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1.
BJOG ; 127(6): 757-767, 2020 05.
Article in English | MEDLINE | ID: mdl-32003141

ABSTRACT

OBJECTIVES: To assess the cost-effectiveness of progesterone compared with placebo in preventing pregnancy loss in women with early pregnancy vaginal bleeding. DESIGN: Economic evaluation alongside a large multi-centre randomised placebo-controlled trial. SETTING: Forty-eight UK NHS early pregnancy units. POPULATION: Four thousand one hundred and fifty-three women aged 16-39 years with bleeding in early pregnancy and ultrasound evidence of an intrauterine sac. METHODS: An incremental cost-effectiveness analysis was performed from National Health Service (NHS) and NHS and Personal Social Services perspectives. Subgroup analyses were carried out on women with one or more and three or more previous miscarriages. MAIN OUTCOME MEASURES: Cost per additional live birth at ≥34 weeks of gestation. RESULTS: Progesterone intervention led to an effect difference of 0.022 (95% CI -0.004 to 0.050) in the trial. The mean cost per woman in the progesterone group was £76 (95% CI -£559 to £711) more than the mean cost in the placebo group. The incremental cost-effectiveness ratio for progesterone compared with placebo was £3305 per additional live birth. For women with at least one previous miscarriage, progesterone was more effective than placebo with an effect difference of 0.055 (95% CI 0.014-0.096) and this was associated with a cost saving of £322 (95% CI -£1318 to £673). CONCLUSIONS: The results suggest that progesterone is associated with a small positive impact and a small additional cost. Both subgroup analyses were more favourable, especially for women who had one or more previous miscarriages. Given available evidence, progesterone is likely to be a cost-effective intervention, particularly for women with previous miscarriage(s). TWEETABLE ABSTRACT: Progesterone treatment is likely to be cost-effective in women with early pregnancy bleeding and a history of miscarriage.


Subject(s)
Abortion, Spontaneous/economics , Abortion, Spontaneous/prevention & control , Progesterone/economics , Progestins/economics , Uterine Hemorrhage/drug therapy , Abortion, Spontaneous/etiology , Adolescent , Adult , Cost-Benefit Analysis , Double-Blind Method , Female , Humans , Live Birth/economics , Pregnancy , Progesterone/therapeutic use , Progestins/therapeutic use , Randomized Controlled Trials as Topic , State Medicine , Treatment Outcome , United Kingdom , Uterine Hemorrhage/complications , Uterine Hemorrhage/economics , Young Adult
2.
Behav Brain Res ; 245: 29-33, 2013 May 15.
Article in English | MEDLINE | ID: mdl-23396147

ABSTRACT

Altered BDNF-mediated synaptogenesis is a major contributor to stress-vulnerability and depression. This study sought to determine patterns of hippocampal BDNF expression in stress-vulnerable and -resilient strains in the chick anxiety-depression model. Socially raised Black Australorp and Production Red strains were tested at 5-6 days post hatch under either 30, 60, 90, or 120 min of social separation stress; chicks tested with 2 social companions for 120 min served as controls. Distress vocalizations were recorded throughout the test session and latency to behavioral despair calculated. Following tests, bilateral hippocampal sections were harvested and analyzed via ELISA for BDNF levels. Black Australorps had shorter latencies to behavioral despair than Production Reds reflecting greater stress vulnerability. No differences were detected in BDNF levels between a No-Test and Social group within or between strains. The stress resilient Production Reds showed stable BDNF levels across the isolation test period whereas the vulnerable Black Australorps showed an increase in hippocampal BDNF levels that peaked at 90 min and declined thereafter. These findings fit well with the notion that strain-dependent stress-vulnerability reflects, in part, poor homeostatic mechanisms controlling synaptogenesis.


Subject(s)
Anxiety/genetics , Anxiety/psychology , Brain-Derived Neurotrophic Factor/metabolism , Chickens/physiology , Depression/genetics , Depression/psychology , Resilience, Psychological , Animals , Data Interpretation, Statistical , Enzyme-Linked Immunosorbent Assay , Hippocampus/metabolism , Male , Social Isolation , Species Specificity , Stress, Psychological/metabolism , Vocalization, Animal
3.
Nepal Med Coll J ; 15(1): 71-3, 2013 Mar.
Article in English | MEDLINE | ID: mdl-24592800

