tbuckley/cabot-search huggingface dataset:
A preliminary study of the structure and function of enlarged parotid glands in chronic relapsing pancreatitis by sialography and biopsy methods.
Authors: J L Alappatt, M D Ananthachari
Journal: Gut (1967)

EDITORIAL SYNOPSIS Enlargement of the parotid glands is associated with calcific pancreatitis in one area of India.Surprisingly, the enlarged parotids showed evidence of hypertrophy and hypersecretion.
<i>Parietaria</i> pollinosis: a review
Authors: G. D'Amato, A. Ruffilli, G. Sacerdoti, S. Bonini
Journal: Allergy (1992)

Species of the genus Parietaria (pellitory) are a prevalent cause of allergy in the Mediterranean area and the most important in some European regions such as southern Italy and coastal Spain (14, 26, 27, 29, 30, 31, 36, 59, 69). Up to now, however, Parietaria has received little attention in northern Europe and the US because of its limited regional distribution. Therefore, less is known about Parietaria allergy than about other inhalant allergens such as those of grasses, ragweed, and mites. During the last 5 years, only 31 reports on Parietaria allergy have appeared in the literature, as compared with 37 papers on birch pollen. This ratio may appear unbalanced, considering that millions of people suffer from pollinosis caused by Parietaria , while a much smaller number have rhinitis and/or asthma caused by birch pollen. The increasing movement of people throughout Europe and to and from the US is reason to broaden our knowledge of patterns of inhalant allergy in each geographic area, especially where tourism and immigration are high. This paper briefly reviews available data and personal studies on the botanical, aerobiological, immunochemical, and clinical features of Parietaria allergy.
Renal Microvascular Disease: Angiographic-Microangiographic Correlates
Authors: R. Brent Harrison
Journal: JAMA (1981)

<i>Renal Microvascular Disease: Angiographic-Microangiographic Correlates</i>is a concise, well-written study of the renal microvascular bed, which should be of wider appeal than the somewhat esoteric title might suggest. Dr Bookstein is a radiologist with an interest in angiography and Dr Clark is a radiologist with interests in pathology and microangiography. Each has combined his own area of interest with meticulous attention to technique and detail to produce a remarkable study of the renal microvascular bed in various disease states. The quality of the illustrations can only be appreciated by an angiographer. By combining the techniques of in vitro microangiography and in vivo magnification angiography, Drs Bookstein and Clark have offered clear, well-illustrated explanations of the various radiographic patterns that are seen at angiography and excretory urography. In the next edition of this text, the authors might consider including urographic examples as well as angiographic patterns, since this work will be
Spontaneous Malignant Transformation of Human Mesenchymal Stem Cells Reflects Cross-Contamination: Putting the Research Field on Track – Letter
Authors: Anja Torsvik, Gro V. Røsland, Agnete Svendsen, Anders Molven, Heike Immervoll, Emmet McCormack, Per Eystein Lønning, Monika Primon, Ewa Sobala, Joerg-Christian Tonn, Roland Goldbrunner, Christian Schichor, Josef Mysliwietz, Tamara T. Lah, Helena Motaln, Stian Knappskog, Rolf Bjerkvig
Journal: Cancer Research (2010)

Several groups, including ours, have published results showing spontaneous transformation of human mesenchymal stem cells (MSC). Recently, we reported in this journal spontaneous transformation of bone marrow-derived human MSC (hMSC), isolated and expanded independently in two laboratories ([1][1
Surgical approaches and drug treatment in the carcinoid syndrome.
Authors: P Siklos
Journal: BMJ (1978)

than an objectively demonstrable entity.Research has been rightly directed to demon- strating the variables which influence the relapse of acute schizophrenia with productive symptoms.What is also needed is an objective assessment of the variables which may influence the development or resolution of schizophrenic defect.Have changes in in- stitutional management changed the development of defect or merely where a schizophrenic lives ?Do long-term phenothiazines influence the postacute course or merely productive symptoms ?Is defect inevitably associated with an organic brain lesion ?
Selective Vagal Denervation of the Atria Eliminates Heart Rate Variability and Baroreflex Sensitivity While Preserving Ventricular Innervation
Authors: Chuen-Wang Chiou, Douglas P. Zipes
Journal: Circulation (1998)

