tbuckley/cabot-search huggingface dataset:
Human mesenchymal stem cells successfully improve skin-substitute wound healing
Authors: H. Nakagawa, S. Akita, M. Fukui, T. Fujii, K. Akino
Journal: British Journal of Dermatology (2005)

Background Large or deteriorated skin defects are sometimes life threatening. There is increasing evidence that adult stem cells are useful for tissue regeneration. Human mesenchymal stem cells (hMSCs) are self‐renewing and are potent in differentiating into multiple cells and tissues. Objectives To investigate the effects of hMSCs in cutaneous wound healing. Methods Wound healing was studied in an hMSC‐populated porcine skin substitute, using a nude rat model to minimize immune reactions. Full‐thickness skin and soft tissue defects of 1·5 × 1·5 cm in size, including the panniculus carnosus, were excised and covered with hMSCs and basic fibroblast growth factor (bFGF)‐soaked skin substitutes and an evaluation was made of wound size, histology and protein expression at 3, 7 and 42 days after injury. Results The wound size was significantly smaller in the hMSC‐treated groups (P < 0·01) and any dose of bFGF (1, 10, 100 μg) enhanced the healing (P < 0·01). The re‐epithelialization markers integrin α3 and skin‐derived antileucoproteinase were remarkably increased with the presence of bFGF in a dose‐dependent manner, while the mesenchymal cell surface markers CD29 and CD44 were downregulated in a time‐dependent manner. Human pancytokeratin, which does not cross‐react with rat antigens, was observed by Western blotting at 38 kDa and 42 kDa from the hMSC‐treated tissues on day 7. The expression levels were elevated by 10 μg bFGF (P < 0·01). The immunohistochemical expression of human pancytokeratin was only observed in the hMSC‐treated groups. Conclusions These data suggest that hMSCs together with bFGF in a skin defect model accelerate cutaneous wound healing as the hMSCs transdifferentiate into the epithelium.
CHANGES IN THE PROTEOLYTIC ENZYMES AND ANTI-ENZYMES OF THE BLOOD SERUM PRODUCED BY SUBSTANCES (CHLOROFORM AND PHOSPHORUS) WHICH CAUSE DEGENERATIVE CHANGES IN THE LIVER
Authors: Eugene L. Opie, Bertha I. Barker, A. R. Dochez
Journal: The Journal of Experimental Medicine (1911)

The observations of Salkowski, 2 which have shown that incubated liver undergoes "self-digestion," have been extended to almost all tissues of the animal body.It is well known that the autolysis of most tissues occurs with maximum activity in a weakly acid medi'am.Biondi ~ has found that disintegration of liver is hastened by addition of weak acid, and Hedin and Rowland, 4 using the expressed juice of various organs, have noted that spleen, kidney, and lymphatic nodes autolyze more actively in acid than in neutral or alkaline media.The trivial autolysis of voluntary muscle is not materially affected by acid or alkali, but the autolysis of heart muscle resembles that of other organs.Levene and Stookey 5 have found that autolysis of brain tissue and of testicle is favored by the presence of acid.The pancreas is not an exception to the foregoing rule.The well-known observations of Heidenhain 6 have shown that trypsin, which exhibits maximum activity in alkali, exists in the pancreas as inactive zymogen, so that fresh extracts of the organ cause little proteolysis under conditions which favor the activity of trypsin.
THE PROPHYLACTIC VALUE OF LEARY'S VACCINE
Authors: HARRY LEE BARNES
Journal: JAMA (1918)

As an institution offers unusual advantages for the study of an epidemic and the measures for its control, a record of our experience with influenza vaccine at the state sanatorium may not be without value. The institution had about 225 patients and ninety-four employees. During the last two weeks of September, 1918, four employees and five patients contracted influenza. These patients were all in one ward of the hospital and were apparently infected from a patient who visited Woonsocket. They were isolated in rooms and a cubicle of the ward, and the disease did not spread.  The four employees were isolated in their rooms. September 29, all patients and employees, with few exceptions, were forbidden to receive visitors or leave the institution. We were free from influenza, which was at the height of the epidemic in the surrounding country, until October 10, when a woman patient admitted on October 9
Direct enumeration and functional assessment of circulating dendritic cells in patients with liver disease
Authors: Anne M. Wertheimer, Antony Bakke, Hugo R. Rosen
Journal: Hepatology (2004)

