tbuckley/cabot-search huggingface dataset:
Distinguishing primary and metastatic carcinomas of the liver: Immunohistochemical updates and reminders
Authors: Neil O. Theise
Journal: Hepatology (1994)

Distinguishing primary hepatocellular carcinoma (HCC) from metastatic carcinomas to the liver is often difficult, if not impossible, particularly in needle biopsy and fine-needle aspiration specimens. In an attempt to identify a specific immunohistochemical profile that would distinguish HCC from metastatic carcinomas, we studied 56 HCCs, 8 cholangio-carcinomas, and 24 metastatic adenocarcinomas with monoclonal antibodies to alpha-fetoprotein (AFP), keratin (AE1, AE3, and CAM5.2), Leu-M1, human milk fat globule (HMFG-2), tumor-associated glycoprotein-72 (B72.3), epithelial specific membrane antigen (Ber-EP4), and BCA-225 (CU-18). Both monoclonal and polyclonal (mCEA and pCEA) antibodies to carcinoembryonic antigen also were used. Metastatic adenocarcinomas were often positive for CU-18 (71%), Leu-M1 (75%), B72.3 (50%), HMFG-2 (67%), Ber-EP4 (83%) and mCEA (71%). Using these antibodies, the frequency of positivity for HCC was 9%, 16%, 11%, 20%, 36%, and 11%, respectively. CU-18 was the only monoclonal antibody in which there was a significant difference in positive rates between HCC and metastatic adenocarcinomas. Most HCCs (71%) revealed a bile canalicular staining pattern with pCEA. Because this staining pattern was absent in metastatic carcinomas, pCEA appears to be useful in confirming a diagnosis of HCC, AE1, AE3 and CAM5.2 antibodies were not useful in distinguishing HCC from metastatic carcinomas. Each cholangiocarcinoma shared a staining profile similar to that of metastatic carcinomas. Hepatocyte paraffin 1 is a monoclonal antibody that has been developed specifically to react with hepatocytes in routine formalin-fixed and paraffin-embedded surgical pathology tissues. It results in a distinct, granular cytoplasmic staining of hepatocytes but fails to react with bile ducts and nonparenchymal liver cells. The antibody decorates a majority of hepatocellular carcinomas, including fibrolamellar variants. It fails to react with a wide variety of other adult malignancies, with the exception of focal staining in a few gastrointestinal malignancies, including a sub-population of gastric carcinomas.
Management of patients with systemic mastocytosis: Review of M. D. Anderson Cancer Center experience
Authors: Bryan Hennessy, Francis Giles, Jorge Cortes, Susan O'Brien, Alessandra Ferrajoli, Gladys Ossa, Guillermo Garcia‐Manero, Stefan Faderl, Hagop Kantarjian, Srdan Verstovsek
Journal: American Journal of Hematology (2004)

Abstract Mastocytosis is characterized by mast cell proliferation that may be limited to the skin (cutaneous mastocytosis) or may involve one or more extracutaneous organs, e.g., the bone marrow (systemic mastocytosis; SM). This study objective is to evaluate the features and outcome of patients referred to M. D. Anderson Cancer Center (MDACC) with SM. A search of the MDACC database from 1944 to 2002 was conducted for patients with SM and review of their clinical charts. Eighteen patients with mastocytosis were identified in the MDACC database; 15 (11 males and 4 females) had SM and available information. Two had associated myelodysplastic syndrome (MDS), and one had acute myeloid leukemia (AML). The median age was 58 years (range 31–80). Nine patients were treated with subcutaneous interferon‐alpha, and only 1 experienced temporary control of the disease. Three of these patients were then treated with imatinib mesylate: transient improvement was noted in two patients. One patient underwent stem cell transplantation as first therapy and achieved complete remission; this patient had associated MDS and is now in complete remission for 8 years. The patient with associated AML was treated with high‐dose cytarabine and idarubicin; he has been in complete remission for 16 months. One patient was treated with induction chemotherapy consisting of high‐dose cytarabine and 2CDA but expired due to sepsis. Three patients received symptomatic therapy only; these were the only 3 patients who presented with normal blood counts. SM is rare and has no effective standard of care. Collaboration among academic centers to accrue enough patients to evaluate novel therapeutic strategies is needed. Am. J. Hematol. 77:209–214, 2004. © 2004 Wiley‐Liss, Inc.
Spermatotoxicity associated with acute and subchronic ethoxyethanol treatment.
Authors: H Zenick, D Oudiz, R J Niewenhuis
Journal: Environmental Health Perspectives (1984)

