Panel report ECIS 2012: publication strategy for junior researchers: quantity vs. quality, importance of the first authorship and collaboration

The publication record is a key component of a successful academic career in IS. Despite its importance, its definition - especially for junior researchers―remains unclear. Is it better to have one A-publication or three Bpublications? Does being the third author on an A-publication carry more weight than being the first author on a Bpublication? Is it better to publish with as few co-authors as possible to demonstrate ability for independent work or is publishing with others a sign of good teamwork and academic excellence? Faced with these uncertainties, young researchers increasingly question the choices they make regarding their publication strategy. If unaddressed, these issues are bound to interfere with the quality of the IS research and scholars’ job satisfaction. This article raises these concerns associated with a publication strategy for junior researchers and reports the views voiced by five academics at a panel session at the European Conference on Information Systems 2012. In particular, the following topics are discussed: quantity vs. quality, value of the first authorship, the “optimal” number of authors, and the issues of co-authorship with an academic supervisor.

Investigation of IL23 (p19, p40) and IL23R highlights nuclear IL23p19 expression as a marker of indolent tumor features and favorable outcome in colorectal cancer patients

Objective: IL23 is involved in chronic inflammation but its role in cancer progression is not fully elucidated. Here we characterize IL23 subunits p40, p19 and IL23 receptor (IL23R) in the normal-adenoma-carcinomametastasis cascade of colorectal cancers and their relationship to clinicopathological and outcome data. Method: Immunohistochemistry for IL23R, IL12p40, IL23 and IL23p19 (monoclonal) was performed on a multi-punch tissue microarray (n=213 patients). Expression differences between normal-adenomas-cancerslymph nodes were evaluated. Correlation with clinicopathological and outcome data was undertaken. Results were validated on an independent cohort (n=341 patients). Results: An increased expression from normal-adenoma-cancer was observed (p<0.0001; all) followed by a marked reduction in lymph nodes (p<0.0001; all). Cytoplasmic and/or membranous staining of all markers was unrelated to outcome. Nuclear IL23p19 staining occurred in 23.1%and was associated with smaller tumor diameter (p=0.0333), early pT (p=0.0213), early TNM (p=0.0186), absence of vascular (p=0.0124) and lymphatic invasion (p=0.01493) and favorable survival (univariate (p=0.014) and multivariable (p=0.0321) analysis). All IL23p19 positive patients were free of distant metastasis (p=0.0146). Survival and metastasis results could be validated in Cohort 2. Conclusion: The presence of nuclear IL23p19 is related to indolent tumor features and favorable outcome supporting a more ‘protective’ role of this protein in colorectal cancer progression

AN IMPLANTABLE MOSFET DOSIMETER MODIFIED TO ACT AS A FIDUCIAL MARKER

In external beam radiation therapy, it is imperative that the prescribed dose is administered to the correct location and in the correct amount. Though several ex vivo methods of quality assurance are currently employed to achieve this goal, verifying that the correct dose is received within the patient in situ is impossible without the capability of measuring dose inside the patient. Recently, a method of measuring dose delivered within the patient has been developed, an implantable MOSFET dosimeter. This dosimeter is implanted within the patient and records the dose received. Since the dosimeter is implanted in the patient, it could serve a dual function as a fiducial marker for image guided radiation therapy (IGRT) treatment if it could be modified to be visible on x-rays. In this study, modifications to the MOSFET dosimeter were made to increase its visibility for IGRT treatment. To test whether the modifications hindered the dosimeter’s ability to accurately measure and transmit dose information, the energy dependence, angular dependence and wireless read range of the modified dosimeter were measured and compared to unmodified dosimeters. It was found that the modified dosimeter performed as well as the unmodified dosimeter while also being suitable for use as a fiducial marker for IGRT treatment.

PANEL DISCUSSION: "Medical Ethics, Eugenics, and the Holocaust"

A panel discussion moderated by Dr. Thomas R. Cole, McGovern Chair in Medical Humanities and Director of the John P. McGovern Center for Humanities and Ethics at the University of Texas Health Science Center in Houston. Panelists include: Rabbi Samuel E. Karff, Rabbi Emeritus of Congregation Beth Israel and Associate Director of the John P. McGovern Center for Humanities and Ethics and Visiting Professor in the Department of Family Medicine at the University of Texas Health Science Center at the Texas Medical Center. Cardinal DiNardo, the second Archbishop of the Archdiocese of Galveston-Houston and the first cardinal archbishop from a diocese in the Southern United States. Dr. Sheldon Rubenfeld, Clinical Professor of Medicine at Baylor College of Medicine. He is Board Certified in Internal Medicine and in Endocrinology, Diabetes, and Metabolism, and is a Fellow in both the American College of Physicians and the American College of Endocrinology. Dr. Rubenfeld has taught "Healing by Killing: Medicine During the Third Reich" for three years and "Jewish Medical Ethics" for seven years at Baylor College of Medicine. He created a six-month program about Medicine and the Holocaust at Holocaust Museum Houston, including an exhibit entitled How Healing Becomes Killing: Eugenics, Euthanasia, Extermination and a series of lectures by distinguished speakers entitled "The Michael E. DeBakey Medical Ethics Lecture Series".

