tbuckley/cabot-search huggingface dataset:
Catch-up Growth
Authors: Bart Boersma, Jan Maarten Wit
Journal: Endocrine Reviews (1997)

I. Introduction II. Catch-up Growth: Theoretical Considerations A. Definition B. Catch-up growth vs. compensatory growth C. Canalization D. Catch-up growth vs. resumption of a normal height velocity E. Types of catch-up growth F. Assessment of duration and success of catch-up growth III. Secondary Growth Disorders and Subsequent Catch-up Growth A. The early studies B. Malnutrition C. Celiac disease D. GH deficiency E. Hypothyroidism F. Corticosteroid excess G. Intrauterine growth retardation (IUGR) IV. Mechanisms Regulating Catch-up Growth A. The neuroendocrine hypothesis B. The growth plate hypothesis V. Determinants of Normal Growth and Their Changes During Catch-up Growth A. Introduction B. The somatotrophic axis C. The epiphyseal growth plate VI. Concluding Remarks
Behavioral and Biochemical Interrelations in Alcoholism
Authors: J H Mendelson, N K Mello
Journal: Annual Review of Medicine (1976)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
DNA-AuNP networks on cell membranes as a protective barrier to inhibit viral attachment, entry and budding
Authors: Chun Mei Li, Lin Ling Zheng, Xiao Xi Yang, Xiao Yan Wan, Wen Bi Wu, Shu Jun Zhen, Yuan Fang Li, Ling Fei Luo, Cheng Zhi Huang
Journal: Biomaterials (2015)
THE MODERN VERSION OF ADULT RESPIRATORY DISTRESS SYNDROME
Authors: Robert H. Demling, M.D
Journal: Annual Review of Medicine (1995)

▪ Abstract Adult respiratory distress syndrome (ARDS) remains a highly lethal complication of autodestructive inflammation. This syndrome originally referred to a single organ failure but is now considered a component, usually the first, of the multisystem organ failure syndrome (MOFS). Cytokines, neutrophils, and endothelial adherence molecules initiate the disease process, with cell injury caused by oxidants and proteases released from inflammatory cells. ARDS, if progressive, will result in pulmonary fibrosis. Improved ventilatory support techniques have not been shown to decrease mortality. Pharmacologic manipulation of the inflammatory response is a more promising method of controlling the disease process.
The functional role of Notch signaling in human gliomas
Authors: M.-T. Stockhausen, K. Kristoffersen, H. S. Poulsen
Journal: Neuro-Oncology (2009)

Gliomas are among the most devastating adult tumors for which there is currently no cure. The tumors are derived from brain glial tissue and comprise several diverse tumor forms and grades. Recent reports highlight the importance of cancer-initiating cells in the malignancy of gliomas. These cells have been referred to as brain cancer stem cells (bCSC), as they share similarities to normal neural stem cells in the brain. The Notch signaling pathway is involved in cell fate decisions throughout normal development and in stem cell proliferation and maintenance. The role of Notch in cancer is now firmly established, and recent data implicate a role for Notch signaling also in gliomas and bCSC. In this review, we explore the role of the Notch signaling pathway in gliomas with emphasis on its role in normal brain development and its interplay with pathways and processes that are characteristic of malignant gliomas.
Evidence-based policy and practice: riding for a fall?
Authors: D. J Hunter
Journal: Journal of the Royal Society of Medicine (2003)

Hard on the heels of evidence-based medicine (EBM) comes evidence-based policy and practice (EBPP). At all levels in healthcare systems there is a hunger for better knowledge to inform policy and practice. Is this yet another of the fashions and fads that continually beset the National Health Service, or does EBPP mark a development that could fundamentally change the way in which health policy is made and implemented?
The effects of splenectomy on engraftment and platelet transfusion requirements in patients with chronic myelogenous leukemia undergoing marrow transplantation
Authors: Meera Banaji, Scott I. Bearman, C. Dean Buckner, Reginald A. Clift, William I. Bensinger, Finn B. Petersen, Sherrill J. Slichter, Robert W. McGuffin, Jean E. Sanders, Patricia S. Stewart, Roger S. Hill, H. Joachim Deeg, Rainer Storb, E. Donnall Thomas
Journal: American Journal of Hematology (1986)

