Bilateral popliteal vein aneurysms

An 82-year-old man was admitted with a left hip fracture sustained in a fall. The fracture was surgically repaired. Ipsilateral leg swelling developed over the following 2 weeks. A lower extremity venous duplex scan demonstrated isolated dilatation of the popliteal veins in both lower extremities. Chronic thrombosis was noted in both popliteal veins at the level of this dilatation. Initial duplex scanning also revealed acute thrombus in the left popliteal, posterior tibial, and peroneal veins. A repeat scan 1 week later identified propagation of thrombus into the superficial femoral vein. Popliteal vein aneurysms, although rare, can cause significant morbidity and mortality. The literature is also reviewed.Presented at the Second Annual Winter Meeting of the Peripheral Vascular Surgery Society, Breckenridge, Colo., January 25–27, 1992.     

花生四烯酸、二十碳五烯酸及二十二碳六烯酸对兔主动脉条张力的影响

外源性AA引起兔动脉条收缩,呈剂量依赖性;EPA抑制AA收缩血管亦呈浓度依赖性;DHA对AA收缩血管作用无明显影响。破坏血管内皮后AA收缩血管作用大为减弱,EPA抑制AA收缩血管作用也几乎消失。吲哚美辛能阻断AA收缩兔主动脉条的作用。兔主动脉6-keto-PGF_1α、TXB₂及其比值随AA浓度升高而增加,低剂量EPA对前列腺素类代谢无明显影响,较大剂量时则降低上述指标。     

Identification of inflections in T-cell counts among HIV-1-infected individuals and relationship with progression to clinical AIDS

Studies of circulating T (CD3⁺) lymphocytes have shown that on a population basis T-cell numbers remain stable for many years after HIV-1 infection (blind T-cell homeostasis), but decline rapidly beginning approximately 1.5–2.5 years before the onset of clinical AIDS. We derived a general method for defining the loss of homeostasis on the individual level and for determining the prevalence of homeostasis loss according to HIV status and the occurrence of AIDS in more than 5,000 men enrolled in the Multicenter AIDS Cohort Study. We used a segmented regression model for log₁₀ CD3⁺ cell counts that included separate T-cell trajectories before and after a time (the T-cell inflection point) where the loss of T-cell homeostasis was most likely to have occurred. The average slope of CD3⁺ lymphocyte counts before the inflection point was close to zero for HIV− and HIV+ men, consistent with blind T-cell homeostasis. After the inflection point, the HIV+ individuals who developed AIDS generally showed a dramatic decline in CD3⁺ cell counts relative to HIV− men and HIV+ men not developing AIDS. A CD3⁺ cell decline of greater than 10 percent per year was present in 77% of HIV+ men developing AIDS but in only 23% of HIV+ men with no onset of AIDS. Our findings at the individual level support the blind T-cell homeostasis hypothesis and provide strong evidence that the loss of homeostasis is an important mechanism in the pathogenesis of the severe immunodeficiency that characterizes the late stages of HIV infection.