tbuckley/cabot-search huggingface dataset:
"THE VITONET QUACKERY"
Authors: Kenneth C. Crain
Journal: JAMA (1928)

<h3>To the Editor:</h3> —In the article on this subject inThe Journal, March 10, mention was made of the fact that this concern, under its former name of the Vit-O-Net Manufacturing Company, had several years ago, before it had begun to make the excessive claims referred to in the article, advertised both inThe Journaland in<i>Hospital Management</i>. Letters addressed to<i>Hospital Management</i>by several hospitals, indicating favorable experience with the Vit-O-Net blanket, which was then offered only as an electric heating pad of large size, have since been used by the Vit-O-Net people as inferential support for its present cure-all claims. This use is not warranted by the letters themselves, and was never contemplated or authorized by<i>Hospital Management</i>or by any of the hospitals concerned. It was out of an excess of caution that we addressed to hospitals who had purchased Vit-O-Net blankets a letter inquiring what
Causes of Death in Patients Receiving Long-Term Hemodialysis
Authors: Jaleel Y. Siddiqui
Journal: JAMA (1970)

From August 1964 to June 1969, fifteen of 41 patients treated by long-term hemodialysis died. Four patients died of intracranial hemorrhage and two had convulsive disorders of unknown etiology which directly contributed to their death. Predialysis hypertension was present in four of these six patients. Five patients died with hyperkalemia and two patients died of infections. Other causes of death were suicide, congestive heart failure, and accidental death. The predominance of central nervous system symptoms in this group of patients suggests strongly that the development of neurologic disorders be considered an ominous sign in the patient receiving dialysis. More extensive dialysis, bilateral nephrectomy for intractable hypertension, and administration of potassium-binding resins will hopefully improve future results.
Bone Marrow–Derived CD11b+Jagged2+ Cells Promote Epithelial-to-Mesenchymal Transition and Metastasization in Colorectal Cancer
Authors: Francisco Caiado, Tânia Carvalho, Isadora Rosa, Leonor Remédio, Ana Costa, João Matos, Beate Heissig, Hideo Yagita, Koichi Hattori, João Pereira da Silva, Paulo Fidalgo, António Dias Pereira, Sérgio Dias
Journal: Cancer Research (2013)

Timely detection of colorectal cancer metastases may permit improvements in their clinical management. Here, we investigated a putative role for bone marrow-derived cells in the induction of epithelial-to-mesenchymal transition (EMT) as a marker for onset of metastasis. In ectopic and orthotopic mouse models of colorectal cancer, bone marrow-derived CD11b(Itgam)(+)Jagged2 (Jag2)(+) cells infiltrated primary tumors and surrounded tumor cells that exhibited diminished expression of E-cadherin and increased expression of vimentin, 2 hallmarks of EMT. In vitro coculture experiments showed that the bone marrow-derived CD11b(+)Jag2(+) cells induced EMT through a Notch-dependent pathway. Using neutralizing antibodies, we imposed a blockade on CD11b(+) cells' recruitment to tumors, which decreased the tumor-infiltrating CD11b(+)Jag2(+) cell population of interest, decreasing tumor growth, restoring E-cadherin expression, and delaying EMT. In support of these results, we found that peripheral blood levels of CD11b(+)Jag2(+) cells in mouse models of colorectal cancer and in a cohort of untreated patients with colorectal cancer were indicative of metastatic disease. In patients with colorectal cancer, the presence of circulating CD11b(+)Jag2(+) cells was accompanied by loss of E-cadherin in the corresponding patient tumors. Taken together, our results show that bone marrow-derived CD11b(+)Jag2(+) cells, which infiltrate primary colorectal tumors, are sufficient to induce EMT in tumor cells, thereby triggering onset of metastasis. Furthermore, they argue that quantifying circulating CD11b(+)Jag2(+) cells in patients may offer an indicator of colorectal cancer progression to metastatic levels of the disease.
Proteinase 3. A distinct human polymorphonuclear leukocyte proteinase that produces emphysema in hamsters.
Authors: R C Kao, N G Wehner, K M Skubitz, B H Gray, J R Hoidal
Journal: Journal of Clinical Investigation (1988)

