tbuckley/cabot-search huggingface dataset:
The Efficacy of Penicillin Regimens
Authors: Donald B. Louria, Robert G. Brayton
Journal: JAMA (1963)

Phenethicillin given orally was found to be an effective agent in the treatment of respiratory tract infections due to pneumococci and beta hemolytic streptococci. Bacteriological superinfection was infrequent in patients treated with 2.4 million units or less of intramuscular aqueous or procaine penicillin G or with oral potassium phenethicillin, 250 mg every six hours. If the dosage of potassium phenethicillin was increased to 500 mg every six hours by mouth, or if 10 million to 20 million units of aqueous or procaine penicillin G was given intravenously, the superinfection rate rose 25% to 28.6%. Forty per cent of those bacteriologically superinfected incurred clinical disease attributed to the superinfection. These studies emphasize that the most advantageous regimen for patients with acute pulmonary infections consists of the smallest amount of a single antibiotic that will suppress or eradicate invading microorganisms.
Letter: Pregnancy after hysterotomy.
Authors: B Astedt, S Furgyik
Journal: BMJ (1974)

0 Esch Proteus Ki.Ps.Salmonela Sh.gella coli spp.aerogenes aeruginosa sppx spp.results it should be remembered that, ac- cording to the independent investigators quoted by the manufacturers, minocycline in standard dosage (an initial oral dose of 200 mg followed by 100 mg twice daily) produces serum concentrations of only 1-3 ,g/ml, 14 that ordinary doses of tetracycline (for example, 250 mg 6-hourly) will produce peak serum levels in the order of 2-4 ,ug/ ml,5 and that with Proteus species neither antibiotic was bactericidal or likely to be therapeutically effective.With the other Gram-negative bacteria the activity of the two antibiotics appeared to be similar.-I
BACTERIAL TOXIN AS A CAUSE OF RETINAL HEMORRHAGE
Authors: Arthur S. Tenner
Journal: JAMA (1918)

In a recent article,<sup>1</sup>Dr. Lewis of Buffalo called attention to the obscure etiology of retinal hemorrhage and set forth a new conception, namely, that there occurs in these cases absorption into the blood of a soluble protein poison, usually given off from a focal infection, which has a solvent effect on the intercellular cement substance of the cell wall, and that the hemorrhage is not due to alteration of the blood pressure but to local lysis in the wall itself. Even if no confirmatory pathologic evidence is presented, this theory is worthy of consideration. The ophthalmologist is often at a loss to assign any cause to his case of retinal hemorrhage.<sup>2</sup>When high blood pressure, arterial sclerosis or constitutional disease coexist, he has been content to attribute the hemorrhage to one of these, without further inquiry as to their mode of action. I am convinced that retinal
Role of IgD in the immune response and tolerance. I. Anti-delta pretreatment facilitates tolerance induction in adult B cells in vitro.
Authors: D W Scott, J E Layton, G J Nossal
Journal: The Journal of Experimental Medicine (1977)

Adult spleen cells from C57BL.Ige mice, which generally are resistant to in vitro tolerance induction in the B-cell compartment, became hyporesponsive (tolerant) when cultured with antigen in the presence of an anti-allotype serum. Both antigen and anti-delta had to be present for this effect, which was hapten-specific and did not occur in C57BL/L mice, which lack the Ig5-1 allotype of the delta-chain detected in this system. Preculture with anti-mu serum plus antigen, in contrast, did not cause tolerance induction in adult spleen B cells of either strain. These results suggest that the surface IgD may act as a failsafe receptor to prevent tolerance induction in adult B cells. Tolerance studies with spleen cells from mice with markedly reduced numbers of IgD+ve cells, because of regimen of repeated injections of anti-delta serum beginning at birth (delta-suppressed mice), confirmed the importance of membrane IgD in preventing tolerance, because such delta-suppressed mice were hypersusceptible to tolerance by antigen alone. Inasmuch as immature B cells lack IgD on their surface, these studies suggest that acquisition of IgD is an important maturational step in the ability of murine B cells to discriminate tolerogenic and immunogenic signals.
Obstructive Sleep Apnea Syndrome Affects Left Ventricular Diastolic Function
Authors: Miguel A. Arias, Francisco García-Río, Alberto Alonso-Fernández, Olga Mediano, Isabel Martínez, José Villamor
Journal: Circulation (2005)

