Diabetes mellitus is a chronic disease and a worldwide public health challenge. It has been shown that 50-80% proportion of T2DM is undiagnosed. In this paper, support vector machines are utilized to screen diabetes, and an ensemble learning module is added, which turns the "black box" of SVM decisions into comprehensible and transparent rules, and it is also useful for solving imbalance problem. Results on China Health and Nutrition Survey data show that the proposed ensemble learning method generates rule sets with weighted average precision 94.2% and weighted average recall 93.9% for all classes. Furthermore, the hybrid system can provide a tool for diagnosis of diabetes, and it supports a second opinion for lay users.

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Aims. Most pulsar nulling observations have been conducted at frequencies lower than 1400 MHz. We aim to understand the nulling behaviors of pulsars at relatively high frequencies, and to decipher whether or not nulling is caused by a global change in the pulsar magnetosphere. Methods. We used the Jiamusi 66 m telescope to observe 20 bright pulsars at 2250 MHz with unprecedented lengths of time. We estimated the nulling fractions of these pulsars, and identified the null and emission states of the pulses. We also calculated the nulling degrees and scales of the emission-null pairs to describe the distributions of emission and null lengths. Results. Three pulsars, PSRs J0248+6021, J0543+2329, and J1844+00, are found to null for the first time. The details of null-to-emission and emission-to-null transitions within the pulse window are observed for the first time for PSR J1509+5531, which is a low-probability event. A complete cycle of long nulls with timescales of hours is observed for PSR J1709−1640. For most of these pulsars, the K-S tests of nulling degrees and nulling scales reject the hypothesis that null and emission are caused by random processes at high significance levels. Emission-null sequences of some pulsars exhibit quasi-periodic, low-frequency or featureless modulations, which might be related to different origins. During transitions between emission and null states, pulse intensities have diverse tendencies for variation. Significant correlations are found between respectively nulling fraction, nulling cadence, and nulling scale and the energy loss rate of the pulsars. Combined with the nulling fractions reported in the literature for 146 nulling pulsars, we find that statistically large nulling fractions are more tightly related to pulsar period than to characteristic age or energy-loss rate.

To evaluate the role of glycogen synthase kinase-3β (GSK-3β) in the apoptosis of cardiomyocytes in diabetic cardiomyopathy (DCM). Diabetes mellitus (DM) in rats was induced by intraperitoneal injection of 1% streptozotocin (STZ), and lithium chloride (LiCl) was used to decrease the expression of GSK-3β. Hematoxylin/eosin (HE) staining and the terminal deoxyribonucleotide transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay was conducted to evaluate the pathological injury and apoptosis of cardiomyocytes respectively. Western blot was applied to detect the protein expressions of Cleaved-caspase 3, caspase 3, Bax and Bcl-2 in rat cardiomyocytes. Real-time polymerase chain reaction (RT-PCR) was applied to detect the gene expressions of phosphoinositide 3-kinases (PI3K), Akt, and GSK-3β in rat cardiomyocytes. DM-induced cardiomyocyte injuries, which were presented as capillary basement membrane thickening, interstitial fibrosis, cardiomyocyte hypertrophy and necrosis in HE staining and increased apoptosis detected by TUNEL assay. When comparing with the control group, the mRNA expression of PI3K and Akt in DM group obviously decreased but the mRNA expression of GSK-3β obviously elevated (P < 0.05). In addition, the ratio of Cleaved-caspase 3/caspase 3 and Bax/Bcl-2 were notably increased in DM group compared with control group (P < 0.05). LiCl, as an inhibitor of GSK-3 apparently reduced the expression of GSK-3β mRNA (P < 0.05) but not the PI3K and Akt comparing with the DM group. LiCl also attenuated the myocardial injury and apoptosis induced by DM. The myocardial injury induced by DM is associated with the up-regulation of GSK-3β. LiCl inhibited the expression of GSK-3β and myocardial apoptosis in diabetic myocardium.