tbuckley/cabot-search huggingface dataset:
Premenstrual Symptoms and Psychiatric Morbidity in Two Italian Health Care Settings
Authors: Giovanni de Girolamo, Giovanni Marchitelli, Rosalia Corbani, Stefano Palazzi
Journal: Psychotherapy and Psychosomatics (1989)

Epidemiological surveys show that a large number of adult females complain of symptoms related to the menstrual cycle. According to the method proposed by another author, we administered the modified version of the Menstrual Distress Questionnaire and the General Health Questionnaire (GHQ), 12-item version, to 101 women attending a family planning clinic and to 92 women attending a general practice in two North Italian towns. A very high rate (about 85% of the total sample) of women complained of moderate to severe symptoms during their premenstrual phase and a substantial proportion of women showed some degree of psychiatric ill health. Comparing the premenstrual complainers and the premenstrual non-complainers, the only significant difference found was related to the score on the GHQ. Half the women reported about 5 symptoms, and a cluster analysis identified a group of women complaining of severe symptoms. Implications of these findings for the current discussion on the premenstrual syndrome are discussed.
Dissecting Aortic Aneurysm Manifested as Fever of Unknown Origin
Authors: Philip A. Mackowiak
Journal: JAMA (1976)

A patient with a dissecting aneurysm of the ascending aorta had fever of unknown origin. Although his clinical picture included a number of classical features of his disorder, these were initially misinterpreted, largely because fever was the patient's chief complaint. Polymorphonuclear leukocytes sequestered within the aortic hemagen as they disintegrated. This case emphasizes the protean nature of the dissecting aortic aneurysm, adding yet another distinct clinical manifestation, fever of unknown origin, with which it may be associated.
347 HEALTHY RANGES FOR SERUM ALANINE AMINOTRANSFERASE CONCENTRATION: TIME FOR A NEW UPDATE?
Authors: P. Prati, F. Cappiello, A. Berzuini, M. Spreaflco, I. Guarnori, L. Raffaele, C. Bonato, P. Duca, A. Colli
Journal: Journal of Hepatology (2011)
Childhood Adiposity as a Predictor of Cardiac Mass in Adulthood
Authors: Xiangrong Li, Shengxu Li, Eralp Ulusoy, Wei Chen, Sathanur R. Srinivasan, Gerald S. Berenson
Journal: Circulation (2004)

The association between left ventricular hypertrophy, an independent predictor of cardiovascular (CV) morbidity and mortality, and CV risk factors has been well documented in childhood and in adulthood. However, information on the relationship between left ventricular mass (LVM) in adults and longitudinal measurements of CV risk factors from childhood to adulthood is limited.
Long-term effects of prenatal indomethacin administration on the pulmonary circulation in rats
Authors: J Herget, V Hampl, V Povysilova, Z Slavik
Journal: European Respiratory Journal (1995)

Mechanical properties of the adult pulmonary vasculature are affected by perinatal experience of hypoxic pulmonary hypertension. In the present study, we followed the long-term effects of perinatal pulmonary hypertension induced by means other than hypoxia in rats. Daily injections of indomethacin (1 mg.kg-1 body weight (BW)) were given to the parturient rats. Their newborn pups had significantly increased number of muscularized peripheral pulmonary vessels. Pulmonary hypertension, however, did not persist to adulthood (mean pulmonary arterial pressure (Ppa) was 17.2 +/- 1.3 torr in the experimental group and 16.4 +/- 0.8 torr in controls). Pulmonary hypertension induced in adult rats by exposure to chronic hypoxia or by acute hypoxic challenges was similar in indomethacin-treated and control rats. Normoxic perfusion pressure/flow (P/Q) plots in isolated lungs were less steep in indomethacin-treated than in control rats. Acute hypoxia increased the slope of P/Q plots in indomethacin treated rats but not in controls. The described changes in the pulmonary vasculature induced by indomethacin are similar to those found previously in adult rats born in hypoxia. We conclude that perinatal pulmonary hypertension permanently modifies the pulmonary vasculature.
Diagnostic Radiologists in Distress
Authors: J. L. Cole, M. Goldman, F. W. Wright
Journal: BMJ (1972)

