tbuckley/cabot-search huggingface dataset:
Exhaled breath temperature in asthmatic and healthy children: A case-control study
Authors: Andrea Bon, Anna Manfredi, Margherita Mauro, Mario Canciani
Journal: European Respiratory Journal (2014)

Introduction:  Exhaled Breath Temperature (EBT) is a promising marker of airway inflammation. Studies on adult asthmatic patients show an increase of the EBT compared to healthy peers, but there are few studies in paediatric patients.   Objective:  The aim of this study is to compare the EBT of asthmatic children versus healthy controls, and to evaluate correlations with spirometry and exhaled nitric oxide (ENO).   Methods:  56 patients were enrolled (36 M 20 F, aged 7-16 ys), 44 asthmatics and 12 controls. Anamnestic data, physical examination, and EBT values with X-halo (Delmedica), along with body and air temperature were evaluated. In asthmatic children we performed pulmonary function tests and ENO, too.   Results:  The median EBT was greater in asthmatics compared to controls (33.35°C vs 29.14°C, p=0.001). The average body temperature was similar in both groups (36.23°C vs 32.38 °C, p> 0.05) but the average air temperature was different (18.9°C vs 23.1°C, p   Conclusions:  There is a significant difference in median EBT between asthmatic and healthy children. We couldn9t find any correlation between EBT and FEV1 or ENO, possibly because the three tests reflect different phases of bronchial inflammation.
Protection Against Guinea Pig Hepatomas by Pretreatment With Subcelluar Fractions of Mycobacterium bovis (BCG)2
Authors: Percy Minden, Mark Wainberg, David W. Weiss
Journal: JNCI Journal of the National Cancer Institute (1974)

A methanol-extraction residue and a supernatant of sonically disrupted cells were derived from killed BCG. Pretreatment with these substances prevented progressive development of line-10 hepatocarcinoma in a significant proportion of syngeneic strain-2 Sewall-Wright guinea pigs challenged with sufficient neoplastic cells to cause fatal disease in all the controls.
Very early detection of small clones harbouring EGFR mutations in NSCLC by 2nd generation sequencing
Authors: Claudia Vollbrecht, Fabian Mairinger, Slave Trajanoski, Iris Halbwedl, Theresa Maierhofer, Gabriele Michelitsch, Elvira Stacher, Martin Filipits, Katharina Schmid, Jens Kollmeier, Thomas Mairinger, Helmut Popper
Journal: European Respiratory Journal (2011)

Activating mutations of the EGFR gene are present in NSCLC and respond to EGFR TKI therapy, but 50% of these patients show disease progression during the course of TKI treatment, possibly due to resistant tumor cell clones primarily present as small clones within the carcinoma. We tested 80 adenocarcinomas of the lung for known and unknown EGFR mutations comparing different methods for mutation analysis, and tried to correlate the new adenocarcinoma classification with EGFR mutation status. The study included 40 samples with proven mutation status and 40 predominantly acinar or papillary adenocarcinomas with undetermined EGFR status. EGFR-mutation analysis was previously done by either Sanger- or pyrosequencing, LightCycler assay, BioFilmChip microarray, IHC with mutant specific antibodies, or by DxS kit. DNA was isolated and EGFR mutations in exon 18 to 21 were tested with 454 sequencing system. Cut-off was set according to Wang et al. (Genome Res. 2007). 1829 mutations were found in 79 patient samples. 77 different previously evaluated mutations could be confirmed. Additional 158 different new mutations were detected in tumor cells. When compared to other methods our results show a better specificity and better sensitivity. Cases analyzed by LightCycler assay and pyrosequencing showed 100% correspondence to 454 sequencing, whereas all other methods showed abberations. Mutations present in small tumor cell clones were not detected by any of the other methods. Furthermore, T790M resistance mutation combined with an activating mutation could be found in 2 untreated patient samples. The results underline the need for higher sensitive methods applicable in in routine diagnostics.
Positivity of quantiferon-TB tests in sarcoidosis patients
Authors: Erdogan Cetinkaya, Mehmet Akif Ozgul, Elif Yelda Ozgun Niksarlioglu, Hilal Onaran, Murat Acat
Journal: European Respiratory Journal (2013)

