tbuckley/cabot-search huggingface dataset:
Healing of chondral and osteochondral defects in a canine model: the role of cultured chondrocytes in regeneration of articular cartilage
Authors: S Shortkroff, L Barone, H P Hsu, C Wrenn, T Gagne, T Chi, H Breinan, T Minas, C B Sledge, R Tubo, M Spector
Journal: Biomaterials (1996)
Prenatal and Postnatal Maternal Stress and Wheeze in Urban Children
Authors: Yueh-Hsiu Mathilda Chiu, Brent A. Coull, Sheldon Cohen, Alana Wooley, Rosalind J. Wright
Journal: American Journal of Respiratory and Critical Care Medicine (2012)

Rationale: Critical periods for programming early wheeze risk may include pregnancy and infancy. Effects of timing remain poorly understood.Objectives: Associations among prenatal and postnatal maternal stress and children's wheeze were prospectively examined in 653 families. Effect modification by maternal sensitization was also examined.Methods: Stress was indexed by a maternal negative life events (NLEs) score (range, 0–9) ascertained during pregnancy and between 1 and 2 years postpartum. Mothers reported child wheeze every 3 months up to age 2 years. Relationships of prenatal and postnatal maternal NLEs with repeated wheeze (≥2 episodes) were examined using logistic regression adjusting for covariates. Penalized splines were implemented to explore possible nonlinear associations. We also examined the interaction between prenatal stress and maternal sensitization indexed by allergen-specific IgE from maternal prenatal serum.Measurements and Main Results: Adjusted models considering prenatal or postnatal NLEs alone both showed an exposure-response relationship between higher stress and child wheeze. When considering prenatal and postnatal stress concurrently, only children of mothers with high stress in both periods were significantly more likely to wheeze (adjusted odds ratio, 3.04; 95% confidence interval, 1.67–5.53) than children of mothers reporting low stress in both periods. Associations between high prenatal stress and wheeze were significant in children born to nonsensitized mothers (any IgE <0.35 kU/L) but not in the sensitized group (P for interaction = 0.03).Conclusions: Although children have heightened sensitivity to maternal stress in utero and in early childhood, those with higher stress in both periods were particularly at risk for wheeze. The prenatal maternal immune milieu modified effects.
Human Chorionic Gonadotropin in Pregnancy and Maternal Risk of Breast Cancer
Authors: Paolo Toniolo, Kjell Grankvist, Marianne Wulff, Tianhui Chen, Robert Johansson, Helena Schock, Per Lenner, Göran Hallmans, Matti Lehtinen, Rudolf Kaaks, Göran Wadell, Anne Zeleniuch-Jacquotte, Eva Lundin, Annekatrin Lukanova
Journal: Cancer Research (2010)

Abstract Full-term pregnancies are associated with long-term reductions in maternal risk of breast cancer, but the biological determinants of the protection are unknown. Experimental observations suggest that human chorionic gonadotropin (hCG), a major hormone of pregnancy, could play a role in this association. A case-control study (242 cases and 450 controls) nested within the Northern Sweden Maternity Cohort included women who had donated a blood sample during the first trimester of a first full-term pregnancy. Total hCG was determined on Immulite 2000 analyzer. Odds ratios (OR) and 95% confidence intervals (CI) were estimated through conditional logistic regression. Maternal breast cancer risk decreased with increasing hCG (upper tertile OR, 0.67; CI, 0.46–0.99), especially for pregnancies before age 25 (upper tertile OR, 0.41; CI, 0.21–0.80). The association diverged according to age at diagnosis: risk was reduced after age 40 (upper tertile OR, 0.60; CI, 0.39–0.91) and seemed to increase before age 40 (upper tertile OR, 1.78; CI, 0.72–4.38). Risk was reduced among those diagnosed 10 years or longer after blood draw (upper tertile OR, 0.60; CI, 0.40–0.90), but not so among those diagnosed within 10 years (upper tertile OR, 4.33; CI, 0.86–21.7). These observations suggest that the association between pregnancy hCG and subsequent maternal risk of breast cancer is modified by age at diagnosis. Although the hormone seems to be a determinant of the reduced risk around or after age 50, it might not confer protection against, or it could even increase the risk of, cancers diagnosed in the years immediately following pregnancy. Cancer Res; 70(17); 6779–86. ©2010 AACR.
Growth Hormone: Metabolic Clearance Rates, Integrated Concentrations, and Production Rates in Normal Adults and the Effect of Prednisone
Authors: Robert G. Thompson, Ana Rodriguez, Avinoam Kowarski, Robert M. Blizzard
Journal: Journal of Clinical Investigation (1972)

