Effect of a low sodium DASH diet, including red meat on blood pressure in post-menopausal women

Background – The DASH type dietary pattern which consists of high fruit, vegetable and dairy products and low saturated fat, is “base-producing” but restricts red meat with no clear justification.
Objective – To compare the BP-lowering effect of Vitality diet (VD), a moderately low sodium, “base” producing modified DASH diet, containing 6 serves/week of lean red meat to a “ high carbohydrate, low fat diet (HCLF diet), with a higher dietary acid load in post-menopausal women.
Design – Ninety-five hypertensive post-menopausal women (46 VD and 49 HCLF) completed a 14-wk randomised parallel study. Home BP was measured daily. Repeat 24-h dietary records and 24-h urine samples were collected fortnightly. Dietary acid load, expressed as potential renal acid load (PRAL), was calculated from nutrient intakes.
Outcomes – During the intervention, the VD group had an average daily consumption of 85 g cooked red meat. They had a mean (± SEM) reduction of 38 ± 7 mmol/d in urinary sodium excretion (P <0.0001), and a 7 ± 4 mmol/d increase in urinary potassium (P = 0.0681), with an estimated 23.1± 2.3 mEq/d lower PRAL than the HCLF group (P <0.0001). The fall in systolic pressure in the VD group tended to be greater by 3 ± 2 mmHg (P = 0.08) than the fall in systolic pressure seen with the HCLF diet. A greater BP-lowering effect of VD was observed among those taking anti-hypertensive medication (n = 17) with a greater 5.5 ± 2.7 mm Hg (P = 0.0518) reduction of systolic BP and greater reduction in diastolic BP by 3.6 ± 1.7 mm Hg (P = 0.0388) compared to the HCLF diet. However, no relationship between BP and PRAL was observed.
Conclusions – A low sodium DASH type dietary pattern with the inclusion of lean red meat was effective in reducing BP in post-menopausal women, particularly in those taking anti-hypertensive medication. This dietary pattern could be recommended for this group who are at increased risk of cardiovascular disease.
This study was funded by Meat & Livestock Australia.

Blood-stage Plasmodium infection induces CD8+ T lymphocytes to parasite-expressed antigens, largely regulated by CD8α+ dendritic cells

Although CD8+ T cells do not contribute to protection against the blood stage of Plasmodium infection, there is mounting evidence that they are principal mediators of murine experimental cerebral malaria (ECM). At present, there is no direct evidence that the CD8+ T cells mediating ECM are parasite-specific or, for that matter, whether parasite-specific CD8+ T cells are generated in response to blood-stage infection. To resolve this and to define the cellular requirements for such priming, we generated transgenic P. berghei parasites expressing model T cell epitopes. This approach was necessary as MHC class I-restricted antigens to blood-stage infection have not been defined. Here, we show that blood-stage infection leads to parasite-specific CD8+ and CD4+ T cell responses. Furthermore, we show that P. berghei-expressed antigens are cross-presented by the CD8α+ subset of dendritic cells (DC), and that this induces pathogen-specific cytotoxic T lymphocytes (CTL) capable of lysing cells presenting antigens expressed by blood-stage parasites. Finally, using three different experimental approaches, we provide evidence that CTL specific for parasite-expressed antigens contribute to ECM.

Truncation of Plasmodium berghei merozoite surface protein 8 does not affect in vivo blood-stage development

Merozoite surface protein 8 (MSP8) has shown promise as a vaccine candidate in the Plasmodium yoelii rodent malaria model and has a proposed role in merozoite invasion of erythrocytes. However, the temporal expression and localisation of MSP8 are unusual for a merozoite antigen. Moreover, in Plasmodium falciparum the MSP8 gene could be disrupted with no apparent effect on in vitro growth. To address the in vivo function of full-length MSP8, we truncated MSP8 in the rodent parasite Plasmodium berghei. PbΔMSP8 disruptant parasites displayed a normal blood-stage growth rate but no increase in reticulocyte preference, a phenomenon observed in P. yoelii MSP8 vaccinated mice. Expression levels of erythrocyte surface antigens were similar in P. berghei wild-type and PbΔMSP8-infected erythrocytes, suggesting that a parasitophorous vacuole function for MSP8 does not involve global trafficking of such antigens. These data demonstrate that a full-length membrane-associated form of PbMSP8 is not essential for blood-stage growth.

Like blood or brown water

Gaylene Perry records the paradox of being a vegetarian in a family of butchers.

Local nitric oxide synthase inhibition reduces skeletal muscle glucose uptake but not capillary blood flow during in situ muscle contraction in rats

OBJECTIVE: We have previously shown in humans that local infusion of a nitric oxide synthase (NOS) inhibitor into the femoral artery attenuates the increase in leg glucose uptake during exercise without influencing total leg blood flow. However, rodent studies examining the effect of NOS inhibition on contraction-stimulated skeletal muscle glucose uptake have yielded contradictory results. This study examined the effect of local infusion of an NOS inhibitor on skeletal muscle glucose uptake (2-deoxyglucose) and capillary blood flow (contrast-enhanced ultrasound) during in situ contractions in rats.

RESEARCH DESIGN AND METHODS: Male hooded Wistar rats were anesthetized and one hindleg electrically stimulated to contract (2 Hz, 0.1 ms) for 30 min while the other leg rested. After 10 min, the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (arterial concentration of 5 µmol/l) or saline was infused into the epigastric artery of the contracting leg.

RESULTS: Local NOS inhibition had no effect on blood pressure, heart rate, or muscle contraction force. Contractions increased (P < 0.05) skeletal muscle NOS activity, and this was prevented by L-NAME infusion. NOS inhibition caused a modest significant (P < 0.05) attenuation of the increase in femoral blood flow during contractions, but importantly there was no effect on capillary recruitment. NOS inhibition attenuated (P < 0.05) the increase in contraction-stimulated skeletal muscle glucose uptake by ~35%, without affecting AMP-activated protein kinase (AMPK) activation.

CONCLUSIONS: NOS inhibition attenuated increases in skeletal muscle glucose uptake during contraction without influencing capillary recruitment, suggesting that NO is critical for part of the normal increase in skeletal muscle fiber glucose uptake during contraction.