Effects of Pre- and Intermittent Warming of Cucumber Fruits on Chilling Injury, Titratable Acidity, Sugar and Ascorbic Acid Contents

1) 1℃及び5℃冷蔵のそれぞれのキュウリ果実に, 18℃, 24時間反復処理(2日おき3回)と, 36℃, 24時間処理(1℃では冷蔵前, また5℃では冷蔵3日後)とを行い, 低温障害並びに滴定酸度, 糖及びビタミンC含量の変化を調査した。2) 低温障害の抑制に関して, 1℃冷蔵においては36℃加温処理の著しい効果に対し, 18℃反復処理の効果はやや劣った。5℃冷蔵では両処理とも著しい抑制効果を示した。3) 滴定酸度, 糖含有量については, 1℃, 5℃いづれの冷蔵においても加温処理の影響は少なかった。4) 1℃及び5℃冷蔵によって, 還元型アスコルビン酸が減少し, 酸化型アスコルビン酸は増加した。ビタミンCの冷蔵による変化に対する抑制効果は, 1℃冷蔵の場合18℃反復処理では少なかったが, 36℃加温処理ではある程度認められた。5℃冷蔵においては両加温処理により, ビタミンCの変化は完全に抑制された。 / 1. Cucumber fruits were warmed at 18℃ for 24 hr three times of 2-day intervals during cold storage at 1 and 5℃, and also warmed at 36℃ for 24 hr before cold storage at 1℃ and after three days in cold storage at 4℃. Their effects on chilling injury, titratable acidity, sugar content and vitamin C content were determined. 2. Both warming treatments reduced chilling injury markedly for the fruit stored at 5℃. For the fruit stored at 1℃, the repeated warming at 18℃ produced only slight effect, but the warming at 36℃ pronounced effect. 3. Titratable acidity and sugar content were little affected by both treatments. 4. A reduction of L-ascorbic acid and an increase of dehydro-L-ascorbic acid during cold storage were completely prevented by both treatments for the fruit stored at 5℃. But there was slightly less effect for the fruit stored at 1℃

Мультипарадигмальний підхід до аналізу феномену нігілізму

У статті розглянуто нігілізм як неоднозначне й поліморфне поняття. Досліджено різні підходи до тлумачення та розв’язання питань, пов’язаних із нігілізмом. Розкрито людиномірність нігілізму в контексті відстеження варіативного смислового навантаження феномену. Встановлено, що нігілізм потрібно позиціонувати як спосіб пробудження людського духу, заперечення деструктивного конформізму й відсутності опору (пасивний песимізм).В статье рассмотрен нигилизм как неоднозначное и полиморфное понятие. Исследованы различные подходы к толкованию и решению вопросов, связанных с нигилизмом. Раскрыта человекомерность нигилизма в контексте отслеживания вариативной смысловой нагрузки феномена. Установлено, что нигилизм нужно позиционировать как способ пробуждения человеческого духа, отрицание деструктивного конформизма и отсутствия сопротивления (пассивный пессимизм).Nihilism is considered as ambiguous and polymorphic concept. Different approaches to the interpretation and solution of issues associated with nihilism are investigated. Human measurement of nihilism in the context of tracking meaning of varied semantic capacity of the phenomenon is revealed. It is determined that nihilism must be positioned as a way of awakening of the human spirit, denial of destructive conformism and absence of resistance (passive pessimism)

Changing current practice in urology: Improving guideline development and implementation through stakeholder engagement

Effective stakeholder integration for guideline development should improve outcomes and adherence to clinical practice guidelines

Unregulated actin polymerization by WASp causes defects of mitosis and cytokinesis in X-linked neutropenia

Specific mutations in the human gene encoding the Wiskott-Aldrich syndrome protein (WASp) that compromise normal auto-inhibition of WASp result in unregulated activation of the actin-related protein 2/3 complex and increased actin polymerizing activity. These activating mutations are associated with an X-linked form of neutropenia with an intrinsic failure of myelopoiesis and an increase in the incidence of cytogenetic abnormalities. To study the underlying mechanisms, active mutant WASpI294T was expressed by gene transfer. This caused enhanced and delocalized actin polymerization throughout the cell, decreased proliferation, and increased apoptosis. Cells became binucleated, suggesting a failure of cytokinesis, and micronuclei were formed, indicative of genomic instability. Live cell imaging demonstrated a delay in mitosis from prometaphase to anaphase and confirmed that multinucleation was a result of aborted cytokinesis. During mitosis, filamentous actin was abnormally localized around the spindle and chromosomes throughout their alignment and separation, and it accumulated within the cleavage furrow around the spindle midzone. These findings reveal a novel mechanism for inhibition of myelopoiesis through defective mitosis and cytokinesis due to hyperactivation and mislocalization of actin polymerization

The von Hippel-Lindau gene is required to maintain renal proximal tubule and glomerulus integrity in zebrafish larvae