Abstract Granulocyte and platelet recovery as well as platelet transfusion requirements following allogeneic marrow transplantation were analyzed in 67 patients with chronic myelogenous leukemia in the chronic phase. Twenty patients had splenectomy prior to transplantation. Forty‐seven patients were transplanted without splenectomy, 21 of whom had splenic enlargement by physical examination. There were no differences in the proportion of patients with granulocyte recovery, but the recovery of peripheral granulocytes to levels of 200, 500 and 1,000/mm 3 occurred more rapidly in the splenectomy group than in the no‐splenectomy group. Patients with splenectomy received platelet transfusions for a mean of 10 (2–36) days as compared to 20 (3–82) days for patients without splenectomy (p &lt; .001). Eighteen (90%) patients with splenectomy became platelet transfusion independent at a median of 16 (2–32) days after transplantation as compared to 40 (85%) patients without splenectomy who became transfusion independent at a median of 28 (15–86) days (p &lt; .001). The proportion of patients achieving platelet levels of 50 and 100 × 10 3 /mm 3 did not differ between the two groups (p = .07), but patients in the splenectomy group achieved these levels more rapidly following transplant (p &lt; .001). One of 17 evaluable patients in the splenectomy group and 31 of 46 in the no‐splenectomy group became refractory to random platelets (p &lt; .001) and required platelets from family members or unrelated completely or partially HLA matched donors. In the no‐splenectomy group, splenic size did not affect the speed of granulocyte or platelet recovery or platelet transfusion requirements. There was no difference in the post‐transplant survival of patients with or without splenectomy.
Prognostic and Predictive Biomarkers for Act (Adjuvant Chemotherapy) in Resected Non-Small Cell Lung Cancer (R-Nsclc): Lace-Bio
Authors: L.K. Seymour, G. Le Teuff, M. Tsao, E. Brambilla, F. Shepherd, J. Soria, R. Kratzke, S. Graziano, J. Douillard, R. Rosell, A. Reiman, B. Lacas, A. Bourredjem, T. Le Chevalier, R. Pirker, M. Filipits, P. Hainaut, P.A. Janne, J. Pignon
Journal: Annals of Oncology (2014)
A CD90+ Tumor-Initiating Cell Population with an Aggressive Signature and Metastatic Capacity in Esophageal Cancer
Authors: Kwan Ho Tang, Yong Dong Dai, Man Tong, Yuen Piu Chan, Pak Shing Kwan, Li Fu, Yan Ru Qin, Sai Wah Tsao, Hong Lok Lung, Maria L. Lung, Daniel K. Tong, Simon Law, Kwok Wah Chan, Stephanie Ma, Xin Yuan Guan
Journal: Cancer Research (2013)

Abstract Tumor-initiating cells (TIC), also known as cancer stem cells, are regarded widely as a specific subpopulation of cells needed for cancer initiation and progression. TICs have yet to be identified in esophageal tumors that have an increasing incidence in developed countries. Here, we report a CD90+ cell population found in esophageal squamous cell carcinoma (ESCC), which is endowed with stem cell–like properties and high tumorigenic and metastatic potential. mRNA profiling of these cells suggested pathways through which they drive tumor growth and metastasis, with deregulation of an Ets-1/MMP signaling pathway and epithelial–mesenchymal transition figuring prominently. These cells possessed higher self-renewal activity and were sufficient for tumor growth, differentiation, metastasis, and chemotherapeutic resistance. CD90+ TICs were isolated and characterized from ESCC clinical specimens as well as ESCC cell lines. In freshly resected clinical specimens, they represented a rare cell population, the levels of which correlated with strong family histories and lymph node metastasis. Our results prompt further study of this CD90+ population of esophageal TICs as potential therapeutic targets. Cancer Res; 73(7); 2322–32. ©2013 AACR.
Tissue kallikrein protects against pressure overload-induced cardiac hypertrophy through kinin B2 receptor and glycogen synthase kinase-3β activation☆
Authors: H LI, H YIN, Y YAO, B SHEN, M BADER, L CHAO, J CHAO
Journal: Cardiovascular Research (2006)

