Numerical Investigation of Negative Temperature Coefficient Effects on Sooting Characteristics in a Laminar Co-flow Diffusion Flame.

It is a common sense that diesel engines produce worse soot emission than gasoline engines, even though gasoline direct injection also brings about terrible sooting tendency. However, reports showed that diesel emits less soot than gasoline in laminar diffusion flames, which implies that soot emission is a combined effect of multiple factors, such as the combustion mode, physical properties of the fuel, and also fuel chemistry. This work, thus, conducted numerical calculations in laminar co-flow diffusion flames of fuels with different negative temperature coefficient (NTC) behaviors in an order of n-heptane > iso-octane > toluene to solely evaluate the chemical effect, especially the role of low-temperature combustion on soot formation. 2-Dimensional simulations were carried out to obtain the soot distributions, and 0-dimensional simulations were performed to analyze the chemical kinetics of polycyclic aromatic hydrocarbon (PAH) formation and low-temperature reaction sensitivities. The grids of the 2-D model converged at 80(r) × 196(z), and the boundary conditions of both models were set to eliminate the influence of physical factors as much as possible. The results showed that there were three main reactions associated to the formation of aromatic hydrocarbons A1 at the first-stage combustion in the n-heptane flame and the iso-octane flame, in which the reaction of C7H15 + O2 = C7H15O2 enhances the NTC behavior. The first two reaction pathways generated larger molecular hydrocarbons and were unfavorable by A1 formation and therefore inhabit the PAH formation, and 49.8% of C7H16 reacted through the large molecular pathways, while the percentage for C8H18, with weaker NTC behavior, was only 37%. Toluene with even weaker NTC behavior showed no low-temperature oxidation. Therefore, in a more general case, fuels with stronger NTC behavior smoke less, and this conclusion could be promising potential to reduce soot emission in future.

Discharge pharmacotherapy for Type 2 diabetic inpatients at two hospitals of different tiers in Zhejiang Province, China.

OBJECTS: To look into the discharge pharmacotherapy for type 2 diabetics admitted to two general hospitals of different ranks and inspect current real-world management of discharge pharmacology and its related factors. METHODS: Type 2 diabetics admitted to a tertiary general hospital (Ningbo Medical Treatment Centre Lihuili Hospital, LHLH) or a secondary general hospital (Simen Hospital, SMH) for intensification of their anti-diabetics were included for retrospective analysis. Patients' demographics, clinical characteristics, admission diabetes therapy and discharge diabetes pharmacology were analyzed and compared among patients in each hospital as well as between two hospitals. RESULTS: 391 patients from LHLH and 164 patients from SMH were included for analyzing. Compared with patients from LHLH, patients from SMH were older, more illiterate and had higher HbA1c concentrations. While there was a nearly equal split of oral anti-diabetes drugs (OADs)-only and Insulin treatment in LHLH's discharge pharmacotherapy, insulin treatment dominated SMH's. Basal-and-bolus insulin assumed the majority of SMH's insulin regimens but only accounted for less than 20% of LHLH's. The principal discrepancy in OADs-only treatment existed in the utilization of newer classes of OADs. Cost and body mass index (BMI) were the main differentiating factors among OADs-only treatments while duration, BMI and HbA1c differ among insulin treatments at LHLH. Clinical characteristics didn't significantly differ among OADs-only treatments and HbA1c was the only differentiating factor among insulin treatments at SMH. Overall, hospital, duration, HbA1c, and vascular diseases were main factors that affect discharge pharmacology. CONCLUSIONS: Great disparities exist in the discharge pharmacotherapy at two hospitals. Diabetes management is mostly glucose-oriented at SMH while multifactorial considerations were reflected in LHLH's discharge pharmacotherapy. Besides differences in patients' demographics, medication availability and diagnosis of early-stage vascular complications, lack of practical algorithm for discharge management in T2DM may be the underlying deficiency and a key part for future improvement.

Palladium(ii)-catalyzed oxidative C(sp3)-P bond formation via C(sp3)-H bond activation.

Disclosed herein is a Pd(ii)-catalyzed C(sp3)-H/P-H oxidative cross-coupling reaction between 8-methylquinolines with H-phosphonates or diarylphosphine oxides via chelation-assisted C(sp3)-H bond activation. The protocol exhibits a relatively broad functional-group tolerance and exclusive chemo- and regioselectivity. Furthermore, detailed mechanistic studies support the proposed reaction pathway.

Newer Perspectives of Mechanisms for Euglycemic Diabetic Ketoacidosis.