AIM:   Sarcoidosis is a multisystemic disease with noncaseifie granuloma in organs with unknown etiology. In this study, we investigated the positivity of Quantiferon-TB test in patients with sarcoidosis.   METHOD:   In this study we investigated 87 patients with newly diagnosed in January 2007-January 2012, retrospectively. Demographic data, stage, diagnosis methods, quantiferon-TB tests and tuberculin skin test (TST) were assesed.   RESULTS:   Mean age was 41.9 (SD11.2) and age range was between 25-71 years. Of the patients 61 (70.1%) were women, 26 (29.9%) were male. Diagnosis methods were transbronchial neddle aspiration (48 cases, 55.2%), EBUS-transbronchial neddle aspiration (18 cases, 20.7%), transbronchial biopsy (9 cases, 10.3%) and mediastinoscopy (9 cases, 10.3%). Majority of the patients were stage I (41, 47.1%) and stage II (40, 46%); 6 (6.9%) were stage III. Quantiferon-TB test positivity was determined in 55 (63.2%) patients and negativity was determined 28(%32.2) patients. Tuberculin skin test was determined in 52 (59.8%) patients as anergic and TST induration diameter was greater than 10mm in 13 (17.2%) patients. In the admission of hospital 15 (17.2%) patients had eritema nodosum. During the study period, no active tuberculosis infection was detected.   CONCLUSION:   In this study, the positivity rate of Quantiferon-TB test was higher in patients with sarcoidosis. This result support that mycobacterium tuberculosis might be a factor in sarcoidosis etiology. Furthermore, there was no active tuberculosis infection in study group; latent tuberculosis should be considered in sarcoidosis in the populations which have higher prevalance of tubercuolsis. country.
Cellular ions in hypertension, insulin resistance, obesity, and diabetes
Authors: L M Resnick
Journal: Journal of the American Society of Nephrology (1992)

The clinical linkage of hypertensive cardiovascular disease, left ventricular hypertrophy, and accelerated atherosclerosis with a spectrum of metabolic disturbances including peripheral insulin resistance, hyperinsulinemia, obesity, and frank non-insulin dependent diabetes mellitus, has been increasingly appreciated. However, the underlying biologic basis mediating this clinical association remains unclear. Nuclear magnetic resonance techniques have been used to measure various intracellular ion species in human erythrocytes and have found that common, shared intracellular abnormalities of cytosolic free calcium, free magnesium, and pH occur in each of these clinical syndromes. Specifically, essential hypertension is characterized by higher fasting free cytosolic calcium concentrations and reciprocally lower intracellular free magnesium and pH levels compared with those of normotensive control subjects. Furthermore, for all subjects, free calcium and free magnesium levels were closely related both to the left ventricular mass and to the degree of insulin resistance present. Moreover, these same intracellular ionic lesions were found in normotensive obese and/or non-insulin diabetic individuals. Last, evidence has recently been provided that the cardiovascular consequences of increased dietary sugar and salt intake may well be determined by their concurrent influence on cellular ion metabolism. These data led to a hypothesis for a central role for altered cellular ion homeostasis in mediating the clinical linkage of cardiovascular and metabolic disease. According to this ionic hypothesis, essential hypertension, non-insulin dependent diabetes, and their frequently associated features of obesity, left ventricular hypertrophy, and accelerated atherosclerosis all derive from and reflect different clinical manifestations of the same underlying cellular lesion, characterized at least in part by elevated cytosolic free calcium and suppressed free magnesium levels.
Hereditary angioedema with normal C1-INH with<i>versus</i>without specific<i>F12</i>gene mutations
Authors: K. Bork, K. Wulff, G. Witzke, J. Hardt
Journal: Allergy (2015)