Investigations of the male reproductive toxicity of ethoxyethanol (ethylene glycol monoethyl ether) have been restricted exclusively to histopathological assessments of the testes. The present study consisted of two experiments designed to document the spermatotoxicity of ethoxyethanol (EE) as reflected in evaluations of ejaculated rat semen. The basic strategy involved the evaluation of individual ejaculates recovered from the genital tract of a female rat prior to exposure of the males to EE. Repeated assessments of the ejaculate were made during the experimental phase according to specified protocols. Adult Long-Evans hooded male rats received 0, 936, 1872 or 2808 mg/kg (PO) of EE for five consecutive days. Semen evaluations were then conducted at weeks 0, 1, 4, 7, 10 and 14 after exposure. Males in the highest two dose groups showed declines in sperm counts by week 4 and were essentially azoospermic by week 7. At this time, males receiving the lowest dose of EE also exhibited decreases in ejaculated sperm counts. An increase in abnormal sperm shapes was also observed. Over the ensuing weeks all males exhibited varying degrees of recovery as reflected by increasing ejaculated sperm counts. In a second experiment, males were treated with 0 or 936 mg/kg of EE daily (5 days/week) for 6 weeks with semen evaluations conducted weekly. By week 5, sperm counts were significantly depressed and there was an increase in the number of abnormal shapes. Sperm motility was depressed by week 6. The temporal trends seen in these experiments suggested a differential sensitivity of the spermatocyte stage to EE toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
Nonstationary Influence of El Niño on the Synchronous Dengue Epidemics in Thailand
Authors: Bernard Cazelles, Mario Chavez, Anthony J McMichael, Simon Hales
Journal: PLoS Medicine (2005)

Background Several factors, including environmental and climatic factors, influence the transmission of vector-borne diseases. Nevertheless, the identification and relative importance of climatic factors for vector-borne diseases remain controversial. Dengue is the world's most important viral vector-borne disease, and the controversy about climatic effects also applies in this case. Here we address the role of climate variability in shaping the interannual pattern of dengue epidemics. Methods and Findings We have analysed monthly data for Thailand from 1983 to 1997 using wavelet approaches that can describe nonstationary phenomena and that also allow the quantification of nonstationary associations between time series. We report a strong association between monthly dengue incidence in Thailand and the dynamics of El Niño for the 2–3-y periodic mode. This association is nonstationary, seen only from 1986 to 1992, and appears to have a major influence on the synchrony of dengue epidemics in Thailand. Conclusion The underlying mechanism for the synchronisation of dengue epidemics may resemble that of a pacemaker, in which intrinsic disease dynamics interact with climate variations driven by El Niño to propagate travelling waves of infection. When association with El Niño is strong in the 2–3-y periodic mode, one observes high synchrony of dengue epidemics over Thailand. When this association is absent, the seasonal dynamics become dominant and the synchrony initiated in Bangkok collapses.
Integrated follow-up is needed
Authors: J. Wass, A. Toogood, G. Brabant, S. Ball, R. Ross
Journal: BMJ (2010)

Jenney and Levitt state that currently 1 in 800 adults is a survivor of cancer and that the late sequelae of treatment is a major issue, highlighting cardiac consequences.1 Other consequences such as effects on the endocrine system are far more common. Indeed, 42% …
'Imported' leprosy in US
Authors: M. F. Goldsmith
Journal: JAMA (1984)

Increasing immigration from developing nations has caused an unprecedented rise in the number of cases of leprosy, or Hansen's disease, in the United States, according to Samuel L. Moschella, MD, senior consultant at the Lahey Clinic, Burlington, Mass. Speaking at the recent American Academy of Dermatology meeting in Chicago, Moschella said 350 new cases were registered in 1982 at the National Hansen's Disease Center in Carville, La. However, he added, extrapolating from this figure to cases not yet diagnosed and, therefore, as yet unreported, indicates that some 750 to 1,000 people may now be arriving from the Third World each year with incipient or active leprosy. While such countries as Mexico and the Philippines have been the point of origin of many "imported" cases of leprosy in the past, most such cases now seen or newly diagnosed have originated in Cuba, Haiti, El Salvador, Nicaragua, and the Southeast Asian countries
Not losing the child
Authors: I. Robertson
Journal: BMJ (1995)

