tbuckley/cabot-search huggingface dataset:
Clear-cell variant of calcifying epithelial odontogenic tumor (Pindborg tumor) in the mandible
Authors: Ching-Yi Chen, Chung-Wei Wu, Wen-Chen Wang, Li-Min Lin, Yuk-Kwan Chen
Journal: International Journal of Oral Science (2013)

We present an uncommon case (female patient aged 59 years) of the clear-cell variant of calcifying epithelial odontogenic tumor (CEOT) (also known as Pindborg tumor) in the mandible. The clinical characteristics and probable origins of the clear tumor cells of previously reported cases of clear-cell variant of intraosseous CEOT are also summarized and discussed.
EDTA‐dependent pseudothrombocytopenia: A clinical and epidemiological study of 112 cases, with 10‐year follow‐up
Authors: Nicola Bizzaro
Journal: American Journal of Hematology (1995)

In the past 10 years, we have observed 112 cases of EDTA-dependent pseudothrombocytopenia (PTCP) due to in vitro platelet clumping at room temperature. 93 patients had antiplatelet antibodies (48 IgM, 30 IgG, 3 IgA, and 12 had two different isotypes concomitantly). In 20% of patients, the presence of IgM antibodies characteristically accompanied platelet agglutination also at 37 degrees C, and in citrated blood. The phenomenon was not age or sex related, nor was it associated with any particular pathology or use of specific drugs, and was present in both healthy subjects and patients with various diseases. Flow cytofluorimetric analysis of CD5-positive B cells, which are responsible for autoantibody production, did not demonstrate any changes in the percentage and absolute number of this lymphocyte subset. Average follow-up was 5 years (6 months-10 years); however, previous clinical records disclosed that PTCP was present for more than 15 years in four cases, and more than 20 years in three others, with no clinical manifestation of disease. This study confirms that EDTA-dependent PTCP is a phenomenon related to the presence of natural autoantibodies with antiplatelet activity, devoid of pathological significance. Its clinical interest resides in the need for its prompt and certain recognition in order to avoid unnecessary examinations and therapeutic interventions. The best and most rapid technique for obtaining accurate platelet counts in PTCP subjects is to collect and examine EDTA blood at 37 degrees C; however, clumping will still be present in about 20% of these cases, and even in citrated blood. To obviate this phenomenon, blood should be collected in ammonium oxalate, and platelets counted in a Burker chamber.
A Nanoparticle System Specifically Designed to Deliver Short Interfering RNA Inhibits Tumor Growth <i>In vivo</i>
Authors: Nobuhiro Yagi, Ichiro Manabe, Tsuneaki Tottori, Atsushi Ishihara, Fusa Ogata, Jong Heon Kim, Satoshi Nishimura, Katsuhito Fujiu, Yumiko Oishi, Keiji Itaka, Yasuki Kato, Masahiro Yamauchi, Ryozo Nagai
Journal: Cancer Research (2009)

Use of short interfering RNA (siRNA) is a promising new approach thought to have a strong potential to lead to rapid development of gene-oriented therapies. Here, we describe a newly developed, systemically injectable siRNA vehicle, the "wrapsome" (WS), which contains siRNA and a cationic lipofection complex in a core that is fully enveloped by a neutral lipid bilayer and hydrophilic polymers. WS protected siRNA from enzymatic digestion, providing a long half-life in the systemic circulation. Moreover, siRNA/WS leaked from blood vessels within tumors into the tumor tissue, where it accumulated and was subsequently transfected into the tumor cells. Because the transcription factor KLF5 is known to play a role in tumor angiogenesis, we designed KLF5-siRNA to test the antitumor activity of siRNA/WS. KLF5-siRNA/WS exhibited significant antitumor activity, although neither WS containing control scrambled-siRNA nor saline containing KLF5-siRNA affected tumor growth. KLF5-siRNA/WS inhibited Klf5 expression within tumors at both mRNA and protein levels, significantly reducing angiogenesis, and we detected no significant acute or long-term toxicity. Our findings support the idea that siRNA/WS can be used to knock down specific genes within tumors and thereby exert therapeutic effects against cancers.
Nab-Paclitaxel Is an Active Drug in Preclinical Model of Pediatric Solid Tumors
Authors: Libo Zhang, Paula Marrano, Sushil Kumar, Michael Leadley, Evelyn Elias, Paul Thorner, Sylvain Baruchel
Journal: Clinical Cancer Research (2013)