A constant withdrawal pump was used to determine the integrated concentration of growth hormone (ICGH) which was used in conjunction with the metabolic clearance rate (MCR) of growth hormone (GH) to calculate the GH production rates (GHPR) in normal adults, acromegalics, and normal controls receiving prednisone. The mean ICGH for 22 premenopausal females on no medication was 3.0+/-1.6 ng/ml (sd) which is significantly lower (P < 0.005) than the mean of 6.6+/-2.9 for 10 women receiving oral contraceptives and significantly higher than the means of 1.5+/-0.75 for 5 postmenopausal females (P < 0.05) and 1.8+/-1.0 for 16 adult males (P < 0.01) which are comparable. The mean GHPR's in mg/24 hr per m(2) for the four groups are: normal females = 0.52+/-0.24 (sd), females receiving contraceptive pills = 1.65+/-0.58 (P < 0.005), postmenopausal females = 0.26+/-0.12 (P < 0.025), and adult males 0.35+/-0.23 (P < 0.025).Three untreated acromegalic patients had ICGH's of 59, 82, and 93 ng/ml and GHPR's ranging from 14.5 to 17.9 mg/24 hr. Prednisone in a dose of 20 mg t.i.d. for 8 days significantly decreased both the ICGH and GHPR. Alternate day prednisone (60 mg in a single q.o.d. dose) resulted in less consistent inhibition of GH release which may play a role in the more normal growth seen in children receiving q.o.d. prednisone.
Intravenous Administration of Human Bone Marrow Stromal Cells Induces Angiogenesis in the Ischemic Boundary Zone After Stroke in Rats
Authors: Jieli Chen, Zheng Gang Zhang, Yi Li, Lei Wang, Yong Xian Xu, Subhash C. Gautam, Mei Lu, Zhenping Zhu, Michael Chopp
Journal: Circulation Research (2003)

We tested the hypothesis that intravenous infusion of human bone marrow stromal cells (hMSCs) promotes vascular endothelial growth factor (VEGF) secretion, VEGF receptor 2 (VEGFR2) expression and angiogenesis in the ischemic boundary zone (IBZ) after stroke. hMSCs (1×10 6 ) were intravenously injected into rats 24 hours after middle cerebral artery occlusion (MCAo). Laser scanning confocal microscopy (LSCM), immunohistochemistry and ELISA were performed to assay angiogenesis and levels of human and rat VEGF in the host brain, respectively. In addition, capillary-like tube formation was measured using mouse brain-derived endothelial cells (MBDECs). Morphological and three dimensional image analyses revealed significant ( P &lt;0.05) increases in numbers of enlarged and thin walled blood vessels and numbers of newly formed capillaries at the boundary of the ischemic lesion in rats (n=12) treated with hMSCs compared with numbers in rats (n=12) treated with PBS. ELISA measurements showed that treatment with hMSCs significantly ( P &lt;0.05) raised endogenous rat VEGF levels in the IBZ from 10.5±1.7 ng/mL in the control group to 17.5±1.6 ng/mL in the hMSC-treated group. In addition, treatment with hMSCs increased endogenous VEGFR2 immunoreactivity. In vitro, when MBDECs were incubated with the supernatant obtained from cultured hMSCs, capillary-like tube formation was significantly ( P &lt;0.01) induced. However, hMSC-induced capillary-like tube formation was significantly ( P &lt;0.01) inhibited when the endothelial cells were incubated with the supernatant from hMSCs in the presence of a neutralizing anti-VEGFR2. These data suggest that treatment of stroke with hMSCs enhances angiogenesis in the host brain and hMSC-enhanced angiogenesis is mediated by increases in levels of endogenous rat VEGF and VEGFR2.
Lung sequestration: report of seven cases and review of 540 published cases
Authors: B Savic, F J Birtel, W Tholen, H D Funke, R Knoche
Journal: Thorax (1979)