Background —The purpose of this study was to test whether radiofrequency catheter ablation (RFCA) of 3 epicardial fat pads that resulted in efferent vagal denervation of the atria and sinus and atrioventricular nodes also denervated the ventricles. Methods and Results —Vagal innervation of the ventricles was determined by measuring prolongation of ventricular effective refractory period induced by bilateral vagal stimulation (20 Hz, 10 V, 4 ms). Changes in heart rate variability (HRV) and baroreflex sensitivity (BRS) were also examined. We found that RFCA of the 3 epicardial fat pads vagally denervated the sinus and AV nodes and atria without affecting vagal innervation of the ventricles, indicating that efferent vagal fibers to the ventricles do not travel through the 3 epicardial fat pads. Parameters of time-domain variables decreased significantly; the total-power, high-frequency, and low-frequency components of frequency-domain variables decreased significantly; and the ratio of the low- and high-frequency components increased significantly after chronic vagal denervation. Vagally modulated sinus arrhythmia and BRS were also eliminated after chronic vagal denervation. These data also indicate that HRV and BRS represent vagal activity at the level of the sinus node and may not accurately reflect efferent vagal activity at the ventricular level. Conclusions —Selective vagal denervation of the sinus and AV nodes and atria decreased HRV and eliminated BRS while preserving ventricular innervation.
Prophylaxis of Recurrent Rheumatic Fever
Authors: Alvan R. Feinstein
Journal: JAMA (1968)

For preventing recurrences of rheumatic fever, a repetitive oral penicillin regimen was planned to mimic the action of monthly injections of long-acting penicillin G benzathine. The oral regimen (TCP) contained a<i>therapeutic</i>high level dose for the first ten days of each month, and a<i>continuous</i>low level dose for the remainder of the month. In 343 young rheumatic patients, observed during four calendar years, the group receiving injections had a streptococcal infection attack rate of 6.6 per 100 patient-years, and a rheumatic recurrence rate of 0.6%. For patients receiving TCP, the corresponding rates were 22.7% and 4.8%; these rates were higher than the injection rates even when assessed in a subgroup of patients who maintained TCP with excellent fidelity. The TCP results were not significantly different from those of previously tested oral regimens, in which lower doses of penicillin were used.
P03.05 * THE HIV-DERIVED PROTEIN VPR(52-96) HAS PRO-APOPTOTIC AND ANTIPROLIFERATIVE ACTIVITY IN GLIOBLASTOMA CELL LINES IN VITRO
Authors: J. M. Kubler, L. Hartmann, M. Engelhardt, S. Kirschner, C. Herskind, C. Schultz, P. Maier, M. A. Brockmann, F. Wenz, F. Giordano
Journal: Neuro-Oncology (2014)

BACKGROUND AND PURPOSE: Patients with actively replicating human immunodeficiency virus (HIV) are highly radiosensitive and exhibit adverse reactions even at low irradiation doses. One of the major underlying causes are high intra- and extracellular levels of a virus-encoded peptide termed viral protein R (Vpr). As Vpr efficiently crosses the blood-brain barrier and accumulates in astrocytes, we examined whether its active subunit (Vpr52-96) may be utilized as drug in the treatment of glioblastoma multiforme. MATERIAL AND METHODS: Four glioblastoma-derived cell lines with and without lentivirus-mediated MGMT-overexpression (U251, U87MG, U251-MGMT, U87-MGMT) were exposed to Vpr52-96, 100 µM of temozolomide (TMZ), conventional photon irradiation (2-6 Gy) or to combinations of the three. Acute toxicities and LD50 were examined using the MTT proliferation assay. Apoptosis was detected using a luminescent reaction measuring caspase-3 and -7 activities (Caspase Glo®). Clonogenic survival (survival fraction, SF) was determined using the colony-forming assay. RESULTS: Treatment of U251 cells with 1, 10 and 20 µM of medium-dissolved Vpr52-96 yielded cell viability rates of 82.4 ± 3.2%, 32.6 ± 9.1% and 10.5 ± 4.8% respectively, corresponding to a LD50 of 4.0 ± 1.1 µM. For U87MG, the corresponding viability rates were 89.3 ± 4.4%, 61.2 ± 12.4% and 43.6 ± 17.8%, resulting in an LD50 of 15.7 ± 7.5 µM. Combined treatment (Vpr + RT and/or TMZ) showed additive, but not synergistic effects in MTT assays. Vpr induced apoptosis in all cell lines within 6-12 hours in a dose-dependent fashion. Clonogenic assays also revealed an additive effect but no sensitization towards irradiation. Vpr alone efficiently inhibited clonogenic survival (SF at 10 µM Vpr: 0.24 ± 0.06 for U251 and 0.35 ± 0.09 for U87MG). In contrast to TMZ, it acts independently from the MGMT expression status (SF of U251-MGMT at 10 µM Vpr: 0.2 vs. 0.9 at 100 µM TMZ; SF of U87-MGMT at 10 µM Vpr: 0.3 vs. 0.7 at 100 µM TMZ). SUMMARY: Vpr52-96 exhibits all traits of a chemotherapeutic drug that may be employed for the treatment of glioblastoma multiforme. The protein acts additively to current standard therapies and shows undiminished antiproliferative activity in MGMT-overexpressing cells.
Heavy Smokers, Smoking Cessation, and Clonidine
Authors: Jack L. Cox
Journal: JAMA (1988)

