bluuebunny/crossref_metadata_2025_split huggingface dataset:
Model study of the leather degradation by oxidation and hydrolysis
Authors: Vyskočilová Gabriela , Ebersbach Matthäa , Kopecká Radka , Prokeš Lubomír , Příhoda Jiří 
Published: May 2019

Abstract
Many objects of culture heritage, comprised of leather, need to receive the right treatment to be restored and to elongate their lifespan. Determination of the degradation degree and even better the type of the degradation is a crucial knowledge for the way of subsequent conservation, exhibition and long-term storage. Collagen based materials are very sensitive to the deterioration and undergo, mainly hydrolysis and oxidation. Namely acid hydrolysis and photooxidation are the most often causes of the disintegration of leather. Contrary to the leather investigation, a few studies dedicated to parchment described some typical features of hydrolysis, oxidation and gelatinization observed applying Attenuated Total Reflection Fourier-Transform Infrared spectroscopy (ATR-FTIR) which is widely used in collagen degradation type research. Except of the collagen secondary structure, followed by IR spectroscopy, we determined the shrinkage temperature of the collagen substrate by Micro Hot Table method (MHT) to reach the degradation level. In this paper, artificially degraded leather samples as a theoretical representative of cultural heritage objects were examined. We discuss the use of both techniques (IR and MHT) as potential methods for fast assessment of oxidation and hydrolysis of vegetable tanned leathers and degradation level. New samples of leather tanned by various vegetable tannins were artificially degraded under controlled conditions. We simulated the photooxidation by means of the Xenon arc lamp exposure, oxidation using the soaking in hydrogen peroxide, acid hydrolysis by the soaking in hydrochloric acid and alkaline hydrolysis using the soaking in natrium hydroxide. ATR-FTIR spectra of reference and tested samples were compared. Oxidation causes increase of the distance between amide I (AI) and amide II (AII) wavenumbers (Δν) above 100 cm−1 and the intensity ratio between AI and AII bands (AI/AII) above 1.6. The AI/AII ratio depends on the type of hydrolysis. The increase above 1.8 proves acid hydrolysis while the decrease under 1 demonstrate alkaline hydrolysis. MHT results are not so obvious. Generally, mainly the hydrolysis causes the decrease of the temperatures. We have found out that knowledge of the whole shrinkage interval is important and provides more appropriate information about the leather disintegration.
Uterine Glands: Developmental Biology and Functional Roles in Pregnancy
Authors: Kelleher Andrew M , DeMayo Francesco J , Spencer Thomas E 
Published: May 2019

AbstractAll mammalian uteri contain glands in the endometrium that develop only or primarily after birth. Gland development or adenogenesis in the postnatal uterus is intrinsically regulated by proliferation, cell–cell interactions, growth factors and their inhibitors, as well as transcription factors, including forkhead box A2 (FOXA2) and estrogen receptor α (ESR1). Extrinsic factors regulating adenogenesis originate from other organs, including the ovary, pituitary, and mammary gland. The infertility and recurrent pregnancy loss observed in uterine gland knockout sheep and mouse models support a primary role for secretions and products of the glands in pregnancy success. Recent studies in mice revealed that uterine glandular epithelia govern postimplantation pregnancy establishment through effects on stromal cell decidualization and placental development. In humans, uterine glands and, by inference, their secretions and products are hypothesized to be critical for blastocyst survival and implantation as well as embryo and placental development during the first trimester before the onset of fetal–maternal circulation. A variety of hormones and other factors from the ovary, placenta, and stromal cells impact secretory function of the uterine glands during pregnancy. This review summarizes new information related to the developmental biology of uterine glands and discusses novel perspectives on their functional roles in pregnancy establishment and success.
Illicit Upregulation of Serotonin Signaling Pathway in Adrenals of Patients With High Plasma or Intra-Adrenal ACTH Levels
Authors: Le Mestre Julie , Duparc Céline , Reznik Yves , Bonnet-Serrano Fidéline , Touraine Philippe , Chabre Olivier , Young Jacques , Suzuki Mari , Sibony Mathilde , Gobet Françoise , Stratakis Constantine A , Raverot Gérald , Bertherat Jérôme , Lefebvre Hervé , Louiset Estelle 
Published: May 2019

Abstract

Context
In the human adrenal, serotonin (5-HT), released by mast cells stimulates corticosteroid secretion through activation of type 4 serotonin receptors (5-HT4R). In primary pigmented nodular adrenocortical disease cells, activation of the cAMP/protein kinase A (PKA) pathway by PRKAR1A mutations triggers upregulation of the 5-HT synthesizing enzyme tryptophan hydroxylase (TPH) and the 5-HT4, 5-HT6, and 5-HT7 receptors. Because ACTH stimulates cortisol secretion through activation of PKA, adrenocortical tissues exposed to sustained stimulation by ACTH may harbor increased expression of TPH and 5-HT4/6/7 receptors.