We present an analysis of 400 intralobar and 133 extralobar sequestrations, six cases presenting intra- and extralobar sequestration simultaneously, five sequestrations of one whole lung, and two bilateral intralobar sequestrations. This anomaly comprises 0·15-6·4% of all congenital pulmonary malformations. Usually the posterior basal segment is affected. The aberrant artery in intralobar sequestration originated in 74% of all cases from the thoracic aorta, and in 14·8% there was more than one anomalous artery. The mean diameter of the aberrant arteries was 6·3-6·6 mm. Usually arteries with predominantly elastic fibres were found. Arteriosclerotic changes were common, even in children. The venous return of the intralobar sequestration is, in 95·7% of all cases, via the pulmonary veins. In 13·7% of all cases other congenital malformations were observed. Symptoms arose within the first decade of life in 37·2% Bronchography and retrograde arteriography are the mainstay of diagnosis. Sequestrations are not supplied by a bronchial artery. Treatment of choice is operation as early as possible. Altogether seven operative deaths were reported, five of which were due to haemorrhage during operation. Of the 133 extralobar sequestrations, 77·4% were located between diaphragm and lower lobe. The arterial supply was provided by branches of the aorta. Some cases were supplied with venous blood by branches of the pulmonary artery. In six cases secondary changes, such as tuberculosis or carcinoma were found. In 60% of all the patients symptoms occurred within the first decade of life. Preoperative diagnosis was correct in only six cases. There were four postoperative deaths.
Determination of Autologus Serum Skin Test and its Association with Clinical and Immunological Markers in Adult Patients with Chronic Urticaria Treated at the Regional Unit of Immunology at the "Dr. Enrique Tejera" Hospital from April to September 2007.
Authors: M.E. Flores Chávez, A. Chacon, M.R. Chacon de Petrola, M.T. Pacheco de Toro
Journal: Journal of Allergy and Clinical Immunology (2009)
Particle Irradiation Suppresses Metastatic Potential of Cancer Cells
Authors: Toshiyuki Ogata, Teruki Teshima, Kazufumi Kagawa, Yoshio Hishikawa, Yutaka Takahashi, Atsuko Kawaguchi, Yuko Suzumoto, Kumie Nojima, Yoshiya Furusawa, Nariaki Matsuura
Journal: Cancer Research (2005)

Abstract Particle radiotherapy such as proton and carbon ion has been producing promising clinical results worldwide. The purpose of this study was to compare metastatic capabilities of malignant tumor cells after irradiation with photon, proton, and carbon ion beams to clarify their ion beam–specific biological effects. We examined the biological properties of highly aggressive HT1080 human fibrosarcoma cells to assess their metastatic processes in terms of cell adhesion capability to extracellular matrix, expression of integrins, cell migration, cell invasive capability, and matrix metalloproteinase-2 activity in vitro. We then assessed the metastatic capabilities of LM8 mouse osteosarcoma irradiated with carbon ion or photon beam in the syngeneic mice. Both proton and carbon ion irradiation decreased cell migration and invasion in a dose-dependent manner and strongly inhibited matrix metalloproteinase-2 activity. On the other hand, lower X-ray irradiation promoted cell migration and invasion concomitant with up-regulation of αVβ3 integrin. For cancer cells treated with carbon ion irradiation, the number of pulmonary metastasis was decreased significantly in vivo. These findings suggest that particle irradiation suppresses metastatic potential even at lower dose, whereas photon irradiation promotes cell migration and invasive capabilities at lower dose level, and provide preclinical evidence that ion beam radiotherapy may be superior to conventional photon beam therapy in possible preventive effects on metastases of irradiated malignant tumor cells.
L-type calcium channels, potassium channels, and novel nonspecific cation channels in a clonal muscle cell line derived from embryonic rat ventricle.
Authors: K R Sipido, E Marban
Journal: Circulation Research (1991)