Studies were designed to explore the possibility that human polymorphonuclear leukocyte granule constituents in addition to elastase (HLE) had the potential to cause emphysema. A two-step purification of three serine proteinases was developed. Granule extract proteins were initially separated by dye-ligand affinity chromatography. Fractions eluted were divided into four pools. Hamsters were given a single intratracheal instillation of saline +/- 0.1 mg protein of each pool. While pool 2 contained HLE and cathepsin G, the most dramatic bullous emphysema developed in animals treated with pool 4. The esterase from pool 4, designated proteinase 3 (PR-3) was purified, characterized in vitro, and tested for its ability to cause emphysema. PR-3 is a neutral serine proteinase with isoenzyme forms. Its ability to degrade elastin at pH 6.5 is slightly greater than that of HLE, but it is less active than HLE at pH 7.4 or 8.9. PR-3 has weak activity against azocasein. Its ability to degrade hemoglobin is intermediate to that of HLE and cathepsin G at pH 7.4. PR-3 has no activity against chromogenic substrates specific for HLE or cathepsin G. Its pI is substantially less than HLE or cathepsin G. It is also immunologically distinct from HLE. It induces emphysema in hamsters commensurate with that of HLE. We conclude that PR-3 may be important in the pathogenesis of human emphysema.
Ex Vivo Examination of the Pancreas by Intraductal Ultrasonography (IDUS)
Authors: J. Menzel, E. C. Foerster, B. Ubrig, R. Keller, S. Kerber, W. Domschke
Journal: Endoscopy (1993)

Pancreas specimens from humans (seven normal autopsy specimens, one surgical resection specimen containing a 15 mm microcystic adenoma in the pancreatic head) were examined by intraductal ultrasonography using flexible, high-resolution ultrasonic catheters (20 MHz, 4.8 and 6.0 French diameter). The catheters were easily inserted into the pancreatic duct in all specimens. The ultrasonographic tissue pattern could be correlated with the histological findings in tissue cross-sections at defined positions. A high degree of resolution was achieved in the differentiation of blood vessels, duct system elements, fibrotic tissue, fatty tissue and pancreatic tissue with a varying fat content. At an average distance of 5.5 mm, structures as small as 0.1 mm could be discriminated. No evidence of ductal trauma due to insertion of the catheters was found either on subsequent radiographic studies or on histologic examination. Clinical studies using this probe during ERCP are necessary to clarify whether intraductal ultrasonography could contribute to the diagnosis of small pancreatic lesions and to the differentiation of indeterminate ductal stenoses.
P24 L-ORNITHINE PHENYLACETATE REDUCES AMMONIA IN PIGS WITH ACUTE LIVER FAILURE THROUGH PHENYLACETYLGLYCINE FORMATION: A NOVEL AMMONIA-LOWERING PATHWAY
Authors: R.G. Kristiansen, C. Rose, O.-M. Fuskevåg, H. Mæhre, A. Revhaug, R. Jalan, L.M. Ytrebø
Journal: Journal of Hepatology (2014)
An Assassin's Diary
Authors: Donald W. Goodwin
Journal: JAMA (1973)

Who is Arthur H. Bremer? When asked to write an introduction to Bremer's diary, Harding Lemay couldn't remember. George Wallace will remember. Bremer's bullet, fired in a Maryland shopping center (Hey George! Over here!), left a crippled candidate and man.  Who Arthur Bremer was in the Presidential primary spring of 1972 becomes slightly clearer from his diary, written during that period. He was 21, five foot six, from Milwaukee. He had a Confederate flag that he used to shine his shoes, and two guns until he lost one. He spent most of the six-week period covered by the diary stalking President Nixon, hoping to kill him and become famous like Oswald. Since the President dislikes demonstrators, it is ironic that demonstrators may have saved his life. They were always coming between Bremer and his target, and Bremer finally abandoned Nixon in disgust to stalk Wallace instead.  But who, really, was Bremer?
Scientists may have identified way of turning off immune response
Authors: S. Gottlieb
Journal: BMJ (2002)

Scientists believe they may have identified a way to turn off the immune response when patients receive a transplanted organ or bone marrow by manipulating T cells, which are key players in initiating and conducting immune responses.

In previous studies researchers identified a special group of T cells, called suppressor T cells, which can shut down the normal function of other important immune system cells called monocytes and dendritic cells.

