Tatsuo Akimura

Chlamydia pneumoniae Infection as a Risk Factor for Subarachnoid Hemorrhage

Many risk factors for subarachnoid hemorrhage (SAH), such as hypertension and recent infection, have already been established. Chlamydia pneumoniae is a common respiratory pathogen that has been implicated as a potential risk factor for hypertension and atherosclerotic diseases. The purpose of the case-control study presented here was to examine the causative relationship between C. pneumoniae infection and SAH. Serum C. pneumoniae IgG and IgA antibodies were measured using an enzyme-linked immunosorbent assay in 52 patients with SAH and in 104 healthy age-matched control subjects. Multivariate analysis revealed a significant association between SAH and both a strong seropositivity for IgG and/or IgA antibodies against C. pneumoniae (odds ratio, OR, 3.62; 95% confidence intervals, CI, 1.06–12.39; p = 0.040), which indicates the presence of acute C. pneumoniae infection, and hypertension (OR, 2.91; 95% CI, 1.42–5.96; p = 0.0035). These results provide evidence that infection with C. pneumoniae may be a risk factor for SAH from a ruptured intracranial aneurysm.

Regeneration of Cerebral Microvessels After Cold Injury: Biological Significance of Edema Fluid

Brain edema is a frequent and serious problem in man. Many investigators have performed morphological studies on various aspects of brain edema, including blood-brain barrier (BBB) damage and vascular permeability, for which they have often employed the cold-lesion model of vasogenic edema. In this cold-injury model, it has been clearly established that edema fluid passes into the brain tissue and accumulates within the abnormally distended extracellular space [1]. Many neurons as well as all other cellular elements are separated from each other by the hematogenous edematous fluid, and eventually begin to float freely in the fluid. However, it seems that little attention has been paid to the biological significance of the edema fluid. Mitosis of astrocytes is observed in edematous tissue. By cinematography, it has also been noted that many cells showing ruffle movement swim about feverishly in the edematous tissue [2]. Obviously, many cells in the edematous tissue will take part in lesion repair, under conditions where the vascular network in the edematous tissue is sparse [3]. However, it is still unknown from where and how many cells receive the energy for lesion repair. In the present study, by revealing sequential changes in endothelial cell kinetics following different types of cold injury using immunohistochemical techniques, we intended to verify if edematous fluid is an important factor for lesion repair. In addition, it was considered important to observe if transferrin receptors (Tf-R) are present when transferrin in edematous fluid is needed. Transferrin is the major serum iron-transport protein and, along with iron, plays an important role in cell growth and metabolism. Key reactions in energy metabolism and DNA synthesis are catalyzed by iron-containing enzymes. The first step in the delivery of iron to cells by transferrin involves its binding to a specific cell-surface receptor [4]. However, synthesis of transferrin does not occur in the brain [5]. In the normal brain, transferrin receptors are expressed on brain capillaries, facilitating transport of transferrin into brain tissues [6].