Objective
To investigate the effects of long-term ACTH stimulation on the serotonergic pathway in adrenals of patients with high plasma or intra-adrenal ACTH levels.

Methods
Adrenal tissues were obtained from patients with Cushing disease, ectopic secretion of ACTH [paraneoplastic Cushing syndrome; (paraCS)], 21-hydroxylase deficiency (21-OHD), primary bilateral macronodular adrenal hyperplasia with intra-adrenal ACTH presence, or cortisol-producing adenomas. TPH and 5-HT4/6/7 receptor expression was investigated using RT-PCR and immunochemistry in comparison with normal adrenals. Primary cultured adrenocortical cells originating from a patient with paraCS were incubated with 5-HT and 5-HTR agonists/antagonists.

Results
TPH and/or 5-HT4/6/7 receptors were overexpressed in the different types of tissues. In paraCS cultured cells, the cortisol response to 5-HT was exaggerated compared with normal adrenal cells and the stimulatory action of 5-HT was reduced by 5-HT4R antagonist.

Conclusion
Our results indicate that prolonged activation of the cAMP/PKA pathway by ACTH induces an aberrant serotonergic stimulatory loop in the adrenal cortex that likely participates in the pathogenesis of corticosteroid hypersecretion.
Impaired Glucose-Stimulated Proinsulin Secretion Is an Early Marker of β-Cell Impairment Before Prediabetes Stage
Authors: Yang Ying , Wang Min , Tong Jingzhi , Dong Zuoliang , Deng Min , Ren Xiaojun , Li Hui , Yang Jing , Meng Zhaowei , Sun Jinhong , He Qing , Liu Ming 
Published: May 2019

AbstractContextEvidence indicates that there is substantial impairment/loss of β-cell function/mass even before prediabetes. Elevated plasma proinsulin is a sign of β-cell dysfunction in patients with diabetes/prediabetes. However, the dynamic changes of glucose stimulated proinsulin secretion (GSPS) among nondiabetic individuals remain obscure.ObjectiveTo examine GSPS and glucose-stimulated insulin secretion (GSIS) among individuals with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT) and to evaluate whether impaired GSPS is an early biomarker of β-cell impairment in individuals with NGT who have subthreshold postprandial plasma glucose (PPG).Design and ParticipantsWe evaluated GSPS and GSIS in 116 Chinese adults without diabetes (mean age ± SD, 33.31 ± 9.10 years; mean BMI, 25.24 ± 4.20 kg/m2) with fasting plasma glucose (FPG) < 5.6 mmol/L. Based on 2hPPG, the participants were divided into three groups: NGT1 (2hPPG < 6.67 mmol/L), NGT2 (6.67 ≤ 2hPPG < 7.78 mmol/L), and IGT (7.78 ≤ 2hPPG<11.1 mmol/L). We analyzed the association of GSIS and GSPS with commonly used indexes of β-cell function, insulin resistance and family history of diabetes.ResultsAlthough not diagnosed with prediabetes, the individuals with NGT2 have clinical characteristics and high diabetes risk factors similar to those of the IGT group. However, unlike individuals with IGT, NGT2 participants did not exhibit a delayed GSIS. Instead, GSPS was impaired in NGT2 groups but not in NGT1 group.ConclusionsThis study suggests that impaired GSPS, but not impaired GSIS, may serve as an early biomarker to identify a subpopulation of NGT with a high risk of diabetes.
Somatic PRKAR1A Gene Mutation in a Nonsyndromic Metastatic Large Cell Calcifying Sertoli Cell Tumor
Authors: Tatsi Christina , Faucz Fabio R , Blavakis Emmanouil , Carneiro Benedito A , Lyssikatos Charalampos , Belyavskaya Elena , Quezado Martha , Stratakis Constantine A 
Published: May 2019