Normally, …
Thermal Cycling Enhances the Accumulation of a Temperature-Sensitive Biopolymer in Solid Tumors
Authors: Matthew R. Dreher, Wenge Liu, Charles R. Michelich, Mark W. Dewhirst, Ashutosh Chilkoti
Journal: Cancer Research (2007)

The delivery of anticancer therapeutics to solid tumors remains a critical problem in the treatment of cancer. This study reports a new methodology to target a temperature-responsive macromolecular drug carrier, an elastin-like polypeptide (ELP) to solid tumors. Using a dorsal skin fold window chamber model and intravital laser scanning confocal microscopy, we show that the ELP forms micron-sized aggregates that adhere to the tumor vasculature only when tumors are heated to 41.5 degrees C. Upon return to normothermia, the vascular particles dissolve into the plasma, increasing the vascular concentration, which drives more ELPs across the tumor blood vessel and significantly increases its extravascular accumulation. These observations suggested that thermal cycling of tumors would increase the exposure of tumor cells to ELP drug carriers. We investigated this hypothesis in this study by thermally cycling an implanted tumor in nude mice from body temperature to 41.5 degrees C thrice within 1.5 h, and showed the repeated formation of adherent microparticles of ELP in the heated tumor vasculature in each thermal cycle. These results suggest that thermal cycling of tumors can be repeated multiple times to further increase the accumulation of a thermally responsive polymeric drug carrier in solid tumors over a single heat-cool cycle. More broadly, this study shows a new approach--tumor thermal cycling--to exploit stimuli-responsive polymers in vivo to target the tumor vasculature or extravascular compartment with high specificity.
A New Self-Expandable and Removable Metal Stent for Biliary Obstruction - A Preliminary Report
Authors: E. Goldin, M. Beyar, T. Safra, O. Globerman, A. Verstandig, D. Wengrower, A. Fich
Journal: Endoscopy (1993)

We report our experience with a new self expandable metallic stent, a coil spring made from a nickel-titanium alloy. The super elastic characteristic of this metal offers a very strong radial force and previous dilatation of biliary strictures is not necessary. The stent is endoscopically inserted constricted over an introducing catheter, expanding spontaneously after release to its original 8 mm diameter. During the last six months, eleven stents were inserted in nine patients with pancreatic carcinoma to relieve jaundice. Another stent was percutaneously implanted treating a benign stricture in a patient with a choledochojejunostomy after a Whipple operation. Clinical improvement was achieved in all the patients except in one who died from liver metastases 5 weeks later. In two patients, although stents were obstructed after 2 and 4 months from insertion, they were easily removed by pulling their distal end through the endoscopic working channel. After a mean follow up of 4.5 months, patients had no evidence of biliary reobstruction. Although follow-up is short, these results are encouraging, and this new metallic stent seems to have several advantages over the current commercially available ones.
What is the optimal management of partial epilepsy uncontrolled by a first choice anticonvulsant?
Authors: D. W Chadwick, G. A Baker, A. Jacoby, A. G Marson, P. E Smith
Journal: BMJ (2008)

Up to 70% of people who are treated with a single anticonvulsant will enter remission within a short time of being diagnosed with epilepsy.1 Optimal first choice treatments have been identified in some comparative randomised controlled trials and guidelines from the National Institute for Health and Clinical Excellence.2 3 Lamotrigine or carbamazepine are usually the preferred initial treatment of seizures with localised onset in the brain, whereas valproate is preferred for generalised epilepsy syndromes.4 5 However, despite optimal doses of a first line anticonvulsant, many patients with localised onset seizures (10-15/100 000 each year worldwide) do not enter remission and continue to have seizures of varying severity and frequency, which are associated with considerable psychosocial distress.6 7 The evidence base to support management of these patients is minimal,2 and it is uncertain which of the following available options is optimal:
Abstract 3039: Identification of a novel biomarker of resistance to lapatinib common to both breast and oesophagogastric cancer
Authors: Irene Chong, Daniel Wetterskog, Kai-Keen Shiu, Titia Meijer, Rachael Natrajan, Lambros Maryou, Jorge Reis-Filho, Lord J. Lord, Cunningham David, Alan Ashworth
Journal: Cancer Research (2011)

