Photodetectors integrating waveguides and semiconductor materials.

Photodetectors integrating substrates and semiconductor materials are increasingly attractive for applications in optical communication, optical sensing, optical computing, and military owing to the unique optoelectronic properties of semiconductor materials. However, it is still a challenge to realize high-performance photodetectors by only integrating substrates and semiconductor materials because of the limitation of incident light in contact with sensitive materials. In recent years, waveguides such as silicon (Si) and silicon nitride (Si3N4) have attracted extensive attention owing to their unique optical properties. Waveguides can be easily hetero-integrated with semiconductor materials, thus providing a promising approach for realizing high-performance photodetectors. Herein, we review recent advances in photodetectors integrating waveguides in two parts. The first involves the waveguide types and semiconductor materials commonly used to fabricate photodetectors, including Si, Si3N4, gallium nitride, organic waveguides, graphene, and MoTe2. The second involves the photodetectors of different wavelengths that integrate waveguides, ranging from ultraviolet to infrared. These hybrid photodetectors integrating waveguides and semiconductor materials provide an alternative way to realize multifunctional and high-performance photonic integrated chips and circuits.

High-performance MoS2phototransistors with Hf1-xAlxO back-gate dielectric layer grown by plasma enhanced atomic layer deposition.

Molybdenum sulfide (MoS2) as an emerging optoelectronic material, shows great potential for phototransistors owing to its atomic thickness, adjustable band gap, and low cost. However, the phototransistors based on MoS2have been shown to have some issues such as large gate leakage current, and interfacial scattering, resulting in suboptimal optoelectronic performance. Thus, Al-doped hafnium oxide (Hf1-xAlx) is proposed to be a dielectric layer of the MoS2-based phototransistor to solve this problem because of the relatively higher crystallization temperature and dielectric constant. Here, a high-performance MoS2phototransistor with Hf1-xAlxO gate dielectric layer grown by plasma-enhanced atomic layer deposition has been fabricated and studied. The results show that the phototransistor exhibits a high responsivity of 2.2 × 104A W-1, a large detectivity of 1.7 × 1017Jones, a great photo-to-dark current ratio of 2.2 × 106%, and a high external quantum efficiency of 4.4 × 106%. The energy band alignment and operating mechanism were further used to clarify the reason for the enhanced MoS2phototransistor. The suggested MoS2phototransistors could provide promising strategies in further optoelectronic applications.

Characteristics of tunable aluminum-doped Ga2O3thin films and photodetectors.

Aluminum-doped Ga2O3(AGO) thin films were prepared by plasma-enhanced atomic layer deposition (PE-ALD). The growth mechanism, surface morphology, chemical composition, and optical properties of AGO films were systematically investigated. The bandgap of AGO films can be theoretically set between 4.65 and 6.8 eV. Based on typical AGO films, metal-semiconductor-metal photodetectors (PDs) were created, and their photoelectric response was examined. The preliminary results show that PE-ALD grown AGO films have high quality and tunable bandgap, and AGO PDs possess superior characterizations to undoped films. The AGO realized using PE-ALD is expected to be an important route for the development of a new generation of gallium oxide-based photodetectors into the deep-ultraviolet.

Postprocedure administration of insulin in canine autologous vein grafting: a potential strategy to attenuate intimal hyperplasia.