Abstract
Large cell calcifying Sertoli cell tumors (LCCSCTs) are rare testicular tumors, representing <1% of all testicular neoplasms. Almost 40% of patients with LCCSCTs will present in the context of an inherited tumor predisposition condition, such as Carney complex (CNC) or Peutz-Jeghers syndrome. We report the case of a 42-year-old man who had presented with a right testicular mass, and was diagnosed with metastatic LCCSCT. The patient underwent radical orchiectomy, achieving initial remission of his disease. However, lymph node and hepatic metastases were identified. He received chemotherapy without response, and he died of complications of his disease 4 years after the initial diagnosis. Genetic analysis of the tumor and a lymph node metastasis identified a somatic frameshift mutation in the PRKAR1A gene (c.319delG, p.E107fs*22). The mutation was predicted to result in premature termination of the PRKAR1A protein and, thus, not be expressed at the protein level, consistent with other PRKAR1A nonsense mutations. The patient was extensively screened for signs of CNC, but he had no stigmata of the complex. To the best of our knowledge, the present report is the first of a somatic mutation in the PRKAR1A gene shown to be associated with a seemingly sporadic case of LCCSCT. Somatic PRKAR1A mutations are rare in sporadic tumors, and it is unknown whether this mutation was causative of LCCSCT in our patient who did not have CNC, or contributed to the malignancy of the tumor, which might have been caused by additional mutations.
SUN-432 A Case of Sellar Plasmacytoma Masquerading as Pituitary Carcinoma with Hypopituitarism
Authors: Lee Christine , Tan Marilyn 
Published: May 2019

Abstract
Background: Sellar plasmacytomas are rare tumors arising from clonal plasma cells localized to the sellar/parasellar region. They may mimic other pituitary pathology such as pituitary adenomas, chordomas, meningiomas or metastatic carcinomas in both clinical manifestations and radiographic evidence. Certain features such as predominance of cranial nerve palsies and absence of hypopituitarism appear to be more common with sellar plasmacytomas. We present an interesting case of a sellar plasmacytoma, initially mistaken for pituitary carcinoma, with rapid development of hypopituitarism and systemic multiple myeloma. Case: A 75 year old healthy male presented with sudden onset left eye diplopia and retro-orbital pain. Left eye ptosis and diplopia with left lateral and upward gaze were noted on exam. Initial MRI brain revealed a 17mm soft tissue mass involving pituitary and clivus, extending into the left superior orbital fissure, concerning for pituitary carcinoma. With the exception of low LH (1.2) and testosterone (25), baseline pituitary hormone labs, complete blood count and metabolic panel were within normal limits. Within 1 month, he acutely presented with fever, confusion, weakness, and bony pains. Repeat pituitary labs showed low ACTH &lt; 5, AM cortisol 4.3, TSH 0.07, FT4 0.5. New findings of acute renal injury, hypercalcemia, anemia with elevated Mspike, Kappa light chain 39.7 (0.3-2.0mg/dl), kappa/lamda ratio 66.2 (0.3-1.6) and beta2microglobulin 4484 were found. Repeat MRI brain noted multifocal osseous metastatic disease with left sellar and cavernous sinus lesion contiguous with clival osseous lesion displacing pituitary gland, concerning for plasmacytoma. PET/CT showed focal lytic lesions in clivus and posterior left iliac bone. Bone marrow biopsy confirmed 70% myeloma involvement with kappa monotypic plasma cell population. He was started on hydrocortisone, levothyroxine, chemotherapy and XRT. Conclusion: The rarity of plasmacytomas, combined with their clinical presentation and imaging characteristics similar to other sellar tumors, can often result in misdiagnosis. Accuracy of diagnosis is critical, as sellar plasmacytomas and underlying multiple myeloma (present in 50% of cases) require XRT and systemic chemotherapy respectively rather than surgery. Although pituitary function is usually preserved in plasmacytomas, our case shows that acute anterior pituitary dysfunction can be an early presenting sign.
Illustrated Connections
Authors: McWilliams Sally 
Published: May 2019

AbstractIn The Magical Life of Long Tack Sam, Ann Marie Fleming creates an illustrated memoir that highlights the connections between generations of diasporic Chinese subjects. Nominally a memoir about her great-grandfather, Fleming uses the politics of vaudeville and her great-grandfather’s career as entry points into an examination of gendered Orientalism, racial exclusion, and nationalism, counterbalanced with depictions of magic, love, family, and creative resistance. The memoir uses three feminist strategies to imaginatively open out the formal and narrative conventions of Chinese diasporic history: it plays with formal timelines and genealogies as memorializing tools to deconstruct history as chronological and teleological; it invents spatial histories to make visible familial relationships; and it explores the power of collaborative memory to open the way for new diasporic forms of history. From these strategies the memoir invokes a feminist interpretation of Chinese diasporic history that emphasizes new configurations of time, space, and bodies in the production of memories for the historical archive.
Making Democracy Real
Authors: Follet Joyce C. 
Published: May 2019

