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Background: A large proportion of treated hypertensive subjects do not achieve target blood pressure (BP) levels. We investigated trends in treatment and BP levels in the population, and among treated hypertensive subjects in northern Sweden., Methods: The six Northern Sweden MONICA population surveys 1986 to 2009, included 6342 subjects aged 45 to 74 years of age, participation rate 79.3%. Factors associated with lack of BP control are presented for 1106 participants in 2009. BP control was defined as a systolic BP <140 and a diastolic BP <90 mm Hg among treated hypertensive patients., Results: Between 1986 and 2009, the proportion of the population that received antihypertensive treatment increased. The proportion of the whole population having BP <140/90 mm Hg increased for all (p < 0.001 for each subgroup), except for men 45-55 years old. In 2009, 62.4% of the population had BP <140/90 mm Hg, 67.2% in women and 58.1% in men (p = 0.002). In the group of treated hypertensive patients, the proportion having BP control increased (p < 0.001) with no difference between sex or age groups. In 2009 52.1% of treated hypertensives had BP control. In 2009, adequate BP control among treated hypertensive patients was 63.9% for those with BMI <25, but only 48.8% for those with BMI > 25 (p = 0.015). Abdominal obesity was associated with less BP control (48.1%) than without abdominal obesity (66.2%, p = 0.007). Women who were physically inactive had better BP control than those who were active (p = 0.03). Men treated with two or more antihypertensive drugs were 50% more likely to reach target BP than men with monotherapy (60.4% vs. 40.0 %, p = 0.035). Rural or urban living, level of education, diabetes mellitus or having a high cardiovascular risk were not associated with better BP control., Conclusion: Antihypertensive treatment and BP control have increased in northern Sweden since 1986, although in 2009 still barely half of the treated patients achieved adequate BP levels. Intensified treatment and weight reduction may help to further improve BP control.

In a patient with chronic corneal ulcer, resistant to conventional therapy, analysis of tear fluid revealed a high plasmin activity which could be inhibited by aprotinin, an inhibitor of serine proteinases. Therapy with topical aprotinin resulted in rapid epithelialization. After this initial patient, within a period of four months tear fluid specimens of altogether 48 patients with corneal lesions were analyzed, and 32 were found to be positive for proteolytic activity. Of these 18 were treated with topical aprotinin which rapidly promoted corneal epithelial healing. Six of these patients had been treated with conventional therapy for 3-10 weeks but proved to be completely therapy-resistant. Our observations on three successfully treated patients with chemical burns of the cornea indicated appearance of plasmin in tear fluid after a few days correlating with cessation of epithelialization. In all patients, in which tear fluid plasmin activity was followed, the activity disappeared during aprotinin therapy correlating with corneal re-epithelialization. In some patients with low proteolytic activity aprotinin was combined with fibronectin with a beneficial therapeutic effect. No proteolytic activity was found in the tear fluid of control individuals. These preliminary data indicate that in patients with treatment-resistant corneal lesions inhibition of proteolytic activity can assist in epithelial healing. Such an inhibition is likely to be a prerequisite for the proteinase-sensitive cell adhesion proteins such as fibronectin to promote epithelialization.

Human leukocyte interferon, purified approximately 1000-fold by affinity chromatography on immobilized anti-interferon globulins and SDS-Sephadex filtration, was resolved into one major and one minor component by adsorption chromatography on hydroxylapatite and electrophoresis in polyacrylamide gels. These components were indistinguishable in their capacity to protect bovine, porcine and murine cells, and the antiviral activities of both were equally susceptible to reduction by beta-mercaptoethanol. They were neutralized to the same degree of rabbit anti-leukocyte interferon but were not neutralized by rabbit antifibroblast interferon serum. Mice immunized with either component developed antibodies to both but failed to form antibodies against human fibroblast interferon. Our present evidence indicates that the two components posses at most only minor structural and antigenic dissimilarities.