We assessed the role of glycogen synthase kinase-3beta (GSK-3beta) and kinin B2 receptor in mediating tissue kallikrein's protective effects against cardiac hypertrophy.We investigated the effect and mechanisms of tissue kallikrein using hypertrophic animal models of rats as well as mice deficient in kinin B1 or B2 receptor after aortic constriction (AC).Intramyocardial delivery of adenovirus containing the human tissue kallikrein gene resulted in expression of recombinant kallikrein in rat myocardium. Kallikrein gene delivery improved cardiac function and reduced heart weight/body weight ratio and cardiomyocyte size without affecting mean arterial pressure 28 days after AC. Icatibant and adenovirus carrying a catalytically inactive GSK-3beta mutant (Ad.GSK-3beta-KM) abolished kallikrein's effects. Kallikrein treatment increased cardiac nitric oxide (NO) levels and reduced NAD(P)H oxidase activity and superoxide production. Furthermore, kallikrein reduced the phosphorylation of apoptosis signal-regulating kinase1, mitogen-activated protein kinases (MAPKs), Akt, GSK-3beta, and cAMP-response element binding (CREB) protein, and decreased nuclear factor-kappaB (NF-kappaB) activation in the myocardium. Ad.GSK-3beta-KM abrogated kallikrein's actions on GSK-3beta and CREB phosphorylation and NF-kappaB activation, whereas icatibant blocked all kallikrein's effects. The protective role of kinin B2 receptor in cardiac hypertrophy was further confirmed in kinin receptor knockout mice as heart weight/body weight ratio and cardiomyocyte size increased significantly in kinin B2 receptor knockout mice after AC compared to wild type and B1 receptor knockout mice.These findings indicate that tissue kallikrein, through kinin B2 receptor and GSK-3beta signaling, protects against pressure overload-induced cardiomyocyte hypertrophy by increased NO formation and oxidative stress-induced Akt-GSK-3beta-mediated signaling events, MAPK and NF-kappaB activation.
A Technical Triade for Proteomic Identification and Characterization of Cancer Biomarkers
Authors: Christian Melle, Günther Ernst, Bettina Schimmel, Annett Bleul, Sven Koscielny, Andreas Wiesner, Ralf Bogumil, Ursula Möller, Dirk Osterloh, Karl-Jürgen Halbhuber, Ferdinand von Eggeling
Journal: Cancer Research (2004)

Abstract Biomarkers are needed to elucidate the biological background and to improve the detection of cancer. Therefore, we have analyzed laser-microdissected cryostat sections from head and neck tumors and adjacent mucosa on ProteinChip arrays. Two differentially expressed proteins (P = 3.34 × 10−5 and 4.6 × 10−5) were isolated by two-dimensional gel electrophoresis and identified as S100A8 (calgranulin A) and S100A9 (calgranulin B) by in-gel proteolytic digestion, peptide mapping, tandem mass spectrometry analysis, and immunodepletion assay. The relevance of these single marker proteins was evaluated by immunohistochemistry. Positive tissue areas were reanalyzed on ProteinChip arrays to confirm the identity of these proteins. As a control, a peak with low P was identified as calgizzarin (S100A11) and characterized in the same way. This technical triade of tissue microdissection, ProteinChip technology, and immunohistochemistry opens up the possibility to find, identify, and characterize tumor relevant biomarkers, which will allow the movement toward the clonal heterogeneity of malignant tumors. Taking this approach, proteins were identified that might be responsible for invasion and metastasis.
Birth Size and the Pathogenesis of Breast Cancer
Authors: Pagona Lagiou, Dimitrios Trichopoulos
Journal: PLoS Medicine (2008)

In a major undertaking reported in this issue of PLoS Medicine, a collaborative group co-ordinated by Isobel dos Santos Silva provide all but conclusive evidence that birth size is a predictor of breast cancer risk in adult life [1]. The researchers compiled and reanalysed individual participant data from 32 studies, comprising 22,058 cases of breast cancer. On the basis of reliable data retrieved from birth records, they found that an increase of birth weight by 500 grams was associated with a statistically significant 6% increase in breast cancer risk; whereas, controlling for birth weight, an increase of birth length by two centimetres was associated with a 9% increase in this risk. The relative size of the effects is small, but the individual studies driving the conclusion were of sound epidemiological design (cohort or nested case-control) and relied on objectively documented birth size parameters, allowing little room for selection or information bias. Now that the question of whether birth size is associated with breast cancer risk appears to be settled, a number of additional questions need to be addressed.
Efficacy and Safety of Prolonged-Release Lanreotide in Patients With Gastrointestinal Neuroendocrine Tumors and Hormone-Related Symptoms
Authors: A.N.M. Wymenga, B. Eriksson, P.I. Salmela, M.B. Jacobsen, E.J.D.G. Van Cutsem, R.H. Fiasse, M.J. Välimäki, J. Renstrup, E.G.E. de Vries, K.E. Öberg
Journal: Journal of Clinical Oncology (1999)

