We describe director distortions in the nematic liquid crystal (LC) caused by a spherical particle with tangential surface orientation of the director and show that light transmittance through the distorted region is a steep function of the particle's size. The effect allows us to propose a real-time microbial sensor based on a nontoxic lyotropic chromonic LC (LCLC) that detects and amplifies the presence of immune complexes. A cassette is filled with LCLC, antibody, and antigen-bearing particles. Small and isolated particles cause no macroscopic distortions of the LCLC. Upon antibody-antigen binding, the growing immune complexes distort the director and cause detectable optical transmittance between crossed polarizers.

We describe director distortions in the nematic liquid crystal (LC) caused by a spherical particle with tangential surface orientation of the director and show that light transmittance through the distorted region is a steep function of the particle's size. The effect allows us to propose a real-time microbial sensor based on a lyotropic chromonic LC (LCLC) that detects and amplifies the presence of immune complexes. A cassette is filled with LCLC, antibody, and antigen-bearing particles. Small and isolated particles cause no macroscopic distortions of the uniformly aligned LCLC. Upon antibody-antigen binding, the growing immune complexes

We examined the effect of fibrinolysis depression on thrombin-induced pulmonary microembolism in awake sheep prepared with chronic lung lymph fistulas. Fibrinolysis was depressed by an intravenous infusion (100 mg) of tranexamic acid [trans-4-(Aminomethyl)cyclohexanecarboxylic acid]. Pulmonary microembolism was induced by an intravenous infusion of alpha-thrombin (80 NIH U/kg) in normal (n = 7) and in tranexamic acid-treated (n = 6) sheep. Thrombin immediately increased pulmonary lymph flow (Qlym) in both groups. The increased Qlym was not associated with a change in the lymph-to-plasma protein concentration (L/P) ratio in the control group and with a small decrease in the tranexamic acid-treated group. The increases in Qlym and pulmonary transvascular protein clearance (Qlym X L/P ratio) in the tranexamic acid-treated group were greater and sustained at four- to fivefold above base line for 10 h after the thrombin and remained elevated at twofold above base line even at 24 h. In contrast, Qlym and protein clearance were transiently increased in the control group. The mean pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (PVR) increased after thrombin in tranexamic acid-treated group; the increases in Ppa and PVR in the control group were transient. Protein reflection coefficient as determined by the filtration independent method decreased after thrombin in tranexamic acid-treated sheep (n = 5), indicating an increased vascular permeability to proteins. We conclude that prolongation of microthrombi retention in the pulmonary circulation results in an increased vascular permeability to proteins. Both increased vascular permeability and vascular hydrostatic pressure are important determinants of the increases in Qlym and transvascular protein clearance after thrombin-induced pulmonary microembolism.

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