A highly sensitive wearable flexible strain sensor based on polycrystalline MoS2 thin film.

The present study investigates the piezoresistive properties of polycrystalline MoS2 film for strain-sensing applications. The gauge factor (GF) of the flexible MoS2 device (MoS2/PET) has been calculated to be 102 ± 5 in the stress range from ~7 MPa to ~14 MPa. In addition, to improve the sensing stress range, the flexible strain sensors are encapsulated by SU-8. The effect of encapsulation layer thickness is reflected in the GF, which is attributed to the shifting of the neutral axis. However, the calculated GF is constant in the higher stress range, 80 ± 2 and 12 ± 1 for 2 µm and 10 µm thick SU-8, respectively. Herein, we report a cost-effective and scalable approach to fabricate large-area polycrystalline MoS2-based flexible sensors for a wider stress range. The encapsulated devices remained undistorted and intact for stress values beyond 14 MPa. Further, we demonstrate the durability of the fabricated sensors with body movements, such as hand gestures, for all the three types of strain sensor.

Thickness Dependent Parasitic Channel Formation at AlN/Si Interfaces.

The performance of GaN-on-Silicon electronic devices is severely degraded by the presence of a parasitic conduction pathway at the nitride-substrate interface which contributes to switching losses and lower breakdown voltages. The physical nature of such a parasitic channel and its properties are however, not well understood. We report on a pronounced thickness dependence of the parasitic channel formation at AlN/Si interfaces due to increased surface acceptor densities at the interface in silicon. The origin of these surface acceptors is analyzed using secondary ion mass spectroscopy measurements and traced to thermal acceptor formation due to Si-O-N complexes. Low-temperature (5 K) magneto-resistance (MR) data reveals a transition from positive to negative MR with increasing AlN film thickness indicating the presence of an inversion layer of electrons which also contributes to parasitic channel formation but whose contribution is secondary at room temperatures.

Chemopreventive potential of synergy1 and soybean in reducing azoxymethane-induced aberrant crypt foci in fisher 344 male rats.

Synergy1, a prebiotic composed of Inulin and Oligofructose (1 : 1). Soybean meal is a natural source of isoflavones. The objective was to investigate the effects of feeding Synergy1 and SM on the incidence of azoxymethane- (AOM-) induced aberrant crypt foci (ACF) in Fisher 344 male rats. Rats (54) were randomly assigned to 9 groups (n = 6). Control group (C) was fed AIN-93G and treatment groups Syn1 and SM at 5% and 10% singly and in combinations. Rats were injected with two s/c injections of AOM at 7 and 8 weeks of age at 16 mg/kg body weight and killed at 17 weeks by CO(2) asphyxiation. Colonic ACF enumeration and hepatic enzyme activities were measured. Reductions (%) in total ACF among treatment groups fed combinations were higher (67-77) compared to groups fed singly (52-64). Synergistic mechanisms among phytochemicals may be responsible suggesting protective role in colon carcinogenesis with implications in food product development.

Hypocomplementemia in chronic idiopathic urticaria.

A discrete evoking factor or presumed pathophysiologic mechanism is not recognized in the majority of patients with chronic urticaria or angioedema. Two cases are reported in which chronic urticaria was the main manifestation of an immune cutaneous vasculitis associated with hypocomplementemia attributable to classic and alternative mechanisms of complement activation. Among 72 consecutive patients evaluated for chronic urticaria, 10 additional patients with idiopathic urticaria were found to have hypocomplementemia. Of these, two had evidence of classic and alternative mechanisms of complement activation, five had evidence of only classic pathway activation, and three evidence of predominately or exclusively alternative pathway activation. Circulating immune complexes were found in the majority of patients with classic pathway activation. Hypocomplementemia may provide clues to pathophysiologic mechanisms operative in some patients with chronic urticaria.

Plasma histamine changes during provoked bronchospasm in asthmatic patients.

