tbuckley/cabot-search huggingface dataset:
Intermittent self catheterisation with hydrophilic, gel reservoir, and non-coated catheters: a systematic review and cost effectiveness analysis
Authors: S. L. Bermingham, S. Hodgkinson, S. Wright, E. Hayter, J. Spinks, C. Pellowe
Journal: BMJ (2013)

We present the case of a patient with a necrotizing multilobar pneumonia caused by community-acquired methicillin-resistant <i>Staphylococcus aureus</i> (MRSA). The patient presented with shortness of breath and a productive cough of 3 days duration. On arrival to the emergency department she was intubated for increased work of breathing and given vasopressors for hypotension refractory to fluid resuscitation. Blood cultures taken at admission, sputum cultures from the patient9s endotracheal tube, and bronchoalveolar lavage cultures all grew <i>S. aureus</i> resistant to penicillinase-resistant penicillins. Over the following days the patient9s respiratory function deteriorated as she grew progressively hypoxemic and hypercarbic despite aggressive mechanical ventilation and intravenous antibiotics. On day 4 of her hospitalization a computed tomogram revealed extensive pulmonary necrosis consistent with necrotizing pneumonia. The patient9s family elected to withdraw support, and the patient rapidly died following cessation of mechanical ventilation.
Myoglobinuric acute renal failure in a cardiac transplant patient taking lovastatin and cyclosporine.
Authors: D S Alejandro, J Petersen
Journal: Journal of the American Society of Nephrology (1994)

Acute renal failure can occur in cardiac transplant patients for a variety of reasons. A case of a patient who developed acute renal failure secondarily to drug-induced rhabdomyolysis is reported. The literature regarding acute renal failure and lovastatin and other 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors is reviewed. The potential mechanisms of myoglobinuria and nephrotoxicity and the therapeutic implications are discussed.
The benefits of amateur boxing--a response
Authors: B. Maydew
Journal: British Journal of Sports Medicine (1975)

As a Physical Educationist I cannot allow Dr. Blonstein's annotation on 'The Benefits of Amateur Boxing' (BJSM Vol. 8 No. 4) to pass without comment, and whilst having every respect for what Dr. Blonstein is saying, it seems that there is much more to be said on this subject.Aggression, as Dr. Blonstein so rightly points out, is inherent in us all; though in varying stages of latency.I disagree, however, with his statement that "the ideal way of getting rid of aggression in boys is by teaching them boxing".Surely many other individual combat sports can, and do, serve the same purpose, Judo, Kendo and Wrestling are but three examples.I am not saying that any of these sports are better in developing a boy's character than three rounds of boxing, what I am saying is that their potential in this respect is equal to that of boxing.The pre-and post-fight rituals of Judo and Kendo etc. are, it seems, especially significant, and parallel Dr. Blonstein's virtuous handshake at the end of a contest.Serving the same purpose, though on a different plane, the team game of rugby must rank high on any list of aggression-cathartic sports.
Common Bile Duct Stones Become Smaller After Endoscopic Biliary Stenting
Authors: A. C. W. Chan, E. K. W. Ng, S. C. S. Chung, C. W. Lai, J. Y. W. Lau, J. J. Y. Sung, J. W. C. Leung, A. K. C. Li
Journal: Endoscopy (1998)

Background and Study Aims: Endoscopic biliary stenting is often used for large or difficult common bile duct (CBD) stones that cannot be extracted at one session. We compared the sizes of the CBD stones after a period of stenting.
736 LAMIVUDINE IN LATE PREGNANCY FOR PREVENTION OF HBV TRANSMISSION: EFFECTIVENESS AND DETECTION OF ANTIVIRAL RESISTANCE
Authors: A. Ayres, L. Yuen, S. Manoharan, A. Glass, R. Nguyen, W. Ng, M. Maley, G. Paven, M.T. Levy, S. Locarnini
Journal: Journal of Hepatology (2011)
Sports in extreme conditions: The impact of exercise in cold temperatures on asthma and bronchial hyper-responsiveness in athletes
Authors: Kai-Håkon Carlsen
Journal: British Journal of Sports Medicine (2012)

