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The goal of this article is to introduce the notion of industrial linguistic heritage into the study of industrial heritage. By combining viewpoints of cultural heritage research and language studies, the article opens new insights into the identities and cultural resources of industrial communities. The linguistic heritage of industry is investigated in the light of two case studies from selected linguistic landscapes of Varkaus, a small industrial community in eastern Finland. The case studies illuminate both multilingualism of the industrial community as industrial linguistic heritage and language as a means to verbalize and commemorate the industrial past of the community. The examination of the linguistic landscape data shows that language is an important strategic means to verbalize the past, to restore shared histories and participatory experiences, and to carry out commemorative identity work in the industrial heritage community.

By using digital oral historical sources, Suominen and Sivula study the domestication of Nintendo console gaming in Finland in the late 1980s and the early 1990s. They analyse how the gaming memories are recollected and attached to particular places. According to Suominen and Sivula, the gaming identity is built around homes, but on the other hand, the domestic gaming is extended in public and mobile environments.

The postglacial land uplift process has been modelled using two different approaches: by modelling the geodynamics of the earth’s crust (also referred to as Glacial Isostatic Adjustment (GIA) modelling) or by fitting mathematical models to existing archaeological and geological data (referred to as semi-empirical modelling). Although the semi-empirical models are not based on the physical properties of the earth’s crust, they are easy to implement and can adapt better to local variations when compared to the GIA models. Semi-empirical models are fitted to the ice retreat data, eustatic sea level dynamics and lake isolation data on past shoreline displacement. As most of these data sources involve uncertainties, the land uplift process can be modelled probabilistically using the Monte Carlo method.

The rich and colorful human history of Eura has been documented based on archaeological findings. The oldest findings from Satakunta are associated with the Suomusjarvi culture, which may have had possible cultural and trading connections to East Karelia. The findings also show that there has been two different types of ceramics in the same place and time period indicating a chance that there have been two populations from different cultures at the same time. Numerous archaeological findings belonging to the later Kiukainen culture show the cultural dependencies with other archaeological finding sites in Finland. In this chapter, four archaeological examples that belong to either Suomusjarvi or Kiukainen culture are presented. Also a brief history of Scandinavian archaeology is presented and the roots of Finnish archaeology are discussed in this chapter.

The landscape reconstruction at four historical sites in Eura: Kolmhaara, Tyttopuisto, Kuninkaanhauta and Luistari is presented in this chapter. The reconstruction focuses on the time periods of the archaeological findings at respective sites: Stone Age in the case of Kolmhaara and Tyttopuisto, Bronze Age in the case of the Kuninkaanhauta and Iron Age in the case of Luistari. Landscape reconstruction results are discussed in relation with the radiocarbon datings of the findings at these sites. It is found that while for the Kuninkaanhauta the land uplift model locates the settlement at a favorable location with respect to the shoreline at approximately the same time period obtained using radiocarbon dating, there is a significant discrepancy between the two methods of estimating the age of the settlements for the Stone Age sites of Kolmhaara and Tyttopuisto.

Tässä artikkelissa tarkastelen kolmen osallistuvasti havainnoimani ja johtamani tilaushistoriahankkeen tuottaman aineiston valossa paikallista historiapolitiikkaa ja paikallishistoriallista identiteettityötä. Artikkeli etenee keskeisten käsitteiden määritelmistä ja tutkimuskysymyksistä historiankirjoituksen typologisointeihin ja tilaushistoriatapausten kuvailuun ja päättyy yritykseen mallintaa kulttuuriperintöä ylläpitävän identiteettityön lajeja ja kulttuuriperintöprosessin logiikkaa.

Cyclooxygenase-2 (COX-2) expression has been found to associate with poor prognosis in several types of carcinomas. HuR is an mRNA stability protein and it regulates the expression of COX-2. Objectives and methods. We analyzed the expression of COX-2 and HuR in 64 mucinous ovarian carcinoma specimens by immunohistochemistry. Results. In mucinous tumors, high COX-2 protein expression was found in epithelial cancer cells in 39% (22/56) and in stromal cells in 24% (13/55) of the specimens. The expression of COX-2 in cancer cells correlated with high grade ( P = 0.0285), but stromal COX-2 expression had no correlation with any clinical parameter tested. Cytoplasmic HuR protein expression was observed in cancer cells in 47% (27/57) and in stromal cells in 7% (4/56) of the mucinous tumors, and it correlated with COX-2 expression in the cancer cells ( P = 0.0162) but not in the stroma. Conclusion. Our results support the hypothesis that cytoplasmic HuR is connected to COX-2 expression in ovarian carcinoma, but that its role is restricted to the transformed epithelial cancer cells.

Expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2) associates with reduced survival in human breast cancer. COX-2 may be directly involved with mammary carcinogenesis, since expression of COX-2 is sufficient for formation of breast tumors in transgenic mice, and COX-2 selective inhibitors can suppress tumorigenesis in rodent models of breast cancer. MMP-2 is an extracellular matrix degrading proteolytic enzyme that bas been linked to invasion and metastasis. A direct link between COX-2 and MMP-2 may exist, since inhibition of COX-2 activity can result in reduction of MMP-2 expression and activity. In this study we analyzed protein expression of COX-2 and MMP-2 in tissue array specimens of 278 invasive breast cancers by immunohistochemistry. Immunopositivity of these two markers was correlated with each other and with various clinicopathological parameters including survival. We found high COX-2 expression in 30% and high MMP-2 expression in 83% of the breast cancer specimens, and there was a positive association between the expression of these two factors (p = 0.003). It was especially evident that whenever COX-2 expression was high, MMP-2 expression was almost invariably high (95%). Furthermore, high expression of either COX-2 or MMP-2 associated with decreased disease specific survival when compared with the COX-2 or MPP-2 low group (p = 0.026 and p = 0.021, respectively). Taken together, our results indicate that expression of COX-2 protein is associated with expression of MMP-2 protein in human breast cancer and that both COX-2 and MMP-2 are markers of poor prognosis in breast cancer.

Based on our previous demonstration that elevated cyclooxygenase-2 (COX-2) expression is a prognostic factor for reduced survival in patients with adenocarcinoma of the esophagus, the aim of our study was to analyze the role of COX-2 expression in esophageal squamous cell carcinoma. We analyzed COX-2 protein expression from 117 consecutive patients by immunohistochemistry using a COX-2 specific monoclonal antibody. Eighty-one patients had not received any therapy before surgery whereas 36 patients received neoadjuvant chemotherapy as part of a randomized controlled trial. In the patients who received no chemotherapy, COX-2 expression was low in 75% and high in 25% of the specimens. In this patient group, high COX-2 expression associated with distal location of the tumor (p = 0.02), but did not correlate with any other clinicopathological parameter tested, including overall survival. In the patient group who received neoadjuvant chemotherapy, postoperative COX-2 expression was low in 69% and high in 31%. Interestingly, in this patient group low COX-2 expression correlated with development of distant metastases (p = 0.03) and to reduced overall survival (p = 0.02). Our results show that the prognostic significance of COX-2 depends on the histological type of esophageal carcinoma and preoperative treatment of the patient. In conclusion, COX-2 is not a prognostic marker in squamous cell carcinoma of the esophagus, but low COX-2 expression is associated with poor prognosis in the neoadjuvant-treated patients.

Epidemiological studies have shown that the use of nonsteroid anti-inflammatory drugs (NSAIDs) is associated with reduced risk of gastric cancer. The best-known target of NSAIDs is the cyclooxygenase (Cox) enzyme. Two Cox genes have been cloned, of which Cox-2 has been connected with gastric carcinogenesis. Expression of Cox-2 is elevated in gastric adenocarcinomas, which correlates with several clinicopathological parameters, including depth of invasion and lymph node metastasis. This suggests that Cox-2-derived prostanoids promote aggressive behavior of adenocarcinomas of the stomach. Cox-2 expression is especially prominent in intestinal-type gastric carcinoma and it is already present in dysplastic precursor lesions of this disease, which suggests that Cox-2 contributes to gastric carcinogenesis already at the preinvasive stage. Our most recent data show that Cox-2 is expressed in gastric adenomas of trefoil factor 1 deficient mice. Treatment of these mice with a Cox-2 selective inhibitor, celecoxib, reduced the size of the adenomas. Taken together these data support efforts to initiate clinical studies to investigate the effect of Cox-2 inhibitors as chemotherapeutic agents and as adjuvant treatment modalities against gastric neoplasias.

Gastrointestinal carcinomas synthesize elevated levels of prostaglandin E(2) (PGE(2)), which has been mechanistically linked to carcinogenesis. Recently, microsomal prostaglandin E synthase-1 (mPGES-1) was cloned, which seems to be inducible and linked to cyclooxygenase-2 (Cox-2) in the biosynthesis of PGE(2). We examined expression of mPGES-1 in intestinal type gastric adenocarcinomas and in gastric cancer cell lines. The transcript for mPGES-1 was elevated in 57% (4/7) of gastric carcinomas as detected by Northern blot analysis. Moderate to strong mPGES-1 immunoreactivity was observed in 56% (5/9) of the carcinomas as detected by immunohistochemistry. Furthermore, mPGES-1 mRNA, protein and microsomal PGES activity were detected in gastric adenocarcinoma cell lines that originated from intestinal type tumors (MKN-7 and MKN-28). In contrast to Cox-2, however, expression of mPGES-1 mRNA or protein were not induced by phorbol 12-myristate 13-acetate (PMA) or interleukin-1beta (IL-1beta) in any of the gastric cancer cell lines tested (MKN-1, -7, -28, -45 and -74). Two gastric cancer cell lines (MKN-45 and MKN-74) did not express mPGES-1 and lacked microsomal PGES activity, but were still able to synthesize PGE(2). Because all gastric cell lines expressed cPGES as detected by immunoblotting, it is possible that Cox-2 can interact with cPGES or with some other yet unidentified PGES in gastric cancer cells. Furthermore, our data show that regulatory mechanisms that drive expression of mPGES-1 and Cox-2 dissociate in gastric cancer cell lines.

