bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anti-fibrinolytic agents in post partum haemorrhage: a systematic review
Authors: Ferrer Pili , Roberts Ian , Sydenham Emma , Blackhall Karen , Shakur Haleema 
Published: July 2009

Abstract

Background
Post partum haemorrhage is a leading cause of maternal death worldwide. It also contributes to maternal morbidity as women may require a hysterectomy to control bleeding, or may require a blood transfusion, which can transmit viral infections. Anti-fibrinolytic agents have been proposed as a treatment for post partum haemorrhage. We conducted a systematic review to assess the effectiveness and safety of anti-fibrinolytic agents in post partum bleeding.

Methods
All randomised controlled trials of anti-fibrinolytic agents given for bleeding during the postpartum period were included in this review. We searched Medline, PubMed, EMBASE, Cochrane Central Register of Controlled trials, Web of Science, metaRegister of controlled trials, LILACS, Reproductive Health Library, African healthline, POPLINE, MedCarib, CINAHL, Clinicaltrials.gov and the reference lists of eligible trials. Two authors extracted data. Methodological quality was assessed by evaluating allocation concealment. The primary outcome was maternal mortality. Secondary outcomes were blood loss, blood transfusion, hysterectomy, mean haemoglobin concentration, thrombo-embolic events and other adverse effects.

Results
We identified three randomised controlled trials involving 461 participants. The trials compared tranexamic acid with no treatment and reported blood loss after delivery. In all three trials, allocation concealment was either inadequate or unclear. The administration of tranexamic acid was associated with a reduction in blood loss of 92 millilitres (95%CI 76 to 109). The most frequently reported adverse effect of tranexamic acid was nausea, although the increase was easily compatible with the play of chance (RR 4.63, 95%CI 0.23 to 95.14).

Conclusion
Tranexamic acid may reduce blood loss in post partum haemorrhage. However, the quality of the currently available evidence is poor. Adequately powered, high quality randomised controlled trials are needed.
Expression of ezrin is associated with invasion and dedifferentiation of hepatitis B related hepatocellular carcinoma
Authors: Yeh Chun-Nan , Pang See-Tong , Chen Tsung-Wen , Wu Ren-Ching , Weng Wen-Hui , Chen Miin-Fu 
Published: July 2009

Abstract

Background
Hepatocellular carcinoma (HCC) is the fifth most common malignancy in the world and constitutes the leading cause of cancer-related death among men, and second among women in Taiwan. Liver cirrhosis and HCC are relatively prevalent, and 80% to 85% of the patients with these conditions have positive results for hepatitis B surface antigen in Taiwan. Only 5% of the general population is seronegative for all hepatititis B virus (HBV) markers. This is the first study to determine the role of ezrin upon HBV HCC cell and patients with HBV HCC undergoing hepatectomy

Methods
Immunohistochemical study with ezrin in 104 human HBV-HCC cases were carried out to investigate its association with the clinicopathological features and the outcomes of 104 HBV-HCC patients undergoing hepatetomy. In addition, DNA constructs including the wild type ezrin (wt-ezrin) and mutant ezrin Tyr353 (Y353) were transfected into Hep3B cell to study its role in tumor invasion and differentiation.

Results
HBV HCC patients with ezrin over-expression independently have smaller tumor size, cirrhotic liver background, poor tumor differentiation, and more vascular invasion. Ezrin expression status has no impact on survival for HBV-HCC patients undergoing hepatectomy. The in vitro assay showed that wt-ezrin Hep3B cells have a significant higher level of AFP secretion and higher invasion ability as compared with the control and Y353- ezrin Hep3B cells.

Conclusion
Ezrin over-expression contributed to de-differentiation and invasion of HBV-HCC cell. HBV-HCC patients with ezrin over-expression were independently associated with tumor with smaller size, cirrhotic liver background, poor differentiation, and vascular invasion.
Breast cancer cells stimulate osteoprotegerin (OPG) production by endothelial cells through direct cell contact
Authors: Reid Penny E , Brown Nicola J , Holen Ingunn 
Published: July 2009

Abstract

Background
Angiogenesis, the sprouting of capillaries from existing blood vessels, is central to tumour growth and progression, however the molecular regulation of this process remains to be fully elucidated. The secreted glycoprotein osteoprotegerin (OPG) is one potential pro-angiogenic factor, and clinical studies have demonstrated endothelial cells within a number of tumour types to express high levels of OPG compared to those in normal tissue. Additionally, OPG can increase endothelial cell survival, proliferation and migration, as well as induce endothelial cell tube formation in vitro. This study aims to elucidate the processes involved in the pro-angiogenic effects of OPG in vitro, and also how OPG levels may be regulated within the tumour microenvironment.