The purpose of this study was to determine the role of obstructive sleep apnea syndrome (OSAS) as an independent risk factor for the development of left ventricular diastolic abnormalities. Moreover, we tested the hypothesis that nasal continuous positive airway pressure (nCPAP) improves such alterations in OSAS patients by eliminating apneic events.In this prospective, randomized, placebo-controlled, double-blind crossover study, 27 consecutive newly diagnosed middle-aged OSAS men with neither controllable factors nor conditions affecting left ventricular diastolic function and 15 healthy control subjects were selected. OSAS patients were randomized to 12 weeks on sham nCPAP and 12 weeks on effective nCPAP application. Echocardiographic parameters, blood pressure recordings, and urinary catecholamine levels were obtained at baseline and after both treatment modalities. At baseline, an abnormal left ventricular filling pattern was present in 15 of the 27 OSAS patients and only in 3 of the 15 control subjects (P=0.020). Impaired relaxation was by far the most common abnormal pattern in both groups (11 and 3 patients, respectively). In OSAS patients, 12 weeks on effective nCPAP induced a significant increase in E/A ratio (P<0.01), as well as reductions in mitral deceleration (P<0.01) and isovolumic relaxation (P<0.05) times.OSAS can affect left ventricular diastolic function independently of other possible factors. Chronic application of nCPAP could avoid the progression of diastolic abnormalities, and indeed, it might reverse these alterations, at least in the initial stages before severe structural changes can be developed.
Diagnostic des tumeurs kystiques pancréatiques par ponction du liquide kystique sous échoendoscopie: validation de nouveaux seuils des marqueurs tumoraux
Authors: A Gillet, B Bournet, P Otal, G Canevet, S Le Guellec, P Andrau, E Sirach, B Suc, N Carrere, J Moreau, J Escourrou, L Buscail
Journal: Endoscopy (2010)

Introduction: Les tumeurs kystiques du pancréas sont de plus en plus fréquemment découverte de façon fortuite. Compte tenu du potentiel dégénératif des lésions mucineuses il est important d'apprécier au mieux le diagnostic étiologique avant de proposer ou non une chirurgie parfois lourde en terme de morbidité. L'analyse du liquide de cytoponction des lésions kystiques permet d'orienter ce diagnostic et nous avons établis de nouvelles valeurs seuils de ces marqueurs (Endoscopy Oct. 2008; supp 1: A55) à partir de prélèvements effectués chez des patients opérés ou non. Les but s de notre étude étaitent: 1°) valider définitivement ces seuils à partir d'une série de patients opérés pour lésions kystiques du pancréas avec confirmation histologique; 2°) comparer les performances de la cytoponction sous échoendoscopie (EE) incluant ces nouvelles valeurs, à l'imagerie classique par échografie, TDM et IRM.
Endoscopic Fine-needle Aspiration Cytology of the Stomach. A New Diagnostic Procedure
Authors: P. Lange, K. Kock, J. Laustsen, E. Arffmann, P.S. Teglbjærg
Journal: Endoscopy (1987)

In order to improve the diagnosis of submucosal gastric malignancies, a new method of endoscopic fine-needle aspiration cytology was evaluated. The method is compared with conventional forceps biopsy and brush cytology, and technical problems are discussed. It is concluded that endoscopic fine-needle aspiration cytology is a simple and safe procedure, but further development of the method and more clinical experience are required before the diagnostic capability of the method can be established.
A Prospective Study of Bone Lead Concentration and Death From All Causes, Cardiovascular Diseases, and Cancer in the Department of Veterans Affairs Normative Aging Study
Authors: Marc G. Weisskopf, Nitin Jain, Huiling Nie, David Sparrow, Pantel Vokonas, Joel Schwartz, Howard Hu
Journal: Circulation (2009)