Background: von Hippel-Lindau (VHL) disease is characterized by the development of benign and malignant tumours in many organ systems, including renal cysts and clear cell renal cell carcinoma. It is not completely understood what underlies the development of renal pathology, and the use of murine Vhl models has been challenging due to limitations in disease conservation. We previously described a zebrafish model bearing inactivating mutations in the orthologue of the human VHL gene. Methods: We used histopathological and functional assays to investigate the pronephric and glomerular developmental defects in vhl mutant zebrafish, supported by human cell culture assays. Results: Here, we report that vhl is required to maintain pronephric tubule and glomerulus integrity in zebrafish embryos. vhl mutant glomeruli are enlarged, cxcr4a+ capillary loops are dilated and the Bowman space is widened. While we did not observe pronephric cysts, the cells of the proximal convoluted and anterior proximal straight tubule are enlarged, periodic acid schiff (PAS) and Oil Red O positive, and display a clear cytoplasm after hematoxylin and eosine staining. Ultrastructural analysis showed the vhl–/– tubule to accumulate large numbers of vesicles of variable size and electron density. Microinjection of the endocytic fluorescent marker AM1–43 in zebrafish embryos revealed an accumulation of endocytic vesicles in the vhl mutant pronephric tubule, which we can recapitulate in human cells lacking VHL. Conclusions: Our data indicates that vhl is required to maintain pronephric tubule and glomerulus integrity during zebrafish development, and suggests a role for VHL in endocytic vesicle trafficking

TCF21 hypermethylation regulates renal tumor cell clonogenic proliferation and migration

We recently identified hypermethylation at the gene promoter of transcription factor 21 (TCF21) in clear cell sarcoma of the kidney (CCSK), a rare pediatric renal tumor. TCF21 is a transcription factor involved in tubular epithelial development of the kidney and is a candidate tumor suppressor. As there are no in vitro models of CCSK, we employed a well-established clear cell renal cell carcinoma (ccRCC) cell line, 786-O, which also manifests high methylation at the TCF21 promoter, with consequent low TCF21 expression. The tumor suppressor function of TCF21 has not been functionally addressed in ccRCC cells; we aimed to explore the functional potential of TCF21 expression in ccRCC cells in vitro. 786-O clones stably transfected with either pBABE-TCF21-HA construct or pBABE vector alone were functionally analyzed. We found that ectopic expression of TCF21 in 786-O cells results in a trend toward decreased cell proliferation (not significant) and significantly decreased migration compared with mock-transfected 786-O cells. Although the number of colonies established in colony formation assays was not different between 786-O clones, colony size was significantly reduced in 786-O cells expressing TCF21. To investigate whether the changes in migration were due to epithelial-to-mesenchymal transition changes, we interrogated the expression of selected epithelial and mesenchymal markers. Although we observed upregulation of mRNA and protein levels of epithelial marker E-cadherin in clones overexpressing TCF21, this did not result in surface expression of E-cadherin as measured by fluorescence-activated cell sorting and immunofluorescence. Furthermore, mRNA expression of the mesenchymal markers vimentin (VIM) and SNAI1 was not significantly decreased in TCF21-expressing 786-O cells, while protein levels of VIM were markedly decreased. We conclude that re-expression of TCF21 in renal cancer cells that have silenced their endogenous TCF21 locus through hypermethylation results in reduced clonogenic proliferation, reduced migration, and reduced mesenchymal-like characteristics, suggesting a tumor suppressor function for transcription factor 21

Genetic predisposition to ductal carcinoma in situ of the breast

Background: Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer. It is often associated with invasive ductal carcinoma (IDC), and is considered to be a non-obligate precursor of IDC. It is not clear to what extent these two forms of cancer share low-risk susceptibility loci, or whether there are differences in the strength of association for shared loci. Methods: To identify genetic polymorphisms that predispose to DCIS, we pooled data from 38 studies comprising 5,067 cases of DCIS, 24,584 cases of IDC and 37,467 controls, all genotyped using the iCOGS chip. Results: Most (67 %) of the 76 known breast cancer predisposition loci showed an association with DCIS in the same direction as previously reported for invasive breast cancer. Case-only analysis showed no evidence for differences between associations for IDC and DCIS after considering multiple testing. Analysis by estrogen receptor (ER) status confirmed that loci associated with ER positive IDC were also associated with ER positive DCIS. Analysis of DCIS by grade suggested that two independent SNPs at 11q13.3 near CCND1 were specific to low/intermediate grade DCIS (rs75915166, rs554219). These associations with grade remained after adjusting for ER status and were also found in IDC. We found no novel DCIS-specific loci at a genome wide significance level of P < 5.0x10-8. Conclusion: In conclusion, this study provides the strongest evidence to date of a shared genetic susceptibility for IDC and DCIS. Studies with larger numbers of DCIS are needed to determine if IDC or DCIS specific loci exist

Cryptococcus: from environmental saprophyte to global pathogen.

Cryptococcosis is a globally distributed invasive fungal infection that is caused by species within the genus Cryptococcus which presents substantial therapeutic challenges. Although natural human-to-human transmission has never been observed, recent work has identified multiple virulence mechanisms that enable cryptococci to infect, disseminate within and ultimately kill their human host. In this Review, we describe these recent discoveries that illustrate the intricacy of host-pathogen interactions and reveal new details about the host immune responses that either help to protect against disease or increase host susceptibility. In addition, we discuss how this improved understanding of both the host and the pathogen informs potential new avenues for therapeutic development

Wnt signalling and cancer stem cells

[Abstract] Intracellular signalling mediated by secreted Wnt proteins is essential for the establishment of cell fates and proper tissue patterning during embryo development and for the regulation of tissue homeostasis and stem cell function in adult tissues. Aberrant activation of Wnt signalling pathways has been directly linked to the genesis of different tumours. Here, the components and molecular mechanisms implicated in the transduction of Wnt signal, along with important results supporting a central role for this signalling pathway in stem cell function regulation and carcinogenesis will be briefly reviewed.Ministerio de Ciencia e Innovación; SAF2008-0060