Gadoxetate uptake as a possible marker of hepatocyte damage after liver resection-preliminary data

AIM: To determine the feasibility of evaluating surgically induced hepatocyte damage using gadoxetate disodium (Gd-EOB-DTPA) as a marker for viable hepatocytes at magnetic resonance imaging (MRI) after liver resection. MATERIAL AND METHODS: Fifteen patients were prospectively enrolled in this institutional review board-approved study prior to elective liver resection after informed consent. Three Tesla MRI was performed 3-7 days after surgery. Three-dimensional (3D) T1-weighted (W) volumetric interpolated breath-hold gradient echo (VIBE) sequences covering the liver were acquired before and 20 min after Gd-EOB-DTPA administration. The signal-to-noise ratio (SNR) was used to compare the uptake of Gd-EOB-DTPA in healthy liver tissue and in liver tissue adjacent to the resection border applying paired Student's t-test. Correlations with potential influencing factors (blood loss, duration of intervention, age, pre-existing liver diseases, postoperative change of resection surface) were calculated using Pearson's correlation coefficient. RESULTS: Before Gd-EOB-DTPA administration the SNR did not differ significantly (p = 0.052) between healthy liver tissue adjacent to untouched liver borders [59.55 ± 25.46 (SD)] and the liver tissue compartment close to the resection surface (63.31 ± 27.24). During the hepatocyte-specific phase, the surgical site showed a significantly (p = 0.04) lower SNR (69.44 ± 24.23) compared to the healthy site (78.45 ± 27.71). Dynamic analyses revealed a significantly lower increase (p = 0.008) in signal intensity in the healthy tissue compared to the resection border compartment. CONCLUSION: EOB-DTPA-enhanced MRI may have the potential to be an effective non-invasive tool for detecting hepatocyte damage after liver resection.

A study of xlcaax-1: Patterns of localization, possible function and usefulness as a developmental marker

Morphogenesis is the process by which the 3-dimensional structure of the developing embryo takes shape. We are studying xlcaax-1, a gene whose product can be used as a molecular marker for several morphogenetic events. We report here the cellular and subcellular localization of the xlcaax-1 protein during development of Xenopus laevis. Whole mount immunocytochemistry and immunoperoxidase staining of tissue sections showed that during development the xlcaax-1 protein accumulation was coincident with the differentiation of the epidermis, pronephros and mesonephros. In the pronephros and mesonephros the xlcaax-1 protein was localized to the basolateral membrane of differentiated tubule epithelial cells. Thus, the xlcaax-1 protein served as a marker for tubule formation and polarization during Xenopus kidney development. Xlcaax-1 may also be used as a marker for the functional differentiation of the epidermis and the epidermally derived portions of the lens and some cranial nerves. The xlcaax-1 protein was most abundant in kidney and immunogold EM analysis showed that the xlcaax-1 protein was highly enriched in the basal infoldings of the basolateral membrane of the epithelial cells in adult kidney distal tubules. The xlcaax-1 protein was also localized in other ion transporting epithelia. The localization pattern and preliminary functional assays of xlcaax-1 suggest that the protein may function in association with an ion transport channel or pump.^ Cell migration and cell-cell interactions play important roles in numerous processes during morphogenesis. One of these is the formation of the pronephric (wolffian) duct (PD), which connects the pronephros to the cloaca. It is currently accepted that in most amphibians the pronephric duct is formed by active migration of the pronephric duct rudiment (PDR) cells along a pre-determined pathway. However, there is evidence that in Xenopus, the PD may be formed entirely by in situ segregation of cells out of the lateral mesoderm. In this study, we showed, using PDR ablation and X. laevis - X. borealis chimeras, that PD elongation in Xenopus required both active cell migration and an induced recruitment of cells from the posterior lateral plate mesoderm. We also showed that PDR cell migration was limited to only a few stages during development and that this temporal control is due, at least in part, to changes in the competence of the PD pathway to support cell migration. In addition, our data suggested that an alkaline phosphatase (APase) adhesion gradient may be involved in determining this competence. ^

Defining the regions of homology between human chromosome 16p12--13 and mouse chromosomes