Exercise-induced asthma (EIA) and bronchial hyper-responsiveness (BHR) are frequently reported among elite athletes of outdoor endurance winter sports, particularly in cross-country and biathlon skiers. The pathogenesis of EIA is related to water loss and heat-loss through the increased respiration during exercise, leading to mediator release, airways inflammation and increased parasympathetic nervous activity in the airways, causing bronchial constriction and BHR. In the competing elite athlete this is presently considered to be due to the frequently repeated increased ventilation during training and competitions in combination with the repeated environmental exposure to cold air in outdoor winter sports. It is important that athletes at risk of asthma and BHR are monitored through regular medical control with assessment of lung function and BHR, and when BHR or asthma is diagnosed, optimal controlling treatment through anti-inflammatory treatment by inhaled steroids should be started and relieving treatment (inhaled ipratropium bromide and inhaled β2-agonists) should be used to relieve bronchial constriction if present.
Clinical Benefit of 2ND EGFR-TKI Retreatment on Overall Survival in Patients with Advanced Non-Small Cell Lung Cancer
Authors: M. Nakashima, T. Hirose, Y. Ohki, Y. Murata, T. Sugiyama, H. Ishida, K. Okuda, T. Yamaoka, T. Ohmori, T. Ohnishi
Journal: Annals of Oncology (2013)
Caveolin-1 Deficiency Inhibits the Basolateral K+ Channels in the Distal Convoluted Tubule and Impairs Renal K+ and Mg2+ Transport
Authors: Lijun Wang, Chengbiao Zhang, Xiaotong Su, Dao-Hong Lin, Wenhui Wang
Journal: Journal of the American Society of Nephrology (2015)

Kcnj10 encodes the inwardly rectifying K+ channel Kir4.1 in the basolateral membrane of the distal convoluted tubule (DCT) and is activated by c-Src. However, the regulation and function of this K+ channel are incompletely characterized. Here, patch-clamp experiments in Kcnj10-transfected HEK293 cells demonstrated that c-Src–induced stimulation of Kcnj10 requires coexpression of caveolin-1 (cav-1), and immunostaining showed expression of cav-1 in the basolateral membrane of parvalbumin-positive DCT. Patch-clamp experiments detected a 40-pS inwardly rectifying K+ channel, a heterotetramer of Kir4.1/Kir5.1, in the basolateral membrane of the early DCT (DCT1) in both wild-type (WT) and cav-1-knockout (KO) mice. However, the activity of this basolateral 40-pS K+ channel was lower in KO mice than in WT mice. Moreover, the K+ reversal potential (an indication of membrane potential) was less negative in the DCT1 of KO mice than in the DCT1 of WT mice. Western blot analysis demonstrated that cav-1 deficiency decreased the expression of the Na+/Cl– cotransporter and Ste20-proline-alanine-rich kinase (SPAK) but increased the expression of epithelial Na+ channel-α. Furthermore, the urinary excretion of Mg2+ and K+ was significantly higher in KO mice than in WT mice, and KO mice developed hypomagnesemia, hypocalcemia, and hypokalemia. We conclude that disruption of cav-1 decreases basolateral K+ channel activity and depolarizes the cell membrane potential in the DCT1 at least in part by suppressing the stimulatory effect of c-Src on Kcnj10. Furthermore, the decrease in Kcnj10 and Na+/Cl– cotransporter expression induced by cav-1 deficiency may underlie the compromised renal transport of Mg2+, Ca2+, and K+.
Model-based Analysis of ChIP-Seq (MACS)
Authors: Yong Zhang, Tao Liu, Clifford A Meyer, Jérôme Eeckhoute, David S Johnson, Bradley E Bernstein, Chad Nusbaum, Richard M Myers, Myles Brown, Wei Li, X Shirley Liu
Journal: Genome biology (2008)

We present Model-based Analysis of ChIP-Seq data, MACS, which analyzes data generated by short read sequencers such as Solexa's Genome Analyzer. MACS empirically models the shift size of ChIP-Seq tags, and uses it to improve the spatial resolution of predicted binding sites. MACS also uses a dynamic Poisson distribution to effectively capture local biases in the genome, allowing for more robust predictions. MACS compares favorably to existing ChIP-Seq peak-finding algorithms, and is freely available.
S100P-Derived RAGE Antagonistic Peptide Reduces Tumor Growth and Metastasis
Authors: Thiruvengadam Arumugam, Vijaya Ramachandran, Sobeyda B. Gomez, Ann M. Schmidt, Craig D. Logsdon
Journal: Clinical Cancer Research (2012)