Results
It has previously been demonstrated that OPG can induce tube formation on growth factor reduced matrigel. In this study, we demonstrate that OPG enhances the pro-angiogenic effects of VEGF and that OPG does not stimulate endothelial cell tube formation through activation of the VEGFR2 receptor. We also show that cell contact between HuDMECs and the T47D breast cancer cell line increases endothelial cell OPG mRNA and protein secretion levels in in vitro co-cultures. These increases in endothelial cell OPG secretion were dependent on ανβ3 ligation and NFκB activation. In contrast, the pro-angiogenic factors VEGF, bFGF and TGFβ had no effect on HuDMEC OPG levels.

Conclusion
These findings suggest that the VEGF signalling pathway is not involved in mediating the pro-angiogenic effects of OPG on endothelial cells in vitro. Additionally, we show that breast cancer cells cause increased levels of OPG expression by endothelial cells, and that direct contact between endothelial cells and tumour cells is required in order to increase endothelial OPG expression and secretion. Stimulation of OPG secretion was shown to involve ανβ3 ligation and NFκB activation.
Malaria ookinetes exhibit multiple markers for apoptosis-like programmed cell death in vitro
Authors: Arambage Shashini C , Grant Karen M , Pardo Ian , Ranford-Cartwright Lisa , Hurd Hilary 
Published: July 2009

Abstract

Background
A wide range of unicellular eukaryotes have now been shown to undergo a form of programmed cell death (PCD) that resembles apoptosis; exhibiting morphological and, in some cases, biochemical markers typical of metazoans. However, reports that sexual and asexual stages of malaria parasites exhibit these markers have been challenged. Here we use a rodent malaria model, Plasmodium berghei, to determine whether, and what proportion of cultured ookinetes show signs of apoptosis-like death and extend the study to examine ookinetes of Plasmodium falciparum in vivo.

Results
Ookinetes displayed the following markers of PCD: loss of mitochondrial membrane potential, nuclear chromatin condensation, DNA fragmentation, translocation of phosphatidylserine to the outer surface of the cell membrane and caspase-like activity. The proportion of parasites expressing apoptosis markers rose with time, particularly when cultured in phosphate buffered saline. Some ookinetes positive for apoptosis markers also had compromised membranes, which could represent a late stage in the process. When these are included a similar proportion of ookinetes display each marker. Over 50% of P. falciparum ookinetes, removed from the mosquito midgut lumen 24 h post-infection, had nuclei containing fragmented DNA.

Conclusion
We have confirmed previous reports that Plasmodium ookinetes display multiple signs that suggest they die by a mechanism resembling apoptosis. This occurs in vivo and in vitro without experimental application of triggers. Our findings support the hypothesis that non-necrotic mechanisms of cell death evolved before the advent of multicellular organisms.
The change and effect of endothelial progenitor cells in pig with multiple organ dysfunction syndromes
Authors: Luo Tian Hang , Wang Yao , Lu Zheng Mao , Zhou Hong , Xue Xu Chao , Bi Jian Wei , Ma Li Ye , Fang Guo En 
Published: July 2009

Abstract
Introduction
The dysfunction and decrease of endothelial progenitor cells (EPCs) may play a very important role in the initiation of organ dysfunction caused by trauma or severe sepsis. We aim to measure the number and function of EPCs in the progression of multiple organ dysfunction syndromes (MODS) caused by severe sepsis, which may help to understand the pathogenesis of MODS by the changing of EPCs.

Methods
A total of 40 pigs were randomly divided into two groups, which were subjected to hemorrhagic shock, resuscitation and endotoxemia (experimental group, n = 20) or acted as a control (control group, n = 20). The number and function of EPCs including adhesive, migratory and angiogenesis capacities were analyzed at different times in both groups.

Results
All the animals in the experimental group developed MODS (100%) and 17 of 20 animals (85%) died due to MODS; the incidence of MODS and death of the animals in the control group were 0% (P < 0.01). The number, migratory and adhesive capacities of EPCs decreased sharply in the animals of the experimental group corresponding to the increasing severities of MODS, but the angiogenesis function increased gradually until death. The decrease in function of EPCs preceded the decrease in number of EPCs. The decrease in number and function of EPCs occurred prior to the occurrence of MODS.