usually refers to the destruction of the fetus per se.But as Dr. Wilkinson points out, many doctors conscientiously consider the needs of the whole person, allowing for the possibility that these needs may conflict with the patient's immediate demands.In my view these two issues are not distinct from each other; the destruction of the fetus must rarely be compatible with the whole patient's needs.If a woman (in one way way or another) procures an abortion, this indicates that we, as doctors, relatives, or citizens, have been failing to help her.-Iam, etc.,
Labour promises to shake up NHS
Authors: J Warden
Journal: BMJ (1994)

A labour government in Britain would abolish fundholding by general practitioners, get rid of the internal market, and set up democratic boards to run NHS trusts. Labour's long awaited consultation paper accepts the separation of providers and purchasers in health care but argues for a shift in emphasis to primary care.

* Labour would shift the emphasis to primary care

(Fig Omitted)

John Smith, the leader of the Labour party, said that it would “rebuild the NHS.” He said that while the United States was …
Allergic lung responses are increased in prostaglandin H synthase–deficient mice
Authors: Stephen H. Gavett, Sharon L. Madison, Patricia C. Chulada, Paula E. Scarborough, Wei Qu, James E. Boyle, Howard F. Tiano, Christopher A. Lee, Robert Langenbach, Victor L. Roggli, Darryl C. Zeldin
Journal: Journal of Clinical Investigation (1999)

To investigate the function of prostaglandin H synthase-1 and synthase-2 (PGHS-1 and PGHS-2) in the normal lung and in allergic lung responses, we examined allergen-induced pulmonary inflammation and airway hyperresponsiveness in wild-type mice and in PGHS-1(-/-) and PGHS-2(-/-) mice. Among nonimmunized saline-exposed groups, we found no significant differences in lung function or histopathology, although PGE(2) was dramatically reduced in bronchoalveolar lavage (BAL) fluid from PGHS-1(-/-) mice, relative to wild-type or PGHS-2(-/-) mice. After ovalbumin sensitization and challenge, lung inflammatory indices (BAL cells, proteins, IgE, lung histopathology) were significantly greater in PGHS-1(-/-) mice compared with PGHS-2(-/-) mice, and both were far greater than in wild-type mice, as illustrated by the ratio of eosinophils in BAL fluid (8:5:1, respectively). Both allergic PGHS-1(-/-) and PGHS-2(-/-) mice exhibited decreased baseline respiratory system compliance, whereas only allergic PGHS-1(-/-) mice showed increased baseline resistance and responsiveness to methacholine. Ovalbumin exposure caused a modest increase in lung PGHS-2 protein and a corresponding increase in BAL fluid PGE(2) in wild-type mice. We conclude that (a) PGHS-1 is the predominant enzyme that biosynthesizes PGE(2) in the normal mouse lung; (b) PGHS-1 and PGHS-2 products limit allergic lung inflammation and IgE secretion and promote normal lung function; and (c) airway inflammation can be dissociated from the development of airway hyperresponsiveness in PGHS-2(-/-) mice.
Peripheral and autonomic neuropathy after treatment with perhexiline maleate.
Authors: D M Fraser, I W Campbell, H C Miller
Journal: BMJ (1977)

the fingers, painful limitation of the hips, and bony swelling of the right knee.Radiographs of the joints showed widespread degenerative changes with no evidence of erosions.His latex test result was negative.Close questioning disclosed that he had been taking two Elestol tablets three times a daNy for at least 15 years for his hands.It also transpired that in 1972 he underwent an open prostatectomy without steroid cover.Ophthalmological examination was performed by Mr B Cobb and showed no retinopathy or loss of central visual acuity.
Anticonvulsant Drugs And Vitamin D Metabolism
Authors: Leo Vincent Gould
Journal: JAMA (1973)

