C-reactive protein is linked to lower cognitive performance in overweight and obese women.

Our objective was to ascertain the nature of the associations between C-reactive protein (CRP) and cognition, and to examine how they are affected by gender and obesity. We evaluated 62 females and 63 males between 42 and 82 years of age. There were 20 lean females with a body mass index (BMI) of <25 kg/m2 and 42 overweight or obese females, with BMIs > or =25 kg/m2. There were 14 lean males and 49 with BMIs >/=25 kg/m2. CRP was associated with lower scores on cognitive tests of frontal lobe function among females and these associations were driven by the overweight/obese female group. In these data no associations between CRP and cognition were found among males. Obesity-associated inflammation is much more prominent in females and it appears to be associated with cognitive dysfunction, particularly of frontal lobe tasks.

High-performance capillary electrophoresis for the determination of trypsin and chymotrypsin inhibitors and their association with trypsin, chymotrypsin and monoclonal antibodies.

High-performance capillary electrophoresis (HPCE) was adapted for the determination of Kunitz soybean trypsin inhibitor, Bowman Birk inhibitor from soybean and protein-type proteinase inhibitors from pea (Pisum sativum L.). The method was developed for the determination and characterization of the inhibitors, the enzymes trypsin and chymotrypsin and the monoclonal antibodies (mAbs) raised against the inhibitors, and also the inhibitor-enzyme and inhibitor-mAb association complexes. The results from studies involving the use of various types of buffers revealed the advantages of having zwitterions such as trimethylammoniumpropyl sulphonate (AccuPure) or taurine included in the buffer. The use of capillaries dynamically coated with zwitterions efficiently reduced the interactions of the proteins with the silica capillary surface, which was important for the analyses for trypsin, chymotrypsin and mAbs and their association complexes with the inhibitors. The influence of temperature, voltage, pH and buffer type on migration times, resolution, peak areas and number of theoretical plates was investigated for the proteins studied. The proposed HPCE method is very suitable for studies of proteinase inhibitors compared with traditional inhibitor studies, and it gives efficient protein separations with the possibility of 245,000 plates/m.

Cell membrane handling of sodium in lymphocytes during salt restriction in normotensives.

Lymphocyte sodium content and sodium efflux were studied in 9 healthy normotensive males without history of essential hypertension before, during and after 5 weeks of severe sodium depletion. Sodium depletion caused a significant increase in sodium content and a slight but non-significant decrease in potassium content. Total and ouabain-sensitive sodium efflux rate constants decreased significantly during sodium depletion, while absolute sodium efflux, derived from cellular sodium concentration and the corresponding sodium efflux rate constants, remained unchanged. A significant reduction in arterial mean and diastolic blood pressure, measured by ambulatory as well as by home readings, was observed during salt restriction. Prolonged severe sodium depletion of normotensive subjects leads to changes in lymphocytic sodium homeostasis, probably due to a primary inhibition of the sodium pump and a secondary intralymphocytic sodium accumulation. The mechanism underlying these changes remains unclarified.

Sodium homeostasis in lymphocytes and blood pressure alterations before and during salt restriction in normotensives and in essential hypertensives.

Blood pressure, lymphocytic sodium content and sodium efflux were studied in hypertensive and normotensive subjects during salt restriction. Diastolic blood pressure decreased significantly in both groups. In essential hypertension the initial high lymphocyte sodium content decreased during salt depletion with a simultaneous decrease in absolute sodium efflux probably due to primary changes in sodium influx. Conversely intralymphocytic sodium content increased in normotensive subjects, which may be caused by an inhibition of the sodium, potassium pump. Our findings indicate that autoregulatory mechanisms with regard to lymphocyte sodium metabolism differs between hypertensive and normotensive subjects.

Lymphocyte cell membrane handling of sodium and blood pressure control during salt restriction in normotensive subjects.

Intralymphocytic sodium and potassium concentrations, 22Na efflux rate constants (EFRC) and blood pressures (BPs) were studied in nine normotensive young males without a history of essential hypertension before, during and after 5 weeks of severe sodium depletion. Diastolic and median BPs decreased significantly as estimated by both ambulatory and home readings. A slight decrease in intralymphocytic potassium content and a significant increase in sodium content was found. Measurements of 22Na-EFRC were reduced by 15% in the ouabain-sensitive component of the sodium pump, while the absolute sodium efflux stayed constant during sodium depletion. These results are evidence of a primary inhibition of the sodium pump during salt restriction in normotensives.

Effects of imipramine of the orthostatic changes in blood pressure, heart rate and plasma catecholamines.

The effect of imipramine on the orthostatic changes in heart rate, blood pressure and plasma catecholamines were examined in six healthy male subjects on two occasions on high sodium balance (Na+ excretion greater than 120 mmol per day) and on low sodium balance (Na+ excretion less than 110 mmol per day), respectively. Orthostatic tests were carried out before and 2 h after ingestion of 150 mg imipramine hydrochloride. Imipramine caused a moderate increase in supine systolic blood pressure, and a pronounced increase in the rise in heart rate, when the subjects assumed erect position. The orthostatic drop in systolic blood pressure was in most cases only moderately increased after ingestion of imipramine, but in three subjects pronounced orthostatic hypotension developed when the sodium balance was low, whereas no clinical symptoms were seen in the same subjects when tested after imipramine ingestion on a high sodium balance. The plasma catecholamine levels in supine and standing position were not influenced by imipramine or by the changes in sodium balance. The data may suggest that inhibition of presynaptic reuptake of noradrenaline and/or alpha 2-adrenoceptor blockade causes the moderate rise in supine blood pressure, whereas alpha 1-adrenoceptor blockade, mainly affecting the venous part of the vascular bed, may explain the orthostatic reactions.