Blood lead concentration has been associated with mortality from different causes in several studies. Many effects of lead exposure that might increase risk of death are likely to result from cumulative exposure, for which bone lead is a better biomarker than blood lead. The association between bone lead levels and mortality has not been explored.We prospectively assessed the association between both blood lead and bone lead, analyzed with the use of K-shell x-ray fluorescence, and mortality among 868 men in the Normative Aging Study. We identified 241 deaths over an average of 8.9 (SD=3.9) years of follow-up. We calculated adjusted hazard ratios and 95% confidence intervals using Cox proportional hazards. Compared with the lowest tertile of patella bone lead, the fully adjusted hazard ratios in the highest tertile for all-cause and cardiovascular mortality (n=137 deaths) were 2.52 (95% confidence interval, 1.17 to 5.41) and 5.63 (95% confidence interval, 1.73 to 18.3), respectively. The age-, smoking-, and race-adjusted hazard ratio for ischemic heart disease mortality (n=62 deaths) in the highest tertile was 8.37 (95% confidence interval, 1.29 to 54.4). Results were similar for tibia lead. Bone lead was not associated with cancer, and blood lead was not associated with any mortality category.We found bone lead to be associated with all-cause and cardiovascular mortality in an environmentally exposed population with low blood lead levels. This study suggests that cumulative lead exposure from prior decades of high environmental exposures continues to significantly affect risk of death despite recent declines in environmental lead exposure.
Randomized Phase II Trial of All-<i>Trans</i>-Retinoic Acid With Chemotherapy Based on Paclitaxel and Cisplatin As First-Line Treatment in Patients With Advanced Non–Small-Cell Lung Cancer
Authors: Oscar Arrieta, Claudia H. González-De la Rosa, Elena Aréchaga-Ocampo, Geraldine Villanueva-Rodríguez, Tania L. Cerón-Lizárraga, Luis Martínez-Barrera, María E. Vázquez-Manríquez, Miguel Ángel Ríos-Trejo, Miguel Á. Álvarez-Avitia, Norma Hernández-Pedro, Carlos Rojas-Marín, Jaime De la Garza
Journal: Journal of Clinical Oncology (2010)

This randomized phase II trial evaluated whether the combination of cisplatin and paclitaxel (PC) plus all-trans retinoic acid (ATRA) increases response rate (RR) and progression-free survival (PFS) in patients with advanced non-small-cell lung cancer (NSCLC) with an acceptable toxicity profile and its association with the expression of retinoic acid receptor beta 2 (RAR-beta2) as a response biomarker.Patients with stages IIIB with pleural effusion and IV NSCLC were included to receive PC, and randomly assigned to receive ATRA 20 mg/m(2)/d (RA/PC) or placebo (P/PC) 1 week before treatment until two cycles were completed. RAR-beta2 expression was analyzed in tumor and adjacent lung tissue.One hundred seven patients were included, 55 in the P/PC group and 52 in the RA/PC group. RR for RA/PC was 55.8% (95% CI, 46.6% to 64.9%) and for P/PC, 25.4% (95% CI, 21.3 to 29.5%; P = .001). The RA/PC group had a longer median PFS (8.9 v 6.0 months; P = .008). Multivariate analysis of PFS showed significant differences for the RA/PC group (hazard ratio, 0.62; 95% CI, 0.4 to 0.95). No significant differences in toxicity grade 3/4 were found between groups, except for hypertriglyceridemia (10% v 0%) in RA/PC (P = .05). Immunohistochemistry and reverse-transcriptase polymerase chain reaction assays showed expression of RAR-beta2 in normal tissues of all tumor samples, but only 10% of samples in the tumor tissue.Adding ATRA to chemotherapy could increase RR and PFS in patients with advanced NSCLC with an acceptable toxicity profile. A phase III clinical trial is warranted to confirm these findings.
The Bispecific SDF1-GPVI Fusion Protein Preserves Myocardial Function After Transient Ischemia in Mice
Authors: Melanie Ziegler, Margitta Elvers, Yvonne Baumer, Christoph Leder, Carmen Ochmann, Tanja Schönberger, Tobias Jürgens, Tobias Geisler, Burkhard Schlosshauer, Oleg Lunov, Stefan Engelhardt, Thomas Simmet, Meinrad Gawaz
Journal: Circulation (2012)