We have characterized the membrane currents in the H9c2 clonal muscle cell line derived from embryonic rat ventricle. These cells, established by selective serial passage and clonal proliferation, have been found by Hescheler and coworkers to express dihydropyridine-sensitive calcium channels that respond to beta-adrenergic stimulation. We have investigated the macroscopic and elementary currents in these cells by using standard patch-clamp methods. In cells that are kept confluent for 3-4 weeks, we have confirmed the expression of L-type calcium channels and additionally establish that the unitary conductance of many, but not all, of these channels (25 pS in 70 mM barium) is equal to that of cardiac rather than skeletal muscle. When the cells are proliferating rapidly, calcium channels are sparse or absent, but at least two distinct potassium channels and a nonspecific cation channel are observed. The nonspecific channel exhibits a conductance of 30 pS in physiological saline and conducts sodium, potassium, and calcium with nearly equal efficacy. Several unusual properties distinguish this nonspecific channel from others described previously. Gating is voltage dependent, with slow activation and marked increases in open probability at positive potentials. Unlike voltage, activation and marked increases in open probability at positive potentials. Unlike voltage, changes in [Ca2+] or in membrane stretch do not noticeably influence activity. In conclusion, our work and that of Hescheler et al indicate that H9c2 cells are potentially valuable surrogates for the investigation of ion channel regulation and muscular gene expression.
Arterial Endothelium-Specific Activin Receptor-Like Kinase 1 Expression Suggests Its Role in Arterialization and Vascular Remodeling
Authors: Tsugio Seki, Jihye Yun, S. Paul Oh
Journal: Circulation Research (2003)

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant vascular disorder characterized by epistaxis, mucocutaneous telangiectases, and arteriovenous malformations (AVM). Two genes are linked to HHT: endoglin ( ENG ) in HHT1 and activin receptor-like kinase 1 ( ACVRL1 ; ALK1 ) in HHT2. Although both genes are involved in the transforming growth factor β signaling pathways, the pathogenetic mechanisms for HHT remain elusive. It was shown that mutations in the Alk1 gene in mice and zebrafish resulted in an embryonic lethal phenotype due to severe dilation of blood vessels. We created a novel null mutant mouse line for Alk1 ( Alk1 lacZ ) by replacing its exons, including the one that encodes the transmembrane domain, with the β-galactosidase gene. Using Alk1 lacZ mice, we show that Alk1 is predominantly expressed in developing arterial endothelium. Alk1 expression is greatly diminished in adult arteries, but is induced in preexisting feeding arteries and newly forming arterial vessels during wound healing and tumor angiogenesis. We also show that hemodynamic changes, which require vascular remodeling, may regulate Alk1 expression. Our studies suggest the role of Alk1 signaling in arterialization and remodeling of arteries. Contrary to the current view of HHT as venous disease, our findings suggest that the arterioles rather than the venules are the primary vessels affected by the loss of an Alk1 allele, and that blood vessels with reduction in Alk1 expression may harbor defects in responding to demands for vascular remodeling.
Proof or Principle? On Economic Modeling to Guide Genomic Testing in Metastatic Colorectal Cancer
Authors: Josh J. Carlson, Scott D. Ramsey
Journal: JNCI Journal of the National Cancer Institute (2012)

