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Prediction in language comprehension has become a key mechanism in recent psycholinguistic theory, with evidence from lexical prediction as a primary source. Less work has focused on whether comprehenders also make structural predictions above the lexical level. Previous research shows that processing is facilitated for syntactic structures which are predictable based on context; however, there is so far no direct evidence that speakers formulate structural predictions ahead of encountering input. We investigated whether subject noun animacy cues comprehenders to predict different verb phrase (VP) structures, with the incompatibility between a low animacy subject and an Agent interpretation of transitives/unergative VPs predicting a derived (passive/unaccusative) VP structure, using Italian auxiliaries. Native Italian speakers read sentences with subject nouns varying from high to low animacy followed by the auxiliary avere HAVE , which is compatible with underived VPs, or essere BE , which is compatible with derived VPs. The auxiliary avere HAVE elicited greater frontal negativity when preceded by a subject noun with lower animacy. The auxiliary essere BE elicited no differential ERP given subject animacy. We propose that this frontal negativity reflects violation of a structural prediction, with amplitude reflecting the strength of initial commitment or difficulty in revising a predicted structure. Differences between auxiliaries are proposed to follow from the more specific distribution of avere HAVE . We argue that this evidence unambiguously supports a predictive mechanism for phrase-level structure. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Do people predict different aspects of a predictable word to the same extent? We tested prediction of phonological and gender information by creating phonological and gender mismatches between an article and a predictable noun in Italian. Native Italian speakers read predictive sentence contexts followed by the expected noun (e.g., un incidente: 'accident') or another plausible, but unexpected noun, either beginning with a different phonological class (consonant vs. vowel, e.g., uno scontro: 'collision'; phonological mismatch) or belonging to a different gender class (e.g., un'inondazione: 'flooding'; gender mismatch). Phonological mismatch articles elicited greater negativity than expected articles at posterior channels around 450-800 ms post-stimulus. In contrast, gender mismatch articles elicited greater negativity than expected articles at left posterior channels around 250-800 ms. Unexpected nouns showed an N400 effect followed by frontal positivity relative to expected nouns. The earlier effect for the gender mismatch articles suggests that people are quicker or more likely to pre-activate gender information vs. phonological information of a predictable word. We interpret the results with respect to production-based prediction accounts., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

As a human-specific trait, language offers a unique window on human cognition. Grammatical constraints on the ways we speak about events, for instance, have long been thought to reveal the representational formats that our minds impose on the ways that we think about events. In recent research, verbs that name events of death have stood out as key counterexamples to standard theories of the grammatical constraints on possible verbs. The special status of these thanatological verbs raises two important questions: why, given the vast number of verbs in any language, is it that verbs of death hold this special status, and what do they tell us about the restrictions on the representational format for possible verbs? This paper reexamines the evidence coming from verbs of death, confirming that they are counterexamples to standard theories, but that their behaviour suggests a more revealing constraint on our mental representations-that our minds impose strict restrictions on the format of asserted meaning. Thus, the constraints on linguistic representation and the human mind offer a unique perspective on the mental representations of thanatological phenomena.This article is part of the theme issue 'Evolutionary thanatology: impacts of the dead on the living in humans and other animals'., (© 2018 The Author(s).)

Do people routinely pre-activate the meaning and even the phonological form of upcoming words? The most acclaimed evidence for phonological prediction comes from a 2005 Nature Neuroscience publication by DeLong, Urbach and Kutas, who observed a graded modulation of electrical brain potentials (N400) to nouns and preceding articles by the probability that people use a word to continue the sentence fragment ('cloze'). In our direct replication study spanning 9 laboratories ( N =334), pre-registered replication-analyses and exploratory Bayes factor analyses successfully replicated the noun-results but, crucially, not the article-results. Pre-registered single-trial analyses also yielded a statistically significant effect for the nouns but not the articles. Exploratory Bayesian single-trial analyses showed that the article-effect may be non-zero but is likely far smaller than originally reported and too small to observe without very large sample sizes. Our results do not support the view that readers routinely pre-activate the phonological form of predictable words., Competing Interests: MN, SP, EH, KS, ED, NK, SV, FB, VK, AI, DM, DB, GR, HF, SB, XF, JT, EK, EH, DD, ZK, SR, FH No competing interests declared, (© 2018, Nieuwland et al.)