To investigate the antitumor effect of nab-paclitaxel, an albumin-stabilized nanoparticle formulation of paclitaxel, on pediatric solid tumor models.A panel of three rhabdomyosarcoma, one osteosarcoma and seven neuroblastoma cell lines were exposed to increasing concentrations of nab-paclitaxel in vitro. Cell viability was evaluated using the Alamar Blue Assay. Antitumor effect was further assessed in vivo in NOD/SCID xenograft and metastatic neuroblastoma mouse models. Tumor sections were analyzed by immunohistochemistry for cleaved caspase-3 and phospho-histone H3. Plasma and intratumoral paclitaxel concentrations were measured by liquid chromatography-mass spectrometry. Ratio of intratumoral and plasma concentration was compared between nab-paclitaxel and paclitaxel treatment groups.Nab-paclitaxel displayed significant cytotoxicity against most pediatric solid tumor cell lines in vitro in a dose-dependent manner. In vivo, nab-paclitaxel showed antitumor activity in both rhabdomyosarcoma (RH4 and RD) and neuroblastoma [SK-N-BE(2) and CHLA-20] xenograft models. In the SK-N-BE(2) metastatic model, nab-paclitaxel treatment significantly extended animal survival compared with control (P < 0.01). Nab-paclitaxel treatment induced tumor cell-cycle arrest and apoptosis in vivo. In the RH4 model, increased local relapse-free intervals were observed with nab-paclitaxel treatment (37.7 ± 3.2 days) comparing with paclitaxel (13.6 ± 2.07 days). Local relapsed tumors following paclitaxel treatment proved to be paclitaxel-resistant and remained responsive to nab-paclitaxel. Mechanistically, a higher tumor/plasma paclitaxel drug ratio in favor of nab-paclitaxel was observed.Nab-paclitaxel showed significant antitumor activity against all pediatric solid tumors associated with an enhanced drug intratumor delivery. Furthermore, testing of nab-paclitaxel in pediatric solid-tumor patient population is under development.
Hyperglycemic Crises in Adult Patients With Diabetes
Authors: Abbas E. Kitabchi, Guillermo E. Umpierrez, John M. Miles, Joseph N. Fisher
Journal: Diabetes Care (2009)

PRECIPITATING FACTORS -The most common precipitating factor in the development of DKA and HHS is infection (1,4,10).Other precipitating factors include discontinuation of or inadequate insulin therapy, pancreatitis, myocardial infarction, cerebrovascular accident, and
Possible contribution to hepatocarcinogenesis of X transcript of hepatitis B virus in japanese patients with hepatitis C virus
Authors: Akihiro Tamori, Shuhei Nishiguchi, Shoji Kubo, Noritoshi Koh, Yoshinori Moriyama, Shunsuke Fujimoto, Tadashi Takeda, Susumu Shiomi, Kazuhiro Hirohashi, Hiroaki Kinoshita, Shuzo Otani, Tetsuo Kuroki
Journal: Hepatology (1999)

Serological research suggests that hepatitis B virus (HBV) and hepatitis C virus (HCV) are associated with the development of hepatocellular carcinoma (HCC). It is unclear how genes of hepatitis viruses participate in hepatocarcinogenesis in patients infected with HCV. We investigated the expression of hepatitis virus-related RNAs in resected liver from 51 patients with HCV antibodies (Ab) and without hepatitis B surface antigen (HBsAg). mRNA transcripts of the genes HBx, HBc, HBs, nonstructural (NS) region 3 of HCV, the 5′–untranslated region (UTR) of HCV, and the 5′–UTR of hepatitis G virus (HGV) were amplified by reverse–transcription polymerase chain reaction (RT–PCR) with specific primers for each gene. The HBx transcript was detected in 19 (37%) tumors and in 8 (16%) specimens of noncancerous tissues ( P = .014). The NS3 gene of HCV was detected in 35 (69%) tumors and 41 (80%) noncancerous tissues. HGV RNA was detected in 3 tumors (6%). Patients with HBx transcripts were younger than patients without HBx transcripts ( P = .012). HBx transcripts were detected in 3 (33%) of 9 well–differentiated HCCs, in 8 (31%) of 26 moderately differentiated HCCs, and in 8 (50%) of 16 poorly differentiated HCCs. Codon 130 (AAG) and codon 131 (GTC) of HBx were changed to ATG and ATC, respectively, in all HCCs with HBx transcripts. In conclusion, we found that the HBx gene was expressed in many HCCs; the gene might promote hepatocarcinogenesis in patients with HCVAb and without HBsAg, but HGV is not closely related to hepatocarcinogenesis in such patients
Effects of statins on vascular wall: vasomotor function, inflammation, and plaque stability
Authors: K K Koh
Journal: Cardiovascular Research (2000)

Clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statin therapy demonstrate an improvement in cardiovascular end points and coronary stenosis. However, an improvement in cardiovascular end points and coronary stenosis is incompletely explained by the baseline or treated LDL cholesterol level. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that modify endothelial function, smooth muscle cells, and monocyte-macrophage: vasomotor function, inflammatory responses, and plaque stability. Augmented bioactivity of NO by statin therapy either indirectly by its effect on lipoprotein levels and protection of LDL from oxidation, or directly by effects on NO synthesis and release, might account for enhancement of endothelium-dependent vasodilation. Recent experimental and animal studies have demonstrated that statins dose-dependently decrease smooth muscle cells migration and proliferation, independently of their ability to reduce plasma cholesterol. Moreover, statins are able to reduce the in vitro cholesterol accumulation in macrophages and expression of matrix metalloproteinase, resulting in plaque stability. These effects of statins were completely prevented by the addition of mevalonate and partially by all-trans farnesol and all-trans geranylgeraniol, confirming the specific role of isoprenoid metabolites, probably through prenylated proteins, in regulating these cellular events. Statins have been shown to prevent the activation of monocytes into macrophages, inhibit the production of pro-inflammatory cytokines, C-reactive protein, and cellular adhesion molecules. Statins decrease the adhesion of monocyte to endothelial cells. Accordingly, statins exert their cardiovascular benefits through a direct antiatherogenic properties in the arterial wall, beyond their effects on plasma lipids.
Differential Gene Expression by <i>Pseudomonas aeruginosa</i> during Interaction with Respiratory Mucus
Authors: Stephen Lory, Shouguang Jin, Jessica M. Boyd, Jennifer L. Rakeman, Philip Bergman
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

Pseudomonas aeruginosa is a common respiratory tract pathogen that causes serious infections in patients with cystic fibrosis. A number of putative virulence factors have been characterized in several laboratories, and some have been implicated in human infections, based on criteria such as the phenotype of isolates from infected patients, an immune response to a particular antigenic factor, and the effect of a virulence factor on infectivity in an animal model. We have developed a series of genetic tools to study the selective regulation of expression of P. aeruginosa genes during interactions of the pathogen with host tissues. These tools are based on direct enrichment of bacteria, when a particular promoter is induced or repressed. We have found that interaction of bacteria with mucus from patients with cystic fibrosis results in marked induction of expression of several genes, including one that encodes a lipopolysaccharide biosynthetic enzyme, a gene for a protein responsible for uptake of the ferric pyochelin siderophore, and a new gene homologous with a class of iron-responsive repressors. The tools described here are useful for identification of induced or repressed genes in various animal models of infection or in controlled laboratory conditions that mimic natural infections of humans. Such genes might not be detectable when bacteria are cultured in laboratory conditions, and these tools are therefore useful for general probing of a bacterial genome for genes regulated during different stages of infection.
Effects of Chronic Ethanol Administration on Rat Liver Proteasome Activities: Relationship With Oxidative Stress
Authors: Virginie Fataccioli, Evelyne Andraud, Monique Gentil, Samuel W. French, Helene Rouach
Journal: Hepatology (1999)