Hereditary angioedema with normal C1-INH may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or mutations in genes that are still unknown (HAE-unknown). To assess the differences in transmission and inheritance, clinical features, and laboratory parameters between patients with HAE-FXII and HAE-unknown.Sixty-nine patients with HAE-FXII from 23 unrelated families and 196 patients with HAE-unknown from 65 unrelated families were studied.Both HAE-FXII and HAE-unknown are inherited as autosomal-dominant traits with incomplete penetrance. The male to female ratio was 1 : 68 in HAE-FXII and 1 : 6.3 in HAE-unknown. The maternal to paternal transmission ratio was 35 : 14 for HAE-FXII and 109 : 12 for HAE-unknown. Mean age at onset of clinical symptoms was 20.3 years in patients with HAE-FXII and 29.6 years in patients with HAE-unknown. The incidence of asphyxiation due to angioedema was similar for HAE-FXII and HAE-unknown. Oral contraceptives and pregnancies had a significantly higher impact on HAE-FXII than on HAE-unknown. Slightly decreased C1-INH activity and C4 concentration were observed in more patients with HAE-FXII than HAE-unknown. Tests for FXI and FXII activity, plasminogen activator inhibitor 1, and activated partial thromboplastin time showed variability but no significant differences between the groups. No abnormalities were found for C1-INH protein, C1q, alpha2-macroglobulin, antithrombin III, and angiotensin-converting enzyme. In families with HAE-FXII, the number of female offspring with F12 mutations was significantly increased and that of male offspring was significantly decreased.HAE-FXII and HAE-unknown differ in various respects, including gender distribution, genetics, symptoms, and estrogen impact.
When Is a Tumor Marker Ready for Prime Time? A Case Study of c-<i>erb</i>B-2 as a Predictive Factor in Breast Cancer
Authors: Hideko Yamauchi, Vered Stearns, Daniel F. Hayes
Journal: Journal of Clinical Oncology (2001)

PURPOSE: c-erbB-2 (HER-2, c-neu) might play a role as a predictive factor in breast cancer. However, the clinical utility of the marker in this disease is still not established. We conducted a critical analysis of the literature, in which we reviewed the factors that contribute to the lack of acceptance of c-erbB-2 for clinical use and attempted to determine the predictive role of c-erbB-2 for response to specific therapies. METHODS: We conducted a MEDLINE literature search using the keywords c-erbB-2, HER2, neu, and breast cancer, reviewed the references included in each publication, and reviewed abstracts that have been reported in the 1997-2000 proceedings to the American Association of Cancer Research and American Society for Clinical Oncology annual meetings. RESULTS: The preclinical and clinical data reported to date suggest that amplification or overexpression of c-erbB-2 is a weak to moderate negative pure prognostic factor. c-erbB-2 seems to be a weak to moderate negative predictive factor for response to endocrine therapy. The marker is also a moderate negative predictive factor for response to alkylating agents and a moderate positive predictive factor for response to anthracyclines. The data regarding response to taxanes or radiotherapy are not sufficient to make recommendations regarding treatment decision making. Finally, c-erbB-2 is a strong predictive factor for response to trastuzumab. CONCLUSION: We conclude that, in the adjuvant setting, c-erbB-2 status should not be used to determine whether a woman should receive adjuvant systemic therapy (weak prognostic factor). In addition, c-erbB-2 status should not be used to determine whether a patient should receive endocrine therapy. When adjuvant chemotherapy is recommended, anthracycline-based therapy should be the preferred regimen for c-erbB-2–positive patients. However, when anthracyclines are contraindicated, alkylating agent–based therapy should not be withheld. To determine the true predictive role and strength of the marker for response to each therapy, prospective randomized clinical trials or formal meta-analyses are required.
Trisomy #15 in Murine Thymomas Induced by Chemical Carcinogens, X-Irradiation, and an Endogenous Murine Leukemia Virus2
Authors: F. P. H. Chan, J. K. Ball, F. R. Sergovich
Journal: JNCI Journal of the National Cancer Institute (1979)

Journal Article Trisomy #15 in Murine Thymomas Induced by Chemical Carcinogens, X-Irradiation, and an Endogenous Murine Leukemia Virus Get access F. P. H. Chan, F. P. H. Chan 3Department of Anatomy, University of Western Ontario, London, Ontario, Canada N6A 5B7. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. K. Ball, J. K. Ball 5 4Cancer Research Laboratory, University of Western Ontario. 5Address reprint requests to Dr. Ball. Search for other works by this author on: Oxford Academic PubMed Google Scholar F. R. Sergovich F. R. Sergovich 6Cytogenetics Laboratory, Children's Psychiatric Research Institute, London, Ontario, Canada. 7We thank Mrs. H. Behr and Mrs. B.Hartford for their technical assistance. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 62, Issue 3, March 1979, Pages 605–610, https://doi.org/10.1093/jnci/62.3.605 Published: 01 March 1979 Article history Received: 31 May 1978 Accepted: 12 August 1978 Published: 01 March 1979
Flagellin potentiates the Ca2+-dependent electrolytes secretion from airway submucosal gland in a TLR4-independent, TLR5-dependent and cGK-dependent manner
Authors: Soshi Muramatsu, Tsutomu Tamada, Masayuki Nara, Koji Murakami, Masahito Ebina
Journal: European Respiratory Journal (2012)