Chronic liver disease has been shown to be associated with diminished humoral and cellular immune function. Although antigen-presenting cells (APC) that initiate immune responses include various cells (B cells, endothelial cells, macrophages, etc.), the dendritic cell (DC) is a professional APC that activates naive T cells most efficiently. To examine the frequency and function of DCs in chronic liver disease, we studied circulating DCs from a cohort of 112 subjects (23 normal subjects, 29 subjects who had spontaneously recovered from hepatitis C virus [HCV] infection, 30 chronically infected HCV patients, and 30 patients with liver disease unrelated to HCV infection). Our analyses revealed significant reduction in both circulating myeloid (mDC) and plasmacytoid dendritic cells (pDC) in patients with liver disease. In contrast, examination of subjects with spontaneously resolved HCV infection revealed no significant difference in either circulating mDCs or pDCs. We found an inverse correlation with serum alanine aminotransferase (ALT) levels and both mDCs and pDCs frequency. In a subset of patients for whom intrahepatic cells were available, paired analysis revealed enrichment for DCs within the intrahepatic compartment. Interferon alfa (IFN-α) production in response to influenza A and poly (I:C) correlated with the frequency of circulating DCs, although IFN-α production was comparable on a per-DC basis in patients with liver disease. In conclusion , patients with liver disease exhibit a reduction in circulating DCs. Considering that DCs are essential for initiation and regulation of innate and adaptive immunity, these findings have implications for both viral persistence and liver disease. (Hepatology 2004;40:335-345.)
CHANGES IN THE NOSE AFTER WIDENING THE PALATAL ARCH
Authors: L. W. DEAN
Journal: JAMA (1910)

If the existing laws do not apply to the grocer as well as to the druggist, then, you doubtless all agree with me in the opinion that the laws should be amended.I leave (his to those better able than I.In conclusion, I beg you to look into your own kitch¬ ens and find whether or not caustic alkalies are used with a reckless disregard of their poisonous nature.
Analysis of Intracorporeal Compared with Extracorporeal Urinary Diversion After Robot-assisted Radical Cystectomy: Results from the International Robotic Cystectomy Consortium
Authors: Kamran Ahmed, Shahid A. Khan, Matthew H. Hayn, Piyush K. Agarwal, Ketan K. Badani, M. Derya Balbay, Erik P. Castle, Prokar Dasgupta, Reza Ghavamian, Khurshid A. Guru, Ashok K. Hemal, Brent K. Hollenbeck, Adam S. Kibel, Mani Menon, Alex Mottrie, Kenneth Nepple, John G. Pattaras, James O. Peabody, Vassilis Poulakis, Raj S. Pruthi, Joan Palou Redorta, Koon-Ho Rha, Lee Richstone, Matthias Saar, Douglas S. Scherr, Stefan Siemer, Michael Stoeckle, Eric M. Wallen, Alon Z. Weizer, Peter Wiklund, Timothy Wilson, Michael Woods, Muhammad Shamim Khan
Journal: European Urology (2013)
Abstract 2120: Secreted protein acidic and rich in cysteine, like 1(SPARCL1), inhibits aggressiveness and relates to better prognosis in colorectal cancers
Authors: Hang Zhang, Hanguang Hu, Weiting Ge, Xiyong Liu, Huarong Chen, Shujing Yu, Suzhan Zhang, Yun Yen, Shu Zheng
Journal: Cancer Research (2011)

Abstract Secreted protein that's acidic and rich in cysteine, like 1(SPARCL1), an extracellular de-adhesion glycoprotein, was down-regulated in several solid cancers such as non-small cell lung cancer and pancreatic cancer. Our previous study revealed that expression of SPARCL1 was negatively related to liver metastasis of colorectal cancer (CRC). To clarify the function of SPARCL1 and its mechanism in CRC, the overexpression cell clone, RKO-SPARCL1, was created for illustrating biological behavior of SPARCL1 in vitro and in vivo. It was shown that SPARCL1 significantly reduced colony formation (p=0.027), invasion ability (p=0.001) and adhesion (p=0.04) of CRC cells in vitro. In comparison with vector control (RKO-pLXSN), RKO-SPARCL1 displayed significantly reduction in liver metastatic nodules in intrasplenic injection nude mice model (p=0.009). Meanwhile, tissue samples from 412 CRC patients were reassembled as tissue microarray for an outcome study. The antibody against SPARCL1 was developed for Immunohistochemistry (IHC) staining to assess the expression level of SPARCL1. Uni- and multivariate Logistic analysis demonstrated that SPARCL1 was negatively related with poorly tumor differentiation (p=0.001), lymph node metastasis (Odds ratio, OR=0.67, 95% 0.45-1.00) and distant metastasis (OR=0.39, 95% 0.18-0.82). The Kaplan-Meier analysis revealed that overexpression of SPARCL1 was significantly related to better overall survival in CRCs (p=0.004). Furthermore, the multivariate COX proportional hazard analysis demonstrated that SPARCL1 significantly reduced the risk of death from CRC (Hazard ratio, HR=0.57, 95% 0.39-0.84). Based on bioinformatics gene ontology analysis for gene expression microarray, overexpression of SPARCL1 significantly inhibited focal adhesion pathway and other tumor-associated oncogenes, such as S100A4 and ERBB3, in RKO cell line. Therefore, it is concluded that SPARCL1 may function as a tumor suppressor inhibiting the aggressiveness of cancer cells and reducing the risk of death from CRCs. It is suggested that SPARCL1 may serve as a prognostic biomarker for CRCs. 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 2120. doi:10.1158/1538-7445.AM2011-2120
Injury consequences from participation in professional rugby league: a preliminary investigation.
Authors: R A Meir, K N McDonald, R Russell
Journal: British Journal of Sports Medicine (1997)