Conclusions
For the first time, it was observed that the number and function of EPCs decreased sharply in the progression of MODS and that it was prior to the occurrence of MODS. The decrease in number and function of EPCs may be one of the main pathogenic factors of MODS.
Alcohol abuse and pulmonary disease
Authors: Boé Darren M , Vandivier R William , Burnham Ellen L , Moss Marc 
Published: July 2009

Abstract
Review on alcohol abuse increasing the risk for acute respiratory distress syndrome through alterations in pulmonary function, and implications to potential therapeutic targets.
ARDS is a severe form of lung injury characterized by increased permeability of the alveolar capillary membrane, diffuse alveolar damage, the accumulation of proteinaceous interstitial and intra-alveolar edema, and the presence of hyaline membranes. These pathological changes are accompanied by physiological alterations, including severe hypoxemia, an increase in pulmonary dead space, and decreased pulmonary compliance. Approximately 200,000 individuals develop ARDS in the United States each year [1], and nearly 50% of these patients have a history of alcohol abuse. We have identified alcohol abuse as an independent risk factor for the development of ARDS [2–5], and more recent studies have validated these findings in patients following lung resection and blood transfusion [2, 3]. In ARDS survivors, alcohol abuse is also associated with an increased duration of mechanical ventilation and prolonged ICU length of stay [5]. Despite studies aimed at improving outcomes in patients with ARDS, the mortality remains high at &gt;40% [6]. For those who abuse alcohol, the mortality is even higher, at 65% [4]. In this review, we will discuss the relationship between alcohol abuse and ARDS, the effects of alcohol abuse on pulmonary function, and future directions and potential therapeutic targets for patients at risk for ARDS as a result of alcohol abuse, which impairs immune function, decreases pulmonary antioxidant capacity, decreases alveolar epithelial cell function, alters activation of the renin angiotensin system, and impairs GM-CSF signaling. These pathways represent potential therapeutic targets for patients at risk for ARDS as a result of alcohol abuse.
Impaired osteoclastogenesis by staphylococcal lipoteichoic acid through Toll-like receptor 2 with partial involvement of MyD88
Authors: Yang Jihyun , Ryu Young Hee , Yun Cheol-Heui , Han Seung Hyun 
Published: July 2009

Abstract
Staphylococcal LTA inhibits osteoclast differentiation primarily through TLR2; and in part through MyD88 signaling, which in turn inhibits activation of ERK, JNK, and AP-1.
Degenerative bone disease, marked by excessive loss of calcified matrix, is often associated with bacterial infections. Osteoclasts, which mediate the bone-resorptive process, are derived mainly from myeloid precursor cells of the monocyte/macrophage lineage, from which cells with phagocytic and inflammatory capacities may alternatively arise. Here, we investigated the effect of LTA, a major cell-wall virulence factor of Gram-positive bacteria, on osteoclast differentiation. Osteoclast precursors were prepared from C57BL/6 mouse BM using M-CSF and RANKL. When osteoclastogenesis was induced in the presence of staphylococcal LTA, LTA dose-dependently inhibited the differentiation of osteoclast precursors to mature osteoclasts. A corresponding inhibition of bone-resorptive function was observed in the reduced resorption area on calcium phosphate-coated culture plates. In contrast, the phagocytic and inflammatory potential of the osteoclast precursors increased in the presence of LTA. TLR2, known to recognize LTA, might be essential for the LTA inhibition of osteoclastogenesis, as the inhibition did not occur in the precursors from TLR2-deficient mice. Importantly, MyD88-dependent and MyD88-independent pathways would participate in the inhibition, as determined using MyD88-deficient cells. Moreover, LTA inhibited phosphorylation of ERK and JNK in osteoclast precursors stimulated with M-CSF and RANKL, concomitantly with a decreased DNA-binding activity of AP-1. These results suggest that staphylococcal LTA inhibits osteoclast differentiation primarily through TLR2 but also in part through MyD88 signaling, which in turn, inhibits activation of ERK, JNK, and AP-1.
Stanniocalcin-1 suppresses superoxide generation in macrophages through induction of mitochondrial UCP2
Authors: Wang Yanlin , Huang Luping , Abdelrahim Maen , Cai Qingsong , Truong Anh , Bick Roger , Poindexter Brian , Sheikh-Hamad David 
Published: July 2009