Intimal hyperplasia (IH) exerts a critical role in vein graft failure after arterial bypassing. Insulin has been demonstrated to remarkably decrease IH in the rat carotid injury model. We hypothesized that postoperative insulin medication prevents the autologous vein graft from IH. Dogs were subjected to jugular-carotid interposition bypass grafting and intravenously infused with vehicle, glucose-insulin-potassium, glucose-potassium, or glucose-insulin-potassium plus Wortmannin 5 minutes before and 4 hours after reperfusion. Then vein grafts were harvested for caspase-3 activation, cell apoptosis, phosphorylated Akt, and endothelial nitric oxide synthase level assays. Other dogs undergoing the same operation were administered with subcutaneous injection of 4 U insulin or 0.5 mL saline two times per day for 1 month postoperatively. Vein grafts were sampled to assess cell proliferation, intimal/medial thickness, and expression of endothelial nitric oxide synthase and [alpha]-smooth muscle actin. Glucose-potassium aggravated apoptosis and caspase-3 activation and decreased Akt and endothelial nitric oxide synthase phosphorylation; however, glucose-insulin-potassium significantly inhibited cell apoptosis and caspase-3 activation and increased phosphorylated Akt and pendothelial nitric oxide synthase levels in canine vein grafts. Wortmannin largely abolished the glucose-insulin-potassium-elicited effects. Moreover, postoperative insulin use greatly inhibited cell proliferation, reduced intimal/medial thickness, upregulated endothelial nitric oxide synthase, and [alpha]-smooth muscle actin expression. Insulin protects autologous vein grafts possibly through the phosphatidylinositol-3 kinase/Akt signaling pathway and prevents IH in autologous vein grafts.

Insulin inhibits beta-adrenergic action in ischemic/reperfused heart: a novel mechanism of insulin in cardioprotection.

OBJECTIVE: Sympathetic overactivity is closely connected with cell injury and contractile dysfunction during myocardial ischemia/reperfusion (MI/R). Insulin exerts protection for the I/R heart and the underlying mechanisms remain unclear. This study aimed to investigate the ability of insulin to modulate beta-adrenergic actions on myocardial contraction and post-ischemic injury in acute MI/R and the underlying mechanism. METHODS: Isolated hearts from adult SD rats were subjected to MI/R (30 min/2 h) and treated with isoproterenol (ISO) or/and insulin. Myocardial contraction, cardiomyocyte apoptosis, myocardial injury and infarction were assessed. In a separate study, isolated ventricular myocytes were subjected to simulated I/R (15/30 min) and myocyte shortening and intracellular Ca2+ transient in response to ISO during reperfusion were assessed with presence or absence of insulin. RESULTS: In isolated I/R hearts, insulin largely reversed the ISO-associated contractile functional impairment at 2 h after MI/R, inhibiting ISO-induced declines in heart rate and left ventricular systolic pressure by 34.0% and 23.0% and preventing ISO-induced elevation in left ventricular end-diastolic pressure by 28.7% respectively (all P < 0.05). In addition, ISO alone resulted in enlarged infarct size, elevated CK and LDH activity and increased apoptotic index in I/R hearts compared with vehicle, which were inhibited by treatment of insulin (all P < 0.05). Interestingly, in SI/R cardiomyocytes, insulin alone at 10(-7 )mol/l increased cell contraction whereas attenuated the positive inotropic response to ISO (10(-9 )mol/l) during R as evidenced by a 18.7% reduction in peak twitch amplitude and a 23.9% reduction in calcium transient amplitude (both P < 0.05). Moreover, insulin blunted ISO-mediated increase in PKA activity, enhanced the PKA-dependent phosphorylation of phospholamban (PLB), resulting in increased sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) activity. CONCLUSION: Insulin attenuated the contractile response to beta-AR stimulation and suppressed ISO-elicited cardiac dysfunction and cell injury in MI/R. The inhibitory effect of insulin on the beta-adrenergic action involved the inhibition of PKA-mediated Ca2+ transient and promotion of post-ischemic Ca2+ handling.

Long-term aerobic exercise protects the heart against ischemia/reperfusion injury via PI3 kinase-dependent and Akt-mediated mechanism.

