Between September 1, 1981, and August 31, 1982, all patients with suspected or confirmed pneumonia among the 46,979 inhabitants of four municipalities in the province of Kuopio, Finland, were reported to a pneumonia register by their attending physicians. In addition, two study pathologists reported all cases of pneumonia found at autopsy, and two permanent registers were checked for retrospective identification of patients. Chest radiographs were obtained from 97% of all patients. The final diagnosis was based on radiologic or autopsy criteria. A total 546 patients (323 males and 223 females) had community-acquired pneumonia; of these, 37% were less than 15 years of age, and 31% were 60 years of age or older. Nineteen percent of the patients had defined chronic conditions, and 42% were admitted to hospital. The case fatality rate was 4%. The overall incidence of community-acquired pneumonia per 1,000 inhabitants per year was 11.6 (13.9 in males, 9.4 in females). The age-specific incidence per 1,000 inhabitants per year was as follows: age < 5 years, 36.0; age 5-14 years, 16.2; age 15-59 years, 6.0; age 60-74 years, 15.4; and age > or = 75 years, 34.2.

Abstract-We studied the expression of lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ), an enzyme capable of hydrolyzing platelet-activating factor (PAF), PAF-like phospholipids, and polar-modified phosphatidylcholines, in human and rabbit atherosclerotic lesions. Oxidative modification of low-density lipoprotein, which plays an important role in atherogenesis, generates biologically active PAF-like modified phospholipid derivatives with polar fatty acid chains. PAF is known to have a potent proinflammatory activity and is inactivated by its hydrolysis. On the other hand, lysophosphatidylcholine and oxidized fatty acids released from oxidized low-density lipoprotein as a result of Lp-PLA 2 activity are thought to be involved in the progression of atherosclerosis. Using combined in situ hybridization and immunocytochemistry, we detected Lp-PLA 2 mRNA and protein in macrophages in both human and rabbit atherosclerotic lesions. Reverse transcriptase-polymerase chain reaction analysis indicated an increased expression of Lp-PLA 2 mRNA in human atherosclerotic lesions. In addition, Ϸ6-fold higher Lp-PLA 2 activity was detected in atherosclerotic aortas of Watanabe heritable hyperlipidemic rabbits compared with normal aortas from control rabbits. It is concluded that (1) macrophages in both human and rabbit atherosclerotic lesions express Lp-PLA 2 , which could cleave any oxidatively modified phosphatidylcholine present in the lesion area, and (2) modulation of Lp-PLA 2 activity could lead to antiatherogenic effects in the vessel wall.

The calcium-binding protein, parvalbumin, was localized immunohistochemically in the human amygdaloid complex. Neuronal cell bodies and fibers that are immunoreactive to parvalbumin were observed in most of the amygdaloid nuclei and cortical areas. Three types of immunoreactive aspiny neurons, ranging from small spherical cells (type 1) to large multipolar cells (type 2) and fusiform cells (type 3), were observed. The densities of the types of neurons that were parvalbumin-immunoreactive varied in the different regions of the amygdala. The highest densities of parvalbumin-immunoreactive neurons were observed in the lateral nucleus, in the magnocellular and intermediate divisions of the basal nucleus, in the magnocellular division of the accessory basal nucleus and in the amygdalohippocampal area. The regions containing the lowest density of parvalbumin-immunoreactive cells were the paralaminar nucleus, the parvicellular division of the basal nucleus, the central nucleus, the medial nucleus and the anterior cortical nucleus. In general, the distribution of immunoreactive fibers and terminals paralleled that of immunoreactive cells. Parvalbumin-immunoreactive varicose fibers formed basket-like plexi and cartridges around the unstained neurons, which suggests that parvalbumin is located in GABAergic basket cells and chandelier cells, respectively. The distribution of parvalbumin-immunoreactive profiles in the human amygdaloid complex was similar to, rather than different from that previously reported in the monkey amygdala (Pitkänen and Amaral [1993] J. Comp. Neurol. 331:14-36). This study provides baseline information about the organization of GABAergic inhibitory circuitries in the human amygdaloid complex.

Background and Purpose-The purpose of the present study was to calculate the prevalence and relative risk of unruptured incidental intracranial aneurysms (IAs) among families with IA case(s) compared with the general population in one geographically defined area in East Finland and to identify the risk group that could benefit most from screening for IAs. We compared these results with our earlier study results of familial IA (FIA) cases, with two or more known IA cases in the same family. Methods-The study groups were collected from the catchment area of the University Hospital of Kuopio in East Finland. The inclusion criteria were age 30 to 70 years and unruptured incidental IAs Ն3 mm. Patients with previous subarachnoid hemorrhage or in whom a ruptured IA was found to be the cause of death were excluded from all study groups. During routine forensic autopsies the circle of Willis was studied for IAs to estimate the number of IAs in the general population. In the families with one known IA case and in FIA families, MR angiography was used as a preliminary screening method for IAs, followed by intra-arterial angiography to verify suspected IAs. Study populations were age and sex adjusted for the statistical calculations. Results-The relative risk for IAs among first-degree relatives in FIA families was 4.2 (95% confidence interval, 2.2 to 8.0) and among first-degree relatives in families with only one affected family member was 1.8 (95% confidence interval, 0.7 to 4.8) compared with the general population in East Finland. Conclusions-First-degree relatives in FIA families constitute a high-risk group for incidental IAs, and this group would benefit from screening studies for IAs. Screening for IAs in families with only one affected member or in the general population is not recommended. (Stroke. 1998;29:359-362.)

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