[Background]

Airway surface fluids are mainly secreted from submucosal glands and play important roles in the airway defense via the upregulation of mucociliary transport. Although Toll-like receptors (TLRs) recognize distinct pathogen-associated molecular patterns, it is not well known whether TLRs directly upregulates the airway secretions. Recently, we have reported that TLR4 works as one of important secretagogue in the airways (AJRCMB 2011). In the present study, we focused on the TLR5 signaling as other candidate for a potentiator of airway secretion.

[Methods]

Freshly isolated swine tracheal submucosal gland cells were prepared and measured their secretory activities as ionic currents by applying a patch-clamp technique. The expression of TLR5 was estimated by both the immunofluorescent staining and RT-PCR. The intracellular mechanisms were investigated by applying some inhibitors of NOS or cGMP-dependent protein kinase (cGK).

[Results]

Flagellin, a TLR5 ligand, showed significant potentiating effects on ACh-evoked ionic currents. These effects were abolished by the pretreatment with anti-TLR5 antibody, but not by specific TLR4 antagonist. Two different inhibitors of each NOS and cGK abolished these effects. We also revealed that the expression of TLR5 on the tracheal submucosal gland cells.

[Conclusion]

Our study showed that flagellin caused the potentiating effects on airway secretions in a TLR5-dependent, TLR4-independent manner and that NO/cGMP/cGK pathway was involved in these intracellular mechanisms. These finding suggest that TLR5 also works as a potentiator of airway secretion in the airway mucosal immune systems.
Clinical characteristics and outcomes of patients with clinically unsuspected pulmonary embolism versus patients with clinically suspected pulmonary embolism
Authors: Michal Shteinberg, Yochai Adir, Miriam Segal-Trabelsy, Arie Laor, Moshe Vardi, Haim Bitterman
Journal: European Respiratory Journal (2012)

Background: The routine use of multidetector computed tomography (MDCT) has led to increased detection of unsuspected pulmonary embolism (UPE). Our aim was to compare the characteristics and prognosis of patients with UPE to patients with suspected PE (SPE).  Methods: We retrospectively reviewed the charts of patients diagnosed with PE in a community-based university hospital between the years 2002-2007. UPE was defined as PE detected on CT scans performed for indications other than PE. We compared patients with UPE to patients with SPE for differences in clinical features, ECG, imaging, and echocardiographic findings. We assessed the long-term outcomes of patients.  Results: Of 500 patients with PE, 408 had SPE and 92 had UPE. Patients with UPE were similar to patients with SPE regarding age and sex distribution. Malignancy was more prevalent in UPE patients (39% vs. 23%, p  Conclusions: We suggest that UPE is more prevalent in patients with a malignancy and is associated with higher mortality despite a less severe clinical presentation. UPE may be a marker of poor prognosis.
Port site recurrences after laparoscopic and thoracoscopic procedures in malignancy.
Authors: P A Johnstone, D C Rohde, S E Swartz, J E Fetter, S D Wexner
Journal: Journal of Clinical Oncology (1996)

PURPOSE AND METHODS A review of the literature was performed to determine the number of cases of port site recurrences (PSR) after laparoscopy or thoracoscopy. CANCERLINE and MEDLINE were searched, as were citings from retrieved and related papers. RESULTS There have been 35 reported cases of PSR after laparoscopic colectomy for colorectal carcinoma, and 23 cases after thoracoscopic procedures for lung neoplasms. All of these have been reported since 1993. Since 1991, 12 cases have been described after laparoscopic cholecystectomy of unsuspected gallbladder carcinoma, and another case after biopsy of a known gallbladder carcinoma. Ten cases of PSR have been reported after laparoscopic procedures for ovarian lesions, often in the presence of peritoneal seeding at diagnosis. Other rare PSRs have been documented after several procedures in various malignancies. CONCLUSION Enrollment of patients onto the ongoing intergroup study evaluating open versus laparoscopic resection of colon cancer should be encouraged. Until valid prospective data on PSR frequency are available, laparoscopic or thoracoscopic resection of malignancy off-protocol should be undertaken with circumspection.
The Past, Present, and Future of Nicotine Addiction Therapy
Authors: Judith J. Prochaska, Neal L. Benowitz
Journal: Annual Review of Medicine (2015)