PURPOSE: To evaluate the prolonged release (PR) of the long-acting somatostatin analog lanreotide in patients with gastrointestinal neuroendocrine tumors and its effect on hormone-related symptomatology, tumor markers, tumor size, tolerability, and quality of life (QOL). PATIENTS AND METHODS: Eligible patients had the following substantial daily symptoms: for patients with carcinoid tumors, three or more stools and/or 1.5 or more flushing episodes; for patients with gastrinoma, greater than 50% elevated basic acid output; and for patients with vasoactive intestinal peptide-secreting tumors (VIPomas), four or more stools and/or a stool volume of ≥ 800 mL, a measurable tumor, and an elevated biochemical tumor marker (≥ two times the upper limit of the normal reference range). Lanreotide PR was administered intramuscularly every 14 days at 30 mg for 6 months. We measured efficacy by studying symptoms, tumor markers, tumor size, and QOL. Side effects were scored according to the National Cancer Institute's toxicity grading system and ultrasound examination of the gallbladder. RESULTS: Fifty-five patients were included in the study (48 patients with carcinoid tumors, six patients with gastrinoma, and one patient with VIPoma). Symptomatic improvement (&gt; 50% reduction) occurred in 38% of the assessable patients with carcinoid tumors, in 67% of the gastrinoma patients, and in the VIPoma patient. Tumor markers normalized in two of 45 assessable patients, 19 patients exhibited a reduction (&gt; 50%), 19 patients exhibited no change, and tumor markers rose by more than 50% in five patients. Tumor size was reduced in two of 31 assessable patients and remained stable in 25 patients; four patients experienced progression. QOL assessments after 1 month showed improvements in emotional and cognitive function, and diminished fatigue, sleeping disorders, and diarrhea. Eight of 30 assessable patients developed gallstones. CONCLUSION: Lanreotide PR is a well-tolerated somatostatin analog with significant clinical, biochemical, and antitumor effects that bring about a significant improvement in QOL for patients with neuroendocrine tumors.
Impact of Ulceration in Stages I to III Cutaneous Melanoma As Staged by the American Joint Committee on Cancer Staging System: An Analysis of the German Central Malignant Melanoma Registry
Authors: Thomas K. Eigentler, Petra G. Buettner, Ulrike Leiter, Claus Garbe
Journal: Journal of Clinical Oncology (2004)

Purpose In 2001, the new American Joint Committee on Cancer classification of cutaneous melanoma (CM) introduced ulceration of the primary melanoma as a new key parameter being represented in respective subcategories of the tumor (T) classification. The present study was performed to validate the prognostic significance of ulceration in relation to T thickness and clinical stages of CM (stages I to III). Patients and Methods Patients (N = 15,158) with incident invasive primary nonmetastatic CM and follow-up data recorded between 1976 and 2000 by the German Central Malignant Melanoma Registry were investigated using survival analysis to evaluate prognostic factors such as T thickness, level of invasion, body site, histologic subtype, ulceration, regression, age, and sex. Results Comparisons of survival probabilities according to the Kaplan-Meier method between ulcerated and nonulcerated CM were not statistically significant for subgroups with T thickness ≤ 1 mm and more than 4.00 mm (P = .2601 and P = .0699, respectively) but were significant for T thickness of 1.01 to 2.00 mm and 2.01 to 4.00 mm (P &lt; .0001 for both). This result was confirmed in the multivariate analysis. For stage III CM, the impact of ulceration on overall survival was statistically significant in the bivariate Cox model (P = .0111) but not in the multivariate Cox model (P = .0522). Conclusion Whereas ulceration seems to have a negative impact on the prognosis of patients with stages T2 and T3, a potential influence for patients with stages T1 and T4 could not be established. If factors of the primary CM were to be taken into consideration to judge prognosis of stage III CM, T thickness but not ulceration should be the focus.
Urinary calcium excretion in familial hypocalciuric hypercalcemia. Persistence of relative hypocalciuria after induction of hypoparathyroidism
Authors: M. F. Attie, J. R. Gill, J. L. Stock, A. M. Spiegel, R. W. Downs, M. A. Levine, S. J. Marx
Journal: Journal of Clinical Investigation (1983)

