Histamine H1- and H2-receptor vasodilation of canine intestinal circulation

Studies were conducted in anesthetized dogs to determine whether the mesenteric vasodilator response to histamine is mediated by H1 receptors alone or whether H2 receptors are also involved in the response. Evidence favoring a role for both receptors included: 1) the vasodilator response to histamine was inhibited by either the H1-receptor antagonist, tripelennamine, or the H2-receptor antagonist, metiamide; 2) both the H1 agonist, 2-methylhistamine, and the H2 agonist, 4-methylhistamine, induced dilator responses in the mesenteric circulation; and 3) two temporal patterns of vasodilation could be distinguished, namely a transient spike and subsequent fade of blood flow (seen with either the H1 agonist or with histamine after H2-receptor blockade) and a sustained and stable increase in flow (seen with either the H2 agonist or with histamine after H1 blockade). Metiamide appeared to be a potent inhibitor of the mesenteric vasodilator response to histamine at least equal to tripelennamine.     

Cognitive performance in conversion hysteria

In order to test some neurobiologically based assumptions pertaining to attention and memory dysfunction in conversion hysteria, a series of tasks was given to 17 hospitalized patients with hysterical conversion reaction and to a control group of nonpsychotic patients under conditions of nonstress and stress. The results indicated significant differences in performance between hysteria and control subjects. The former group, in comparison to controls, had heightened suggestibility, greater field dependency, and greater impairment of recent memory and vigilance-attention. A discriminant analysis indicated the feasibility of using such tests as objective diagnostic criteria for hysteria.     

Analytical model of interaction between contention-based and deterministic channel access mechanisms in Wi-Fi Mesh networks

A new analytical model was developed to estimate the degree of mutual influence of the links between the stations of Wi-Fi Mesh networks which use different channel access methods specified by the IEEE 802.11s standard, namely, contention-based channel access mechanism and the deterministic channel access mechanism based on the preliminary reservation of channel resources. The model was used to compare the efficiency of different backoff counting methods proposed in the paper for providing the interaction between two channel access methods. Additionally, the model was also used to analyze the effect of different techniques for arranging the time intervals reserved by means of the deterministic channel access mechanism on the performance of stations using contention-based channel access mechanism.     

Protein 4.1R-deficient mice are viable but have erythroid membrane skeleton abnormalities

A diverse family of protein 4.1R isoforms is encoded by a complex gene on human chromosome 1. Although the prototypical 80-kDa 4.1R in mature erythrocytes is a key component of the erythroid membrane skeleton that regulates erythrocyte morphology and mechanical stability, little is known about 4.1R function in nucleated cells. Using gene knockout technology, we have generated mice with complete deficiency of all 4.1R protein isoforms. These 4.1R-null mice were viable, with moderate hemolytic anemia but no gross abnormalities. Erythrocytes from these mice exhibited abnormal morphology, lowered membrane stability, and reduced expression of other skeletal proteins including spectrin and ankyrin, suggesting that loss of 4. 1R compromises membrane skeleton assembly in erythroid progenitors. Platelet morphology and function were essentially normal, indicating that 4.1R deficiency may have less impact on other hematopoietic lineages. Nonerythroid 4.1R expression patterns, viewed using histochemical staining for lacZ reporter activity incorporated into the targeted gene, revealed focal expression in specific neurons in the brain and in select cells of other major organs, challenging the view that 4.1R expression is widespread among nonerythroid cells. The 4.1R knockout mice represent a valuable animal model for exploring 4.1R function in nonerythroid cells and for determining pathophysiological sequelae to 4.1R deficiency.