Teachers as writers: a systematic review

This paper is a critical literature review of empirical work from 1990-2015 on teachers as writers. It interrogates the evidence on teachers’ attitudes to writing, their sense of themselves as writers and the potential impact of teacher writing on pedagogy or student outcomes in writing. The methodology was carried out in four stages. Firstly, educational databases keyword searches located 438 papers. Secondly, initial screening identified 159 for further scrutiny, 43 of which were found to specifically address teachers’ writing identities and practices. Thirdly, these sources were screened further using inclusion/exclusion criteria. Fourthly, the 22 papers judged to satisfy the criteria were subject to in-depth analysis and synthesis. The findings reveal that the evidence base in relation to teachers as writers is not strong, particularly with regard to the impact of teachers’ writing on student outcomes. The review indicates that teachers have narrow conceptions of what counts as writing and being a writer and that multiple tensions exist, relating to low self-confidence, negative writing histories, and the challenge of composing and enacting teacher and writer positions in school. However, initial training and professional development programmes do appear to afford opportunities for reformulation of attitudes and sense of self as writer

Phospholipids Trigger Cryptococcus neoformans Capsular Enlargement during Interactions with Amoebae and Macrophages

A remarkable aspect of the interaction of Cryptococcus neoformans with mammalian hosts is a consistent increase in capsule volume. Given that many aspects of the interaction of C. neoformans with macrophages are also observed with amoebae, we hypothesized that the capsule enlargement phenomenon also had a protozoan parallel. Incubation of C. neoformans with Acanthamoeba castellanii resulted in C. neoformans capsular enlargement. The phenomenon required contact between fungal and protozoan cells but did not require amoeba viability. Analysis of amoebae extracts showed that the likely stimuli for capsule enlargement were protozoan polar lipids. Extracts from macrophages and mammalian serum also triggered cryptococcal capsular enlargement. C. neoformans capsule enlargement required expression of fungal phospholipase B, but not phospholipase C. Purified phospholipids, in particular, phosphatidylcholine, and derived molecules triggered capsular enlargement with the subsequent formation of giant cells. These results implicate phospholipids as a trigger for both C. neoformans capsule enlargement in vivo and exopolysaccharide production. The observation that the incubation of C. neoformans with phospholipids led to the formation of giant cells provides the means to generate these enigmatic cells in vitro. Protozoan- or mammalian-derived polar lipids could represent a danger signal for C. neoformans that triggers capsular enlargement as a non-specific defense mechanism against potential predatory cells. Hence, phospholipids are the first host-derived molecules identified to trigger capsular enlargement. The parallels apparent in the capsular response of C. neoformans to both amoebae and macrophages provide additional support for the notion that certain aspects of cryptococcal virulence emerged as a consequence of environmental interactions with other microorganisms such as protists

EFFECTS OF CHANGING GONADOTROPHIN-RELEASING HORMONE PULSE FREQUENCY ON GONADOTROPHIN SECRETION IN MEN

To investigate the effects of alterations in GnRH pulse frequency on gonadotro-phin secretion, we administered low dose GnRH pulses (25 ng/kg) at hourly or 2-hourly frequencies to eight normal men. All subjects received GnRH pulses i.v. every 2 h for 88 h. Following this, exogenous GnRH was discontinued in four normal men (Group A, GnRH withdrawal), and the frequency of GnRH injections was increased to one pulse every hour for 24 h in the other four normal men (Group B, hourly GnRH). Blood samples were obtained every 20 min for LH and FSH and every 12 h for testosterone (T) and oestradiol (E2). Plasma LH increased in all subjects during injection of GnRH pulses every 2h. Withdrawal of GnRH pulses in Group A men was accompanied by a fall in mean LH, reductions in LH pulse amplitude (X¯± SEM: control 6.5±1.0; GnRH withdrawal 4.0 ± 0.5 mlU/ml) and pulse frequency (control 5.5 ± 0.2; GnRH withdrawal 3.5 ± 0.7 pulses/12 h), and an increase in plasma E 2 (control 122 ± 15; GnRH withdrawal 340 ± 37 pmol/l). Gonadotrophin responses to GnRH (25 ng/kg) were normal when tested 32 h after GnRH withdrawal. Injection of hourly GnRH pulses in Group B men was accompanied by a time-dependent change in mean LH, which transiently rose, then fell, and subsequently rose to a plateau during the second 12 h period of hourly GnRH. The final rise in LH was accompanied by an increase in LH frequency to 11.8 ± 0.3 pulses/12 h. These data suggest that: (1) increases in gonadal steroids decrease LH secretion by reducing the amplitude and frequency of endogenous GnRH pulses; and (2) the normal adult male pituitary requires approximately 12 h to initiate a sustained increase in LH secretion in response to a doubling in GnRH pulse frequency.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71865/1/j.1365-2265.1988.tb03857.x.pd

The Inflammatory Relationship Between Hepatitis C Virus With Coronary and Carotid Atherosclerosis.

Hepatitis C virus (HCV), a global health concern, has been linked to various hepatic and extrahepatic deleterious manifestations. Several observational studies have either supported the increased likelihood of coronary and carotid atherosclerosis after infection with HCV or refuted it. To date, there has been no clear consensus to support either train of thought, as randomized, controlled clinical trials have not been completed. In this review, we first discuss articles that support the notion that HCV infection leads to increased plaque formation due to systemic inflammation and then focus on articles that refute this idea. From the literature, we do know that both inflammatory and lipid processes play a role in plaque formation, and thus both components are important in the successful treatment of atherosclerosis. Based on our review of the literature, we do believe that HCV-infected individuals are at an increased risk for more severe coronary artery disease than their healthy counterparts. Although there is no irrefutable evidence that links HCV infection with plaque formation and/or rupture, cardioprotective measures should be taken to reduce poor health outcomes, especially in those individuals who are already at risk of coronary disease

The Inflammatory Relationship between Hepatitis C Virus with Coronary and Carotid Atherosclerosis

Hepatitis C virus (HCV), a global health concern, has been linked to various hepatic and extrahepatic deleterious manifestations. Several observational studies have either supported the increased likelihood of coronary and carotid atherosclerosis after infection with HCV or refuted it. To date, there has been no clear consensus to support either train of thought, as randomized, controlled clinical trials have not been completed. In this review, we first discuss articles that support the notion that HCV infection leads to increased plaque formation due to systemic inflammation and then focus on articles that refute this idea. From the literature, we do know that both inflammatory and lipid processes play a role in plaque formation, and thus both components are important in the successful treatment of atherosclerosis. Based on our review of the literature, we do believe that HCV-infected individuals are at an increased risk for more severe coronary artery disease than their healthy counterparts. Although there is no irrefutable evidence that links HCV infection with plaque formation and/or rupture, cardioprotective measures should be taken to reduce poor health outcomes, especially in those individuals who are already at risk of coronary disease