AbstractMammalian stanniocalcin-1, a secreted phosphogylcoprotein that targets the mitochondria, suppresses superoxide and may function as an LPS antagonist in macrophages.Mammalian STC1 decreases the mobility of macrophages and diminishes their response to chemokines. In the current experiments, we sought to determine the impact of STC1 on energy metabolism and superoxide generation in mouse macrophages. STC1 decreases ATP level in macrophages but does not affect the activity of respiratory chain complexes I–IV. STC1 induces the expression of mitochondrial UCP2, diminishing mitochondrial membrane potential and superoxide generation; studies in UCP2 null and gp91phox null macrophages suggest that suppression of superoxide by STC1 is UCP2-dependent yet is gp91phox-independent. Furthermore, STC1 blunts the effects of LPS on superoxide generation in macrophages. Exogenous STC1 is internalized by macrophages within 10 min and localizes to the mitochondria, suggesting a role for circulating and/or tissue-derived STC1 in regulating macrophage function. STC1 induces arrest of the cell cycle at the G1 phase and reduces cell necrosis and apoptosis in serum-starved macrophages. Our data identify STC1 as a key regulator of superoxide generation in macrophages and suggest that STC1 may profoundly affect the immune/inflammatory response.
Growth Hormone and Sex Steroid Effects on Serum Glucose, Insulin, and Lipid Concentrations in Healthy Older Women and Men
Authors: Münzer Thomas , Harman S. Mitchell , Sorkin John D. , Blackman Marc R. 
Published: July 2009

Context: With aging, GH, IGF-I, and sex steroid concentrations and glucose tolerance decrease, and body fat and serum lipids increase.Objective: The aim of the study was to assess GH and/or sex steroid administration effects on serum glucose, insulin, insulin sensitivity, and lipids in older individuals.Design: A double-masked, 2 × 2 factorial, placebo-controlled, double-dummy design was used for the study.Intervention: GH and/or sex steroid [transdermal estradiol plus oral medroxyprogesterone acetate in women (HRT); testosterone enanthate (T) in men] were administered for 6 months.Participants: Healthy, community-dwelling women (n = 57) and men (n = 74) ages 65–88 yr (mean, 72 yr) participated in the study.Main Outcome Measures: We measured serum glucose, insulin, and insulin sensitivity [quantitative insulin sensitivity check index (QUICKI) and insulin sensitivity index (ISI)] before and during an oral glucose tolerance test and lipid profiles.Results: In women, GH did not alter oral glucose tolerance test 120 min or 2-h area under the curve (AUC) glucose values, but it increased 120 min insulin and AUC insulin. There were no significant effects of HRT or GH+HRT. ISI and QUICKI decreased after GH. In men, GH increased 120 min and AUC glucose and insulin AUC. GH+T increased 120 min glucose and glucose and insulin AUCs. T alone did not affect glucose or insulin. ISI decreased after GH and GH+T, whereas QUICKI decreased after GH. GH in women and men and GH+T in men decreased QUICKI by 4 wk. In women, HRT decreased total cholesterol and low-density lipoprotein (LDL)-cholesterol, and GH decreased LDL-cholesterol. In men, total cholesterol decreased after T and GH+T. LDL-cholesterol decreased after GH and GH+T. GH increased serum triglycerides.Conclusions: GH administration to healthy older individuals for 6 months increased insulin resistance with moderately beneficial effects on lipids.Chronic GH administration to healthy older individuals increases insulin resistance with moderately beneficial effects on lipids.
The Clinical, Radiological and Pathological Aspects of Pulmonary Hæmosiderosis
Authors: Park S. D. Scott 
Published: July 2009

Abstract
The first radiological recognition of pulmonary hæmosiderosis was apparently by Rosenhagen, in 1928. Since then recorded cases have been few and the condition is generally regarded as being rare. Most of the cases described are in mitral stenosis, but more recently some of a different etiology have been recognised, usually in children with a fairly severe anæmia. In many of the recorded cases of both types, miliary tuberculosis has been diagnosed on the X-ray film, even in those where the patient had mitral stenosis, and usually the diagnosis was not corrected until post-mortem.
The Radiological Anatomy of the Labyrinth
Authors: Pygott F. 
Published: July 2009