Background & Aims: Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced risk of cancer in the digestive tract. Cyclooxygenase (COX) is the best-known target of NSAIDs, and expression of the COX-2 isoform is elevated in esophageal carcinomas but its clinical significance remains unclear. We examined COX-2 expression in esophageal adenocarcinomas and its relation to clinicopathologic parameters. Methods: Tumor sections from 145 consecutive patients undergoing intentionally curative surgery for an adenocarcinoma arising from a Barrett's esophagus were immunohistochemically stained using a COX-2–specific anti-human monoclonal antibody. The specimens were scored based on the intensity and extent of COX-2 immunopositivity. Results: COX-2 immunoreactivity was negative to weak in 21% (COX-2 low) and moderate to strong in 79% (COX-2 high) of the carcinomas. Patients with high COX-2 expression were more likely to develop distant metastases ( P = 0.02) and local recurrences ( P = 0.05), and survival was significantly reduced ( P = 0.002, log-rank test) among patients with high COX-2 expression when compared with the COX-2 low group. Five-year survival rates were 35% (95% confidence interval [CI], 23–47) and 72% (95% CI, 53–90) in COX-2 high and COX-2 low categories, respectively. Furthermore, expression of COX-2 was recognized as an independent prognostic factor by multivariate analysis (relative risk, 3.5; 95% CI, 1.6–7.9). Conclusions: Elevated expression of COX-2 protein is associated with significantly reduced survival of patients undergoing surgery for esophageal adenocarcinoma. These findings support the effort to initiate clinical studies to investigate the effect of COX-2 inhibitors as a novel (adjuvant) chemotherapeutic modality for the treatment of adenocarcinoma arising from Barrett's esophagus. GASTROENTEROLOGY 2002;122:1800-1807

Multiple epidemiological studies indicate that the use of aspirin and other NSAIDs are associated with reduced risk of malignancies especially in the digestive tract. In addition, another NSAID sulindac causes regression of colorectal adenomatous polyps in patients with familial adenomatous polyposis (FAP) [1, 2]. Recent studies suggest that COX-2 is a rational target of NSAIDs in prevention of colorectal cancer. First, elevated levels of COX-2 mRNA and protein, but not those of COX-1, were found in colorectal adenocarcinomas and in their adenomatous precursors [3–5]. Second, selective COX-2 inhibitors suppress neoplasia formation in rodent models of colorectal cancer [6–10]. Importantly, genetic disruption of COX-2 suppresses the polyp formation in ApcΔ716-knockout and in Min mice, which are models for FAP [6, 11]. However, it should be noted that disruption of COX-1 gene also reduced the polyp burden in the Min mouse model [11]. Finally, elevated COX-2 expression was shown to associate with poor prognosis in colorectal carcinoma [12].

Cyclooxygenase-2 (COX-2) expression has been shown to associate with poor prognosis in ovarian cancer, and an mRNA stability protein HuR has been shown to enhance expression of COX-2 in tissue culture conditions. We found cytoplasmic immunoreactivity for HuR protein in 52% (233 of 445) of serous-type ovarian carcinoma specimens, and it associated with high COX-2 expression (P = 0.0045) and with clinicopathological variables, including poor prognosis (P0.0001) and high grade (P0.0001). In ovarian cancer cells in vitro, a small interfering RNA against HuR and leptomycin B, an inhibitor of nucleocytoplasmic translocation of HuR, inhibited COX-2 expression. Our results show that cytoplasmic HuR expression associates with poor outcome in ovarian cancer, and one plausible explanation for this finding may be related to the ability of HuR to induce COX-2 expression.

