Effect of moisture content and drying method on the amylose content of rice

Rice is a primary source to all human beings. It gives energy and supply carbohydrate in human daily life. It is also one of the main sources of employment for people living in the rural area to generate incomes. In this study, determinations of quality of rice dried in an oven and in a Laterally Aerated Moving Bed (LAMB) dryer were performed., tTe drying in an oven was performed with initial moisture content (MC) of 18% reduced to 14% w.b. at temperatures of 35, 45, 55, 65 and 75 0C. The amylose contents of the rice were 20.78, 21.81, 21.53, 21.63 and 22.50%, respectively. Furthermore, drying of paddy with temperature of 45 0C and initial moisture content of 15% w.b was performed with different final moisture content of 14, 12, 10 and 8% w.b using oven drying. The amylose content were 21.79, 20.17, 20.85, 26.35%, respectively. As for paddy dried in LAMB dryer, it was found that the amylose content were in the intermediate range (20 - 25.50%). The drying temperature of the LAMB dryer was at 25 0C with 100 to 200 L/min of air flowrate resulted in the intermediate amylose content of the rice despite the final moisture content reduced to 8% w.b

Lack of interaction between ErbB2 and insulin receptor substrate signaling in breast cancer

Background: ErbB2 Receptor Tyrosine Kinase 2 (ErbB2, HER2/Neu) is amplified in breast cancer and associated with poor prognosis. Growing evidence suggests interplay between ErbB2 and insulin-like growth factor (IGF) signaling. For example, ErbB2 inhibitors can block IGF-induced signaling while, conversely, IGF1R inhibitors can inhibit ErbB2 action. ErbB receptors can bind and phosphorylate insulin receptor substrates (IRS) and this may be critical for ErbBmediated anti-estrogen resistance in breast cancer. Herein, we examined crosstalk between ErbB2 and IRSs using cancer cell lines and transgenic mouse models. Methods: MMTV-ErbB2 and MMTV-IRS2 transgenic mice were crossed to create hemizygous MMTV-ErbB2/MMTVIRS2 bigenic mice. Signaling crosstalk between ErbB2 and IRSs was examined in vitro by knockdown or overexpression followed by western blot analysis for downstream signaling intermediates and growth assays. Results: A cross between MMTV-ErbB2 and MMTV-IRS2 mice demonstrated no enhancement of ErbB2 mediated mammary tumorigenesis or metastasis by elevated IRS2. Substantiating this, overexpression or knockdown of IRS1 or IRS2 in MMTV-ErbB2 mammary cancer cell lines had little effect upon ErbB2 signaling. Similar results were obtained in human mammary epithelial cells (MCF10A) and breast cancer cell lines. Conclusion: Despite previous evidence suggesting that ErbB receptors can bind and activate IRSs, our findings indicate that ErbB2 does not cooperate with the IRS pathway in these models to promote mammary tumorigenesis

Dynamic Temporal Change of Cerebral Microbleeds: Long-Term Follow-Up MRI Study

Background: Cerebral microbleeds (MBs) are understood as an important radiologic marker of intracerebral hemorrhage. We sought to investigate the temporal changes of MBs and clinical factors associated with the changes using long-term follow-up MRI. Methods/Principal Findings: From October 2002 to July 2006, we prospectively enrolled patients with stroke or transient ischemic attack, and followed-up their brain MRIs with an interval.12 mo. We compared demographic factors, vascular risk factors, laboratory findings, and radiologic factors according to the presence or changes of MBs. A total of 224 patients successfully completed the follow-up examinations (mean, 27 months). Newly developed MBs were noted in 10 patients (6.8%) among those without MBs at baseline (n = 148), and in those with MBs at baseline (n = 76), the MB count had decreased in 11 patients (14.5%), and increased in 41 patients (53.9%). The estimated annual rate of change of MB numbers was 0.80 lesions per year in all patients, a value which became greater in those patients who exhibited MBs at baseline (MBs$5, 5.43 lesions per year). Strokes due to small vessel occlusion and intracerebral hemorrhage, as well as white matter lesions were independently associated with an increased MB count, whereas the highest quartile of low-density lipoprotein (LDL) cholesterol was associated with a decreased MB count. Conclusion: During the follow-up period, most of MBs showed dynamic temporal change. Symptomatic or asymptomati

A moderate elevation of circulating levels of IGF-I does not alter ErbB2 induced mammary tumorigenesis

Background Epidemiological evidence suggests that moderately elevated levels of circulating insulin-like growth factor-I (IGF-I) are associated with increased risk of breast cancer in women. How circulating IGF-I may promote breast cancer incidence is unknown, however, increased IGF-I signaling is linked to trastuzumab resistance in ErbB2 positive breast cancer. Few models have directly examined the effect of moderately high levels of circulating IGF-I on breast cancer initiation and progression. The purpose of this study was to assess the ability of circulating IGF-I to independently initiate mammary tumorigenesis and/or accelerate the progression of ErbB2 mediated mammary tumor growth. Methods We crossed heterozygous TTR-IGF-I mice with heterozygous MMTV-ErbB2 mice to generate 4 different genotypes: TTR-IGF-I/MMTV-ErbB2 (bigenic), TTR-IGF-I only, MMTV-ErbB2 only, and wild type (wt). Virgin females were palpated twice a week and harvested when tumors reached 1000 mm3. For study of normal development, blood and tissue were harvested at 4, 6 and 9 weeks of age in TTR-IGF-I and wt mice. Results TTR-IGF-I and TTR-IGF-I/ErbB2 bigenic mice showed a moderate 35% increase in circulating total IGF-I compared to ErbB2 and wt control mice. Elevation of circulating IGF-I had no effect upon pubertal mammary gland development. The transgenic increase in IGF-I alone wasn\u27t sufficient to initiate mammary tumorigenesis. Elevated circulating IGF-I had no effect upon ErbB2-induced mammary tumorigenesis or metastasis, with median time to tumor formation being 30 wks and 33 wks in TTR-IGF-I/ErbB2 bigenic and ErbB2 mice respectively (p = 0.65). Levels of IGF-I in lysates from ErbB2/TTR-IGF-I tumors compared to ErbB2 was elevated in a similar manner to the circulating IGF-I, however, there was no effect on the rate of tumor growth (p = 0.23). There were no morphological differences in tumor type (solid adenocarcinomas) between bigenic and ErbB2 mammary glands