In this study, the evolutionary relationship between human chromosome 16p12-p13 and mouse chromosomes was investigated by determining the order of marker loci in the region and then identifying the chromosomal locations of the homologous loci in mice. Eighteen genes from human 16 were mapped to fifteen subchromosomal regions by a variety of mapping approaches.^ Thirteen of the genes were mapped in the mouse. Linkage analysis with backcross mice and segregation analysis in a mouse - Chinese Hamster Ovary (CHO) somatic cell hybrid panel informative for different regions of mouse genome were used. The results assigned the thirteen genes to three different mouse chromosomes.^ A group of six genes on mouse 16 was found to be closely linked to Scid. The order of Myh11 and Mrp remains ambiguous since no recombination was detected in backcross analysis. Their relative position in human is also uncertain since they were shown to be very close to each other. For the other mouse loci, an unambiguous gene order could be determined and was found to be identical to that in human. Therefore, they comprise a new conserved linkage group between the two species. The orientation of the group was inverted relative to the centromeres, i.e. the proximal loci in one species become distal in another. The size of the group was estimated to be from 4.4 to 8 Mb and 10 to 32 cM in human. In mouse, it was about 21 cM in the backcross analysis. The two boundaries of the conserved linkage were defined within a 1 Mb range. It is now possible to predict the locations of mouse homologs for some human disease genes based on their locations on human 16p.^ The six human 16p genes that map to MMU7 showed a different gene order in mouse than in human. No recombination was found between Crym and Umod while Crym was distal to D16S79A and proximal to D16S92. The location of Stp and Cdr2 with respect to the above four loci was not determined since they were not mapped in the same set of backcross mice. These genes greatly expanded an existing conserved synteny group between the human 16p12-p13 region and the MMU7. It now consists of eleven loci that span a region of probably more than 10 Mb in human. The gene order derived from this study provided further evidence for chromosomal rearrangements within the conserved synteny. (Abstract shortened by UMI.) ^

Delineation of a novel genetic region at 5q11 harboring tumor suppressor gene(s) and identification of the telomeric DNA as a marker for human prostate cancer

Prostate cancer is the most commonly diagnosed cancer and the second leading cause of cancer mortality in American men. The distinction between those cases of prostate cancer destined to progress rapidly to lethal metastatic disease and those with little likelihood of causing morbidity and mortality is a major goal of current research. Some type of diagnostic method is urgently needed to identify which histological prostate cancers have completed the progression to a stage that will produce a life-threatening disease, thus requiring immediate therapeutic intervention. The objectives of this dissertation are to delineate a novel genetic region harboring tumor suppressor gene(s) and to identify a marker for prostate tumorigenesis. I first established an in vitro cell model system from a human prostate epithelial cells derived from tissue fragments surrounding a prostate tumor in a patient with prostatic adenocarcinoma. Since chromosome 5 abnormality was present in early, middle and late passages of this cell model system, I examined long-term established prostate cancer cell lines for this chromosome abnormality. The results implicated the region surrounding marker D5S2068 as the locus of interest for further experimentation and location of a tumor suppressor gene in human prostate cancer. ^ Cancer is a group of complex genetic diseases with uncontrolled cell; division and prostate cancer is no exception. I determined if telomeric DNA, and telomerase activity, alone or together, could serve as biomarkers of prostate tumorigenesis. I studied three newly established human prostate cancer cell lines and three fibroblast cell cultures derived from prostate tissues. In conclusion, my data reveal that in the presence of telomerase activity, telomeric repeats are maintained at a certain optimal length, and analysis of telomeric DNA variations might serve as early diagnostic and prognostic biomarkers for prostate cancer. (Abstract shortened by UMI.)^

CHROMOSOMAL MAPPING, LINKAGE RELATIONSHIPS, AND EVOLUTIONARY STUDIES OF THE HUMAN ANONYMOUS DNA CLONE D1S1 (IN SITU HYBRIDIZATION, PRIMATES, GENE MAPPING, AUTOSOMAL DOMINANT RETINITIS PIGMENTOSA, GENE DUPLICATION)

D1S1, an anonymous human DNA clone originally called (lamda)Ch4-H3 or (lamda)H3, was the first single copy mapped to a human chromosome (1p36) by in situ hybridization. The chromosomal assignment has been confirmed in other laboratories by repeating the in situ hybridization but not by another method. In the present study, hybridization to a panel of hamster-human somatic cell hybrids revealed copies of D1S1 on both chromosomes 1 and 3. Subcloning D1S1 showed that the D1S1 clone itself is from chromosome 3, and the sequence detected by in situ hybridization is at least two copies of part of the chromosome 3 copy. This finding demonstrates the importance of verifying gene mapping with two methods and questions the accuracy of in situ hybridization mapping.^ Non-human mammals have only one copy of D1S1, and the non-human primate D1S1 map closely resembles the human chromosome 3 copy. Thus, the human chromosome 1 copies appear to be part of a very recent duplication that occurred after the divergence between humans and the other great apes.^ A moderately informative HindIII D1S1 RFLP was mapped to chromosome 3. This marker and 12 protein markers were applied to a linkage study of autosomal dominant retinitis pigmentosa (ADRP). None of the markers proved linkage, but adding the three families examined to previously published data raises the ADRP:Rh lod score to 1.92 at (THETA) = 0.30. ^