Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
9,340
result(s) for
"Collins, Peter"
Sort by:
Modals and quasi-modals in English
\"Modals and Quasi-modals in English reports the findings of a corpus-based study of the modals and a set of semantically-related 'quasi-modals' in English. The study is informed by recent developments in the study of modality, including grammaticalization and recent diachronic change. The selection of the parallel corpora used, representing British, American and Australian English, was designed to facilitate the exploration of both regional and stylistic variation.\"--Jacket.
Book
Identifying and Managing Malnutrition, Frailty and Sarcopenia in the Community: A Narrative Review
Malnutrition, frailty and sarcopenia are becoming increasingly prevalent among community-dwelling older adults; yet are often unidentified and untreated in community settings. There is an urgent need for community-based healthcare professionals (HCPs) from all disciplines, including medicine, nursing and allied health, to be aware of, and to be able to recognise and appropriately manage these conditions. This paper provides a comprehensive overview of malnutrition, frailty and sarcopenia in the community, including their definitions, prevalence, impacts and causes/risk factors; and guidance on how these conditions may be identified and managed by HCPs in the community. A detailed description of the care process, including screening and referral, assessment and diagnosis, intervention, and monitoring and evaluation, relevant to the community context, is also provided. Further research exploring the barriers/enablers to delivering high-quality nutrition care to older community-dwelling adults who are malnourished, frail or sarcopenic is recommended, to inform the development of specific guidance for HCPs in identifying and managing these conditions in the community.
Journal Article
Genetic alterations in uncommon low-grade neuroepithelial tumors: BRAF, FGFR1, and MYB mutations occur at high frequency and align with morphology
Low-grade neuroepithelial tumors (LGNTs) are diverse CNS tumors presenting in children and young adults, often with a history of epilepsy. While the genetic profiles of common LGNTs, such as the pilocytic astrocytoma and ‘adult-type’ diffuse gliomas, are largely established, those of uncommon LGNTs remain to be defined. In this study, we have used massively parallel sequencing and various targeted molecular genetic approaches to study alterations in 91 LGNTs, mostly from children but including young adult patients. These tumors comprise dysembryoplastic neuroepithelial tumors (DNETs;
n
= 22), diffuse oligodendroglial tumors (d-OTs;
n
= 20), diffuse astrocytomas (DAs;
n
= 17), angiocentric gliomas (
n
= 15), and gangliogliomas (
n
= 17). Most LGNTs (84 %) analyzed by whole-genome sequencing (WGS) were characterized by a single driver genetic alteration. Alterations of
FGFR1
occurred frequently in LGNTs composed of oligodendrocyte-like cells, being present in 82 % of DNETs and 40 % of d-OTs. In contrast, a
MYB
-
QKI
fusion characterized almost all angiocentric gliomas (87 %), and
MYB
fusion genes were the most common genetic alteration in DAs (41 %). A BRAF:p.V600E mutation was present in 35 % of gangliogliomas and 18 % of DAs. Pathogenic alterations in
FGFR1/2/3
,
BRAF
, or
MYB/MYBL1
occurred in 78 % of the series. Adult-type d-OTs with an
IDH1/2
mutation occurred in four adolescents, the youngest aged 15 years at biopsy. Despite a detailed analysis, novel genetic alterations were limited to two fusion genes,
EWSR1
-
PATZ1
and
SLMAP
-
NTRK2
, both in gangliogliomas. Alterations in BRAF, FGFR1, or MYB account for most pathogenic alterations in LGNTs, including pilocytic astrocytomas, and alignment of these genetic alterations and cytologic features across LGNTs has diagnostic implications. Additionally, therapeutic options based upon targeting the effects of these alterations are already in clinical trials.