To conduct a preliminary investigation to determine if injuries sustained while playing professional rugby league have long term consequences for players after retirement from their playing careers.Twenty eight retired players, who had competed in the professional Australian Rugby League competition, responded to a 23 item survey. Respondents were asked to recall all injuries that resulted in them being unable to play for five or more consecutive games. The survey asked players to provide information about age, playing weight, number of games played, position played, number and type of major injuries sustained during their career, and the effects of these injuries both during their career and after retirement.Within the limitations of this study's small sample, it is suggested that players with long term consequences of injury may experience a variety of detrimental effects into retirement, including job limitations, reduced income earning potential, and increased personal medical costs.Although research relating to the type and severity of injuries sustained while playing rugby league has been previously undertaken, investigation into the effect injuries sustained during a professional career have on players after retirement has been neglected. This preliminary investigation suggests that retired professional rugby league players may have at least one long term consequence of injuries sustained during their playing career.
Inactivation of Fac in mice produces inducible chromosomal instability and reduced fertility reminiscent of Fanconi anaemia
Authors: Ming Chen, Darrell J. Tomkins, Wojtek Auerbach, Colin McKerlie, Hagop Youssoufian, Lili Liu, Olga Gan, Madeleine Carreau, Anna Auerbach, Tim Groves, Cynthia J. Guidos, Melvin H. Freedman, Jay Cross, Dean H. Percy, John E. Dick, Alexandra L. Joyner, Manuel Buchwald
Journal: Nature Genetics (1996)
Recycling and Recycled Paper
Authors: Nawin Gupta
Journal: JAMA (1992)

Mention using recycled paper and many people think of tall trees in pristine forests being saved from a lumberjack's saw. While it is true that when paper is recycled fewer trees need to be cut, that is not the real issue. Trees used for making paper are a renewable resource. They are planted and harvested much like any other crop. More central to the issue of recycling is reducing the amount of paper waste going into landfills by making paper products easier to recycle, recycling them, and of course, using recycled paper when possible. According to the US Environmental Protection Agency, Americans generate more than 180 million tons of garbage each year; nearly 75% of this garbage ends up in municipal landfills. Paper and paperboard products constitute nearly 40% of the total garbage generated. The magazine industry's share of the total waste is 2.5% (4.5 million tons). Within the last
Effect of tranexamic acid on mortality in patients with traumatic bleeding: prespecified analysis of data from randomised controlled trial
Authors: I. Roberts, P. Perel, D. Prieto-Merino, H. Shakur, T. Coats, B. J. Hunt, F. Lecky, K. Brohi, K. Willett
Journal: BMJ (2012)