AbstractThis essay offers a historical overview of African American women’s efforts to gain access to contraception, from the early stirrings of the campaign to legalize birth control in the 1910s to the eve of mass movements for racial equality and women’s rights in the 1960s. The birth control struggle becomes a window on the racial, gender, and economic structures black women negotiated in pursuit of sexual and reproductive self-determination at that time. Taking us back a century, and with emphasis on resilience and resistance, their story reminds us of the deep roots and broad vision of black women’s leadership in what has become a women-of-color–led human rights movement for reproductive justice today.
New Frontiers of Electronic Textual Research in the Humanities: Investigating Classical Allusions in Chinese Poetry through Digital Methods
Authors: Huang Yi-Long , Zheng Bingyu 
Published: May 2019

Abstract
By investigating two literary allusions, chuzhi 蜍志 and lüdai 呂袋, found in poems from the Ming-Qing period, this article seeks to discover new ways to combine traditional philological techniques and digital research methodologies in the study of Chinese literature. The article illustrates several procedures through which scholars today can use digitized versions of large compendia such as the Peiwen yunfu 佩文韻府 (Thesaurus Arranged by Rhymes) to efficiently and rapidly find solutions to their questions regarding obscure historical or literary references. In addition, through a thorough study of one of the poems composed by Yiquan 宜泉, a close friend of Cao Xueqin 曹雪芹, and an individual called “Fourth Brother Li” that the poem was dedicated to, this article also shows the special power of electronic textual research to analyze the different ways social networks were formed and how they functioned during this era.
The cancer-associated meprin β variant G32R provides an additional activation site and promotes cancer cell invasion
Authors: Schäffler Henning , Li Wenjia , Helm Ole , Krüger Sandra , Böger Christine , Peters Florian , Röcken Christoph , Sebens Susanne , Lucius Ralph , Becker-Pauly Christoph , Arnold Philipp 
Published: May 2019

ABSTRACT
The extracellular metalloprotease meprin β is expressed as a homodimer and is primarily membrane bound. Meprin β can be released from the cell surface by its known sheddases ADAM10 and ADAM17. Activation of pro-meprin β at the cell surface prevents its shedding, thereby stabilizing its proteolytic activity at the plasma membrane. We show that a single amino acid exchange variant (G32R) of meprin β, identified in endometrium cancer, is more active against a peptide substrate and the IL-6 receptor than wild-type meprin β. We demonstrate that the change to an arginine residue at position 32 represents an additional activation site used by furin-like proteases in the Golgi, which consequently leads to reduced shedding by ADAM17. We investigated this meprin β G32R variant to assess cell proliferation, invasion through a collagen IV matrix and outgrowth from tumor spheroids. We found that increased meprin β G32R activity at the cell surface reduces cell proliferation, but increases cell invasion.
DLC3 suppresses MT1-MMP-dependent matrix degradation by controlling RhoB and actin remodeling at endosomal membranes
Authors: Noll Bettina , Benz David , Frey Yannick , Meyer Florian , Lauinger Manuel , Eisler Stephan A. , Schmid Simone , Hordijk Peter L. , Olayioye Monilola A. 
Published: May 2019

ABSTRACT
Cancer cells degrade the extracellular matrix through actin-rich protrusions termed invadopodia. The formation of functional invadopodia requires polarized membrane trafficking driven by Rho GTPase-mediated cytoskeletal remodeling. We identify the Rho GTPase-activating protein deleted in liver cancer 3 (DLC3; also known as STARD8) as an integral component of the endosomal transport and sorting machinery. We provide evidence for the direct regulation of RhoB by DLC3 at endosomal membranes to which DLC3 is recruited by interacting with the sorting nexin SNX27. In TGF-β-treated MCF10A breast epithelial cells, DLC3 knockdown enhanced metalloproteinase-dependent matrix degradation, which was partially rescued by RhoB co-depletion. This was recapitulated in MDA-MB-231 breast cancer cells in which early endosomes demonstrated aberrantly enriched F-actin and accumulated the metalloproteinase MT1-MMP (also known as MMP14) upon DLC3 knockdown. Remarkably, Rab4 (herein referring to Rab4A) downregulation fully rescued the enhanced matrix degradation of TGF-β-treated MCF10A and MDA-MB-231 cells. In summary, our findings establish a novel role for DLC3 in the suppression of MT1-MMP-dependent matrix degradation by inactivating RhoB signaling at endosomal membranes. We propose that DLC3 function is required to limit endosomal actin polymerization, Rab4-dependent recycling of MT1-MMP and, consequently, matrix degradation mediated by invadopodial activity.
Peroxisomes control mitochondrial dynamics and the mitochondrion-dependent apoptosis pathway
Authors: Tanaka Hideaki , Okazaki Tomohiko , Aoyama Saeko , Yokota Mutsumi , Koike Masato , Okada Yasushi , Fujiki Yukio , Gotoh Yukiko 
Published: May 2019