Seven patients with bronchial asthma underwent bronchial inhalation challenge with aerosolized allergen extracts and methacholine. Simultaneously, venous blood samples were collected and histamine was measured. Each patient was challenged on successive days with an allergen extract to which he had no skin-sensitizing antibody (skin test-negative allergen), followed by methacholine and skin test-positive allergen. Bronchospasm was not induced by inhalation of skin test-negative allergens but was observed in all patients after methacholine and in the majority of patients after skin test-positive allergens. No changes in plasma histamine were detected after challenges with methacholine and skin test-negative allergens. After challenge with skin test-positive allergens, significant rises in plasma histamine were detected in 5 of 7 patients. Plasma histamine was elevated within the first 5 min after inhalation of aerosolized allergen, and elevations persisted as long as 30 min. These studies showing that histamine increases significantly in the plasma during allergen-induced asthma in man suggest that histamine should be considered as at least one of the mediators of bronchospasm in allergic asthma. Bronchospasm induced by the cholinergic drug methacholine, unlike allergen-induced bronchospasm, is not associated with changes in plasma histamine.

Activation of the alternative pathway of the complement system by radiographic contrast media.

Nine patients who underwent radiographic contrast media (RCM) infusion for diagnostic purposes were studied. Simultaneously, venous blood samples were collected and complement was measured. None of the patients had a clinical history of allergy to previous infusion of RCM. A significant drop in plasma complement (CH50) levels was detected in five of nine patients. The drop in CH50 was observed within the first 20 min after the initiation of RCM infusion. All five patients in whom a drop in complement was found showed a decrease in hemolytic C3, properdin, and factor B. In addition, by radial immunodiffusion low levels of C3, C6, properdin, and factor B were observed and split products of C3 and factor B were identified by immunoelectrophoresis. No significant changes in C1q and C4 were detected by radial immunodiffusion during the study of these five patients. This study strongly suggested that in some patients undergoing RCM infusion, activation of the complement system occurred and this activation appears to be through the alternative pathway.

Oral aspirin challenges in asthmatic patients: a study of plasma histamine.

Under carefully controlled conditions, seven aspirin-intolerant asthmatic patients were challenged with oral aspirin and experienced respiratory tract reactions with a decline in forced expiratory volume in 1 sec (FEV1) ranging from 26 to 64%. Venous blood samples, which were collected during the challenges, showed a rise in plasma histamine in all seven patients. The increase in plasma histamine occurred at the onset of their respiratory reactions and those patients with the most severe asthmatic responses were found to have the highest and most prolonged levels of plasma histamine. The aspirin-intolerant asthmatic patients were able to ingest Maalox or sodium salicylate without untoward effects, decline in FEV1 values or changes in plasma histamine levels. Ten non-asthmatic individuals and eight out of ten asthmatic control patients were able to ingest aspirin without any reactions or changes in their plasma histamine levels. However, two asthmatic control individuals, with severe asthma requiring treatment with moderate dosages of corticosteroids, were found to have elevated pre-challenge plasma histamine levels which increased during their ASA challenges despite the absence of respiratory reactions or changes in FEV1 values. It is possible that these two individuals were unsuspected aspirin-intolerant asthmatics. These studies demonstrate that asthmatic reactions to acetylsalicylates are associated with release of histamine into plasma in the subgroup of asthmatic patients with the aspirin-intolerance syndrome. Such a finding suggests that histamine may be one of the mediators of bronchospasm in aspirin-induced asthma.

Reaction to radiographic contrast agents: new developments in etiology.

Although a significant amount of histamine is released into plasma during contrast media injections, there still is no evidence to support an immunologic basis underlying contrast media reactions. This study supports previous observations that suggest in vitro leucocyte challenge may be of predictive value in contrast media reactions. Lassar's study in dogs and this study in humans clearly shows that complement activation by alternative pathway occurs during contrast agent administration. However, pathophysiological significance of this observation is not clear.