<h3>To the Editor.—</h3> The physicianly caution of Dr. Livingston et al (224:1634, 1973) is to be commended. The doubtful logic of their argument against anticonvulsant rickets and osteomalacia is affected by their caution, in that they state that these cases of rickets<i>may</i>have represented merely a coincidental occurrence. A cursory reader of this article would conclude that within the last 30 years no rickets occurred in patients receiving anticonvulsant therapy under their care. In fact, the report establishes only that no<i>clinically evident</i>rickets was discovered in these patients, and no biochemical evidence of rickets was demonstrated in only 28 patients receiving diphenylhydantoin or primidone treatment. These conclusions hardly contradict the large amount of available evidence that there is such a thing as anti-convulsant-induced bone disease. It would be pertinent to ask if suspicion of rickets arose in the minds of all the physicians who saw these patients over
Acute Doxorubicin Cardiotoxicity Is Associated With p53-Induced Inhibition of the Mammalian Target of Rapamycin Pathway
Authors: Wuqiang Zhu, Mark H. Soonpaa, Hanying Chen, Weihua Shen, R. Mark Payne, Edward A. Liechty, Randall L. Caldwell, Weinian Shou, Loren J. Field
Journal: Circulation (2008)

Doxorubicin is used to treat childhood and adult cancer. Doxorubicin treatment is associated with both acute and chronic cardiotoxicity. The cardiotoxic effects of doxorubicin are cumulative, which limits its chemotherapeutic dose. Free radical generation and p53-dependent apoptosis are thought to contribute to doxorubicin-induced cardiotoxicity.Adult transgenic (MHC-CB7) mice expressing cardiomyocyte-restricted dominant-interfering p53 and their nontransgenic littermates were treated with doxorubicin (20 mg/kg cumulative dose). Nontransgenic mice exhibited reduced left ventricular systolic function (predoxorubicin fractional shortening [FS] 61+/-2%, postdoxorubicin FS 45+/-2%, mean+/-SEM, P<0.008), reduced cardiac mass, and high levels of cardiomyocyte apoptosis 7 days after the initiation of doxorubicin treatment. In contrast, doxorubicin-treated MHC-CB7 mice exhibited normal left ventricular systolic function (predoxorubicin FS 63+/-2%, postdoxorubicin FS 60+/-2%, P>0.008), normal cardiac mass, and low levels of cardiomyocyte apoptosis. Western blot analyses indicated that mTOR (mammalian target of rapamycin) signaling was inhibited in doxorubicin-treated nontransgenic mice but not in doxorubicin-treated MHC-CB7 mice. Accordingly, transgenic mice with cardiomyocyte-restricted, constitutively active mTOR expression (MHC-mTORca) were studied. Left ventricular systolic function (predoxorubicin FS 64+/-2%, postdoxorubicin FS 60+/-3%, P>0.008) and cardiac mass were normal in doxorubicin-treated MHC-mTORca mice, despite levels of cardiomyocyte apoptosis similar to those seen in doxorubicin-treated nontransgenic mice.These data suggest that doxorubicin treatment induces acute cardiac dysfunction and reduces cardiac mass via p53-dependent inhibition of mTOR signaling and that loss of myocardial mass, and not cardiomyocyte apoptosis, is the major contributor to acute doxorubicin cardiotoxicity.
Regulation of the rat liver sodium-dependent bile acid cotransporter gene by prolactin. Mediation of transcriptional activation by Stat5.
Authors: T C Ganguly, M L O'Brien, S J Karpen, J F Hyde, F J Suchy, M Vore
Journal: Journal of Clinical Investigation (1997)