Parity-induced decrease in systemic growth hormone alters mammary gland signaling: A potential role in pregnancy protection from breast cancer

Early full-term pregnancy is an effective natural protection against breast cancer in both humans and experimental rodents. The protective effect of an early pregnancy is in part linked to changes in circulating hormones that are involved in both normal breast development and breast cancer. For example, a reduction in circulating growth hormone (GH) has been shown to protect rats from carcinogen-induced mammary tumors. We examined the ability of a full-term pregnancy to alter the endocrine GH/IGF-I axis and how this change affected normal mammary gland function in two commonly used rat models (Sprague-Dawley and Wistar-Furth). Circulating GH and IGF-I were measured in blood drawn every 30 minutes from parous and aged-matched virgin (AMV) female rats. Mean serum GH levels were significantly decreased (

Scaffold attachment factor B1 (SAFB1) heterozygosity does not influence Wnt-1 or DMBA-induced tumorigenesis

<p>Abstract</p> <p>Background</p> <p>Scaffold Attachment Factor B1 (SAFB1) is a multifunctional protein which has been implicated in breast cancer previously. We recently generated SAFB1 knockout mice (SAFB1^-/-), but pleiotropic phenotypes including high lethality, dwarfism associated with low IGF-I levels, and infertility and subfertility in male and female mice, respectively, do not allow for straightforward tumorigenesis studies in these mice. Therefore, we asked whether SAFB1 heterozygosity would influence tumor development and progression in MMTV-Wnt-1 oncomice or DMBA induced tumorigenicity, in a manner consistent with haploinsufficiency of the remaining allele.</p> <p>Methods</p> <p>We crossed female SAFB1^+/-(C57B6/129) mice with male MMTV-Wnt-1 (C57B6/SJL) mice to obtain SAFB1^+/+/Wnt-1, SAFB1^+/-/Wnt-1, and SAFB1^+/-mice. For the chemical induced tumorigenesis study we treated 8 weeks old SAFB1^+/-and SAFB^+/+BALB/c mice with 1 mg DMBA once per week for 6 weeks. Animals were monitored for tumor incidence and tumor growth. Tumors were characterized by performing H&E, and by staining for markers of proliferation and apoptosis.</p> <p>Results</p> <p>We did not detect significant differences in tumor incidence and growth between SAFB1^+/+/Wnt-1 and SAFB1^+/-/Wnt-1 mice, and between DMBA-treated SAFB1^+/+and SAFB1^+/-mice. Histological evaluation of tumors showed that SAFB1 heterozygosity did not lead to changes in proliferation or apoptosis. There were, however, significant differences in the distribution of tumor histologies with an increase in papillary and cribriform tumors, and a decrease in squamous tumors in the SAFB1^+/-/Wnt-1 compared to the SAFB1^+/+/Wnt-1 tumors. Of note, DMBA treatment resulted in shortened survival of SAFB1^+/-mice compared to their wildtype littermates, however this trend did not reach statistical significance.</p> <p>Conclusion</p> <p>Our data show that SAFB1 heterozygosity does not influence Wnt-1 or DMBA-induced mammary tumorigenesis.</p

Patterns of Care Quality and Prognosis Among Hospitalized Ischemic Stroke Patients With Chronic Kidney Disease

Background: Relatively little is known about the quality of care and outcomes for hospitalized ischemic stroke patients with chronic kidney disease (CKD). We examined quality of care and in‐hospital prognoses among patients with CKD in the Get With The Guidelines–Stroke (GWTG‐Stroke) program Methods and Results: We analyzed 679 827 patients hospitalized with ischemic stroke from 1564 US centers participating in the GWTG‐Stroke program between January 2009 and December 2012. Use of 7 predefined ischemic stroke performance measures, composite “defect‐free” care compliance, and in‐hospital mortality were examined based on glomerular filtration rate (GFR) categorized as a dichotomous (+CKD as <60) or rank‐ordered variable: normal (≥90), mild (≥60 to <90), moderate (≥30 to <60), severe (≥15 to <30), and kidney failure (<15 or dialysis). There were 236 662 (35%) ischemic stroke patients with CKD. Patients with severe renal dysfunction or failure were significantly less likely to receive guideline‐based therapies. Compared with patients with normal kidney function (≥90), those with CKD (adjusted OR 0.91 [95% CI: 0.89 to 0.92]), moderate dysfunction (adjusted OR 0.94 [95% CI: 0.92 to 0.97]), severe dysfunction (adjusted OR 0.80 [95% CI: 0.77 to 0.84]), or failure (adjusted OR 0.72 [95% CI: 0.68 to 0.0.76]), were less likely to receive 100% defect‐free care measure compliance. Inpatient mortality was higher for patients with CKD (adjusted odds ratio 1.44 [95% CI: 1.40 to 1.47]), and progressively rose with more severe renal dysfunction. Conclusions: Despite higher in‐hospital mortality rates, ischemic stroke patients with CKD, especially those with greater severity of renal dysfunction, were less likely to receive important guideline‐recommended therapies