<b>Objectives</b> To examine whether the effect of tranexamic acid on the risk of death and thrombotic events in patients with traumatic bleeding varies according to baseline risk of death. To assess the extent to which current protocols for treatment with tranexamic acid maximise benefits to patients. <b>Design</b> Prespecified stratified analysis of data from an international multicentre randomised controlled trial (the CRASH-2 trial) with an estimation of the proportion of premature deaths that could potentially be averted through the administration of tranexamic acid. <b>Participants</b> 13 273 trauma patients in the CRASH-2 trial who were treated with tranexamic acid or placebo within three hours of injury and trauma patients enrolled in UK Trauma and Audit Research Network, stratified by risk of death at baseline (&lt;6%, 6-20%, 21-50%, &gt;50%). <b>Intervention</b> Tranexamic acid (1 g over 10 minutes followed by 1 g over eight hours) or matching placebo. <b>Main outcome measure</b> Odds ratios and 95% confidence intervals for death in hospital within four weeks of injury, deaths from bleeding, and fatal and non-fatal thrombotic events associated with the use of tranexamic acid according to baseline risk of death. Unless there was strong evidence against the null hypothesis of homogeneity of effects (P&lt;0.001), the overall odds ratio was used as the most reliable guide to the odds ratios in all strata. <b>Results</b> Tranexamic acid was associated with a significant reduction in all cause mortality and deaths from bleeding. In each stratum of baseline risk, there were fewer deaths among patients treated with tranexamic acid. There was no evidence of heterogeneity in the effect of tranexamic acid on all cause mortality (P=0.96 for interaction) or deaths from bleeding (P=0.98) by baseline risk of death. In those treated with tranexamic acid there was a significant reduction in the odds of fatal and non-fatal thrombotic events (odds ratio 0.69, 95% confidence interval 0.53 to 0.89; P=0.005) and a significant reduction in arterial thrombotic events (0.58, 0.40 to 0.83; P=0.003) but no significant reduction in venous thrombotic events (0.83, 0.59 to 1.17; P=0.295). There was no evidence of heterogeneity in the effect of tranexamic acid on the risk of thrombotic events (P=0.74). If the effect of tranexamic acid is assumed to be the same in all risk strata (&lt;6%, 6-20%, 21-50%, &gt;50% risk of death at baseline), the percentage of deaths that could be averted by administration of tranexamic acid within three hours of injury in each group is 17%, 36%, 30%, and 17%, respectively. <b>Conclusions</b> Tranexamic acid can be administered safely to a wide spectrum of patients with traumatic bleeding and should not be restricted to the most severely injured. <b>Trial registration</b>ISRCTN86750102.
Mitochondrial dysfunction induced by fatty acid ethyl esters, myocardial metabolites of ethanol.
Authors: L G Lange, B E Sobel
Journal: Journal of Clinical Investigation (1983)

Mechanisms responsible for alcohol-induced heart muscle disease have been difficult to elucidate partly because of previously obscure, demonstrable cardiac metabolism of ethanol. Recently, fatty acid ethyl esters were identified in our laboratory and found to be myocardial metabolites of ethanol. In the present study, they have been shown to induce mitochondrial dysfunction. Incubation of isolated myocardial mitochondria with fatty acid ethyl esters led to a concentration-dependent reduction of the respiratory control ratio index of coupling of oxidative phosphorylation and decrement of maximal rate of oxygen consumption. Furthermore, fatty acid ethyl esters were demonstrated to bind to mitochondria in vitro, and, importantly, 72% of intracellularly synthesized ethyl esters were found to bind to mitochondria isolated from intact tissue incubated with ethanol. Protein binding of fatty acid ethyl esters was markedly less than that of fatty acids. Because uncoupling of mitochondrial oxidative phosphorylation correlated with the cleavage of fatty acid ethyl ester shown to be initially bound to mitochondria, with resultant generation of fatty acid, a potent uncoupler, in a locus in or near the mitochondrial membrane, fatty acid ethyl esters may contribute to a potentially toxic shuttle for fatty acid with transport from physiological intracellular binding sites to the mitochondrial membrane; direct effects of fatty acid ethyl esters may also be deleterious. Operation of this shuttle as a result of ethanol ingestion and subsequent accumulation of fatty acid ethyl esters may account for the impaired mitochondrial function and inefficient energy production associated with toxic effects of ethanol on the heart.
Greg and the BB Gun
Authors: C. B. Clark
Journal: JAMA (1982)

Greg is 12 years old now, and as mature as any 12-year-old boy can be. He has been going to the hospital and office with his dad ever since he could walk, and exposure to medical practice can teach a young person a lot. Recently, Greg decided that he was ready for a BB gun. Despite vigorous opposition from his parents, Greg was determined to have his wish. He was quite definite that he wasn't going to shoot any of the neighbor kids. The plan was to put a target up on a tree and shoot at the target. The other day, a man in his 40s was at the office. I noticed that one of his eyes didn't look quite right. I asked him about it, and he told me that he lost the eye when he was 14. He was setting up cans on a railroad track and
Medical leaders call for debate on funding NHS in England
Authors: G. Iacobucci
Journal: BMJ (2014)

Senior leaders of the NHS in England have called on political leaders to hold a national debate with the public on how the health service should be funded in the future in an attempt to shore up a system that they say is currently “creaking at the seams.”

