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Background Neuroinflammation is a recognized hallmark of Alzheimer’s disease, along with accumulation of amyloid-β plaques, neurofibrillary tangles and synaptic loss. n-3 polyunsaturated fatty acids (PUFA) and molecules derived from them, including eicosapentaenoic acid-derived eicosanoids and docosahexaenoic acid-derived docosanoids, are known to have both anti-inflammatory and pro-resolving properties, while human observational data links consumption of these fatty acids to a decreased risk of Alzheimer’s disease. Few studies have examined the neuroinflammation-modulating effects of n-3 PUFA feeding in an Alzheimer’s disease-related model, and none have investigated whether these effects are mediated by changes in brain eicosanoids and docosanoids. Here, we use both a fat-1 transgenic mouse and a fish oil feeding model to study the impact of increasing tissue n-3 PUFA on neuroinflammation and the production of pro-inflammatory and pro-resolving lipid mediators. Methods Fat-1 mice, transgenic animals that can convert n-6 to n-3 PUFA, and their wildtype littermates were fed diets containing either fish oil (high n-3 PUFA) or safflower oil (negligible n-3 PUFA) from weaning to 12 weeks. Animals then underwent intracerebroventricular infusion of either amyloid-β 1-40 or a control peptide. Hippocampi were collected from non-surgery and surgery animals 10 days after infusion. Microarray was used to measure enrichment of inflammation-associated gene categories and expression of genes involved in the synthesis of lipid mediators. Results were validated by real-time PCR in a separate cohort of animals. Lipid mediators were measured via liquid chromatography tandem mass spectrometry. Results Fat-1 and wildtype mice fed fish oil had higher total hippocampal DHA than wildtype mice fed the safflower oil diet. The safflower-fed mice, but not the fat-1 or fish oil-fed mice, had significantly increased expression in gene ontology categories associated with inflammation in response to amyloid-β infusion. These effects were independent of changes in the expression of genes involved in the synthesis of eicosanoids or docosanoids in any group. Gene expression was replicated upon validation in the wildtype safflower and fish oil-fed, but not the fat-1 mice. Protectin, maresin and D and E series resolvins were not detected in any sample. There were no major differences in levels of other eicosanoids or docosanoids between any of the groups in response to amyloid-β infusion. Conclusions Fish oil feeding decreases neuroinflammatory gene expression in response to amyloid-β. Neither amyloid-β infusion or increasing brain DHA affects the brain concentrations of specialized pro-resolving mediators in this model, or the concentrations of most other eicosanoids and docosanoids.

Increases in astrocytes and one of their markers, glial fibrillary acidic protein (GFAP) have been reported in the brains of patients with Alzheimer's disease (AD). N-3 polyunsaturated fatty acids (PUFA) modulate neuroinflammation in animal models; however, their effect on astrocytes is unclear.Fat-1 mice and their wildtype littermates were fed either a fish oil diet or a safflower oil diet deprived of n-3 PUFA. At 12 weeks, mice underwent intracerebroventricular infusion of amyloid-β 1-40. Astrocyte phenotype in the hippocampus was assessed at baseline and 10 days post-surgery using immunohistochemistry with various microscopy and image analysis techniques.GFAP increased in all groups in response to amyloid-β, with a greater increase in fish oil-fed mice than either fat-1 or wildtype safflower oil-fed mice. Astrocytes in this group were also more hypertrophic, suggesting increased activation. Both fat-1- and fish oil-fed mice had greater increases in branch number and length in response to amyloid-β infusion than wildtype safflower animals.Fish oil feeding, and to a lesser extent the fat-1 transgene, enhances the astrocyte activation phenotype in response to amyloid-β 1-40. Astrocytes in mice fed fish oil were more activated in response to amyloid-β than in fat-1 mice despite similar levels of hippocampal n-3 PUFA, which suggests that other fatty acids or dietary factors contribute to this effect.

SummaryOver the last 5 years approximately 2000 women suffering from premenstrual syndrome have been studied and treated as part of an on-going research programme into the syndrome and its management. From a preliminary analysis of the results of treatment in the first 500 cases, it is estimated that dydrogesterone (10 mg twice daily from Day 12 to Day 26 of the cycle) produced an overall response rate of 70 %, assessed as those cured or greatly relieved of their symptoms. Overall response (55 %) with pyridoxine (40 mg twice daily) was not as satisfactory but some patients in whom the progestagen had been ineflective benefitted greatly. Spironolactone, bromocriptine and MAOIs were used in selected patients. It is recommended that dydrogesterone is best employed first when symptoms of fluid retention and depression predominate, and pyridoxine is best tried first when breast discomfort is the major problem. At least 3-months' treatment is necessary for a reasonable assessment to be made.

The perinatal mortality rates of mothers who delivered at St. Thomas's Hospital from 1969 to 1976 have been examined. The rate in the West Indian population was significant higher than in the United Kingdom white population. The increased West Indian mortality was confined to infants with a birth weight of more than 2.0 kg and a gestational age of more than 37 weeks. The relative risk of perinatal death for West Indian mothers compared with UK white mothers was 1.4 at birth weights of 2.5 kg to 2.9 kg, rising to 4.3 at 4.0 + kg. West Indian perinatal mortality in term babies of normal birth weight was higher in all maternal age and parity groups except parity 3, but the difference was greatest in women aged 30 or over. The African perinatal mortality rate was not significantly greater than the UK white rate although it followed the West Indian trends. Pre-eclampsia and forceps delivery were associated with a greatly increased perinatal mortality in West Indian babies. The excess West Indian mortality could not be explained completely by differences in the proportions of stillbirths and early neonatal deaths nor by the distribution of births by parity, maternal age, or social class. Possible explanations for the differences in mortality are discussed.

(1855). XLII. On certain curious motions observable at the surfaces of wine and other alcoholic liquors. The London, Edinburgh, and Dublin Philosophical Magazine and Journal of Science: Vol. 10, No. 67, pp. 330-333.

(1889). The Mechanical Coaling of Steamers. Royal United Services Institution. Journal: Vol. 33, No. 150, pp. 977-990.

A very large number of fetal abnormalities may now be detected by antenatal ultrasound, many cases being discovered incidentally during examinations to check fetal growth and maturity. Fetal hydrocele has been previously reported, detected at 39 weeks (Conrad & Sheshagiri, 1978) and at term (Miller & Thomas, 1979). In none of these cases was there any associated testicular abnormality. We wish to report a case of in utero torsion of the testis which presented with the typical ultrasound appearances of fetal hydrocele. The ultrasound appearances of the testis after birth are described. The mother was a 23-year-old primigravida who had previously been in good health, but had a family history of diabetes. Early pregnancy was uneventful. An ultrasound examination performed on 2.12.81 confirmed the gestational age. Gestational diabetes was diagnosed at 29 weeks, following an episode of glycosuria. Insulin therapy was then commenced which produced good control of maternal blood glucose. Serial scans at fortnigh...

The duration of lochia and its association with a number of obstetric variables was studied in 236 women. Each woman completed a diary sheet describing the colour and duration of her lochia for up to 60 days post partum. The phases of lochia were divided according to the classical description; lochia rubra, serosa and alba. The median total duration of lochia was 33 days, lochia rubra 4 days and lochia serosa 22 days. Lochia persisted to 60 days in 13% of women. The duration of lochia was shorter in parous women and women with smaller babies.