ABSTRACT

Bloodstream infections in neonates are life-threatening emergencies. Identification of the common bacteria causing such infections and their susceptibility patterns will provide necessary information for timely intervention. This study was done to determine the prevalence of neonatal septicaemia, identify the bacterial isolates and study their antimicrobial susceptibility pattern in neonates admitted to the neonatal intensive care unit of Nepal Medical College Teaching Hospital (NMCTH), Kathmandu, Nepal. This descriptive-analytical study was conducted in NMCTH from July 2011 to January 2012. Blood culture of all neonates who were suspected for neonatal sepsis was performed. Bacterial isolation, identification and antimicrobial susceptibility testing were done by standard microbiological method. Out of 120 neonates suspected of having neonatal sepsis, 30.8% (37/120) were blood culture positive (i.e. prevalence = 30.8%). The most common causative agents of neonatal sepsis was Staphylococcus aureus (56.8%; 21/37) followed by Klebsiella pneumoniae (21.7%; 8/37), Pseudomonas aeruginosa (13.4%; 5/37) and others. Neonatal sepsis was more frequent in male neonates (32.5%) while (26.5%) in female neonates in the ratio of 1.2:1 (p > 0.05). Neonatal sepsis was significantly higher (58.3%) in low birth weight (LBW) (< 2.5kg) neonates compared with good birth weight (GBW) (23.9%) (< 0.05). Prevalence was higher in preterm neonates (57.8%; 11/19) as compared with term-babies (25.7%) (P = 0.05). Generally, all of the isolates were sensitive to most of the antibiotics used as the first line drugs like amikacin, gentamicin, cefotaxime and ampicillin except Acinetobacter baumannii. This organisms was only sensitive towards cotrimoxazole, azithromicin, cefotaxime and ceftazidime.


Subject(s)
Anti-Bacterial Agents/therapeutic use , Infant, Newborn, Diseases/drug therapy , Infant, Newborn, Diseases/microbiology , Sepsis/drug therapy , Sepsis/microbiology , Female , Humans , Infant, Newborn , Infant, Newborn, Diseases/epidemiology , Male , Microbial Sensitivity Tests , Nepal/epidemiology , Prevalence , Prospective Studies , Risk Factors , Sepsis/epidemiology
4.
Article in French | AIM (Africa) | ID: biblio-1264269

ABSTRACT

Calotropis procera (Ait.) Ait.f. (Asclepiadacea) est une plante medicinale traditionnelle bien connue dans le monde en general et; particulierement utilisee en Afrique occidentale dans le traitement de nombreuses affections. Dans le cadre des connaissances sur le niveau de toxicite de la plante; nous avons entrepris la presente etude qui a permis d'effectuer un tri phytochimique de son latex et de determiner son niveau de toxicite standard chez le rat OFA (Oncin France Souche A). Quatre vingt (80) rats ont fait l'objet de tests de toxicite realises a partir de l'administration d'une dose unique; de 0;9 ml de solution preparee sur la base de concentrations de plus en plus croissantes de latex. Les resultats des tests phytochimiques ont montre que le latex de C. procera contenait des sterols; des poly phenols; des flavonoides et surtout des alcaloides. La DL50 determinee par la relation de BERHENS et KARBER etait de 2611;75 mg/kg de poids avec une DL5 de 2110 mg/kg et une DL95 de 2950 mg/kg. Le latex de C. procera serait donc tolere par le rat dans l'experimentation. Le rapport DL5/DL95 de 0;71 traduisait l'existence d'une marge entre l'indice therapeutique et l'indice toxicologique du latex de C. procera. Cette plante n'est probablement pas toxique

6.
J Neurol Sci ; 75(1): 23-32, 1986 Aug.
Article in English | MEDLINE | ID: mdl-3746339

ABSTRACT

Three groups of dystrophic and non-dystrophic mice 129/Re were used for studying the effect of the myotoxic agent iodoacetate on dystrophic muscle. The mice of the first group were given intramuscular injections of iodoacetate. The mice of the second group were injected with normal saline and the third group was maintained as untreated controls. The most severe histopathological changes were found in the dystrophic mice treated with iodoacetate. The non-dystrophic mice of the same group showed a significant increase in the number of internal nuclei. Moderate changes were observed in saline-treated dystrophic controls. There was no significant decrease in the life expectancy in any of the groups. The body weight of dystrophic mice was reduced throughout the experiment. On the contrary the non-dystrophic group showed an increased in weight, regardless of the treatment. The aggravation of the histopathological changes of dystrophic mice by iodoacetate would probably give support to the cyclical necrosis/abnormal regeneration theory of pathogenesis of muscular dystrophy.


Subject(s)
Iodoacetates/toxicity , Muscles/drug effects , Muscular Dystrophy, Animal/chemically induced , Animals , Cell Nucleus/drug effects , Cell Nucleus/ultrastructure , Iodoacetic Acid , Mice , Mice, Inbred Strains , Muscles/pathology , Muscular Dystrophy, Animal/pathology , Necrosis , Regeneration/drug effects
7.
J Neurol Neurosurg Psychiatry ; 47(2): 213-5, 1984 Feb.
Article in English | MEDLINE | ID: mdl-6423776

ABSTRACT

The clinical and laboratory findings of a patient with juvenile acid maltase deficiency are presented. The patient died from respiratory muscle weakness at age 31 years. Muscle biopsy shortly prior to his death showed remarkable vacuolation affecting exclusively type I fibres and mild myopathic changes of both types of muscle fibres, while the muscle biopsy at age 26 years had shown no evidence of acid maltase deficiency.


Subject(s)
Glucan 1,4-alpha-Glucosidase/deficiency , Glucosidases/deficiency , Muscle Hypotonia/enzymology , Muscular Atrophy/enzymology , Adult , Biopsy , Electromyography , Humans , Male , Muscle Hypotonia/pathology , Muscles/enzymology , Muscles/pathology , Muscular Atrophy/pathology , Respiratory Insufficiency/enzymology
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