Abstract Purpose: The receptor for advanced glycation end products (RAGE) contributes to multiple pathologies, including diabetes, arthritis, neurodegenerative diseases, and cancer. Despite the obvious need, no RAGE inhibitors are in common clinical use. Therefore, we developed a novel small RAGE antagonist peptide (RAP) that blocks activation by multiple ligands. Experimental Design: RAGE and its ligands were visualized by immunohistochemical analysis of human pancreatic tissues, and siRNA was used to analyze their functions. Interactions between RAGE and S100P, S100A4, and HMGB-1 were measured by ELISA. Three S100P-derived small antagonistic peptides were designed, synthesized, and tested for inhibition of RAGE binding. The effects of the peptide blockers on NFκB-luciferase reporter activity was used to assess effects on RAGE-mediated signaling. The most effective peptide was tested on glioma and pancreatic ductal adenocarcinoma (PDAC) models. Results: Immunohistochemical analysis confirmed the expression of RAGE and its ligands S100P, S100A4, and HMGB-1 in human PDAC. siRNA silencing of RAGE or its ligands reduced the growth and migration of PDAC cells in vitro. The most effective RAP inhibited the interaction of S100P, S100A4, and HMGB-1 with RAGE at micromolar concentrations. RAP also reduced the ability of the ligands to stimulate RAGE activation of NFκB in cancer cells in vitro and in vivo. Importantly, systemic in vivo administration of RAP reduced the growth and metastasis of pancreatic tumors and also inhibited glioma tumor growth. Conclusion: RAP shows promise as a tool for the investigation of RAGE function and as an in vivo treatment for RAGE-related disorders. Clin Cancer Res; 18(16); 4356–64. ©2012 AACR.
Effect of bisphosphonates on viability, proliferation, and dexamethasone-induced apoptosis of articular chondrocytes
Authors: J F Van Offel
Journal: Annals of the Rheumatic Diseases (2002)

Bisphosphonates (BP) increase bone mass in patients with rheumatoid arthritis and are effective in the prevention and treatment of steroid-induced osteoporosis. However, little is known about their direct effects on chondrocytes.To study the influence of BP on articular chondrocytes in vitro and to investigate whether BP can prevent steroid-induced apoptosis of articular chondrocytes.Bovine articular chondrocytes were cultured and incubated with different concentrations of clodronate, pamidronate, risedronate, or dexamethasone. In the second part of the study, BP were added to the chondrocyte cultures one hour before co-incubation with dexamethasone. Viability and proliferation were evaluated using propidium iodide staining and tritium labelled thymidine incorporation. Apoptosis was measured with annexin V staining or the TUNEL method.Only high concentrations (>10(-6) mol/l) of clodronate, pamidronate, and risedronate induced a decrease in the viability and proliferation of chondrocytes. None of the BP at concentrations ranging from 10(-12) to 10(-3) mol/l induced apoptosis. Growth retardation and apoptosis induced by dexamethasone (10(-7) mol/l) was prevented by addition of pamidronate (10(-6) mol/l) or risedronate (10(-8) or 10(-6) mol/l).Bisphosphonates in therapeutic concentrations are safe for articular chondrocytes in vitro. Moreover, pamidronate and risedronate prevent dexamethasone-induced growth retardation and apoptosis of chondrocytes. These findings add evidence for a chondroprotective effect of nitrogen-containing BP, especially in patients treated with corticosteroids.
NRF-1 genotypes and endurance exercise capacity in young Chinese men
Authors: Z He, Y Hu, L Feng, Y Li, G Liu, Y Xi, L Wen, A Lucia
Journal: British Journal of Sports Medicine (2008)

Background: Nuclear respiratory factor 1 (NRF-1) is a critical component of the energy-sensing mechanism in mammalian cells, and translates physiological signals (particularly those induced by exercise) into increased capacity for mitochondrial biogenesis and oxidative phosphorylation. Objective: To study the possible association between rs2402970, rs6949152 and rs10500120 NRF-1 genotypes and several phenotypes indicative of maximum (VO 2max ) and submaximum aerobic capacity (ventilatory threshold (VT) and metabolic cost of submaximum running at 12 km/hour (running economy; RE)) both at baseline and in response to a 18-week endurance training programme in young Chinese men of Han origin (n = 102; 19 (SD 1) years). Results: For rs2402970, a significant genotype effect was seen for VT (p = 0.004) and RE (p = 0.027). For rs6949152, a significant interaction (genotype×training) effect (p = 0.047) was found for VT. Conclusions: There is an association between NRF-1 genotypes (rs2402970 and rs6949152 polymorphisms) and the baseline and/or training response of human aerobic capacity. More research is needed to corroborate our data in other ethnic groups with lower fitness levels at the pre-training state (particularly Caucasians) and to identify the molecular mechanisms involved in the genotype–phenotype associations we found.
Minocycline and N-methyl-4-isoleucine cyclosporin (NIM811) mitigate storage/reperfusion injury after rat liver transplantation through suppression of the mitochondrial permeability transition
Authors: Tom P. Theruvath, Zhi Zhong, Peter Pediaditakis, Venkat K. Ramshesh, Robert T. Currin, Andrey Tikunov, Ekhson Holmuhamedov, John J. Lemasters
Journal: Hepatology (2007)