It has been well established that subject-verb number agreement can be disrupted by local noun phrases that differ in number from the subject head noun phrase. In sentence production, mismatches in the grammatical number of the head and local noun phrases lead to agreement errors on the verb as in: the key to the cabinets are. Similarly, although ungrammaticality typically causes disruption in measures of sentence comprehension, the disruption is reduced when the local noun phrase has a plural feature. Using a forced-choice comprehension question method, we report two experiments that provide evidence that comprehenders were likely to misinterpret the number information on the head noun phrase when morphosyntactic number markings on the local noun phrase and verb did not match the head. These results are consistent with a growing body of research that suggests that comprehenders often arrive at a final interpretation of a sentence that is not faithful to the linguistic input.

Previous research regarding the neural basis of semantic composition has relied heavily on violation paradigms, which often compare implausible sentences that violate world knowledge to plausible sentences that do not violate world knowledge. This comparison is problematic as it may involve extralinguistic operations such as contextual repair and processes that ultimately lead to the rejection of an anomalous sentence, and these processes may not be part of the core language system. Also, it is unclear if violations of world knowledge actually affect the linguistic operations for semantic composition. Here, we compared two types of sentences that were grammatical, plausible, and acceptable and differed only in the number of semantic operations required for comprehension without the confound of implausible sentences. Specifically, we compared complement coercion sentences (the novelist began the book), which require an extra compositional operation to arrive at their meaning, to control sentences (the novelist wrote the book), which do not have this extra compositional operation, and found that the neural response to complement coercion sentences activated Brodmann's area 45 in the left inferior frontal gyrus more than control sentences. Furthermore, the processing of complement coercion recruited different brain regions than more traditional semantic and syntactic violations (the novelist astonished/write the book, respectively), suggesting that coercion processes are a part of the core of the language faculty but do not recruit the wider network of brain regions underlying semantic and syntactic violations.

Background and Purpose: Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists, such as rosiglitazone and pioglitazone, sensitize cells to insulin, and are therefore used to treat type 2 diabetes. However, in some patients, these drugs induce oedema, and the present study tests the hypothesis that this side effect reflects serum and glucocorticoid-inducible kinase 1 (SGK1)-dependent enhancement of epithelia Na(+) absorption., Experimental Approach: Na(+) absorbing epithelial cells (H441 cells, mpkCCD cells) on permeable membranes were mounted in Ussing chambers, and the effects of rosiglitazone (2 microM) and pioglitazone (10 microM) on transepithelial Na(+) absorption were quantified electrometrically. Changes in SGK1 activity were assessed by monitoring phosphorylation of residues within an endogenous protein., Key Results: Both cell types absorbed Na(+) via an electrogenic process that was enhanced by insulin. In mpkCCD cells, this stimulation of Na(+) transport was associated with increased activity of SGK1, whereas insulin regulated Na(+) transport in H441 cells through a mechanism that did not involve activation of this kinase. Rosiglitazone and pioglitazone had no discernible effect on transepithelial Na(+) absorption in unstimulated or insulin-stimulated cells and failed to alter cellular SGK1 activity., Conclusions and Implications: Our results do not support the view that PPARgamma agonists stimulate epithelial Na(+) absorption or alter the control of cellular SGK1 activity. It is therefore likely that other mechanisms are involved in PPARgamma-mediated fluid retention, and a better understanding of these mechanisms may help with the identification of patients likely to develop oedema or heart failure when treated with these drugs.

