Insulin requirement profiles and related factors of insulin pump therapy in patients with type 2 diabetes

Continuous subcutaneous insulin infusion(CSII) is an effective therapy to control hyperglycemia in both patients with type 1 diabetes and type 2 diabetes.However,there is little data investigating the insulin dose setting during CSII therapy in type 2 diabetes to achieve optimal glycemic control and avoid the risk of hypoglycemia.Thus,this study is aimed to assess the dose characteristics of insulin requirement and explore the related clinical factors in patients with type 2 diabetes who were treated with CSII.A total of 327 patients(195 males) aged 52.9±12.5 years old were included in this study.Patients were treated with CSII to achieve the target fasting capillary blood glucose(4.4-7.0 mmol L ~(-1)) and 2-h postprandial capillary blood glucose(4.4-10.0 mmol L ~(-1)) by adjusting insulin infusion according to the seven-point capillary blood glucose profiles.Total daily insulin dose(TDD),total daily insulin dose per kilogram(TDD kg-1) and the ratio of total basal insulin dose(TBD) to TDD(%TBa) were calculated after patients achieved the glucose targets for at least 3 days via 1-2 weeks of CSII treatment.And insulin dose,insulin dosing patterns and the relevant clinical factors were analyzed.The mean ratio of basal/bolus insulin distribution of all patients was 40%:60%.Patients with central obesity needed more TDD(51.3±17.1 U versus 43.5±14.0 U,P0.05) and TDD kg ~(-1)(0.8±0.3 U kg ~(-1) versus 0.7±0.2 U kg ~(-1),P0.05) than those without central obesity.Pearson's correlation analysis demonstrated that TDD was positively correlated with body mass index(BMI),waist circumference(WC),baseline fasting plasma glucose(FPG),fasting C-peptide level,2 h-postprandial C-peptide level and time to achieve glycemic target(all P0.05);TDD kg ~(-1) was positively correlated with waist-to-hip ratio(WHR),baseline FPG,glycosylated hemoglobin Ale(HbAlc),fasting C-peptide level and time to achieve glycemic target,and negatively correlated with BMI(all P0.05).Multiple linear regression analyses revealed that BMI(β=1.796,P0.01),WC(β=0.109,P0.01),baseline FPG(β=1.459,P0.01) and HbAlc(β=0.930,P=0.021) were independently related to TDD.Gender(β=-0.107,P=0.003),WC(β=0.005,P=0.029),baseline FPG(β=0.025,P0.01) and HbAlc(β=0.016,β=0.007) were independently associated with TDD kg ~(-1).Gender(β=-0.015,P=0.048) and disease duration(β=0.134,P=0.029) were independently associated with %TBa.%TBa is around 40% in Chinese patients with type 2 diabetes treated with CSII when glycemic control is achieved.In addition to body weight or BMI,WC and glucose levels before CSII should be considered to set TDD.Patients with central obesity or poor glycemic control might need more TDD.Higher %TBa should be considered in female patients or patients with longer disease duration.     

Glycolytic enzymes localize to ribonucleoprotein granules in Drosophila germ cells,bind Tudor and protect from transposable elements

Germ cells give rise to all cell lineages in the next‐generation and are responsible for the continuity of life. In a variety of organisms, germ cells and stem cells contain large ribonucleoprotein granules. Although these particles were discovered more than 100 years ago, their assembly and functions are not well understood. Here we report that glycolytic enzymes are components of these granules in Drosophila germ cells and both their mRNAs and the enzymes themselves are enriched in germ cells. We show that these enzymes are specifically required for germ cell development and that they protect their genomes from transposable elements, providing the first link between metabolism and transposon silencing. We further demonstrate that in the granules, glycolytic enzymes associate with the evolutionarily conserved Tudor protein. Our biochemical and single‐particle EM structural analyses of purified Tudor show a flexible molecule and suggest a mechanism for the recruitment of glycolytic enzymes to the granules. Our data indicate that germ cells, similarly to stem cells and tumor cells, might prefer to produce energy through the glycolytic pathway, thus linking a particular metabolism to pluripotency.     

Effects of heat shock on survival and predation of an important whitefly predator,Serangium japonicum

Climate change is expected to increase the frequency of periods of extreme weather events, including heat waves that are harmful to arthropod natural enemies. We studied the thermotolerance of the ladybeetle Serangium japonicum Chapin (Coleoptera: Coccinellidae), an important native predator of the whitefly Bemisia tabaci (Gennadius) (Hemiptera: Aleyrodidae) in China. Serangium japonicum eggs, first‐ and fourth‐instar larvae, pupae, and adults were subjected to a range of high temperatures (36, 39, 42, 43.5, and 45 °C) at intervals between 15 and 720 min. Survival was compromised and declined sharply for all life stages at temperatures of 42 °C and higher. First instars were the least heat tolerant, and eggs were typically the most resistant. Egg predation by S. japonicum did not differ whether the adult beetles were subjected to either heat shock or starvation first. Heat shock treatments at 36 °C did not impede adult egg consumption, treatments at 39 °C crippled ladybeetle's egg consumption for 8 h following treatment but recovered predatory capacity within 24 h after treatment. However, treatments at 42 °C greatly impaired ladybeetle's predatory capacity. After experiencing heat shock at 39 and 42 °C, adults significantly increased the amount of time they spent resting, which is the probable cause of predation decline after heat exposure. These results demonstrate that short periods of extreme heat exposures have a detrimental impact on S. japonicum survival and predation, but the effect was dependent on duration and life stage. Overall, these findings can help predict population dynamics and success of biological control of whitefly by S. japonicum in a warming world.     