Familial hypocalciuric hypercalcemia (FHH) is an autosomal dominant trait comprising hypercalcemia, hypophosphatemia, parathyroid hyperplasia, and unusually low renal clearance of calcium. We evaluated the role of parathyroid hormone in the relative hypocalciuria of FHH and characterized the renal transport of calcium in this disorder using three previously hypercalcemic FHH patients with surgical hypoparathyroidism and three controls with surgical hypoparathyroidism. Intravenous infusion of calcium chloride in two patients with FHH and in three controls increased serum calcium from a mean basal of 5.0 to a mean peak of 6.8 meq/liter in two FHH patients and from 4.2 to 5.7 in three control subjects. Urinary calcium in a third FHH patient was studied without calcium infusion during recovery from hypercalcemia of vitamin D intoxication. At all serum concentrations of calcium, calcium clearance was lower in FHH than in controls; at base-line serum calcium, the ratio of calcium clearance to inulin clearance (CCa/CIN) in FHH subjects was 32% of that in controls and decreased to 19% during hypercalcemia. Calcium infusion increased the ratio of sodium clearance to inulin clearance in controls from a base line of 0.020 to 0.053 at peak concentrations of calcium in serum, but did not affect this parameter in FHH (0.017 at base-line serum calcium vs. 0.019 at peak).
Parental Schizophrenia Spectrum Disorders in Childhood-Onset and Adult-Onset Schizophrenia
Authors: Rob Nicolson, Frances B. Brookner, Marge Lenane, Peter Gochman, Loring J. Ingraham, Michael F. Egan, Kenneth S. Kendler, David Pickar, Daniel R. Weinberger, Judith L. Rapoport
Journal: American Journal of Psychiatry (2003)

Childhood onset of "adult" psychiatric disorders may be caused, in part, by more salient genetic risk. In this study, the rates of schizophrenia spectrum disorders among parents of patients with childhood-onset and adult-onset schizophrenia and parents of community comparison subjects were compared.To assess the presence of axis I and axis II disorders associated with schizophrenia, parents of patients with childhood-onset schizophrenia (95 parents), patients with adult-onset schizophrenia (86 parents), and community comparison subjects (123 parents) were interviewed directly by using semistructured instruments. Information on 19 additional parents (parents of childhood-onset patients, N=2; parents of adult-onset patients, N=11; parents of community comparison subjects, N=6) was obtained by using a family history interview with the same instruments. Transcribed interviews were scored by a rater blind to group membership, and the morbid risks for schizophrenia spectrum disorders in the three groups were compared.Parents of patients with childhood-onset schizophrenia had a significantly higher morbid risk of schizophrenia spectrum disorders (24.74%) than parents of patients with adult-onset schizophrenia (11.35%), and parents of both patient groups had a greater risk of schizophrenia spectrum disorders than did parents of comparison subjects (1.55%).Parents of patients with childhood-onset schizophrenia have a higher rate of schizophrenia spectrum disorders than parents of patients with adult-onset illness. This is consistent with the hypothesis that a childhood onset of schizophrenia is due, at least in part, to a greater familial diathesis for the disorder.
Historical, present, and future significance of corticosteroid in the treatment of acute liver failure
Authors: Keiichi Fujiwara, Shin Yasui, Osamu Yokosuka
Journal: Hepatology (2014)

We read with interest the article by Karkhanis et al.,1 who reported no survival benefit of corticosteroid (CS) for patients with acute liver failure (ALF) of autoimmune, drug-induced, or indeterminate etiology and applaud their efforts for treating this intractable syndrome. In the 1970s, randomized, clinical trials indicated a significant negative effect of CS treatment in ALF, and CS use in ALF has been almost abandoned in the United States and European countries. However, the treatment decision against CS in ALF is difficult in Japan, where the serious problem of a shortage of donor livers exists. CS has been introduced in 70.6% of ALF between 1998 and 2010 according to a Japanese nationwide survey for the purpose of suppressing inflammatory cytokines. Our recent study demonstrated that the introduction of high-dose CS in "the early stage" of viral ALF was effective in suppressing the destruction of hepatocytes (P < 0.05) without significant differences in rates of survival (P = 0.36) and liver regeneration (P = 0.13), although the sample size was small and multicenter studies are also needed in the future.2 The data should be analyzed based on each etiology and the timing of starting CS for precise evaluation of the efficacy of CS in ALF, although the timing of CS administration was decided by the site principal investigator and the specific criteria were not available in this article. We have realized that the timing for starting CS in ALF is limited to the early stage of illness when aminotransferase is high, total bilirubin is low, and international normalized ratio begins to be prolonged, even in autoimmune ALF. No therapy, except liver transplantation, is effective in the late stage of impaired liver regeneration, regardless of etiology.3, 4 Regarding infectious complications, Czaja reported that the assessment of CS can be made over a 2-week interval after introduction, which is sufficiently short to avoid infectious complications.5 As Lee, one of authors of this article, described, the most important problem worldwide is that few hepatologists or intensivists have in-depth experience with ALF patients.6 Keiichi Fujiwara, M.D., Ph.D. Shin Yasui, M.D., Ph.D. Osamu Yokosuka, M.D., Ph.D. Department of Gastroenterology and Nephrology Graduate School of Medicine Chiba University Chiba, Japan