<b>Objective:</b> To evaluate the effectiveness of a preseason physical training programme that taught landing and falling skills in improving landing skills technique and preventing injury in junior elite Australian football players. <b>Methods:</b> 723 male players who participated in an under 18 elite competition were studied prospectively in a non-randomised controlled trial over two consecutive football seasons. There were 114 players in the intervention group and 609 control players. The eight session intervention programme taught players six landing, falling, and recovery skills, which were considered fundamental for safe landing in Australian football. Landing skills taught in these sessions were rated for competence by independent and blinded assessors at baseline and mid-season. <b>Results:</b> Evaluation of landing skills found no significant differences between the groups at baseline. Evaluation after the intervention revealed overall improvement in landing skills, but significantly greater improvement in the intervention group (z = −7.92, p = 0.001). Players in the intervention group were significantly less likely (relative rate 0.72, 95% confidence interval 0.52 to 0.98) to sustain an injury during the season than the control group. In particular, the time to sustaining a landing injury was significantly less for the intervention group (relative rate 0.40, 95% confidence interval 0.17 to 0.92) compared with the control group. <b>Conclusions:</b> Landing and falling ability can be taught to junior elite Australian football players. Players in the intervention group were protected against injury, particularly injuries related to landing and falls.
Metrizamide Cisternography-Reply
Authors: D. P. Wesolowski
Journal: JAMA (1982)

ABSTRACT In Reply.— I appreciate and fully concur with the comments by Dr Heimburger. In paragraph 3 of my previous letter, I listed some of the drawbacks of the lumbar approach for metrizamide cisternography and their influence on the dose-related complications of metrizamide. These are the very reasons for using the lateral C1-2 approach, which allows for the smallest total dose to be used.I heartily join Dr Heimburger in his admonition to all those who use metrizamide to be constantly aware of its potential complications and would add that this awareness must accompany the use of any contrast agent used in invasive neuroradiological procedures, since none is totally innocuous.
A randomized trial of somatostatin (S) versus vasopresin plus nitroglycerin (V/N) in the treatment of acute variceal bleeding (AVB)
Authors: F. Rguez-Moreno, F. Santolaria, E. Glez-Reimers, J.L. Gómez, N. Banista, A. Conde, A. Martínez, E. Rodríguez
Journal: Journal of Hepatology (1991)
Insulin Resistance in Skeletal Muscles in Patients With NIDDM
Authors: Henning Beck-Nielsen, Allan Vaag, Peter Damsbo, Aase Handberg, Ole Hother Nielsen, Jan Erik Henriksen, Peter Thye-Rønn
Journal: Diabetes Care (1992)

Skeletal muscles in patients with non-insulin-dependent diabetes mellitus (NIDDM) are resistant to insulin; i.e., the effect of insulin on glucose disposal is reduced compared with the effect in control subjects. This defect has been found to be localized to the nonoxidative pathway of glucose disposal; hence, the deposition of glucose, as glycogen, is abnormally low. This defect may be inherited, because it is present in first-degree relatives to NIDDM patients two to three decades before they develop frank diabetes mellitus. The cellular defects responsible for the abnormal insulin action in NIDDM patients is reviewed in this article. The paper focuses mainly on convalent insulin signaling. Insulin is postulated to stimulate glucose storage by initiating a cascade of phosphorylation and dephosphorylation events, which results in dephosphorylation and hence activation of the enzyme glycogen synthase. Glycogen synthase is the key enzyme in regulation of glycogen synthesis in the skeletal muscles of humans. This enzyme is sensitive to insulin, but in NIDDM patients it has been shown to be completely resistant to insulin stimulation when measured at euglycemia. The enzyme seems to be locked in the glucose-6-phosphate (G-6-P)-dependent inactive D-form. This hypothesis is favored by the finding of reduced activity of the glycogen synthase phosphatase and increased activity of the respective kinase CAMP-dependent protein kinase. A reduced glycogen synthase activity has also been found in normoglycemic first-degree relatives of NIDDM patients, indicating that this abnormality precedes development of hyperglycemia in subjects prone to develop NIDDM. Therefore, this defect may be of primary genetic origin. However, it does not appear to be a defect in the enzyme itself, but rather a defect in the covalent activation of the enzyme system. Glycogen synthase is resistant to insulin but may be activated allosterically by G-6-P. This means that the defect in insulin activation can be compensated for by increased intracellular concentrations of G-6-P. In fact, we found that both hyperinsulinemia and hyperglycemia are able to increase the G-6-P level in skeletal muscles. Thus, insulin resistance in the nonoxidative pathway of glucose processing can be overcomed (compensated) by hyperinsulinemia and hyperglycemia. In conclusion, we hypothesize that insulin resistance in skeletal muscles may be a primary genetic defect preceding the diabetic state. The cellular abnormality responsible for that may be a reduced covalent insulin activation of the enzyme glycogen synthase. The compensation results in nearnormalization of glycogen synthesis, but the price diabetic subjects must pay to obtain this is hyperglycemia.
Liver Metastases Detected by Tc-99m Sestamibi During Routine Cardiac Imaging
Authors: SAHAR AL-SEBAIE, CHRIS RUSH
Journal: Clinical Nuclear Medicine (1995)