CXCR4-positive bone marrow cells (BMCs) are critically involved in cardiac repair mechanisms contributing to preserved cardiac function. Stromal cell-derived factor-1 (SDF-1) is the most prominent BMC homing factor known to augment BMC engraftment, which is a limiting step of stem cell-based therapy. After myocardial infarction, SDF-1 expression is rapidly upregulated and promotes myocardial repair.We have established a bifunctional protein consisting of an SDF-1 domain and a glycoprotein VI (GPVI) domain with high binding affinity to the SDF-1 receptor CXCR4 and extracellular matrix proteins that become exposed after tissue injury. SDF1-GPVI triggers chemotaxis of CXCR4-positive cells, preserves cell survival, enhances endothelial differentiation of BMCs in vitro, and reveals proangiogenic effects in ovo. In a mouse model of myocardial infarction, administration of the bifunctional protein leads to enhanced recruitment of BMCs, increases capillary density, reduces infarct size, and preserves cardiac function.These results indicate that administration of SDF1-GPVI may be a promising strategy to treat myocardial infarction to promote myocardial repair and to preserve cardiac function.
Connexin43 Gene Transfer Reduces Ventricular Tachycardia Susceptibility After Myocardial Infarction
Authors: Ian D. Greener, Tetsuo Sasano, Xiaoping Wan, Tomonori Igarashi, Maria Strom, David S. Rosenbaum, J. Kevin Donahue
Journal: Journal of the American College of Cardiology (2012)
Response to Antibiotic prophylaxis of endocarditis: the rest of the world and NICE
Authors: Prakash Nanjaiah, Ellen Farmer, Rajwinder Singh Jutley
Journal: Journal of the Royal Society of Medicine (2011)

We read with interest the recent editorial by Chambers et al.1 Like the authors we strongly support antibiotic prophylaxis in at least the high-risk population but have met with resistance from local dental practices who invariably quote NICE guidelines in their defence. However, we noted that the resistance to prescribing antibiotics was variable despite the guidelines being in place for three years. To establish current practice, we undertook a telephone and email survey of 200 randomly selected dental practices in all counties of Great Britain. A response rate of 46.5% (93/200) was generated. Ninety-six percent of the responders reported being aware of NICE guidelines. However, 37% still prescribed prophylactic antibiotics contradictory to recommendations of NICE. On detailed questioning, there remained ambiguity about which patients constituted the high-risk group. Only 21% and 15% correctly identified congenital heart disease and postoperative valve replacement, respectively, as being high-risk patients. Interestingly, 6% of those surveyed still prescribed antibiotics to all preoperative and postoperative open-heart surgery patients.

Three years have passed since NICE recommended no antibiotic prophylaxis irrespective of risk profile in direct contrast to international guidelines.2 However, it appears the message is yet to infiltrate the dental ranks or indeed there is dissent among the ranks. All is therefore not lost. If the respective societies can ‘re-educate’ the dentists on the relative merits of prophylaxis at least in the high-risk group, we may still get the message across.
The Principles of Local Treatment in Diseases of the Upper Air Passages
Authors: S. H. Habershon
Journal: BMJ (1901)