The intracellular mechanism(s) underlying the upregulation of the hepatic Na+/taurocholate cotransporting polypeptide (ntcp) by prolactin (PRL) are unknown. In this report, we demonstrate a time-dependent increase in nuclear translocation of phosphorylated liver Stat5 (a member of the ignal ransducers and ctivators of ranscription family) that correlated with suckling-induced increases in serum PRL levels. In electrophoretic mobility gel shift assays, nuclear Stat5 exhibited specific DNA-binding ability towards IFN-gamma-activated sequence (GAS)-like elements (GLEs; 5'TTC/A-PyNPu-G/TAA-3') located in the -937 to -904 bp region of the ntcp promoter. Transient cotransfections in HepG2 cells revealed that PRL inducibility (2.5-3-fold) required coexpression of the long form of the PRL receptor (PRLRL) and Stat5. Deletion analysis mapped the PRLinducible region to -1237 to -758 bp of the ntcp promoter. Linking this 0.5-kb region to a heterologous thymidine kinase (tk) promoter, or linking multimerized ntcp GLEs either upstream of the ntcp minimal promoter (-158 to +47 bp) or the heterologous promoter conferred dose-dependent PRL responsiveness. The short form of the PRL receptor failed to transactivate ntcp GLEs. These results indicate that PRL acts via the PRLRL to facilitate Stat5 binding to ntcp-GLEs and to transcriptionally regulate ntcp.
Establishment of a highly efficient gene transfer system for mouse fetal hepatic progenitor cells
Authors: Kentaro Yasuchika, Tetsuro Hirose, Hideaki Fujii, Shoshiro Oe, Koichi Hasegawa, Takahisa Fujikawa, Hisaya Azuma, Yoshio Yamaoka
Journal: Hepatology (2002)

Because of a donor shortage problem in liver transplantation, cell transplantation has been anticipated as a useful bridge or substitute therapy, and has necessitated the development of cell sources other than donated organs. Therefore, the use of fetal hepatic progenitor cells (HPCs) is now being focused on. In this study, we intended to establish an efficient ex vivo nonviral gene-transfer system using a newly developed isolation and culture system for mouse fetal HPCs. Fetal HPCs, characterized using immunocytochemistry and reverse-transcription polymerase chain reaction (RT-PCR) for lineage markers, were collected from E13.5 Balb/c mice using change in size because of cell aggregation by their homophilic cell-to-cell binding occurring during suspension culture. Optimal conditions for culture and ex vivo gene transfection for fetal HPCs were determined by (3)H-thymidine incorporation and the expression efficacy of transfected red fluorescent protein (DsRed) gene in different culture media. The optimum timing for gene transfection was also evaluated. To evaluate the in vivo expression of the transferred gene, DsRed-transferred fetal HPCs were transplanted into 70% partially hepatectomized allogenic mice. The highest efficacy of DsRed gene transfection into fetal HPCs in vitro (45% +/- 12.3%) was achieved with culture media, which also enabled the highest (3)H-thymidine incorporation, containing the deleted form of hepatocyte growth factor (dHGF) and insulin, and when transfection was performed immediately after isolation. In vivo DsRed expression in fetal HPCs was maintained concomitantly with albumin expression even after HPC transplantation. In conclusion, we established a highly efficient in vitro gene transfer system for mouse fetal HPCs using a newly developed isolation and culture system.
Drug misuse: GPs' pivotal role
Authors: R. Scott
Journal: BMJ (1997)

At a recent postgraduate meeting for psychiatrists I had to propose the motion, “The management of drug addiction should not be within the remit of the psychiatrist.” After some reflection, I decided that there were three reasons why this was so.

The first is that most people with drug problems are not mad. The second is that psychiatrists have neither the knowledge, the skills, nor the appropriate attitudes to manage drug misusers. And the third reason is that general practitioners are far better at doing it.