Liver metastases from an islet cell tumor of the pancreas were incidentally detected in a 75-year-old man who underwent Tc-99m sestamibi imaging for suspected ischemic heart disease, images of the thorax and upper abdomen showed no significant cardiac perfusion abnormality, but multiple foci of increased uptake were demonstrated in the right upper quadrant. Further investigations demonstrated the islet cell tumor with liver metastases.
Low Renin Hypertension and the Adrenal Cortex
Authors: Daniel Deykin, Christine Balko, Richard F. Spark
Journal: New England Journal of Medicine (1972)

THE concept that the adrenal cortex might be involved in the development of hypertension has been speculated upon by endocrinologists for approximately 60 years. In the early 1900's, Achard and Thiers1 described a patient with hypertension and marked hirsutism who at autopsy was found to have bilaterally enlarged adrenal glands. They implied that the hypertension and the hirsutism were due to some abnormality within the adrenal glands. This concept lay dormant for about 20 years, until Cushing2 reported the syndrome that is now named after him. Hypertension was a prominent part of this syndrome, and the implication was that the . . .
A METHOD OF PERFORMING GASTRO-JEJUNOSTOMY
Authors: K. Black
Journal: BMJ (1913)

I SHALL endeavour to explain a method, slightly different from the ordinary one, of performing the operation of gastro-jejunostomy-a method adopted in 26 consecutive operations for the following lesions: Operations.Gastric ulcer, with or without adhesions 11 Pyloric stenosis and gastric dilatation the result of simple ulceration ... ... ... ... 6 Gastric dilatation associated with enteroptosis 1 Severe haematemesis from simple ulceration ... 1 Duodenal ulcer ... ... ... ... 1 Carcinoma of the stomach ... ... ... 1 Carcinoma of pylorus ...... ... ... 5 26Of these operations two only had fatal results.In one case (of very advanced carcinoma of the pylorus) the patient died from exhaustion, two days after the operation; and in the other (of duodenal ulcer) the patient, who had previously undergone an operation for some pelvic disease, died, three weeks after an apparently successful gastro- jejunostomy operation, from the effects of an abdominal
S74 Effect of pulmonary rehabilitation on the Short Physical Performance Battery (SPPB) in COPD
Authors: M. S. Patel, A. L. Clark, K. A. Ingram, R. P. Fowler, A. V. Donaldson, S. S. Kon, M. I. Polkey, W. D. Man
Journal: Thorax (2010)

<h3>Introduction</h3> The Short Physical Performance Battery (SPPB) is a simple objective assessment tool developed by the National Institute on Ageing for evaluating lower extremity function in older persons. It comprises tests of standing balance, normal gait speed and timed sit-to-stand with a maximum score of 12, and predicts nursing home admission rates and mortality. Lower extremity dysfunction is well recognised in COPD, and hence the SPPB may be a useful functional outcome measure in COPD patients. Pulmonary rehabilitation (PR) is a highly effective intervention in COPD and ameliorates lower limb dysfunction. We hypothesised that the SPPB would improve after PR. <h3>Methods</h3> 35 COPD (18M:17F) patients underwent an 8 week outpatient pulmonary rehabilitation programme. The SPPB, incremental shuttle walk (ISW) and St George9s Respiratory Questionnaire (SGRQ) were measured immediately before and after a PR programme. Paired <i>t</i>-test (or non-parametric equivalent) was used to test the effect of PR. <h3>Results</h3> Baseline characteristics are expressed as mean (SD) or median (25th, 75th percentiles): age 69 (8), FEV1% 43 (23), MRC Dyspnoea 4 (3, 4), ISW 130 (60, 270), and SGRQ 57 (16). Following PR, there was a significant improvement in ISW (mean 70 m; p&lt;0.001) and SGRQ (−7.0; p&lt;0.005). SPPB also significantly improved from a median of 9 (6, 11) pre-PR to a median of 11 (7, 12; p&lt;0.004) post-PR. Change in SPPB did not correlate with change in ISW (r=0.22; p=0.20). <h3>Conclusions</h3> The SPPB may be a useful functional outcome measure in COPD, and gives different information from the ISW. Larger studies are required to determine the minimum clinically significant change in the SPPB.
Radioimmunoassay study of hepatic clearance and disappearance half-time of somatostatin and vasoactive intestinal peptide in dogs.
Authors: J A Chayvialle, P L Rayford, J C Thompson
Journal: Gut (1981)