<h3>Abstract</h3> Angiotensin-converting enzyme 2 (ACE2) has been suggested to be the cellular receptor for the new coronavirus (2019-nCoV) that is causing the coronavirus disease 2019 (COVID-19). Like other coronaviruses such as the SARS-CoV, the 2019-nCoV uses the receptor binding domain (RBD) of the surface spike glycoprotein (S protein) to engage ACE2. We most recently determined the structure of the full-length human ACE2 in complex with a neutral amino acid transporter B<sup>0</sup>AT1. Here we report the cryo-EM structure of the full-length human ACE2 bound to the RBD of the 2019-nCoV at an overall resolution of 2.9 Å in the presence of B<sup>0</sup>AT1. The local resolution at the ACE2-RBD interface is 3.5 Å, allowing analysis of the detailed interactions between the RBD and the receptor. Similar to that for the SARS-CoV, the RBD of the 2019-nCoV is recognized by the extracellular peptidase domain (PD) of ACE2 mainly through polar residues. Pairwise comparison reveals a number of variations that may determine the different affinities between ACE2 and the RBDs from these two related viruses.
Hypercalcemia after Renal Transplantation
Authors: David S. David, Soichi Sakai, B. Lawrence Brennan, Robert A. Riggio, Jhoong Cheigh, Kurt H. Stenzel, Albert L. Rubin, Louis M. Sherwood
Journal: New England Journal of Medicine (1973)

In 64 patients followed for more than one year after renal transplantation hypercalcemia occurred in more than 1/3 of those whose creatinine clearances reached levels greater than 30 ml per minute. The onset of the hypercalcemia occurred between one day and one year after transplantation, the severity of the hypercalcemia being worse in the first two weeks after operation. Once hypercalcemia became manifest it persisted in some cases as long as two to three years after transplantation. Evidence of persistent secondary hyperparathyroidism with raised serum parathyroid hormone was noted in all the hypercalcemic patients as long as two to three years after transplantation. Good renal function, hypophosphatemia and resolution of soft-tissue calcification also contributed to the frequency and severity of the hypercalcemia. Severe hypercalcemia (calcium concentrations of 13 mg per 100 ml and above) necessitated subtotal parathyroidectomy in four patients because of adverse effects on renal function. Persistent mild to moderate hypercalcemia (calcium concentration of 12 mg per 100 ml or less), despite its duration, was easily managed by oral phosphate supplements, without adverse effects on graft function or renal osteodystrophy. (N Engl J Med 289:398–401, 1973)
Clinical outcome following cardioverter defibrillator implantation in patients with hypertrophic cardiomyopathy
Authors: T.J. Lobo, P.A. Friedman, R.F. Rea, T.M. Munger, S.C. Hammill, M.J. Osborn, D.L. Packer, M.S. Stanton, W.K. Shen
Journal: Journal of the American College of Cardiology (1998)
Perforation in Typhoid.
Authors: Theo. L. Hatch
Journal: JAMA (1904)

Owatonna, Minn., Aug. 9, 1904. <h3>To the Editor:</h3> —The matter of perforation in typhoid cases has been discussed very extensively of late, both in society meetings, and in the medical journals. In your editorial of August 6 you have also referred to the symptoms. As the question of operation hinges on the diagnosis, of course for the time being that becomes the most important feature. There is one symptom that I have noticed to be invariably present, both in perforation from typhoid and from gastric ulcer, that I have never heard spoken of. During an experience extending over something over 33 years I have seen perhaps some six or eight of these cases, but have never seen a case in which the pulse was not greatly accelerated—running from 160 up to such a rate that it was not susceptible of being counted. Another feature is that one may pour all
Abstract 3429: AKAP12/SSeCKS inhibits peritoneal metastasis by regulating chemokine production
Authors: Shin Akakura, Masashi Muramatsu, Hyun Kyung Ko, Irwin H. Gelman
Journal: Cancer Research (2012)