We previously reported that ethanol elicits an increased protein oxidation in the liver of rats receiving chronic ethanol by continuous intragastric infusion (Tsukamoto–French method). This accumulation of oxidized proteins could result from a decrease in the cytosolic proteolysis, related specifically to alkaline protease and its major components, the proteasomes. Because several studies suggest that intracellular proteolysis depends on the severity of oxidative stress, we investigated the cytosolic proteolytic activity under two chronic ethanol treatment paradigms associated with varying degrees of oxidative stress. For 4 weeks, male rats received chronic ethanol by continuous intragastric infusion or by oral administration (10% ethanol ad libitum as sole drinking fluid). A significant decrease was evident for alkaline protease activity as well as for sodium dodecyl sulfate (SDS)–activated latent 20S proteasome (chymotrypsine–like [ChT–L] and peptidylglutamyl peptide hydrolase [PGPH] activities) in the liver of rats receiving ethanol by continuous intragastric infusion. Free radical production and related processes appeared to be contributing events in proteolysis inhibition, because phenethyl isothiocyanate (PIC), an inhibitor of cytochrome P4502E1 (CYP2E1), reduced the inhibition of the ethanol–related ChT–L activity. Moreover, the lipid peroxidation level was inversely correlated with ChT–L activity. In contrast, no such changes were observed in ChT–L and PGPH activities or in cellular free radical targets following the oral ad libitum consumption of 10% ethanol. It appears, thus, that only the alcohol treatment paradigm associated with an overt oxidative stress produced a significant inhibition of the proteasome activity. The mechanisms of proteasome inhibition could involve the formation of an endogenous inhibitor such as protein aggregates or aldehyde–derivative peptides. Whatever the mechanism, the inhibition of cytosolic proteolysis and the subsequent accumulation of damaged proteins may be involved in the oxidatively challenged alcoholic livers and play a pathogenic role in experimental alcoholic liver disease.
Effect of Vagal Stimulation and Acetylcholine on the Ventricle
Authors: WILLEM KLIP
Journal: Circulation Research (1961)

It is shown that in the presence of a marginal zone, which is free of corpuscles and which has a width independent of the tube radius, the existence in the central zone of unsheared laminae of finite thickness, which also is independent of the tube radius, tends to increase rather than decrease the apparent viscosity when the radius of the tube becomes smaller.
A Whisper on the wind spawns a storm
Authors: K Weber
Journal: Cardiovascular Research (2000)

The heart, like many other organs, is composed of parenchyma surrounded by stroma. In this case, highly differentiated and very specialized cardiac myocytes are connected to and tethered within a three dimensional scaffolding of structural protein. Cardiac myocytes number one-third of cells found in the heart. Noncardiomyocytes, such as fibroblasts, endothelial and vascular smooth muscle cells, account for the majority of the remaining two-thirds. Interstitial fibroblasts are responsible for normal synthesis and degradation of this extracellular network, an albeit slow yet nonetheless ongoing process [1]. Fibroblasts are undifferentiated and pluripotent with a diverse portfolio of phenotypic expressions and functions. Myofibroblasts are an example of specialized fibroblast-like cells that appear at sites of tissue repair to carry out fibrogenesis and other functions [2].

Type I collagen is the dominant fibrillar collagen of the heart’s extracellular matrix. Its tensile strength of steel imparts cardiac tissue with an ability to resist deformation. Type III collagen, a more flexible fibrillar collagen, is present in lesser proportion while the heart’s concentration of elastin is modest, quite unlike normally distensible blood vessels. Various functions of this structural protein network in health and disease have been reviewed previously [3].

Matrix and fibroblasts are bathed by tissue fluid that contains a filtrate of blood as well as substances derived from myocytes and noncardiomyocytes. Circulating and locally generated substances may serve as signals that govern cell differentiation, growth, apoptosis, and metabolic behavior. Also present in the interstitial space are glycosaminoglycans, proteoglycans and self-aggregating molecules called into play following injury. Such molecules include a family of transforming growth factor-β polypeptides and matrix metalloproteinases, each of which reside … 

* Corresponding author. Tel.: +901-448-5759; fax: +901-448-8084 KTWeber{at}utmem.edu
Observations on Blood Group Distribution in Peptic Ulcer and Gastric Cancer
Authors: R. Doll, B. F. Swynnerton, A. C. Newell
Journal: Gut (1960)

There is increasing evidence that blood group substances play a rôle in the causation of disease or in the protective mechanism against it. This paper records the special liability for patients of blood group O to develop stomal ulceration. Other data studied failed to confirm previous work suggesting that in gastric ulceration or neoplasm blood group A was a characteristic of an antral lesion.
Suicide Among Regular-Duty Military Personnel: A Retrospective Case-Control Study of Occupation-Specific Risk Factors for Workplace Suicide
Authors: Martin J Mahon, John P Tobin, Denis A Cusack, Cecily Kelleher, Kevin M Malone
Journal: American Journal of Psychiatry (2005)