ABSTRACT
Peroxisomes cooperate with mitochondria in the performance of cellular metabolic functions, such as fatty acid oxidation and the maintenance of redox homeostasis. However, whether peroxisomes also regulate mitochondrial fission–fusion dynamics or mitochondrion-dependent apoptosis remained unclear. We now show that genetic ablation of the peroxins Pex3 or Pex5, which are essential for peroxisome biogenesis, results in mitochondrial fragmentation in mouse embryonic fibroblasts (MEFs) in a manner dependent on Drp1 (also known as DNM1L). Conversely, treatment with 4-PBA, which results in peroxisome proliferation, resulted in mitochondrial elongation in wild-type MEFs, but not in Pex3-knockout MEFs. We further found that peroxisome deficiency increased the levels of cytosolic cytochrome c and caspase activity under basal conditions without inducing apoptosis. It also greatly enhanced etoposide-induced caspase activation and apoptosis, which is indicative of an enhanced cellular sensitivity to death signals. Taken together, our data unveil a previously unrecognized role for peroxisomes in the regulation of mitochondrial dynamics and mitochondrion-dependent apoptosis. Effects of peroxin gene mutations on mitochondrion-dependent apoptosis may contribute to pathogenesis of peroxisome biogenesis disorders.
This article has an associated First Person interview with the first author of the paper.
β1 integrin is a sensor of blood flow direction
Authors: Xanthis Ioannis , Souilhol Celine , Serbanovic-Canic Jovana , Roddie Hannah , Kalli Antreas C. , Fragiadaki Maria , Wong Raymond , Shah Dhruv R. , Askari Janet A. , Canham Lindsay , Akhtar Nasreen , Feng Shuang , Ridger Victoria , Waltho Jonathan , Pinteaux Emmanuel , Humphries Martin J. , Bryan Matthew T. , Evans Paul C. 
Published: May 2019

ABSTRACT
Endothelial cell (EC) sensing of fluid shear stress direction is a critical determinant of vascular health and disease. Unidirectional flow induces EC alignment and vascular homeostasis, whereas bidirectional flow has pathophysiological effects. ECs express several mechanoreceptors that respond to flow, but the mechanism for sensing shear stress direction is poorly understood. We determined, by using in vitro flow systems and magnetic tweezers, that β1 integrin is a key sensor of force direction because it is activated by unidirectional, but not bidirectional, shearing forces. β1 integrin activation by unidirectional force was amplified in ECs that were pre-sheared in the same direction, indicating that alignment and β1 integrin activity has a feedforward interaction, which is a hallmark of system stability. En face staining and EC-specific genetic deletion studies in the murine aorta revealed that β1 integrin is activated and is essential for EC alignment at sites of unidirectional flow but is not activated at sites of bidirectional flow. In summary, β1 integrin sensing of unidirectional force is a key mechanism for decoding blood flow mechanics to promote vascular homeostasis.
This article has an associated First Person interview with the first author of the paper.
GGA2 and RAB13 promote activity-dependent β1-integrin recycling
Authors: Sahgal Pranshu , Alanko Jonna , Icha Jaroslav , Paatero Ilkka , Hamidi Hellyeh , Arjonen Antti , Pietilä Mika , Rokka Anne , Ivaska Johanna 
Published: May 2019

ABSTRACT
β1-integrins mediate cell–matrix interactions and their trafficking is important in the dynamic regulation of cell adhesion, migration and malignant processes, including cancer cell invasion. Here, we employ an RNAi screen to characterize regulators of integrin traffic and identify the association of Golgi-localized gamma ear-containing Arf-binding protein 2 (GGA2) with β1-integrin, and its role in recycling of active but not inactive β1-integrin receptors. Silencing of GGA2 limits active β1-integrin levels in focal adhesions and decreases cancer cell migration and invasion, which is in agreement with its ability to regulate the dynamics of active integrins. By using the proximity-dependent biotin identification (BioID) method, we identified two RAB family small GTPases, i.e. RAB13 and RAB10, as novel interactors of GGA2. Functionally, RAB13 silencing triggers the intracellular accumulation of active β1-integrin, and reduces integrin activity in focal adhesions and cell migration similarly to GGA2 depletion, indicating that both facilitate active β1-integrin recycling to the plasma membrane. Thus, GGA2 and RAB13 are important specificity determinants for integrin activity-dependent traffic.