The effects of hepatic transit on concentrations of synthetic cyclic (ovine) somatostatin and of highly purified (porcine) vasoactive intestinal peptide were studied in five conscious dogs prepared with indwelling portal catheters. The peptides were infused via peripheral vein catheters or the portal catheters for 40 minutes at actual integrated doses of 2.8 pmol/kg/min for vasoactive intestinal peptide an 8.2 pmol/kg/min for somatostatin. Specific radioimmunoassays were used for the measurement of the circulating peptides. As estimated from the plateau peptide concentrations achieved a hindleg vein during the portal and the peripheral infusions, the transhepatic loss of immunoreactive vasoactive intestinal peptide was 72.9 +/- 2.1%, against 27.5 +/- 12.5% for somatostatin. For the given doses of peptides infused systematically, the half-life, metabolic clearance rate, and distribution volume were, respectively, 1.80 +/- 0.1 minutes, 39.3 +/- 5.2 ml/kg/min, and 103.7 +/- 14.8 ml/kg for vasoactive intestinal peptide, and 1.0 +/- 0.2 minutes, 95.2 +/- 12.5 ml/kg/min, and 114.7 +/- 6.0 ml/kg for somatostatin. These results indicate that (ovine) somatostatin and (porcine) vasoactive intestinal peptide are both readily cleared from plasma in dogs. In the present experimental conditions, vasoactive intestinal peptide, but not somatostatin, was rapidly altered through hepatic transit so that it escaped recognition by the assay system.
Platinum Sensitivity–Related Germline Polymorphism Discovered via a Cell-Based Approach and Analysis of Its Association with Outcome in Ovarian Cancer Patients
Authors: R. Stephanie Huang, Sharon E. Johnatty, Eric R. Gamazon, Hae Kyung Im, Dana Ziliak, Shiwei Duan, Wei Zhang, Emily O. Kistner, Peixian Chen, Jonathan Beesley, Shuangli Mi, Peter H. O'Donnell, Yarden S. Fraiman, Soma Das, Nancy J. Cox, Yi Lu, Stuart MacGregor, Ellen L. Goode, Robert A. Vierkant, Brooke L. Fridley, Estrid Hogdall, Susanne K. Kjaer, Allan Jensen, Kirsten B. Moysich, Matthew Grasela, Kunle Odunsi, Robert Brown, Jim Paul, Diether Lambrechts, Evelyn Despierre, Ignace Vergote, Jenny Gross, Beth Y. Karlan, Anna deFazio, Georgia Chenevix-Trench, M. Eileen Dolan
Journal: Clinical Cancer Research (2011)

Cell-based approaches were used to identify genetic markers predictive of patients' risk for poor response prior to chemotherapy.We conducted genome-wide association studies (GWAS) to identify single-nucleotide polymorphisms (SNP) associated with cellular sensitivity to carboplatin through their effects on mRNA expression using International HapMap lymphoblastoid cell lines (LCL) and replicated them in additional LCLs. SNPs passing both stages of the cell-based study were tested for association with progression-free survival (PFS) in patients. Phase 1 validation was based on 377 ovarian cancer patients receiving at least four cycles of carboplatin and paclitaxel from the Australian Ovarian Cancer Study (AOCS). Positive associations were then assessed in phase 2 validation analysis of 1,326 patients from the Ovarian Cancer Association Consortium and The Cancer Genome Atlas.In the initial GWAS, 342 SNPs were associated with carboplatin-induced cytotoxicity, of which 18 unique SNPs were retained after assessing their association with gene expression. One SNP (rs1649942) was replicated in an independent LCL set (Bonferroni adjusted P < 0.05). It was found to be significantly associated with decreased PFS in phase 1 AOCS patients (P(per-allele) = 2 × 10(-2)), with a stronger effect in the subset of women with optimally debulked tumors (P(per-allele) = 4 × 10(-3)). rs1649942 was also associated with poorer overall survival in women with optimally debulked tumors (P(per-allele) = 9 × 10(-3)). However, this SNP was not significant in phase 2 validation analysis with patients from numerous cohorts.This study shows the potential of cell-based, genome-wide approaches to identify germline predictors of treatment outcome and highlights the need for extensive validation in patients to assess their clinical effect.