Cold - induced platelet aggregation in vivo and its inhibition by a nonionic surface active substance

With a photoelectric technique the effect of different temperatures on platelets has been studied in flowing canine blood. By passage through an extracorporeal cooling system this blood was cooled stepwise from 36 to 5°C. Platelets were found to aggregate spontaneously at temperatures of around 20°C. A maximum of aggregation was observed at a blood temperature of 15°C whereas further cooling down to 10 or 5°C was followed by a decrease in aggregate count. Platelet aggregation present at a blood temperature of 15°C was seen to disappear upon intravenous injection of an industrial surfactant (Pluronic^R F 6B) in a dose dependent fashion. Since this substance is supposed to stabilize platelet membrane proteins the results may support the hypothesis that the effect of cold on platelets is due to conformational changes of the membrane proteins.     

The light-induced rise in cytosolic calcium starts later than the receptor current of the Limulus ventral photoreceptor.

The intracellular arsenazo signal indicating the transient light-evoked change in cytosolic Ca2+ (or Sr2+) concentration was measured in Limulus ventral photoreceptors simultaneously with the receptor current under voltage clamp conditions at 15 degrees C. The latency of the light-evoked arsenazo response was consistently more than 25 msec longer than the latency of the electrical light response (receptor current or -potential). Replacing calcium by strontium in the superfusate caused, within 30-40 min, reversible changes: an enlargement of the arsenazo response and a considerable prolongation of both latencies, that of the electrical and that of the arsenazo response; the difference between the two latencies, however, stayed essentially constant.     

The influence of genetic factors associated with the immunoglobulin heavy chain locus on the development of benign monoclonal gammapathy in ageing IgH-congenic mice.

The role of genetic factors associated with the immunoglobulin heavy chain locus (Igh) in the development of benign monoclonal gammapathy (BMG), a benign B-cell proliferative disorder, was investigated in six Igh congenic mouse strains during ageing. The strains used had a C57BL or BALB background: C57BL/6, BALB.Igb and CB-20 carrying the C57BL Igh (Ighb allotype), BALB/c and C57BL/6.Iga carrying the BALB/c Igh (Igha allotype) and BAB-14, that is of BALB/c origin with the exception of the constant part of the Igh, which is of C57BL origin. The frequency of homogeneous immunoglobulins (H-Ig), both single and multiple, was the highest in C57BL/6 mice, followed by C57BL/6.Iga. The frequencies of H-Ig in BALB.Igb and CB-20 mice were higher than those of BALB/c and BAB-14, although somewhat lower than in C57BL/6.Iga mice. Multiple H-Ig were found especially in the sera of C57BL/6 mice. Categorization of the monoclonal gammapathies (MG) on the basis of their origin showed a single transient monoclonal B-cell proliferation in 0-8% of the mice of all strains. Persistent, non-progressive MG, presumably BMG, were detected in 64% of C57BL/6, 30% of C57BL/6.Iga, 22% of BALB.Igb, 17% of CB-20, 13% of BAB-14 and 6% of BALB/c mice. Multiple myeloma or Waldenström-like B-cell lymphoma were found to be responsible for 2-4% of the paraproteinemias in all strains. The remaining H-Ig, varying from 11% of the C57BL/6 to 70% of the BAB-14 mice, could not be evaluated in time. The most frequent isotypes of the BMG within C57BL/6 and C57BL/6.Iga were IgG2a and IgG2b, respectively; IgM was the most frequent isotype within the four BALB congenic strains. The immunoglobulin heavy chain allotypes under investigation appeared to be only partly related to the onset, occurrence, multiplicity and persistence of the BMG developing in these Igh congenic C57BL and BALB strains during ageing. The immunoglobulin heavy chain allotypes, however, were not related to the major isotype of the BMG. The results obtained in CB-20 and BALB.Igb on the one hand, and in BAB-14 on the other hand, may suggest a role for the variable part of the Igh in the development of BMG. Since no absolute influence could be ascribed to the Igh, we assume that primarily other genetic sequences regulating proliferative B-cell functions account for the pathogenesis of BMG.     

Solid state line scan cameras for measuring strain in soft tissues and implants

The line scan camera, or LSC, is an inexpensive and easily applied technique for optical strain measurement of soft biomaterials. The LSC is based on a linear array of photodiodes; in gauging applications, where measurements between dark/light interfaces are important, the digital nature of the array can be exploited. Advantages of the LSC include low cost, high frequency response, applicability to front- or backlighted samples, insensitivity to stray and nonuniform lighting as well as to accidental overexposure, ease and linearity of calibration, and lack of temperature sensitivity. With the 1024 element arrays used herein, the relative resolution is theoretically limited to 1 part in 1024, or 0.1%; in practice, the relative resolution is somewhat poorer. LSCs have been successfully used in mechanical tests to measure the diameter of arteries and compliant vascular grafts, the longitudinal strain of vascular grafts, and the dynamic diameter of elastic tube models of graft/artery systems in pulsatile flow visualization experiments.     

Induction of aryl hydrocarbon hydroxylase in rodent lung by cigarette smoke: a potential short-term bioassay.

Aryl hydrocarbon hydroxylase (AHH) activity was increased several fold in the lungs of hamsters, mice and rats after inhalation of cigarette smoke. Hamsters had low basal activity of lung AHH but showed the greatest inducibility (the ratio of induced to noninduced enzyme). Inducibility was lower but the actual levels of enzyme activity, both basal and induced, were higher in mice and highest in rats. Several criteria were met which could qualify the lung AHH assay as a short-term bioassay to aid in the measurement of cigarette toxicity. (1) Within a relatively narrow range, AHH activity increased with the number of cigarettes smoked. (2) In tests with standard reference cigarettes and three commercial brands, cigarettes which delivered high levels of total particulate matter (TPM) in the smoke induced AHH in lung to the highest degree; measures which reduced the TPM, primarily filtering methods, reduced the enzyme-inducing effect. (3) Also, with regard to filtering methods, the type of cigarettes which have been reported to cause the most extensive damage to the respiratory tract of animals in chronic inhalation studies caused the greatest enzyme induction in acute experiments. (4) Assay results can be obtained rapidly; maximum induction occurs within 24 hr after smoke exposure.