Gastrointestinal carcinomas synthesize elevated levels of prostaglandin E(2) (PGE(2)), which has been mechanistically linked to carcinogenesis. Recently, microsomal prostaglandin E synthase-1 (mPGES-1) was cloned, which seems to be inducible and linked to cyclooxygenase-2 (Cox-2) in the biosynthesis of PGE(2). We examined expression of mPGES-1 in intestinal type gastric adenocarcinomas and in gastric cancer cell lines. The transcript for mPGES-1 was elevated in 57% (4/7) of gastric carcinomas as detected by Northern blot analysis. Moderate to strong mPGES-1 immunoreactivity was observed in 56% (5/9) of the carcinomas as detected by immunohistochemistry. Furthermore, mPGES-1 mRNA, protein and microsomal PGES activity were detected in gastric adenocarcinoma cell lines that originated from intestinal type tumors (MKN-7 and MKN-28). In contrast to Cox-2, however, expression of mPGES-1 mRNA or protein were not induced by phorbol 12-myristate 13-acetate (PMA) or interleukin-1beta (IL-1beta) in any of the gastric cancer cell lines tested (MKN-1, -7, -28, -45 and -74). Two gastric cancer cell lines (MKN-45 and MKN-74) did not express mPGES-1 and lacked microsomal PGES activity, but were still able to synthesize PGE(2). Because all gastric cell lines expressed cPGES as detected by immunoblotting, it is possible that Cox-2 can interact with cPGES or with some other yet unidentified PGES in gastric cancer cells. Furthermore, our data show that regulatory mechanisms that drive expression of mPGES-1 and Cox-2 dissociate in gastric cancer cell lines.

Background: Adenocarcinomas of the gastric cardia and distal oesophagus are at present often considered as one clinical entity because of their comparable increasing incidence, prognosis, and optimal treatment options. However, it is still a matter of debate whether these malignancies have the same pathogenesis and genotype. Aims: The aim of this study was to analyse expression of cyclooxygenase 2 (COX-2) in cardia carcinomas, and correlate this expression with clinicopathological parameters and survival. The results were compared with the prognostic value of COX-2 found for Barrett carcinomas. Methods: Tumour sections of 134 consecutive patients undergoing potentially curative surgery for an adenocarcinoma of the gastric cardia and substantially invading the distal oesophagus were immunohistochemically stained using a COX-2 monoclonal antibody. Specimens were blindly scored based on intensity and extent of COX-2 immunopositivity. Results: COX-2 expression was negative to weak in 59% (“COX-2 low”) and moderate to strong in 41% (“COX-2 high”) of tumours. This was significantly lower than in Barrett carcinomas (p

Cyclooxygenase-2 (Cox-2) expression can induce mammary tumorigenesis in transgenic mice, and selective Cox-2 inhibitors are both chemopreventive and chemotherapeutic in rat models of breast cancer. We analyzed the expression of Cox-2 protein by immunohistochemistry in tissue array specimens of 1576 invasive breast cancers. Moderate to strong (elevated) expression of Cox-2 protein was observed in 37.4% of the tumors, and it was associated with unfavorable distant disease-free survival (P0.0001). Elevated Cox-2 expression was associated with a large tumor size, a high histological grade, a negative hormone receptor status, a high proliferation rate (identified by Ki-67), high p53 expression, and the presence of HER-2 oncogene amplification (P0.0001 for all comparisons), along with axillary node metastases and a ductal type of histology (P = 0.0001 and P = 0.0017, respectively). Interestingly, association with the unfavorable outcome was especially apparent in the subgroups defined by estrogen receptor positivity, low p53 expression, and no HER-2 amplification (P0.0001 for all comparisons). These results indicate that elevated Cox-2 expression is more common in breast cancers with poor prognostic characteristics and is associated with an unfavorable outcome. The present findings support efforts to initiate clinical trials on the efficacy of Cox-2 inhibitors in adjuvant treatment of breast cancer.

Tämä artikkeli käsittelee ihmistieteissä tapahtuneita julkaisukäytännön muutoksia. Erityisenä mielenkiinnon kohteena ovat 2000-luvulla voimaan tulleiden yliopistojen uusien rahoitusmallien vaikutukset ja niiden omaksuminen käyttöön. Artikkeli perustuu vuonna 2014 tehtyyn verkkokyselyyn, jossa kartoitettiin miten tutkijat ovat suhtautuneet tiede- ja kustannusmaailman muutoksiin sekä millaisia uusia toimintatapoja ne ovat tutkimustyössä synnyttäneet. Merkittävimpiin löydöksiin kuuluvat ne moninaiset keinot, joilla uusia järjestelmiä on käytännössä sovellettu (ja myös väärinkäytetty), sekä ihmistieteilijöiden jakautuminen erilaisiin ryhmiin, joilla on usein jopa täysin päinvastainen suhtautuminen muutoksiin. Lisäksi esiin nousee se, kuinka hyvin tulosjärjestelmät tunnetaan eri yliopistoissa, ja kuinka järjestelmät ovat herättäneet runsaasti kriittistäkin keskustelua.