Studies of HeLa cells and serum- and glucocorticoid-regulated kinase 1 (SGK1) knockout mice identified threonine residues in the n-myc downstream-regulated gene 1 protein (NDRG1-Thr(346/356/366)) that are phosphorylated by SGK1 but not by related kinases (Murray et al., Biochem J 385:1-12, 2005). We have, therefore, monitored the phosphorylation of NDRG1-Thr(346/356/366) in order to explore the changes in SGK1 activity associated with the induction and regulation of the glucocorticoid-dependent Na(+) conductance (G (Na)) in human airway epithelial cells. Transient expression of active (SGK1-S422D) and inactive (SGK1-K127A) SGK1 mutants confirmed that activating SGK1 stimulates NDRG1-Thr(346/356/366) phosphorylation. Although G (Na) is negligible in hormone-deprived cells, these cells displayed basal SGK1 activity that was sensitive to LY294002, an inhibitor of 3-phosphatidylinositol phosphate kinase (PI3K). Dexamethasone (0.2 muM) acutely activated SGK1 and the peak of this response (2-3 h) coincided with the induction of G (Na), and both responses were PI3K-dependent. While these data suggest that SGK1 might mediate the rise in G (Na), transient expression of the inactive SGK1-K127A mutant did not affect the hormonal induction of G (Na) but did suppress the activation of SGK1. Dexamethasone-treated cells grown on permeable supports formed confluent epithelial sheets that generated short circuit current due to electrogenic Na(+) absorption. Forskolin and insulin both stimulated this current and the response to insulin, but not forskolin, was LY294002-sensitive and associated with the activation of SGK1. While these data suggest that SGK1 is involved in the control of G (Na), its role may be minor, which could explain why sgk1 knockout has different effects upon different tissues.

Electrophysiological studies of H441 human distal airway epithelial cells showed that thapsigargin caused a Ca(2+)-dependent increase in membrane conductance (G(Tot)) and hyperpolarization of membrane potential (V(m)). These effects reflected a rapid rise in cellular K(+) conductance (G(K)) and a slow fall in amiloride-sensitive Na(+) conductance (G(Na)). The increase in G(Tot) was antagonized by Ba(2+), a nonselective K(+) channel blocker, and abolished by clotrimazole, a KCNN4 inhibitor, but unaffected by other selective K(+) channel blockers. Moreover, 1-ethyl-2-benzimidazolinone (1-EBIO), which is known to activate KCNN4, increased G(K) with no effect on G(Na). RT-PCR-based analyses confirmed expression of mRNA encoding KCNN4 and suggested that two related K(+) channels (KCNN1 and KCNMA1) were absent. Subsequent studies showed that 1-EBIO stimulates Na(+) transport in polarized monolayers without affecting intracellular Ca(2+) concentration ([Ca(2+)](i)), suggesting that the activity of KCNN4 might influence the rate of Na(+) absorption by contributing to G(K). Transient expression of KCNN4 cloned from H441 cells conferred a Ca(2+)- and 1-EBIO-sensitive K(+) conductance on Chinese hamster ovary cells, but this channel was inactive when [Ca(2+)](i) was <0.2 microM. Subsequent studies of amiloride-treated H441 cells showed that clotrimazole had no effect on V(m) despite clear depolarizations in response to increased extracellular K(+) concentration ([K(+)](o)). These findings thus indicate that KCNN4 does not contribute to V(m) in unstimulated cells. The present data thus establish that H441 cells express KCNN4 and highlight the importance of G(K) to the control of Na(+) absorption, but, because KCNN4 is quiescent in resting cells, this channel cannot contribute to resting G(K) or influence basal Na(+) absorption.

Local excision of early rectal tumours is an attractive proposition, avoiding the morbidity and mortality of major resection and possible permanent stoma. This study was designed to investigate the incidence of lymph node metastases associated with tumours that are locally confined to the bowel wall. A total of 454 rectal excision specimens were reviewed. Twenty-two (20 per cent) of 109 patients with tumours locally confined to the bowel wall had metastases in local lymph nodes, although 14 of these had only one or two involved nodes. Three of 27 patients with tumours that did not penetrate through the submucosa had lymph node metastases. Less well differentiated tumours were more likely to have metastasized but there was no significant difference in the height or size of tumours or in the depth of invasion between patients with or without lymph node metastases.

