Vascular surgery, risk assessment and gastrointestinal surgery were the areas of focus for 59% of the contemporary most cited emergency abdominal surgery manuscripts. By providing the most influential references this work serves as a guide to what makes a citable emergency surgery paper.

Summary Barrett’s esophagus (BE) is the main pathological precursor of esophageal adenocarcinoma (EAC). Progression to high-grade dysplasia (HGD) or EAC from nondysplastic BE (NDBE), low-grade dysplasia (LGD) and indefinite for dysplasia (IND) varies widely between population-based studies and specialized centers for many reasons, principally the rigor of the biopsy protocol and the accuracy of pathologic definition. In the Republic of Ireland, a multicenter prospective registry and bioresource (RIBBON) was established in 2011 involving six academic medical centers, and this paper represents the first report from this network. A detailed clinical, endoscopic and pathologic database registered 3,557 patients. BE was defined strictly by both endoscopic evidence of Barrett’s epithelium and the presence of specialized intestinal metaplasia (SIM). A prospective web-based database was used to gather information with initial and follow-up data abstracted by a data manager at each site. A total of 2,244 patients, 1,925 with no dysplasia, were included with complete follow-up. The median age at diagnosis was 60.5 with a 2.1:1 male to female ratio and a median follow-up time of 2.7 years (IQR 1.19–4.04), and 6609.25 person years. In this time period, 125 (5.57%) progressed to HGD/EAC, with 74 (3.3%) after 1 year of follow-up and 38 (1.69%) developed EAC, with 20 (0.89%) beyond 1 year. The overall incidence of HGD/EAC was 1.89% per year; 1.16% if the first year is excluded. The risk of progression to EAC alone overall was 0.57% per year, 0.31% excluding the first year, and 0.21% in the 1,925 patients who had SIM alone at diagnosis. Low-grade dysplasia (LGD) progressed to HGD/EAC in 31% of patients, a progression rate of 12.96% per year, 6.71% with the first year excluded. In a national collaboration of academic centers in Ireland, the progression rate for NDBE was similar to recent population studies. Almost one in two who progressed was evident within 1 year. Crucially, LGD diagnosed and confirmed by specialist gastrointestinal pathologists represents truly high-risk disease, highlighting the importance of expertise in diagnosis and management, and providing indirect support for ablative therapies in this context.

Bibliometric analysis highlights key topics and publications that have shaped the understanding and management of esophageal cancer (EC). Here, the 100 most cited manuscripts in the field of EC are analyzed. The Thomson Reuters Web of Science database with the search terms 'esophageal cancer' or 'esophageal carcinoma' or 'oesophageal cancer' or 'oesophageal carcinoma' or 'gastroscopy' was used to identify all English language full manuscripts for the study. The 100 most cited papers were further analyzed by topic, journal, author, year, and institution. A total of 121,556 eligible papers were returned and the median (range) citation number was 406.5 (1833 to 293). The most cited paper focused on the role of perioperative chemotherpy in EC (1833 citations). Gastroenterology published the highest number of papers (n = 15, 6362 citations) and The New England Journal of Medicine received the most citations (n = 12, 12125 citations). The country and year with the greatest number of publications were the USA (n = 50), and 1998, 1999, and 2000 (n = 7). The most ubiquitous topic was the pathology of EC (n = 66) followed by management of EC (n = 54), and studies related to EC prognosis (n = 44). The most cited manuscripts highlighted the pathology, management, and prognosis of EC and this bibliometirc review provides the most influential references serving as a guide to popular research themes.

Uterine fibroids are the commonest of pelvic neoplasms and therefore should command the interest of all gynecologists. What is the source of these tumors is a question that is asked daily and one which can be answered only in generalities. I n three former contributions (1, 2, 3) excessive stimulation of the myometrium by the ovarian follicular hormone has been suggested as a cause. That the action of this hormone is not specific for the endometrium, as demonstrated by the endometrial changes during the normal menstrual cycle, but that it affects the genital tract as a whole, is easily proved (4). When the action on the endometrium is abnormal, with resulting endometri a1 hyperplasia, there is an equally abnormal action upon the myometrium, which, if it is prolonged sufficiently, results in cellular metaplasia of the uterine muscle cell or cells, with the subsequent development of uterine fibroids.According to Meyer (5), the histogenetic study of fibroids does not reveal any distinctive myoma mother cells in the uterine muscle from which a proliferating myoma might develop. He reports that the earliest appearance of a myoma is represented by a thickening of the uterine muscle buiidles which a r e directly connected with the normal musculature of the uterus. De Snoo (6), on the other hand, claims that the uterus is a very primitive special organ which contains many nndifferentiated cells, genitoblasts. During embryonic life these cells form the uterus proper, while in later life they provide the means of gestational hyperplasia and of regeneration of the endometrium during the puerperium. Under pathological conditions, due. to ovarian hormonal dysfunction, these genitoblasts can give rise to the formation of uterine fibroids, endometriomns, or adenomyomas.It is not the object of this paper to enter into a discussion of the primary source of the uterine fibroid, whether it be from myoma mother cells, as genitoblasts, or from cellular metaplasia of normal uterine muscle cells. The actual origin of the fibroid is unimportant ; the paramount question is the determination of the exciting factor which controls the cellular change or which stimulates the geiiitoblasts to tumor proliferation. The hypothesis is here set forth that this exciting cause has its origin in excessive stimulation on the uterine muscle tissue by the ovarian folliculsr hormone. Grttves (7) has aptly observed that uterine fibroids possess certain attributes that seem to place them in a borderland between physiologic hypertrophy and true neoplastic growths. " Their great frequency 402

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