<h3>To the Editor.—</h3> The article entitled "Heavy Smokers, Smoking Cessation, and Clonidine" by Glassman et al<sup>1</sup>raised interesting questions about using a nonnicotine medication as an adjunct in smoking cessation. However, there were several points that could have been clarified to help with evaluating the trial. First, the authors mention eligibility criteria for the study, using a modified Fagerström<sup>2</sup>tolerance scale to determine those individuals who were heavily nicotine dependent, but excluding smokers who had not cut down to 50% of baseline level. This inclusion criterion may have selected out those smokers who were the most nicotine dependent, simply because they were unable to tolerate the withdrawal period. Including these individuals may have influenced the outcome, positively or negatively. Comparing a numerical score from the Fagerström scale would clarify this. Second, although serum nicotine and cotinine levels were measured at the end of four week's of clonidine treatment,
Effect of thrombin inhibition on synovial inflammation in antigen induced arthritis
Authors: P. A. Varisco
Journal: Annals of the Rheumatic Diseases (2000)

<h3>OBJECTIVE</h3> To determine the effect of the thrombin inhibitor, hirudin, on the pathogenesis of murine antigen induced arthritis (AIA). <h3>METHODS</h3> AIA was induced by intra-articular injection of methylated bovine serum albumin in the knee joints of previously immunised mice. Hirudin (injected subcutaneously 3 × 200 μg/mouse/day) was given over 13 days, starting three days before arthritis onset, and its anticoagulant effect monitored by clotting times. Arthritis severity was evaluated by technetium-99m (<sup>99m</sup>Tc) uptake in the knee joints and by histological scoring. In addition, intra-articular fibrin deposition was examined by immunohistochemistry, and synovial cytokine mRNA expression measured by RNase protection. <h3>RESULTS</h3> Joint inflammation, measured by <sup>99m</sup>Tc uptake, was significantly reduced in hirudin treated mice at days 7 and 10 after arthritis onset. Histologically, synovial thickness was markedly decreased in hirudin treated mice compared with untreated ones. By contrast, no difference in articular cartilage proteoglycan content was found between both groups. Intra-articular fibrin deposition and synovial interleukin 1β mRNA levels, were slightly reduced (∼20%) in arthritic joints from hirudin treated mice compared with untreated ones at day 10 of AIA. <h3>CONCLUSION</h3> Hirudin reduces joint inflammation associated with AIA by fibrin-dependent and independent mechanisms.
Is biomedical research a good investment?
Authors: Norman R. Augustine
Journal: Journal of Clinical Investigation (2014)

As the US addresses its budget dilemma, the easiest items to cut are those with the longest-term payoff. Research stands out among this group. Biomedical research has already been markedly reduced, and further reductions appear to be in store. As a frequent witness in Congressional hearings on such matters, here I discuss the challenge of assessing the value of investments in biomedical research.
Gene expression profiling of CD34+ cells identifies a molecular signature of chronic myeloid leukemia blast crisis
Authors: C Zheng, L Li, M Haak, B Brors, O Frank, M Giehl, A Fabarius, M Schatz, A Weisser, C Lorentz, N Gretz, R Hehlmann, A Hochhaus, W Seifarth
Journal: Leukemia (2006)
Relation between Recurrence of Tuberculosis and Transitional Changes in IFN-γ Release Assays
Authors: Yugo Kaneko, Katsutoshi Nakayama, Akira Kinoshita, Yusuke Kurita, Kyuto Odashima, Zenya Saito, Yutaka Yoshii, Tsugumi Horikiri, Aya Seki, Yoshitaka Seki, Hiroshi Takeda, Kazuyoshi Kuwano
Journal: American Journal of Respiratory and Critical Care Medicine (2015)
Integration Frequency and Intermolecular Recombination of rAAV Vectors in Non-human Primate Skeletal Muscle and Liver
Authors: Ali Nowrouzi, Magalie Penaud-Budloo, Christine Kaeppel, Uwe Appelt, Caroline Le Guiner, Philippe Moullier, Christof von Kalle, Richard O Snyder, Manfred Schmidt
Journal: Molecular Therapy (2012)