Journal Article
أهم خمسة أسئلة لبيتر دراكر : حكمة دائمة للقادة الشباب
كثيرا ما سأل بيتر إف. دراكر الأشخاص الذين عمل معهم سؤالا بسيطا : كيف تريدون أن يتذكركم الناس ؟. وفي معهد فرانسيس هيسبين للقيادة، وافقنا بالإجماع على مدى أهمية أن نلعب دورا في إلهام الجيل التالي من القادة. وفي عام 2009، اشترك معهد هيسبين مع جامعة بيتسبرج في إطلاق مشروع أكاديمية هيسبين العالمية للقيادة الطلابية والمشاركة المدنية، الذي استقطب 300 طالب موهوب من جميع القارات وعرض عليهم أعمال بيتر دراكر وفرانسيس هيسبين. إن الجيل الأصغر سنا في يومنا هذا-المعروف بجيل الألفية أو الجيل واي، المولود في الفترة ما بين عامي 1980 و 2000-ليس هو الجيل الأكبر بعد، ولكنه أكثر الأجيال تعلما وتنوعا ؛ فقد ضخم حجم التكنولوجيا وسهولة السفر حول العالم من أحلامهم بالعديد من الطرق. وجعلتهم حركة شبكات التواصل الاجتماعي والإعلام الرقمي، بدءا من القنوات المشفرة التقليدية ووصولا إلى مواقع ألفيس بوك وتويتر متواصلين مع بقية العالم بحيث يمكنهم ارتداء الماركات العالمية وكذلك التفاعل مع القضايا حول العالم بطرق استباقية جديدة. كما طوروا شبكات أصدقاء لم تتضمن الجيران أو رفقاءهم في صفوف الرياضة فقط بل تضمنت أصدقاء من أماكن نائية من العالم. ربما لم يلتقوا بهؤلاء الأصدقاء من قبل وجها لوجه، ولكن التواصل فيما بينهم كان له تأثير كبير على حيواتهم، كما نمى لديهم شعورا بالتعاطف العالمي، ولهذا أنا غالبا ما أشير إلى جيل الألفية بأنه الجيل العالمي الأول.
BOOK
Pilocytic astrocytoma: pathology, molecular mechanisms and markers
Pilocytic astrocytomas (PAs) were recognized as a discrete clinical entity over 70 years ago. They are relatively benign (WHO grade I) and have, as a group, a 10-year survival of over 90 %. Many require merely surgical removal and only very infrequently do they progress to more malignant gliomas. While most show classical morphology, they may present a spectrum of morphological patterns, and there are difficult cases that show similarities to other gliomas, some of which are malignant and require aggressive treatment. Until recently, almost nothing was known about the molecular mechanisms involved in their development. The use of high-throughput sequencing techniques interrogating the whole genome has shown that single abnormalities of the mitogen-activating protein kinase (MAPK) pathway are exclusively found in almost all cases, indicating that PA represents a one-pathway disease. The most common mechanism is a tandem duplication of a ≈2 Mb-fragment of #7q, giving rise to a fusion between two genes, resulting in a transforming fusion protein, consisting of the N-terminus of KIAA1549 and the kinase domain of BRAF. Additional infrequent fusion partners have been identified, along with other abnormalities of the MAP-K pathway, affecting tyrosine kinase growth factor receptors at the cell surface (e.g., FGFR1) as well as BRAF V600E, KRAS, and NF1 mutations among others. However, while the KIAA1549-BRAF fusion occurs in all areas, the incidence of the various other mutations identified differs in PAs that develop in different regions of the brain. Unfortunately, from a diagnostic standpoint, almost all mutations found have been reported in other brain tumor types, although some retain considerable utility. These molecular abnormalities will be reviewed, and the difficulties in their potential use in supporting a diagnosis of PA, when the histopathological findings are equivocal or in the choice of individualized therapy, will be discussed.