In the spectrum of substance use, starting with experimentation, passing through recreation, and then on to dependence, problems may appear at any time. “It seems improbable, however, that gross mental illness is …
Genetic Factors Influencing Irradiation Protection by Bone Marrow. I. The F&lt;sub&gt;1&lt;/sub&gt; Hybrid Effect
Authors: Delta E. Uphoff
Journal: JNCI Journal of the National Cancer Institute (1957)

Journal Article Genetic Factors Influencing Irradiation Protection by Bone Marrow. I. The F1 Hybrid Effect Get access Delta E. Uphoff Delta E. Uphoff National Cancer Institute,2Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 19, Issue 1, July 1957, Pages 123–130, https://doi.org/10.1093/jnci/19.1.123 Published: 01 July 1957 Article history Received: 29 April 1957 Published: 01 July 1957
Sirt1 acts in association with PPAR to protect the heart from hypertrophy, metabolic dysregulation, and inflammation
Authors: A. Planavila, R. Iglesias, M. Giralt, F. Villarroya
Journal: Cardiovascular Research (2010)

A complex set of metabolic and inflammatory processes are involved in the development of cardiac hypertrophy. Accumulating evidence indicates an important role for Sirt1 in cardiac function, whereas peroxisome proliferator-activated receptor-α (PPARα) is a master controller of cardiac lipid metabolism and plays a protective role on cardiac hypertrophy. The objective of the present study was to explore the relationships between Sirt1 and PPARα in the control of hypertrophy, metabolism, and inflammation processes in the heart. Neonatal cardiomyocytes (NCMs) were used for studies in vitro. Both the activation of Sirt1 with resveratrol (RSV) and overexpression of Sirt1 inhibited phenylephrine (PE)-induced NCM hypertrophy and prevented PE-induced down-regulation of fatty acid oxidation genes. Sirt1 also inhibited the PE-induced increase in mRNA levels of the pro-inflammatory cytokine monocyte chemoattractant protein-1 in NCMs and blocked the enhanced nuclear factor-κB (NF-κB) activity associated with exposure to PE. Importantly, inhibition of PPARα suppressed the beneficial effects of Sirt1 on hypertrophy, fatty acid metabolism, and inflammation. Co-immunoprecipitation studies revealed that overexpression of Sirt1 enhanced PPARα binding to the p65 subunit of NF-κB and led to p65-deacetylation in NCMs. Moreover, Sirt1 overexpression led to the deacetylation of the PPARα co-activator PGC-1α. Consistent with these observations in vitro, isoproterenol-induced cardiac hypertrophy, metabolic dysregulation, and inflammation in vivo were prevented by RSV in wild-type mice but not in PPARα-null mice. Collectively, these findings reveal a major involvement of the Sirt1–PPARα interaction in the protective role of Sirt1 against cardiac hypertrophy.
PEDIATRIC RESOURCE EXPENDITURES IN CARDIAC SPECIALTY ENCOUNTERS (PRECISE): DEVELOPMENT OF A COST ADJUSTMENT MODEL FOR CONGENITAL CARDIAC CATHETERIZATION
Authors: Lisa Bergersen, Kimberlee Gauvreau, Jean Connor, Cheryl O'Connell, Melvin Almodovar, James DiNardo, Puja Banka, John Mayer
Journal: Journal of the American College of Cardiology (2013)
Carbon Monoxide Poisoning in a Motel-Reply
Authors: Bruce B. Dan
Journal: JAMA (1989)

<h3>In Reply.—</h3> Dr Harlan seems to have taken offense when none was given, but more unfortunately he has missed the central point of the article and its accompanying editorial. Both were meant to draw attention to a potentially preventable cause of morbidity and mortality. Carbon monoxide is responsible for almost half of all deaths from poisoning, and it is the most frequent cause of chemical asphyxiation. A major reason that several thousand people die every year from its effects is that carbon monoxide poisoning is not considered as often as it should be as a cause for unexplained coma. Dr Harlan illustrates that point when he says that after one person was found dead on the floor of a motel room with cherry-red livor mortis and another person lay a few feet away in coma, that carbon monoxide poisoning tended to be ruled out because they were found in an
Academic Geriatrics for the Year 2000
Authors: John W. Rowe, Esta Grossman, Enriqueta Bond
Journal: New England Journal of Medicine (1987)