Abstract AKAP12/SSeCKS/Gravin (AKAP12) is thought to act as a metastasis suppressor through its direct scaffolding of major signaling proteins such as PKC, PKA and Src, in a spatiotemporal manner (1). For example, AKAP12 inhibition of Src-mediated oncogenic signaling, including induction of VEGF secretion by tumor cells, correlates with inhibition of neovascularization at metastatic sites (2). We have established AKAP12-null (KO) mice and demonstrated that they are cancer-prone in regards to the formation of spontaneous prostatic dysplasia and to carcinogen-induced skin cancer formation (3, 4). However, the role of AKAP12 in host microenvironment in regards to tumor or metastasis control has yet to be elucidated. In this study, we utilized an orthotropic, subcutaneous injection model of B16F10 melanoma to address whether the loss of AKAP12 in the host facilitates metastasis. Although the size of the primary tumors was similar in WT vs. KO mice, KO mice exhibited increased rates of peritoneal metastasis. The peritoneal fluid (PF) of KO mice was more potent than WT-PF in inducing in vitro chemotaxis. Comparison of the cytokines/chemokines using antibody arrays showed a severe upregulation of multiple potential chemoattractants in the KO-PF, including CXCL9/10/11, known ligands for CXCR3, a chemokine receptor upregulated 12-fold in B16F10 versus the low-metastatic B16F0 variant. Pre-injection of KO-PF, but not WT-PF, into WT mice was sufficient to induce high levels of peritoneal metastasis from subcutaneous sites. Taken together, our study suggests that AKAP12 controls metastasis by regulating the production of chemoattractants in the peritoneum, produced either by local microenvironmental cells or by recruited inflammatory cells. References: (1) Gelman, I. H. (2002) Front Biosci 7, 1782-1797. (2) Su, B., Zheng, Q., Vaughan, M.M., Bu, Y., and Gelman, I.H. (2006) Cancer Res. 66, 5599-5607 (3) Akakura, S., Huang, C., Nelson, P. J., Foster, B., and Gelman, I. H. (2008) Cancer Res. 68, 5096-5103. (4) Akakura, S., Bouchard, R., Bshara, W., Morrison, C., and Gelman, I. H. (2011) Int. J. Can. 129, 2025-2031. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3429. doi:1538-7445.AM2012-3429
Combined Use of Systemic Agents for Psoriasis
Authors: Celine Busard, Jeffrey Zweegers, Jacqueline Limpens, Miranda Langendam, Phyllis I. Spuls
Journal: JAMA Dermatology (2014)

Combined use of systemic agents may be necessary to achieve disease control in therapy-resistant patients. However, to our knowledge, an overview of evidence, including quality assessments, is not yet available, and no guidance on monitoring, contraindications, and interactions exists.To summarize and critically appraise the evidence on efficacy and safety of combination therapy with systemic agents in plaque-type psoriasis.Through March 2013, an electronic search limited to randomized clinical trials was performed in MEDLINE, EMBASE, The Cochrane Library, and ongoing trial registers. The quality of evidence was evaluated using the Grading of Recommendations Assessment, Development and Evaluation approach.The initial search retrieved 2583 records, of which 17 met the inclusion criteria. Most studies favored combination therapy, albeit with low significance and low quality of evidence. Etanercept plus methotrexate was the only combination therapy investigated with an adequate sample size (n = 478). In the short term, this combination had superior efficacy with a moderate quality of evidence compared with etanercept monotherapy (Psoriasis Area and Severity Index, 75; relative risk, 1.28; 95% CI, 1.14-1.45). Although this finding coincided with an increase in adverse events (relative risk, 1.25; 95% CI, 1.10-1.42), the overall safety profile remained acceptable.This systematic review provides a comprehensive overview on the validity of different systemic combination therapies. For most combinations, insufficient evidence is available. Initial results indicate that combined therapy with etanercept plus methotrexate may be beneficial in patients that are therapy resistant under intensive follow-up. Dose reductions should be taken into account to minimize adverse effects.