Silencing interleukin 1α underlies a novel inhibitory role of miR-181c-5p in alleviating low-grade inflammation of rats with irritable bowel syndrome

Irritable bowel syndrome (IBS) is a common disorder of unknown etiology. Studies have found a close relation between IBS and microRNAs (miRNAs), but the study concerning the relationship between IBS and miR-181c-5p in IBS is still blank. Thus, this study aims to explore the role of miR-181c-5p in IBS via interleukin 1α (IL1A). Initially, microarray analysis was used to retrieve the genes related to IBS and to predict miRNAs regulating IL1A gene. IBS model was then established with abdominal withdraw reflection (AWR) and Bristol stool grading in mice measured. Afterwards, the functional role of miR-181c-5p in IBS was determined using the ectopic expression, depletion and reporter assay experiments, as well as miR-181c-5p and IL1A expression detected. Subsequently, expression of tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2), and IL-6 were detected to further determine the effects of miR-181c-5p and IL1A on inflammation in IBS. miR-181c-5p and IL1A might be involved in IBS. miR-181c-5p was found to be decreased while IL1A was increased in IBS rats. In addition, miR-181c-5p could target and inhibit expression of IL1A, and IBS mice exhibited elevated AWR and Bristol stool grading, namely 6 to 7 points (70.4 [38 of 54]). Moreover, with the overexpression of miR-181c-5p or silencing of IL1A, the expression of TNF-α, IL-2, and IL-6 was decreased. Collectively, this study suggested that overexpressed miR-181c-5p could silence IL1A, thus inhibiting low-grade inflammation in IBS rats. miR-181c-5p/IL1A is expected to serve as a novel target for the treatment of IBS.     

Identification of proteins from feeder conditioned medium that support human embryonic stem cells

The maintenance of undifferentiated human embryonic stem cells (hESC) requires feeder cells, either in co-culture or feeder-free with conditioned medium (CM) from the feeders. In this study, we compared the CM of a supporting primary mouse embryonic feeder (MEF) and an isogenic but non-supporting MEF line (DeltaE-MEF) in order to gain an insight to the differential expression profile of secreted factors. Using two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption/ionization-time of flight (MALDI) tandem mass spectrometry, 13 protein identities were found to be downregulated in DeltaE-MEF compared to MEF, of which 4 were found to be soluble factors and 3 proteins were membrane-associated or related to the extracellular matrix. In addition, four other proteins were identified to be differentially expressed in MEF-CM using high pressure liquid chromatography (HPLC) and cytokine arrays. In functional experiments where CM was replaced with six of the factors identified, hESC were able to proliferate for five continuous passages whilst maintaining 68-82% and 74-98% expression of pluripotent markers, Oct-4 and Tra-1-60, respectively. Using proteomic tools, important proteins from CM that supports hESC culture have been identified, which when replaced with recombinant proteins, continue to support undifferentiated hESC growth in a feeder-free culture platform.     

Tea polyphenols-loaded nanocarriers: preparation technology and biological function

Biotechnology Letters - Tea polyphenols (TP) have various biological functions including anti-oxidant, anti-bacterial, anti-apoptotic, anti-inflammatory and bioengineered repair properties....     

MAPK‐mediated upregulation of fibrinogen‐like protein 2 promotes proliferation,migration, and invasion of colorectal cancer cells

Fibrinogen‐like protein 2 (FGL2) has been reported to play a key role in the development of human cancers. However, it is still unmasked whether FGL2 plays a potential role in colorectal carcinogenesis. In this study, the messenger RNA and protein expression levels were measured by quantitative real‐time polymerase chain reaction and western blot. Cell counting kit‐8 assay, transwell migration, and invasion assay were carried out to evaluate the proliferation, migration, and invasion of LOVO and SW620 cells. FGL2 was upregulated in colorectal cancer (CRC) tissues, as well as cell lines. Mitogen‐activated protein kinase (MAPK) signaling was activated in CRC tissues and cell lines. FGL2 was confirmed to be downregulated by MAPK signaling inhibitor U0126. Further, we determined that knockdown of FGL2 caused a reduction of proliferation, migration, and invasion in LOVO and SW620 cells. Consistently, treatment of LOVO and SW620 cells with U0126 led to a decrease in cell proliferation, migration, and invasion. However, these changes initiated by U0126 were abolished by FGL2 overexpression. To conclude, MAPK‐mediated upregulation of FGL2 promotes the proliferation, migration, and invasion of CRC cells.