Euglycemic diabetic ketoacidosis (EDKA) was considered a rare condition with its specific definition and precipitating factors. However, with the wide use of sodium glucose cotransporter 2 (SGLT-2) inhibitors, the newest class of antidiabetic agents, EDKA has come back into the spotlight. Relevant cases are increasingly being reported along with insights into the mechanism of EDKA. It seems increasingly clear that EDKA is more common than we used to believe. The SGLT-2 inhibitor-associated EDKA also indicates a necessary review of our previous understanding of "diabetic" ketoacidosis, since the SGLT-2 inhibitor predisposes patients to DKA in a "starvation" way. Actually, there are growing reports about starvation-induced ketoacidosis as well. The previously "exclusive" nomenclature and cognition of these entities need to be reexamined. That the hormonal interactions in DKA may differ from the severity of insulin deficiency also may have served in the scenario of EDKA. The SGLT-2 inhibitors are newly approved in China. The main purpose of this work is to have a better understanding of the situation and update our knowledge with a focus on the pathogenesis of EDKA.

Amidoselenation and Amidotelluration of Alkenes using Oxygen as Terminal Oxidant.

A protocol has been established for oxygen-mediated amidoselenation and amidotelluration of alkenes under mild conditions. This method provides a simple route to a series of structurally diverse ß-amido selenides and ß-amido tellurides in moderate to high yields. The wide substrate scope, good functional group tolerance, ease of large-scale preparation and potential for product derivatization make this reaction attractive for the synthesis of nitrogen-, selenium- and tellurium-containing molecules.

Glucose fluctuation increased hepatocyte apoptosis under lipotoxicity and the involvement of mitochondrial permeability transition opening.

Oxidative stress is considered to be an important factor in producing lethal hepatocyte injury associated with nonalcoholic fatty liver disease (NAFLD). Glucose fluctuation, more pronounced in patients with diabetes, has been recognized as an even stronger oxidative stress inducer than the sustained hyperglycemia. Here, we investigated the role of glucose variability in the development of the NAFLD based on hepatocyte apoptosis and possible mechanisms. To achieve this goal we studied C57BL/6J mice that were maintained on a high fat diet (HFD) and injected with glucose (3 g/kg) twice daily to induce intermittent high glucose (IHG). We also studied hepatic L02 cells incubated with palmitic acid (PA) to induce steatosis. The following experimental groups were compared: normal glucose (NG), sustained high glucose (SHG) and IHG with or without PA. We found that, although hepatic enzyme levels and liver lipid deposition were comparable between HFD mice injected with glucose or saline, the glucose injected mice displayed marked hepatocyte apoptosis and inflammation, accompanied by increased lipid peroxide in liver. In vitro, in the presence of PA, IHG increased L02 cell apoptosis and oxidative stress and produced pronounced mitochondrial dysfunction relative to the NG and SHG groups. Furthermore, treatment with the mitochondrial permeability transition (MPT) inhibitor, cyclosporin A (1.5 µmol/l), prevented mitochondrial dysfunction, oxidative stress and hepatocyte apoptosis. Our data suggests that IHG under lipotoxicity might contribute to the development of NAFLD by increasing oxidative stress and hepatocyte apoptosis via MPT and its related mitochondrial dysfunction.

Regulation of insulin resistance and adiponectin signaling in adipose tissue by liver X receptor activation highlights a cross-talk with PPARγ.

Liver X receptors (LXRs) have been recognized as a promising therapeutic target for atherosclerosis; however, their role in insulin sensitivity is controversial. Adiponectin plays a unique role in maintaining insulin sensitivity. Currently, no systematic experiments elucidating the role of LXR activation in insulin function based on adiponectin signaling have been reported. Here, we investigated the role of LXR activation in insulin resistance based on adiponectin signaling, and possible mechanisms. C57BL/6 mice maintained on a regular chow received the LXR agonist, T0901317 (30 mg/kg.d) for 3 weeks by intraperitoneal injection, and differentiated 3T3-L1 adipocytes were treated with T0901317 or GW3965. T0901317 treatment induced significant insulin resistance in C57BL/6 mice. It decreased adiponectin gene transcription in epididymal fat, as well as serum adiponectin levels. Activity of AMPK, a key mediator of adiponectin signaling, was also decreased, resulting in decreased Glut-4 membrane translocation in epididymal fat. In contrast, adiponectin activity was not changed in the liver of T0901317 treated mice. In vitro, both T0901317 and GW3965 decreased adiponectin expression in adipocytes in a dose-dependent manner, an effect which was diminished by LXRα silencing. ChIP-qPCR studies demonstrated that T0901317 decreased the binding of PPARγ to the PPAR-responsive element (PPRE) of the adiponectin promoter in a dose-dependent manner. Furthermore, T0901317 exerted an antagonistic effect on the expression of adiponectin in adipocytes co-treated with 3 µM Pioglitazone. In luciferase reporter gene assays, T0901317 dose-dependently inhibited PPRE-Luc activity in HEK293 cells co-transfected with LXRα and PPARγ. These results suggest that LXR activation induces insulin resistance with decreased adiponectin signaling in epididymal fat, probably due to negative regulation of PPARγ signaling. These findings indicate that the potential of LXR activation as a therapeutic target for atherosclerosis may be limited by the possibility of exacerbating insulin resistance-related disease.