OBJECTIVE: Physical activity has been shown to improve cardiovascular function and to be beneficial to type 2 diabetic patients. However, the effects of aerobic exercise (AE) on myocardial ischemia/reperfusion (MI/R) are largely unclear. Therefore, the aims of the present study were to determine whether long-term AE can protect the heart against I/R injury, and if so, to investigate the underlying mechanism. METHODS: Adult male Sprague-Dawley rats were randomly subjected to 8 weeks of either sedentary or free-loading swimming exercise (3 h/day, 5 d/week). Then the animals were subjected to 30 min MI followed by 4 h R. Arterial blood pressure and left ventricular pressure (LVP) were monitored throughout the whole MI/R procedure. Plasma creatine kinase (CK) and lactate dehydrogenase (LDH) activities were measured spectrophotometrically. Myocardial infarction and myocardial apoptosis (TUNEL analysis) were determined in a blinded manner. RESULTS: MI/R caused significant cardiac dysfunction and myocardial apoptosis (strong TUNEL-positive staining). Compared with sedentary group, rats subjected to 8 weeks of AE showed protection against MI/R as evidenced by reduced myocardial infarction (26.8 +/- 1.5% vs. 35.3 +/- 2.4%, n = 8, P < 0.05), inhibited cardiomyocyte apoptosis (decreased apoptotic index (12.4 +/- 1.1% vs. 21.0 +/- 1.7%, n = 8, P < 0.01) and decreased myocardial caspase-3 activity), decreased plasma CK and LDH activities and improved recovery of cardiac systolic/diastolic function (including LVSP and +/-LVdP/dt) at the end of R. Moreover, exercise resulted in 1.7-fold, 2.5-fold and 2.5-fold increases in Akt expression, Akt phosphorylation and glycogen synthase kinase-3beta phosphorylation in I/R myocardium, respectively (n = 3, all P < 0.05). More importantly, treatment with wortmannin, a PI3 kinase inhibitor, 15 min before R not only significantly blocked Akt phosphorylation (P < 0.05) in exercise rats, but also abolished long-term AE-induced cardioprotection for the I/R heart as manifested by increased apoptosis and myocardial infarction, and reduced cardiac function. CONCLUSION: Long-term AE exerts cardioprotective effect against MI/R injury, including anti-cardiomyocyte apoptosis, which is at least partly via PI3 kinase-dependent and Akt-mediated mechanism.

Acute hyperglycemia exacerbates myocardial ischemia/reperfusion injury and blunts cardioprotective effect of GIK.

There is a close association between hyperglycemia and increased risk of mortality after acute myocardial infarction (AMI). However, whether acute hyperglycemia exacerbates myocardial ischemia/reperfusion (MI/R) injury remains unclear. We observed the effects of acute hyperglycemia on MI/R injury and on the cardioprotective effect of glucose-insulin-potassium (GIK). Male rats were subjected to 30 min of myocardial ischemia and 6 h of reperfusion. Rats were randomly received one of the following treatments (at 4 ml.kg(-1).h(-1) iv): Vehicle, GIK (GIK during reperfusion; glucose: 200g/l, insulin: 60 U/l, KCL: 60 mmol/l), HG (high glucose during ischemia; glucose:500 g/l), GIK + HG (HG during I and GIK during R) or GIK + wortmannin (GIK during R and wortmannin 15 min before R). Blood glucose, plasma insulin concentration and left ventricular pressure (LVP) were monitored throughout the experiments. Hyperglycemia during ischemia not only significantly increased myocardial apoptosis (23.6 +/- 1.7% vs. 18.8 +/- 1.4%, P < 0.05 vs. vehicle), increased infarct size (IS) (45.6 +/- 3.0% vs. 37.6 +/- 2.0%, P < 0.05 vs. vehicle), decreased Akt and GSK-3beta phosphorylations (0.5 +/- 0.2 and 0.6 +/- 0.1% fold of vehicle, respectively, P < 0.05 vs. vehicle) following MI/R, but almost completely blocked the cardioprotective effect afforded by GIK, as evidenced by significantly increased apoptotic index (19.1 +/- 2.0 vs. 10.3 +/- 1.2%, P < 0.01 vs. GIK), increased myocardial IS (39.2 +/- 2.8 vs. 27.2 +/- 2.1%, P < 0.01 vs. GIK), decreased Akt phosphorylation (1.1 +/- 0.1 vs. 1.7 +/- 0.2%, P < 0.01 vs. GIK) and GSK-3beta phosphorylation (1.4 +/- 0.2 vs. 2.3 +/- 0.2%, P < 0.05 vs. GIK). Hyperglycemia significantly exacerbates MI/R injury and blocks the cardioprotective effect afforded by GIK, which is, at least in part, due to hyperglycemia-induced decrease of myocardial Akt activation.