Graft failure after liver transplantation may involve mitochondrial dysfunction. We examined whether prevention of mitochondrial injury would improve graft function. Orthotopic rat liver transplantation was performed after 18 hours' cold storage in University of Wisconsin solution and treatment with vehicle, minocycline, tetracycline, or N -methyl-4-isoleucine cyclosporin (NIM811) of explants and recipients. Serum alanine aminotransferase (ALT), necrosis, and apoptosis were assessed 6 hours after implantation. Mitochondrial polarization and cell viability were assessed by intravital microscopy. Respiration and the mitochondrial permeability transition (MPT) were assessed in isolated rat liver mitochondria. After transplantation with vehicle or tetracycline, ALT increased to 5242 U/L and 4373 U/L, respectively. Minocycline and NIM811 treatment decreased ALT to 2374 U/L and 2159 U/L, respectively ( P &lt; 0.01). Necrosis and terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) also decreased from 21.4% and 21 cells/field, respectively, after vehicle to 10.1% and 6 cells/field after minocycline and to 8.7% and 5.2 cells/field after NIM811 ( P &lt; 0.05). Additionally, minocycline decreased caspase-3 activity in graft homogenates ( P &lt; 0.05). Long-term graft survival was 27% and 33%, respectively, after vehicle and tetracycline treatment, which increased to 60% and 70% after minocycline and NIM811 ( P &lt; 0.05). In isolated mitochondria, minocycline and NIM811 but not tetracycline blocked the MPT. Minocycline blocked the MPT by decreasing mitochondrial Ca2+ uptake, whereas NIM811 blocks by interaction with cyclophilin D. Intravital microscopy showed that minocycline and NIM811 preserved mitochondrial polarization and cell viability after transplantation ( P &lt; 0.05). Conclusion: Minocycline and NIM811 attenuated graft injury after rat liver transplantation and improved graft survival. Minocycline and/or NIM811 might be useful clinically in hepatic surgery and transplantation. (Hepatology 2007.)
SPIRIT 2013 explanation and elaboration: guidance for protocols of clinical trials
Authors: A.-W. Chan, J. M. Tetzlaff, P. C. Gotzsche, D. G. Altman, H. Mann, J. A. Berlin, K. Dickersin, A. Hrobjartsson, K. F. Schulz, W. R. Parulekar, K. Krleza-Jeric, A. Laupacis, D. Moher
Journal: BMJ (2013)

High quality protocols facilitate proper conduct, reporting, and external review of clinical trials. However, the completeness of trial protocols is often inadequate. To help improve the content and quality of protocols, an international group of stakeholders developed the SPIRIT 2013 Statement (Standard Protocol Items: Recommendations for Interventional Trials). The SPIRIT Statement provides guidance in the form of a checklist of recommended items to include in a clinical trial protocol. This SPIRIT 2013 Explanation and Elaboration paper provides important information to promote full understanding of the checklist recommendations. For each checklist item, we provide a rationale and detailed description; a model example from an actual protocol; and relevant references supporting its importance. We strongly recommend that this explanatory paper be used in conjunction with the SPIRIT Statement. A website of resources is also available (www.spirit-statement.org). The SPIRIT 2013 Explanation and Elaboration paper, together with the Statement, should help with the drafting of trial protocols. Complete documentation of key trial elements can facilitate transparency and protocol review for the benefit of all stakeholders.
George Inglis Manson
Authors: L D Ritchie
Journal: BMJ (2008)

After junior hospital posts at Stracathro, George Inglis Manson went to Peterhead in 1945 as a general practitioner, where he practised faithfully for over 40 years, retiring in 1986. He was appointed medical officer to Peterhead prison in 1955, where he served with …
User Error in Blood Glucose Monitoring: The National Steering Committee for Quality Assurance Report
Authors: Anne Nettles
Journal: Diabetes Care (1993)

Since the invention of patient-operated blood glucose testing devices, professionals have expressed concern about the accuracy of the results (1). In part, their concern relates to the impact of patient results on diabetes management decisions. Numerous authors and investigators have examined potential sources of error ranging from the devices themselves to deterioration in operator technique (2–5).
Mitochondrial functionality in reproduction: from gonads and gametes to embryos and embryonic stem cells
Authors: J. Ramalho-Santos, S. Varum, S. Amaral, P. C. Mota, A. P. Sousa, A. Amaral
Journal: Human Reproduction Update (2009)

