDate not supplied

Struma ovarii: MR findings.

PURPOSE: The purpose of this study was to determine the MR appearance of struma ovarii correlating with the pathological features. METHOD: MR findings of two patients with struma ovarii were retrospectively reviewed and compared with the pathological findings. RESULTS: Both tumors were complex masses composed of multiple cysts and solid components. The size and signal intensity of multiple cysts varied within the tumor. Hyperintense cystic areas on T1-weighted images were thought to correspond pathologically to hemorrhagic cysts and follicles containing viscous proteinaceous colloid. Solid components had as high a signal intensity as did uterine endometrium on T2-weighted images and as intermediate a signal intensity as did uterine muscle layer on T1-weighted images. After intravenous administration of gadolinium-DTPA, the solid components showed marked contrast enhancement. There was also ascitic fluid associated with adhesion and peritoneal thickening. CONCLUSION: The characteristic MR appearance of struma ovarii is thought to be a mixed mass composed of T2-hyperintense solid components with intense contrast enhancement and multiple T1-hyperintense cystic areas suggestive of hemorrhagic degeneration and viscous proteinaceous colloid.

Adult↗