Abstract HER2 is amplified and/or overexpressed in 15% and 20% of breast and oesophagogastric (OG) cancers, respectively. Results from the recently published ToGA trial reveal that trastuzumab plus standard chemotherapy improves survival in patients with advanced HER2-positive OG cancer compared with chemotherapy alone, which mirrors the survival benefit shown with trastuzumab plus chemotherapy in metastatic breast cancer. The clinical value of lapatinib, already confirmed in advanced trastuzumab-resistant breast cancer, is currently being evaluated in prospective phase III trials for HER2-positive OG cancer in the metastatic setting. Despite improvements in outcome with anti-HER2 therapy, less than half of patients respond to treatment, and predictive biomarkers to lapatinib for breast and OG cancer have not yet been identified. We sought to identify predictive biomarkers of resistance to lapatinib treatment, common to both breast and OG cancer, by using a siRNA screen of genes identified in a primary siRNA screen to sensitise lapatinib-resistant breast cancer cell lines to lapatinib. These genes are found recurrently amplified and overexpressed in 45 HER2-amplified primary breast cancers and 13 HER2-amplified breast cancer cell lines. OG junction cell lines were treated with lapatinib and screened using the siRNA library. We found that silencing of TP53INP1, a gene target of TP53 which is known to be a reactive oxygen species scavenger, resulted in significant sensitisation to lapatinib in two of the most lapatinib-resistant HER2-positive cell lines derived from the OG junction. TP53INP1 was over-expressed, but not amplified, in the sensitised OG junction cell lines. Our results suggest that genes which mediate resistance to anti-HER2 therapy in breast cancer may be relevant to OG cancer. We are currently developing assays for TP53INP1 in tumours for validation within the context of prospective randomised controlled clinical trials for OG cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3039. doi:10.1158/1538-7445.AM2011-3039
P2-17-09: A Prospective Assessment of Loss of Grip Strength by Baseline BMI in Breast Cancer Patients Receiving Adjuvant Aromatase Inhibitors or Tamoxifen.
Authors: A Lintermans, A-S Dieudonné, J Vanderhaegen, NL Henry, A Laenen, H Wildiers, R Paridaens, M-R Christiaens, A Smeets, K Leunen, F Amant, I Vergote, P Neven
Journal: Cancer Research (2011)

Abstract Background The 3rd generation aromatase inhibitors (AIs) induce or enhance musculoskeletal problems. Underlying mechanisms are probably multiple, but remain unknown. We have previously reported that loss of grip strength together with tenosynovial abnormalities are more important in AI- than in tamoxifen-users (Morales et al, JCO 2008) and that musculoskeletal changes in AI-users are more pronounced in women with extremes in baseline BMI (Lintermans et al, Ann Oncol 2011) We here report preliminary results from a larger population and plan to validate findings in patients from University of Michigan. Patients and methods In this prospective observational study, postmenopausal early breast cancer patients scheduled to start adjuvant hormonal therapy with any of the third generation AIs or tamoxifen were recruited. After providing informed consent, a functional assessment test of grip strength was performed with a modified sphygmomanometer. Re-evaluation was done after 3, 6 and 12 months of therapy. BMI and waist to hip ratio (WHR) were assessed and a rheumatological questionnaire was completed at each visit. Results Ninety-four (79 AI; 15 tamoxifen) of the planned 200 patients were included in this preliminary study. 18% of AI-users discontinued their treatment due to musculoskeletal symptoms compared with none of the tamoxifen-users. 62% of patients on AI and 35% of tamoxifen patients complained of new or worsened joint pain. Table 1 shows the proportion of patients that attribute their complaints to their endocrine therapy. Grip strength significantly decreased over time (p=0.03), with patients under AI treatment having a larger loss of grip strength than patients under tamoxifen treatment (p=0.04). We confirm our previously reported results on the shape of the curve “BMI AI-induced loss of grip strength”. Years past menopause and age showed a significant effect on grip strength (p&amp;lt;0.001 and p=0.0007, respectively), whereas no significant relationship was found between WHR with grip strength or joint pain. Detailed results will be presented. Conclusion Our preliminary results confirm that a majority of patients treated with an AI experience musculoskeletal problems, which are considered due to the therapy by most patients. Grip strength decreased over time, with a significantly larger loss of grip strength in the AI-users compared with the tamoxifen-users. AI-induced loss of grip strength and baseline BMI showed an inverted U-shaped association, although differences between quartiles were small. Further results should be awaited as this is only a preliminary analysis. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-17-09.
EPIDEMIC INFECTION BY A GENTAMICIN-RESISTANT STAPHYLOCOCCUS AUREUS IN THREE HOSPITALS
Authors: D.C.E. Speller, Mary Stephens, D. Raghunath, AnnetteC. Viant, D.S. Reeves, J.M. Broughall, P.J. Wilkinson, H.A. Holt
Journal: The Lancet (1976)
Temocapril treatment ameliorates autoimmune myocarditis associated with enhanced cardiomyocyte thioredoxin expression
Authors: Z Yuan
Journal: Cardiovascular Research (2002)