Journal Article
X-Men: Legion : Shadow King rising
David Haller is no ordinary mutant. Son of Charles Xavier, founder of the X-Men, David's incredible mental powers fractured his mind and now, each of his personalities controls a different ability! And they're not all friendly, as Xavier and the New Mutants find out the hard way! But as Legion struggles to control the chaos in his head, he attracts the attention of one of Xavier's oldest and most malevolent foes: Amahl Farouk, the Shadow King, who's secretly been stalking and manipulating the X-Men and their allies. When the Shadow King sinks his hooks deep into David's mind, will two teams of X-Men be enough to defeat him -- or will David be the key to the villain's ultimate victory? Includes the Muir Island Saga storyline.
BOOK
Intratumor heterogeneity in human glioblastoma reflects cancer evolutionary dynamics
Glioblastoma (GB) is the most common and aggressive primary brain malignancy, with poor prognosis and a lack of effective therapeutic options. Accumulating evidence suggests that intratumor heterogeneity likely is the key to understanding treatment failure. However, the extent of intratumor heterogeneity as a result of tumor evolution is still poorly understood. To address this, we developed a unique surgical multisampling scheme to collect spatially distinct tumor fragments from 11 GB patients. We present an integrated genomic analysis that uncovers extensive intratumor heterogeneity, with most patients displaying different GB subtypes within the same tumor. Moreover, we reconstructed the phylogeny of the fragments for each patient, identifying copy number alterations in EGFR and CDKN2A/B/p14ARF as early events, and aberrations in PDGFRA and PTEN as later events during cancer progression. We also characterized the clonal organization of each tumor fragment at the single-molecule level, detecting multiple coexisting cell lineages. Our results reveal the genome-wide architecture of intratumor variability in GB across multiple spatial scales and patient-specific patterns of cancer evolution, with consequences for treatment design.
Journal Article
Pursuit : the Balvenie stories collection
\"What is it to pursue a goal, to strive for an ideal, to follow a dream? These are the questions explored by The Balvenie in this unique collection compiled by award-winning novelist Alex Preston. The stories - from some of the brightest and most exciting voices writing today - tell of determination, endeavour and perseverance against the odds. They range across wildly different contexts and cultures, from the epic to the intimate, in fiction and non-fiction, illustrating and illuminating the outer limits of human character and achievement.\"--Publisher description.
BOOK
Human parainfluenza virus type 3 expressing the respiratory syncytial virus pre-fusion F protein modified for virion packaging yields protective intranasal vaccine candidates
Human respiratory syncytial virus (RSV) and parainfluenza virus type 3 (HPIV3) are among the most common viral causes of childhood bronchiolitis and pneumonia worldwide, and lack effective antiviral drugs or vaccines. Recombinant (r) HPIV3 was modified to express the RSV fusion (F) glycoprotein, the major RSV neutralization and protective antigen, providing a live intranasal bivalent HPIV3/RSV vaccine candidate. This extends previous studies using a chimeric bovine-human PIV3 vector (rB/HPIV3). One advantage is that rHPIV3 expresses all of the HPIV3 antigens compared to only two for rB/HPIV3. In addition, the use of rHPIV3 as vector should avoid excessive attenuation following addition of the modified RSV F gene, which may occur with rB/HPIV3. To enhance its immunogenicity, RSV F was modified (i) to increase the stability of the prefusion (pre-F) conformation and (ii) by replacement of its transmembrane (TM) and cytoplasmic tail (CT) domains with those of HPIV3 F (H3TMCT) to increase incorporation in the vector virion. RSV F (+/- H3TMCT) was expressed from the first (F/preN) or the second (F/N-P) gene position of rHPIV3. The H3TMCT modification dramatically increased packaging of RSV F into the vector virion and, in hamsters, resulted in significant increases in the titer of high-quality serum RSV-neutralizing antibodies, in addition to the increase conferred by pre-F stabilization. Only F-H3TMCT/preN replication was significantly attenuated in the nasal turbinates by the RSV F insert. F-H3TMCT/preN, F/N-P, and F-H3TMCT/N-P provided complete protection against wt RSV challenge. F-H3TMCT/N-P exhibited the most stable and highest expression of RSV F, providing impetus for its further development.
Journal Article