The tobacco addiction treatment field is progressing through innovations in medication development, a focus on precision medicine, and application of new technologies for delivering support in real time and over time. This article reviews the evidence for combined and extended cessation pharmacotherapy and behavioral strategies including provider advice, individual counseling, group programs, the national quitline, websites and social media, and incentives. Healthcare policies are changing to offer cessation treatment to the broad population of smokers. With knowledge of the past and present, this review anticipates what is likely on the horizon in the clinical and public health effort to address tobacco addiction.
miR-21: a miRaculous Socratic paradox
Authors: P. A. da Costa Martins, L. J. De Windt
Journal: Cardiovascular Research (2010)

This editorial refers to ‘Ischaemic preconditioning-regulated miR-21 protects heart against ischaemia/reperfusion injury via anti-apoptosis through its target PDCD4’ by Y. Cheng et al. , pp. 431–439, this issue. 

The molecular biology dogma that chromosomal DNA transcribes its genetic information to large messenger RNAs (mRNAs), yielding proteins as the chief actors within the cell, carrying out the duties specified by the information encoded in genes, failed to consider the recent evidence that the majority of the genomes of eukaryotes are, in fact, transcribed into non-coding RNA (ncRNA), many of which are alternatively spliced and/or processed into very small (18–100 nucleotides in length), yet fully functional RNA molecules. MicroRNAs (miR or miRNAs) are one such class of evolutionarily conserved, small ncRNAs, on average 22 nucleotides in length. miRNAs are post-transcriptional regulators that bind to complementary sequences in the 3′ untranslated regions (3′ UTRs) of target mRNAs in a sequence-specific manner, usually resulting in gene silencing.

Through forward genetic screening in the nematode Caenorhabditis elegans , the first prototypical miRNAs, lin-4 and let-7, were uncovered as regulators of developmental timing. Subsequent studies in vertebrates suggested that miRNAs, rather than functioning as decisive regulatory on–off switches, more commonly function to modulate or fine-tune expression of proteins and cellular phenotypes.1 On the basis of sequence conservation and the ability to fold into a hairpin structure, the human genome is predicted to encode as many as a thousand miRNAs, some tissue- or cell type-specific, others considered as house-keeping molecules, and combined they are estimated to regulate as many as 30% of all cellular proteins.2

In several recent studies, microarray analyses were performed to determine whether miRNAs are misexpressed in hypertrophic and failing hearts. These studies point to a collection of miRNAs that are up- or down-regulated during pathological cardiac remodelling in rodents and humans.3 … 

*Corresponding author. Tel: +31 43 388 4308; fax: +31 43 387 1055, Email: l.dewindt{at}maastrichtuniversity.nl
Childhood obstructive sleep apnoea and elevated blood pressure: A longitudinal follow-up study
Authors: Albert Li, Chun T. Au, Crover Ho, Yun K. Wing
Journal: European Respiratory Journal (2012)

Background and Objective: Childhood obstructive sleep apnoea (OSA) is a prevalent condition, and is associated with raised blood pressure (BP) in cross-sectional studies. This study aimed to investigate if baseline or changes in OSA severity could predict BP changes over a 4-year period.  Methods and Results: Children who participated in our previous OSA prevalence study were invited to undergo repeat overnight sleep study and ambulatory 24-hr BP monitoring at 4-year follow-up. One hundred and ninety-one (62% out of 306) subjects took part in this follow-up study. Children with baseline moderate-to-severe OSA (OAHI >5/hr) had significantly higher BP at follow-up than controls. The change in OAHI was positively associated with the changes in wake and sleep systolic BP. Path analysis revealed a best-fit model in which log-transformed baseline OAHI and change in OAHI were both independent predictors for change in sleep systolic BP, after adjusting for baseline sleep systolic BP, gender, height and body mass index z score.  Conclusions: In the first longitudinal study that examined relationship between OSA and BP in children, we found baseline OSA severity could predict systolic BP at 4-year follow-up. The change in OAHI was associated with the change in sleep systolic BP, independent of obesity and weight gain. The results are clinically relevant since elevated BP in childhood is a well-known risk factor for future cardiovascular adverse events. Early diagnosis and intervention should thus be advocated in the management of childhood OSA.