Estimates of the number of older Americans who will need specialized care by the year 2000 and the number of physicians who will be trained to provide that care foretell a serious disparity. In response to the projected gap, the Institute of Medicine created an ad hoc committee to identify the types of physicians likely to be needed to care for the older population, the training these physicians should receive, and ways to develop academic leaders to shape and deliver that training. This article summarizes the committee's final report, including the findings of a conference that brought together representatives of . . .
Brain natriuretic peptide as a novel cardiac hormone in humans. Evidence for an exquisite dual natriuretic peptide system, atrial natriuretic peptide and brain natriuretic peptide.
Authors: M Mukoyama, K Nakao, K Hosoda, S Suga, Y Saito, Y Ogawa, G Shirakami, M Jougasaki, K Obata, H Yasue
Journal: Journal of Clinical Investigation (1991)

Using a specific radioimmunoassay for human brain natriuretic peptide (hBNP) with a monoclonal antibody, we have investigated its synthesis, secretion, and clearance in comparison with those of atrial natriuretic peptide (ANP) in normal subjects and patients with congestive heart failure (CHF). Mean BNP-like immunoreactivity (-LI) levels in normal atrium and ventricle were 250 and 18 pmol/g, respectively. The plasma BNP-LI level in normal subjects was 0.90 +/- 0.07 fmol/ml, which was 16% of the ANP-LI level. In contrast, the plasma BNP-LI level markedly increased in patients with CHF in proportion to its severity, and surpassed the ANP-LI level in severe cases. There was a significant step-up of the plasma BNP-LI level in the coronary sinus (CS) compared with that in the aortic root (Ao) and the difference between these BNP-LI levels, delta(CS-Ao)BNP, also increased with the severity of CHF. In addition, the step-up of the BNP-LI level in the anterior interventricular vein [delta(AIV-Ao)BNP] was comparable to delta(CS-Ao)BNP, indicating that BNP is secreted mainly from the ventricle. Predominant BNP synthesis in the ventricle was also confirmed by Northern blot analysis. Catheterization and pharmacokinetic studies revealed that hBNP is cleared from the circulation more slowly than alpha-hANP; this was in part attributed to lower (about 7%) binding affinity of hBNP to clearance receptors than that of alpha-hANP. A predominant molecular form of BNP-LI in the heart and plasma was a 3-kD form corresponding to hBNP. These results indicate that BNP is a novel cardiac hormone secreted predominantly from the ventricle, and that the synthesis, secretion and clearance of BNP differ from those of ANP, suggesting discrete physiological and pathophysiological roles of BNP in a dual natriuretic peptide system.
Effect of Genome Size on AAV Vector Packaging
Authors: Zhijian Wu, Hongyan Yang, Peter Colosi
Journal: Molecular Therapy (2009)

Adeno-associated virus (AAV) vector genomes have been limited to 5 kilobases (kb) in length because their packaging limit was thought to be similar to the size of the parent AAV genome. Recent reports claim that significantly larger vector genomes can be packaged intact. We examined the packaged vector genomes from plasmid-encoded AAV vectors that ranged from 4.7 to 8.7 kb in length, using AAV types 2, 5, and 8 capsids. Southern blot analysis indicated that packaged AAV vector genomes never exceeded 5.2 kb in length irrespective of the size of the plasmid-encoded vector or the capsid type. This result was confirmed by vector genome probing with strand-specific oligonucleotides. The packaged vector genomes derived from plasmid-encoded vectors exceeding 5 kb were heterogeneous in length and truncated on the 5' end. Despite their truncated genomes, vector preparations produced from plasmid-encoded vectors exceeding 5.2 kb mediated reporter gene expression in vitro at high multiplicity of infection (MOI). The efficiency of expression was substantially lower than that of reporter vectors with genomes <5 kb in length. We propose that transcriptionally functional, intact vector genomes are generated in cells transduced at high MOI from the fragmentary genomes of these larger vectors, probably by recombination.