In a letter to the Times published on 7 July,1 doctors and other leading figures said that urgent action was essential to meet the challenge of caring …
“But Doctor, What Have I Got to Lose. . . ?”
Authors: Gregory P. Kalemkerian
Journal: Journal of Clinical Oncology (2001)

Article Tools SPECIAL DEPARTMENTS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2001.19.18.3904 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 11559729 “But Doctor, What Have I Got to Lose. . . ?” Gregory P. KalemkerianxGregory P. KalemkerianSearch for articles by this author Show More University of Michigan, Ann Arbor, MI https://doi.org/10.1200/JCO.2001.19.18.3904 Full Text PDF Figures and Tables "“But Doctor, What Have I Got to Lose. . . ?”." Journal of Clinical Oncology, 19(18), p. 3904© 2001 by American Society of Clinical Oncology
856 Bile acid feeding protects cholangiocytes from hepatic artery ligation-induced apoptosis by stimulating cholangiocyte VEGF secretion through a PI3K/AKT dependent mechanism
Authors: S GLASER, H FRANCIS, S TAFFETANI, J PHINIZY, D ALVARO, E GAUDIO, T HORST, M MARZIONI, G LESAGE, B BAUMANN
Journal: Hepatology (2003)

Most cholestatic disorders are caused by defects in cholangiocytes. The type 3 isoform of the inositol 1,4,5-trisphosphate receptor (ITPR3) is the most abundant intracellular calcium release channel in cholangiocytes. ITPR3 is required for bicarbonate secretion by bile ducts, and its expression is reduced in intrahepatic bile ducts of patients with cholestatic disorders. We investigated whether the nuclear factor, erythroid 2-like 2 (NFE2L2 or NRF2), which is sensitive to oxidative stress, regulates expression of ITPR3.The activity of the ITPR3 promoter was measured in normal human cholangiocyte (NHC) cells and primary mouse cholangiocytes. Levels of ITPR3 protein and messenger RNA were examined by immunoblot and polymerase chain reaction analyses, respectively. ITPR3 activity was determined by measuring calcium signaling in normal human cholangiocyte cells and secretion in isolated bile duct units. Levels of NRF2 were measured in liver tissues from rats with cholestasis (induced by administration of α-napthylisothiocyanate) and from patients with biliary diseases.We identified a musculo-aponeurotic fibrosarcoma recognition element in the promoter of ITPR3 that bound NRF2 directly in NHC cells and mouse cholangiocytes. Increasing binding of NRF2 at this site resulted in chromatin remodeling that reduced promoter activity. Mutant forms of the musculo-aponeurotic fibrosarcoma recognition element did not bind NRF2. Activation of NRF2 with quercetin or by oxidative stress reduced expression of ITPR3 and calcium signaling in NHC cells; quercetin also reduced secretion by bile duct units isolated from rats. Knockdown of NRF2 with small interfering RNAs restored expression and function of ITPR3 in NHC cells incubated with quercetin. Bile ducts from rats with cholestasis and patients with cholangiopathic disorders expressed higher levels of NRF2 and lower levels of ITPR3 than ducts from control rats or patients with other liver disorders.The transcription factor NRF2 binds to the promoter of ITPR3 to inhibit its expression in cholangiocytes, leading to reduced calcium signaling and bile duct secretion. This could be a mechanism by which oxidative stress inhibits these processes and contributes to cholangiopathies.
Prevalence of obesity is low in people who do not eat meat
Authors: T. Key, G. Davey
Journal: BMJ (1996)

Table 1-Number of subjects in each category of body mass index (calculated from self reported weights and heights*) when different and common thresholds were used for men and woment Men (n = 1536) Women (n = 1864) Total (n = 3400) Different Common Different Common Different Common threshold threshold threshold threshold threshold threshold Underweight
INCUBATIONAL CHANGES IN THE RED CELL COUNT IN INOCULATED MALARIA: (Preliminary Note.)
Authors: A. Pijper, B. D. Russell
Journal: BMJ (1924)

A radiograph takeln about a month after admission showed a great diminution in the size of ,lie abscess.He was diselharged two montlhs after admission, free from all symiptoms of abscess and displayinig no physical signs beyond some impairiment of resonanice over the riglht lower lobe anid somie diminlution of breath sounds in the same regioin.W 1heni nxext seen, two moniths later, lhe was in goodl healtlh and back at work.All abnormizal physical FIG.3-Fouir months after admission--no trace of abscess.Lung fields normal.signs hiad th-en completely disappeared, and an x-iray examiinationi (Fig. 3) failed to show any trace of his forsmer lesioni.My object in publishiing this case is to call attention to the strikisig and immediate benefit which followed the efficienit di aining of the abscess by the assumption of a suLitable posture by the patient; there is nothing niew in tliat.