Our intention was to examine if subnormal testosterone levels in older men were associated with a reduction in quality of life and physical and mental health, and secondly to examine if testosterone treatment could improve these conditions. We performed a nested case-control study and a 1-year testosterone intervention study. Men with subnormal testosterone had significantly higher weight, fat mass and abdominal adipose tissue. They also had significantly higher glucose and insulin levels, and they had higher triglyceride levels. Testosterone treatment had a large impact on body composition with reduced fat mass and abdominal adipose tissue and increased fat-free mass, but it did not affect weight and glucose and lipid metabolism. Bone mineral density in the hip was significantly higher after the testosterone treatment. Older men with subnormal testosterone levels had an unfavorable metabolic profile. Testosterone treatment improved body composition, but it did not reverse the unfavorable metabolic profile.

Increased plasma- and tissue levels of endothelin-1 (ET-1) during inflammatory diseases, have suggested a role of ET-1 in the pathophysiology of inflammatory reactions. The authors have studied the effect of ET-1 on cytokine release from monocytes and monocyte-derived macrophages. ET-1 increased secretion of TNF-α, IL-1β and IL-6 in a dose- and time-dependent manner. Optimal ET-1 concentration ranged from 0.01 to 1 nM. The maximal response was a 200 to 400% increase in cytokine release. A time-course study revealed that the pattern of cytokines induced by ET-1 was different in monocytes and macrophages, although an early increase in TNF-α was observed in both monocyte and macrophage supernatants. In conclusion, ET-1 stimulates monocytes and macrophages to release cytokines thereby demonstrating a potential role for ET-1 in regulation of inflammatory responses.

In the present study we examined whether endothelin-1 stimulation of human monocytes causes release of chemotactic factors. It was found that monocytes released neutrophil- and monocyte-chemotactic activity in a dose- and time-dependent manner in response to ET-1. ET-1 did not show any chemotactic activity by itself. NCA was detected in monocyte supernatants in response to ET-1 (0.01–100 nM) after 1, 4, 8 and 24 h stimulation. MCA was detected only after 24 h stimulation with ET-1 (0.1–100 nM). Preincubation of the monocyte cultures with the lipoxygenase inhibitors nordihydroguaiaretic acid (10−4 M) or diethylcarbamazine (10−9 M) completely abolished the appearance of NCA and MCA. NCA was neutralized by > 75% using a polyclonal antibody against human interleuktn-8. The ET-1 induced release of IL-8 was confirmed by IL-8 ELISA. A monoclonal antibody against human monocyte chemotactic protein-1 neutralized MCA by > 80%. It is concluded that ET-1 stimulation of monocytes in vitro causes release of neutrophil- and monocyte-chemotactic activity identified as IL-8 and MCP-I respectively. An intact lipoxygenase pathway is crucial for this effect of ET-1 to occur.

At present, 16-slice MDCT cannot replace selective angiography for assessment of coronary bypass graft patency since 24% of bypasses could not be evaluated by this method, and an error rate of 6% is unacceptable.

Background: Hoffmann's syndrome is a rare form of hypothyroid myopathy. Only a few cases of fasciotomy in this setting have previously been reported. Case presentation: A 41-year-old Caucasian man under treatment for hypothyroidism presented with acute-onset severe pain in his forearm for no obvious reason and was admitted to our emergency room. He eventually developed compartment syndrome which necessitated surgical decompression. Soon after surgery he complained of similar symptoms in his calves. By the time his hypothyroid status was confirmed, conservative treatment and orally administered levothyroxine gradually made the pain from his calves disappear, without further surgical treatment. Conclusion: Hoffmann's syndrome may precipitate a compartment syndrome in the absence of trauma.