Objective: Thioredoxin (TRX) is a redox regulatory protein that protects cells from various stresses. Angiotensin-converting enzyme (ACE) inhibitor was reported to enhance endogenous antioxidant enzyme activities. This study was carried out to investigate whether temocapril, a novel non-sulfhydryl-containing ACE inhibitor, reduces the severity of myocarditis via redox regulation mechanisms involving TRX. Methods and Results: In normal rat myocytes in vitro and in vivo, Western blot showed that temocapril enhanced cytosolic redox regulatory protein TRX expression, but that neither mitochondrial TRX2 nor antioxidant enzymes, such as copper–zinc superoxide dismutase (Cu/Zn-SOD) or manganese superoxide dismutase (Mn-SOD) expression, was up-regulated by the preconditioning treatment. In rats with experimental autoimmune myocarditis (EAM), the severity of myocarditis and the protein carbonyl contents were less increased in temocapril treatment (10 mg/kg/day, orally) from day 1 to day 21, but not in temocapril treatment from day 15 to day 21. An immunohistochemical study showed that TRX stain was enhanced in infiltrating inflammatory cells and in damaged myocytes. Considering the characteristics of this model that myocardial inflammation begins around day 15 and increases until day 21, temocapril treatment for 3 weeks might be thought of as a preconditioning treatment. Conclusions: The results suggest that TRX and the redox state modified by TRX may play a crucial role in the pathophysiology of EAM. Temocapril ameliorates myocarditis associated with inducing TRX up-regulation in a preconditioning manner, although the mechanism of TRX up-regulation by temocapril remains to be elucidated.
Special deLIVERy: podocyte injury promotes renal angiotensin II generation from liver-derived angiotensinogen
Authors: David I. Ortiz-Melo, Robert F. Spurney
Journal: Kidney International (2014)

The role of the circulating renin-angiotensin system (RAS) in regulating systemic blood pressure and sodium balance is well established. More recently, researchers have turned their focus to the local generation of angiotensin II (Ang II) in specific tissues. Matsusaka et al. revisit the renal RAS and provide evidence that liver-derived angiotensinogen (AGT) is a major determinant of renal Ang II levels in a model of podocyte injury.
Transmural dispersion in LQT and arrhythmogenesis
Authors: T OPTHOF, R CORONEL
Journal: Cardiovascular Research (2005)

At the end of the 19th century Einthoven described the configuration of the human ECG [1] and in later papers he elaborated on the magnitude and direction of its components [2]. From an intellectual point of view it is in fact unacceptable that we still do not know exactly how the T wave emerges. More precisely, we may understand how (dispersion in) repolarization within the ventricles transforms into the T wave in the ECG, but we have to live with the fact that we cannot translate the T wave into dispersion in repolarization. Biophysicists recognize this as ‘the inverse problem’ [3] and it might be that it will never be solved, because multiple cardiac repolarization orders may translate into one and the same T wave. This may be based on the fact that 90% …
EphB4 Overexpression in B16 Melanoma Cells Affects Arterial-Venous Patterning in Tumor Angiogenesis
Authors: Xiaoyong Huang, Yoshihiro Yamada, Hiroyasu Kidoya, Hisamichi Naito, Yumi Nagahama, Lingyu Kong, Shin-Ya Katoh, Weng-lin Li, Masaya Ueno, Nobuyuki Takakura
Journal: Cancer Research (2007)

Abstract EphB4 receptor and its ligand ephrinB2 play an important role in vascular development during embryogenesis. In blood vessels, ephrinB2 is expressed in arterial endothelial cells (EC) and mesenchymal supporting cells, whereas EphB4 is only expressed in venous ECs. Previously, we reported that OP9 stromal cells, which support the development of both arterial and venous ECs, in which EphB4 was overexpressed, could inhibit ephrinB2-positive (ephrinB2+) EC development in an embryonic tissue organ culture system. Although the EphB4 receptor is expressed in a variety of tumor cells, its exact function in regulating tumor progression has not been clearly shown. Here we found that overexpression of EphB4 in B16 melanoma cells suppressed tumor growth in a s.c. transplantation tumor model. Histologic examination of these tumors revealed that EphB4 overexpression in B16 cells selectively suppressed arterial ephrinB2+ EC development. By coculturing ephrinB2-expressing SV40-transformed mouse ECs (SVEC) with EphB4-overexpressing B16 cells, we found that EphB4 induced the apoptosis of SVECs. However, ephrinB2 did not induce the apoptosis of EphB4-overexpressing B16 cells. Based on results from these experiments, we concluded that EphB4 overexpression in B16 tumor cells suppresses the survival of arterial ECs in tumors by a reverse signaling via ephrinB2. [Cancer Res 2007;67(20):9800–8]