A total of 46 patients with duodenal ulcer were randomly assigned, without the knowledge of the investigators, to treatment with cimetidine 200 mg three times daily and 400 mg at night or sucralfate 1 g four times daily followed by one year of maintenance treatment with cimetidine 400 mg at night or sucralfate 1 g twice daily, respectively, in those patients with healed ulcers. The endoscopic healing rates and relapse rates during the maintenance period were similar, four relapses occurring in each group. All four relapses in the sucralfate group occurred at 12 months and only two were symptomatic. All the cimetidine relapses were symptomatic, two occurring at six months, one at nine months, and one at 12 months. Following the one year maintenance period, 13 cimetidine patients and 11 sucralfate patients were followed up for 36 months. During the first two years, nine of 13 (69 percent) cimetidine-treated and two of 11 (18 percent) sucralfate-treated patients had relapses. During the third year, three more sucralfate-treated patients and one more cimetidine-treated patient had relapses, making a total of 10 of 13 (77 percent) and five of 11 (45 percent) in the cimetidine and sucralfate groups, respectively. Duodenal biopsy specimens obtained before and after healing and after one year of maintenance were examined by light and electron microscopy. The sucralfate group showed greater improvement after one year of maintenance therapy than did the cimetidine group, although the appearances in either group were not predictive of subsequent relapse. The results show that relapses are less frequent and occur later after sucralfate therapy and also that the morphologic appearances are more normal after treatment with sucralfate than after treatment with cimetidine.

Forty six patients with endoscopically diagnosed duodenal ulceration were randomly allocated to treatment with either sucralfate 1 g qds (n = 24) or cimetidine 200 mg tds and 400 mg nocte (n = 22). When the ulcers healed, a maintenance dose of sucralfate 1 g bd or cimetidine 400 mg nocte was given for one year (or until relapse if earlier). Biopsies of duodenal mucosa adjacent to ulcer sites for light and electron microscopy were obtained before and after healing and again after one year's maintenance if the ulcer remained healed. Duodenal biopsies were also taken from 20 age and sex matched controls. Rates of healing and relapse during maintenance did not differ between the two treatments, although relapses occurred earlier with cimetidine. In the three year post-maintenance follow up period 10/13 cimetidine patients relapsed compared with four of 11 sucralfate patients (p less than 0.05), the relapses occurring significantly earlier in the cimetidine treated patients (p less than 0.05). Mucosal biopsies from both treatment groups still showed considerable abnormalities after healing. During maintenance, however, the sucralfate scores fell significantly (p less than 0.02) to near control levels unlike the cimetidine scores which remained raised at pretreatment values. The histological and ultrastructural changes were not predictive of later relapse. These findings favour the use of sucralfate in preference to cimetidine for maintenance treatment in the prevention of relapse of healed duodenal ulcers.

Five cases of a distinctive tumor located in the soft tissues of the lower neck in adults are described. The lesion is characterized microscopically by the presence of four components: cellular areas made up of spindle elements; epithelial islands composed of solid nests, trabeculae and cysts; mature adipose tissue; and lymphocytes, sometimes arranged in a Hassall's corpuscle-like fashion. Electron microscopy and immunostaining for keratin showed that the spindle cell component was of epithelial nature. These tumors were supraclavicular or suprasternal in location, and no local recurrence has developed in any case following local resection. We interpret these lesions as benign tumors arising on the basis of a developmental defect. We think that they are derived from the third branchial arch and that they are composed of abnormal thymic tissue.

Five cases are described where minute foci of adenocarcinoma have been demonstrated in the mesorectum several centimetres distal to the apparent lower edge of a rectal cancer. In 2 of these there was no other evidence of lymphatic spread of the tumour. In orthodox anterior resection much of this tissue remains in the pelvis, and its is suggested that these foci might lead to suture-line or pelvic recurrence. Total excision of the mesorectum has, therefore, been carried out as a part of over 100 consecutive anterior resections. Fifty of these, which were classified as 'curative' or 'conceivably curative' operations, have now been followed for over 2 years with no pelvic or staple-line recurrence.

The histological and histochemical features of a primary chemodectoma of lung are described and compared with previously reported pulmonary chemodectomata. The tumour is of interest because, although there is physiological evidence that chemoreceptors are present in the lung, they have not yet been located anatomically.