The purpose of this study was to examine the epidemiology, phenomenology, and occupation-specific risk factors for suicide among regular-duty military personnel as a model for other professions at risk for workplace suicide.Suicide incidence and methods were determined in a retrospective military cohort comprising all deaths (N=732) of regular-duty military personnel in the Irish Defence Forces between 1970 and 2002. A retrospective, case-control study using pair-matched military comparison subjects was conducted to determine occupation-specific risk factors for suicide, particularly by firearm, among military personnel. Risk factors were subjected to chi-square analysis or independent t tests and entered into a binary logistic regression analysis model.The period-averaged suicide rate for the cohort was 15.3/100,000. Firearm suicides accounted for 53% of the cases. Suicides that took place on duty occurred predominantly when personnel were alone shortly after duty commencement in the morning. Bivariate and logistic regression analyses identified psychiatric illness and a past history of deliberate self-harm, morning duty (shortly after duty assumption and consequent access to firearms), and a recent medical downgrading as independent risk factors predicting firearm suicide among military personnel.Occupation influences suicide method. Access to and opportunity to use lethal means in the workplace are distinct but related occupation-specific suicide risk factors in the military and in other at-risk professions. In professions where access to lethal means is inevitable, moderating opportunity for suicide is crucially important. In regular-duty military personnel, a medical downgrading, combined with risk factors established in civilians such as younger age, male gender, psychiatric illness, and past self-harm, increases the risk of suicide. The findings may be used to guide military harm-reduction strategies and have applicability in strategies for other professions at risk for workplace suicide.
Scanning electron microscope study of the development of the human respiratory acinus.
Authors: S A Dilly
Journal: Thorax (1984)

Plastic corrosion casts were made of lungs from fetuses aged from 19 weeks9 gestation to term and of lungs from a child and two adults to study the development of the respiratory acinus. To achieve reliable infusion of the most peripheral airspaces a high viscosity plastic was used that is not known to have been employed previously for corrosion casting of lungs. The casts were examined in the scanning electron microscope and showed the increase both in number and in length of the airways distal to the terminal bronchiole and also the change in shape and complexity of the most peripheral airspaces as the lung matures. The terminal airspaces change from short, simple, tubular endings at 19 weeks9 gestation to short, shallow saccules from around 30 weeks9 gestation to full term and contrast with the deep cup shaped alveoli in the adult. Measurements of the size of the terminal airspace at various stages of development are presented. This new approach, allowing three dimensional study of the peripheral airspaces of the developing lung, will be useful for investigating the lung pathology of neonates.
BET bromodomain inhibition targets both c-Myc and IL7R in high-risk acute lymphoblastic leukemia
Authors: Christopher J. Ott, Nadja Kopp, Liat Bird, Ronald M. Paranal, Jun Qi, Teresa Bowman, Scott J. Rodig, Andrew L. Kung, James E. Bradner, David M. Weinstock
Journal: Blood (2012)
Projections of AIDS Morbidity and Mortality in San Francisco
Authors: G F Lemp, S F Payne, G W Rutherford, N A Hessol, W Winkelstein, J A Wiley, A R Moss, R E Chaisson, R T Chen, D W Feigal
Journal: JAMA (1990)

To develop a model for predicting acquired immunodeficiency syndrome (AIDS) morbidity in San Francisco, Calif, through June 1993, we combined annual human immunodeficiency virus seroconversion rates for homosexual and bisexual men and for heterosexual intravenous drug users with estimates of the cumulative proportion of the population with AIDS by duration of human immunodeficiency virus infection and with estimates of the size of the at-risk populations. We projected AIDS mortality by applying Kaplan-Meier estimates of survival time following diagnosis to the projected number of cases. The median incubation period for AIDS among homosexual and bisexual men infected with the human immunodeficiency virus was estimated to be 11.0 years (mean, 11.8 years; 95% confidence interval, 10.6 to 13.0 years). The model projects 12,349 to 17,022 cumulative cases of AIDS in San Francisco through June 1993, with 9,966 to 12,767 cumulative deaths.