The comprehensive characterization of recombinant adeno-associated viral (rAAV) integration frequency and persistence for assessing rAAV vector biosafety in gene therapy is severely limited due to the predominance of episomal rAAV vector genomes maintained in vivo. Introducing rAAV insertional standards (rAIS), we show that linear amplification-mediated (LAM)-PCR and deep sequencing can be used for validated measurement of rAAV integration frequencies. Integration of rAAV2/1 or rAAV2/8, following intramuscular (IM) or regional intravenous (RI) administration of therapeutically relevant vector doses in nine adult non-human primates (NHP), occurs at low frequency between 10−4 and 10−5 both in NHP liver and muscle, but with no preference for specific genomic loci. High resolution mapping of inverted terminal repeat (ITR) breakpoints in concatemeric and integrated vector genomes reveals distinct vector recombination hotspots, including large deletions of up to 3 kb. Moreover, retrieval of integrated rAAV genomes indicated approximately threefold increase in liver compared to muscle. This molecular analysis of rAAV persistence in NHP provides a promising basis for a reliable genotoxic risk assessment of rAAV in clinical trials. The comprehensive characterization of recombinant adeno-associated viral (rAAV) integration frequency and persistence for assessing rAAV vector biosafety in gene therapy is severely limited due to the predominance of episomal rAAV vector genomes maintained in vivo. Introducing rAAV insertional standards (rAIS), we show that linear amplification-mediated (LAM)-PCR and deep sequencing can be used for validated measurement of rAAV integration frequencies. Integration of rAAV2/1 or rAAV2/8, following intramuscular (IM) or regional intravenous (RI) administration of therapeutically relevant vector doses in nine adult non-human primates (NHP), occurs at low frequency between 10−4 and 10−5 both in NHP liver and muscle, but with no preference for specific genomic loci. High resolution mapping of inverted terminal repeat (ITR) breakpoints in concatemeric and integrated vector genomes reveals distinct vector recombination hotspots, including large deletions of up to 3 kb. Moreover, retrieval of integrated rAAV genomes indicated approximately threefold increase in liver compared to muscle. This molecular analysis of rAAV persistence in NHP provides a promising basis for a reliable genotoxic risk assessment of rAAV in clinical trials.
Abstract 2611: Cisplatin negatively affects CNS progenitor cells and behavior in the adult mouse
Authors: Nunes T. Ana, Ruolan Han, Kelcie Sprentall, Ornella Santoni, Mark Noble
Journal: Cancer Research (2010)

Abstract Patients that are treated with chemotherapy exhibit long term changes in cognitive function, decreasing quality of life (Van Dam et al 1998). Although much work has been done characterizing these changes in the patient, there is little research on the possible cellular changes. Additionally, little has been done studying the effects of a single chemotherapeutic agent on cognitive function. Our laboratory has previously shown that chemotherapy, including cisplatin, decreases neural progenitor cell division and increases cell death in the mouse brain (Dietrich et al 2006; Han et al., 2008). Here, we have studied the effects of cisplatin on CNS progenitor cells and also on behavior. We found that cisplatin negatively affects progenitor cells throughout the CNS: progenitor cells migrating from the subventricular zone to the olfactory bulb, the olfactory epithelium, the dentate gyrus of the hippocampus and the corpus callosum. The subventricular zone, rostral migratory stream and olfactory bulb all showed increases in cell death and decreases in the neuroblast population. This change in progenitor cell numbers remained significant compared to vehicle control for as long as six months. In the olfactory epithelium, we found a significant decrease in proliferation of olfactory receptor neuron (ORN) progenitor cells. There was also a decrease in proliferation and an increase in cell death in the oligodendrocyte precursor cell (OPC) population of the corpus callosum and in the dentate gyrus. Using a fixed interval-60s operant schedule we examined the effects of cisplatin on performance. This schedule allows for the operant response rate to vary widely without altering the rate of reinforcement. When compared to the vehicle control, we found significant changes in response rate. These findings demonstrate that even in the absence of underlying cancer, cisplatin has adverse effects on CNS progenitor cells in multiple regions and negatively impacts behavioral outcomes. This work provides animal models of potential value in developing treatments to prevent the neurotoxic side effects of cisplatin, thus improving quality of life in recipients of this therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2611.
Impaired interferon production and natural killer cell activation in patients with the skin cancer-prone disorder, xeroderma pigmentosum.
Authors: A A Gaspari, T A Fleisher, K H Kraemer
Journal: Journal of Clinical Investigation (1993)