Mitochondria are multitasking organelles involved in ATP synthesis, reactive oxygen species (ROS) production, calcium signalling and apoptosis; and mitochondrial defects are known to cause physiological dysfunction, including infertility. The goal of this review was to identify and discuss common themes in mitochondrial function related to mammalian reproduction. The scientific literature was searched for studies reporting on the several aspects of mitochondrial activity in mammalian testis, sperm, oocytes, early embryos and embryonic stem cells. ATP synthesis and ROS production are the most discussed aspects of mitochondrial function. Metabolic shifts from mitochondria-produced ATP to glycolysis occur at several stages, notably during gametogenesis and early embryo development, either reflecting developmental switches or substrate availability. The exact role of sperm mitochondria is especially controversial. Mitochondria-generated ROS function in signalling but are mostly described when produced under pathological conditions. Mitochondria-based calcium signalling is primarily important in embryo activation and embryonic stem cell differentiation. Besides pathologically triggered apoptosis, mitochondria participate in apoptotic events related to the regulation of spermatogonial cell number, as well as gamete, embryo and embryonic stem cell quality. Interestingly, data from knock-out (KO) mice is not always straightforward in terms of expected phenotypes. Finally, recent data suggests that mitochondrial activity can modulate embryonic stem cell pluripotency as well as differentiation into distinct cellular fates. Mitochondria-based events regulate different aspects of reproductive function, but these are not uniform throughout the several systems reviewed. Low mitochondrial activity seems a feature of 'stemness', being described in spermatogonia, early embryo, inner cell mass cells and embryonic stem cells.
Benefit of anti-TNFalpha treatment for nephrotic syndrome in a patient with juvenile inflammatory bowel disease associated spondyloarthropathy complicated with amyloidosis and glomerulonephritis
Authors: P Verschueren
Journal: Annals of the Rheumatic Diseases (2003)

Cerebellar granule neurons are highly susceptible to injury in vivo and in vitro, and primary cultures are widely used to characterize relevant receptors and signaling pathways. However, there are problems associated with their use. In particular, cultures are typically grown in medium supplemented with elevated KCl levels because it improves survival, but accumulating evidence indicates that this causes profound neuroadaptations. For example, growth in elevated KCl levels renders neurons electrically silent. Thus, they cannot be used to examine excitotoxicity of synaptic origins. On the other hand, cultures grown in physiological medium are rarely studied because a proportion undergoes apoptosis. Herein, we provide evidence that mature neurons cultured in physiological KCl develop spontaneous action potentials that support survival through <i>N</i>-methyl-d-aspartate (NMDA) receptor-mediated mechanisms. Furthermore, the cdk inhibitor roscovitine enhances the coupling between tetrodotoxin-sensitive action potentials and P/Q-type voltage-dependent calcium channels (VDCCs), thereby converting this survival program to excitotoxicity of synaptic origin. Therefore, roscovitine-triggered necrosis requires spontaneous Na<sup>+</sup>-based action potentials (tetrodotoxin inhibits, (±)-2-amino-4-phosphonobutyric acid enhances), P/Q-type VDCC currents (ω-agatoxin-IVA and ω-conotoxin-MVIIC inhibit, but not ω-conotoxin-GVIA), intact vesicle fusion processes (tetanus toxin inhibits), and transmitter-filled vesicles (concanamycin and bafilomycin inhibit). From a postsynaptic standpoint, roscovitine-mediated excitotoxicity requires the functionally linked activation of α-amino-3-hydroxy-5-methyl-isoxazole-4-propionate/kainate (AMPA/KA) and NMDA receptors, which is consistent with evidence that activated AMPA/KA receptors relieve the voltage-dependent Mg<sup>2+</sup> block of NMDA receptors, resulting in excitotoxic Ca<sup>2+</sup> influx. In the end, NMDA receptor-linked pathways transduce excitotoxicity. On the other hand, L-type VDCC blockers are not protective. Further characterization of this new model is expected to provide important insights about excitotoxicity of synaptic origins and about roscovitine as a selective modulator of this process.
Industry spending on continuing medical education in US falls further
Authors: B. Roehr
Journal: BMJ (2012)

The drug and medical devices industries’ spending on continuing medical education (CME) activities in the United States has fallen for the fourth consecutive year, shows the latest annual report from the Accreditation Council for Continuing Medical Education.1

The report found that overall industry support for CME was $736m (£470m; €590m) in 2011, a decrease of $94m (11.4%) from 2010. At its peak in 2006 the industry’s contribution to CME spending was a half, but that is down to a third today.

Despite the decline of industry support, the number of CME activities and hours of instruction …