Abstract
By sectioning a disarticulated temporal bone in two parallel planes I was able to wire the labyrinth and catheterise the canal of the facial nerve from the internal auditory meatus to the stylomastoid foramen. The first section passed vertically through the external auditory meatus and the Eustachian canal. The second ran along the ridge of the petrous and vertically throught the tip of the mastoid.
The bone was radiographed with its fellow of the opposite side in positions as nearly as possible corresponding to those used in the Law, Granger, Stenvers, and Mayer projections.
The Law projection is obtained by positioning the head so that the orbito-meatal line is at right angles to the centre line of the couch, with the Sagittal plane parallel to the table top. The central ray is directed through the external meatus at an angle of 15° to the face and 15° downwards to the feet. I find in practice that this is unnecessarily complicated; the double tilt prevents the use of Bucky or grid and increases the difficulty of securing corresponding views of the opposite mastoid on the same film. I allow the patient's head to rest naturally on its side on the table with the orbito-meatal line at right angles to the centre line of the table and the Sagittal plane rotated from the horizontal. The position is best assumed with the body in the Sims' semi-prone position, with the arm of the corresponding side lying by the side of the body.
Medical Members' Meeting
Authors: A. M. R.  
Published: July 2009

Abstract
This meeting took place in the Reid Knox Hall of the Institute, on Friday, January 17, 1947, and was attended by about thirty members. Dr. J. Duncan White was in the Chair.
Dr. R. Connell showed films of a case. A man, aged 27 years, a professional footballer, with a history of epileptiform fits. Subject to minor accidents on the football field, but no definite history of fracture. First seen after a football accident in which he sustained a cut over the eyebrow. There was no clinical sign of fracture.
A X ray of the skull was taken and revealed a roughly rounded hiatus in the left temporo-parietal region of the vault. The margins of the hole were smooth and not sclerosed, and the both tables of the bone appeared to be deficient. No sign of fracture was evident. There was, in addition, hyperostosis frontales interna.
Dr. H. Courtney Gage
Authors: Williams Rohan 
Published: July 2009

Abstract
It is given to few men of determined character and of high principles to pass through life and yet to make no enemies, to be regarded by all with sincere and deep affection. Courtney Gage was such a man. After a life devoted to the service of others, Gage died a few days before his sixty-second birthday on October 4, 1947. His death leaves a gap in British radiology that will not be filled.
Before 1914, Gage worked with Sir James Mackenzie Davidson, one of the great pioneer radiologists; he went to France in 1914 with the Essex Yeomanry, was wounded early in the war, and was invalided out of the army. But before long he was back in France with the American Red Cross as an X-ray Technician and was responsible for a great volume of radiographic work for war casualties at Ris Orangis, near Paris; he also covered the work of two large French civil hospitals in that area. His work was recognised by the French Government when he was made “Officier de l'Instruction publique”. He originated a number of techniques for the adequate investigation of spinal injuries and the localisation of foreign bodies, which were published in the French Journal de Radiologie in 1916–1918.
Courtney Gage joined St. Mary's Hospital Medical School in 1919 and qualified in 1924. Thus, on achieving his medical qualification, he came to medical radiology with an unrivalled technical experience behind him.
Carcinoma of the Bronchus with Especial Reference to its Treatment by Radiotherapy
Authors: Shorvon L. M. 
Published: July 2009

Abstract
1. The incidence, ætiology, pathology, symptomatology and diagnosis of carcinoma of the bronchus are briefly described, and the extreme importance of early diagnosis emphasised.
2. Although pneumonectomy is the treatment of choice in suitable cases, it is pointed out that the number of operable cases is small, not more than about 10 per cent.
3. The contradictory opinions as to the value of radiotherapy are referred to.
4. The techniques of treatment by deep X-rays, which I have employed, are described, and the value of penicillin during the course of treatment stressed.
5. A series of 213 cases of carcinoma of the bronchus, seen in Mount Vernon Hospital during the years 1942–6, is analysed.
6. The results of radiotherapy are evaluated under the headings of possibility of cure, prolongation of life, and relief of symptoms.
The Inhibition of Ribo-and Thymo-Nucleic Acid Synthesis in Tumour Tissue by Irradiation with X rays
Authors: Holmes Barbara E. 
Published: July 2009

Abstract
1. The uptake of radioactive phosphorus in the thymonucleic acid fraction of rat tumour tissue is markedly inhibited by X rays.
2. The uptake of radioactive phosphorus in the ribonucleic acid fraction is also inhibited, but to a smaller extent.
3. Nembutal inhibits the uptake of radioactive phosphorus in both these fractions and should, therefore, not be used as a sedative during the irradiation.
4. The observation of Hevesy, that irradiation of one tumour can affect the nucleic acid metabolism of another tumour in the same animal, has been confirmed.