Xeroderma pigmentosum (XP) is a rare autosomal recessive disorder with sun sensitivity, markedly increased skin cancer susceptibility, and defective DNA repair without consistently identified symptoms of immune deficiency. We examined natural killer (NK) cell activity and interferon production in peripheral blood lymphocytes (PBL) of eight XP patients who had multiple primary skin cancers. The XP patients had normal numbers of T cells and NK cells, as well as normal lymphokine-activated killer cell activity and normal tumor necrosis factor-alpha production. Unstimulated NK cell function was 40% of normal controls in five XP patients, but was normal in three other XP patients. However, PBL from all the XP patients tested showed no enhancement of NK activity by the interferon inducer, polyinosinic acid:polycytidilic acid (polyIC) but enhancement by interferon-alpha was normal, suggesting an impairment in interferon production. Parallel studies in non-XP skin cancer patients revealed that both unstimulated and polyIC-enhanced NK activity were normal. Further investigation using PBL from XP patients revealed that the production of interferon-gamma after stimulation with interferon inducers (polyIC, interleukin 2, or K562 tumor cells) was 13-43% of normals. These data indicate that XP lymphocytes have a defect in production of interferons and suggest that defective interferon production, as well as DNA repair defects, may play an important role in the susceptibility of XP patients to skin cancer.
Nalorphine in opiate poisoning.
Authors: N. Wright, C. W. Syme
Journal: BMJ (1969)

for any published account of these misfortunes, which are presumably theoretical.I have used the gingival sulcus route of administration of oxytocin with complete success, and, may I dare to suggest, much greater comfort, satisfaction, and safety to the patients.'Ritchie and Brudenell have also published papers describing the satisfactory use of oxytocin administered by absorption through the buccal mucous membrane.2' It would be interesting to know why absorption of a drug through the buccal mucosa is more dangerous than giving the same drug intravenously.-Iam, etc., Croydon,
TRAUMATIC PARAPLEGIA: Observations on Cases with Reference to Treatment and Prognosis
Authors: O. H. Gotch
Journal: BMJ (1923)

TRAU.'MA.TIC PARAPLEGIA.TMEDxICBLJoums 049true respiratory quotient owing to irregularities of the breathing.Yet in such cases as the above there is another factor to be considered.The liberation of alkali in the blood consequent upon the removal of the ketolie bodies would result in a compensatory retenition of carbon dioxide.This might easily be sufficient in amount not only to mask any rise but even to produce a fall in the respiratory quotient.It will be noted in Fig. 1 that there is a conspicuous fall in the respiratory quotient at the time the increase of bicarbonate reserve is most rapid.The above results form part of a larger scheme of research undertaken on behalf of the Medical Research Council.
Bax and Bak Are Required for Apoptosis Induction by Sulforaphane, a Cruciferous Vegetable–Derived Cancer Chemopreventive Agent
Authors: Sunga Choi, Shivendra V. Singh
Journal: Cancer Research (2005)

Abstract Sulforaphane, a constituent of many edible cruciferous vegetables, including broccoli, effectively suppresses proliferation of cancer cells in culture and in vivo by causing apoptosis induction, but the sequence of events leading to cell death is poorly defined. Here, we show that multidomain proapoptotic Bcl-2 family members Bax and Bak play a critical role in apoptosis induction by sulforaphane. This conclusion is based on the following observations: (a) sulforaphane treatment caused a dose- and time-dependent increase in the protein levels of both Bax and Bak and conformational change and mitochondrial translocation of Bax in SV40-transformed mouse embryonic fibroblasts (MEF) derived from wild-type mice to trigger cytosolic release of apoptogenic molecules (cytochrome c and Smac/DIABLO), activation of caspase-9 and caspase-3, and ultimately cell death; (b) MEFs derived from Bax or Bak knockout mice resisted cell death by sulforaphane, and (c) MEFs derived from Bax and Bak double knockout mice exhibited even greater protection against sulforaphane-induced cytochrome c release, caspase activation, and apoptosis compared with wild-type or single knockout cells. Interestingly, sulforaphane treatment also caused a dose- and time-dependent increase in the protein level of Apaf-1 in wild-type, Bax−/−, and Bak−/− MEFs but not in double knockout, suggesting that Bax and Bak might regulate sulforaphane-mediated induction of Apaf-1 protein. A marked decline in the protein level of X-linked inhibitor of apoptosis on treatment with sulforaphane was also observed. Thus, it is reasonable to postulate that sulforaphane-induced apoptosis is amplified by a decrease in X-linked inhibitor of apoptosis level, which functions to block cell death by inhibiting activities of caspases. In conclusion, the results of the present study indicate that Bax and Bak proteins play a critical role in initiation of cell death by sulforaphane.