The use of molecular testing to personalize cancer treatment selection is on the rise and has been heralded as a panacea for patients diagnosed with cancer. In principle, the scenario for molecular testing is clearly positive: a relatively inexpensive test that identifies “responders” to expensive therapeutics can improve outcomes for those who receive it while sparing other patients (and society) the risk and expense of medicines that ultimately will not help and sometimes can harm. As with all major advancements in the treatment landscape, a fuller picture of molecular testing can only emerge through experience. That experience inevitably leads to a more nuanced understanding of molecular testing’s impact on outcomes, costs, and value for patients and populations. A prime example of the evolution of knowledge from promise to reality can be seen with KRAS mutation testing in metastatic colorectal cancer (mCRC). KRAS, and to a lesser extent BRAF, mutation testing is used to identify mCRC patients who do not benefit from two costly anti-epidermal growth factor receptor (EGFR) therapies: cetuximab and panitumumab. The intent of testing is to avoid unnecessary drug exposure and the associated toxicity and cost for the 30% to 40% of mCRC patients unlikely to respond to these drugs (ie, patients with tumors harboring KRAS mutations). Both the National Comprehensive Cancer Network and the American Society of Clinical Oncology clinical guidelines support the use of KRAS testing in clinical practice based on level 2 evidence from retrospective analyses of clinical trial data and other observational study designs (1,2). However, the real-world impact of screening for both KRAS and BRAF prior to treatment initiation is not yet fully understood. Simulation modeling can be a useful way to estimate the impact of molecular testing on population health outcomes, costs, and value, as well as to identify factors that fundamentally drive the benefits and drawbacks of molecular
AB0731 Does dynamic contrast-enhanced magnetic resonance (dce-mri) aid the diagnosis of early rheumatoid arthritis in the wrist?
Authors: L. Medrud, A. Nielsen, M. Boesen, U. Fredberg, T. Ellingsen
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatoidarthritis (RA) patients are at risk of developing irreversible joint damage. Modern treatment strategies prevent or reduce the permanent joint damage(1). DCE- MRI is a method evaluating perfusions characteristic and might give extra information for the diagnosis. <h3>Objectives</h3> Evaluate the clinical consequence of DCE-MRI in early DMARD and steroid naïve RA in the wrist joint, compared to standard-MRI / Ultrasound (US) and clinical evaluation. <h3>Methods</h3> Nine patients with early RA by an rheumatologist (2009 ACR/EULAR criteria) were referred to standard-MRI, DCE- MRI and US of the most affected hand before start of treatment. We used 1.5 T Siemens Avanto Magnetom for the MRI sequences. DCE-MRI is based on sequential acquisition of MRI sequences during infusion of a contrast agent. Active arthritis was defined as: initial rate of enhancement (IRE) &gt; 0,01, maximum enhancement (ME) &gt;1,7 and perfusion with wash out- or plateau pattern in a small region of interest (ROI). Standard MRI were analyzed using the OMERACT RA MRI scoring system (RAMRIS) (3). Cut –off: synovitis &gt;2, or edema in min. two bones, or edema in one bone and one erosion. <h3>Results</h3> <h3>Conclusions</h3> The good correlation between arthritis scored by RAMRIS and DCE- MRI resembles findings from the literature (2). Furthermore in two patients DCE- MRI showed sign of inflammation in equivocal cases where RAMRIS could not define arthritis. This suggests DCE- MRI can confirm the clinical diagnosis of arthritis earlier in some patients with early RA. In a high proportion of patients DCE-MRI and ultrasound gave the same result (8 out of 9). This might be expected because they are both methods for evaluating perfusions characteristic. <h3>References</h3> Lard LR.JM. Am J Med. 2001 Oct Boesen M. Rheumatology. 2012 Jan Østergaard M.Ann Rheum Dis. 2005 Feb <h3>Disclosure of Interest</h3> L. Medrud: None Declared, A. Nielsen: None Declared, M. Boesen Consultant for: M Boesen has acted as an independant nonpaid clinical advisor for Image Analysis LTD., U. Fredberg: None Declared, T. Ellingsen: None Declared
Possession and jinn
Authors: Najat Khalifa, Timothy Hardie
Journal: Journal of the Royal Society of Medicine (2005)

Religion remains a powerful influence on notions of health and disease.1 One Islamic concept that has entered into western mythology is that of the jinn or genies, as in the story of Aladdin. However, according to Islamic belief, jinn are real creatures that form a world other than that of mankind, capable of causing physical and mental harm to human beings. An example of such harm is possession.2,3 As defined by Littlewood,4 possession is the belief that an individual has been entered by an alien spirit or other parahuman force, which then controls the person or alters that person's actions and identity. To the observer, this would be manifested as an altered state of consciousness. In the UK, jinn possession is most likely to be seen among people from Pakistan, Bangladesh, the Middle East or North Africa.4

Some commentators claim that possession is a culture-bound syndrome but others argue that, although the manifestations may differ according to culture, the underlying theme is always the same.5 According to Whitwell and Barker,6 the word possession is used in two different ways. The first refers to 'true' possession invoking the supernatural. The second, which makes no such assumptions, has been applied to several different states. One example of the second is a syndrome consisting of clouding of consciousness, changed demeanour and tone of voice and subsequent amnesia. Another is a trance that may be induced deliberately in a certain cult setting. According to Prins,7 true possession consists of occult experience, invitation and unknown influences. Very little has appeared on jinn possession in medical publications. Here we describe cultural and religious and psychiatric aspects and offer guidance on management in clinical practice.