Increased forearm blood flow during glucose clamp is related neither to insulin sensitivity nor to hyperinsulinemia in borderline hypertensive young men

It is controversial whether raised insulin within the physiological concentration range increases forearm blood flow (FBF). The aim of the present study was therefore to examine the effect of the isoglycemic hyperinsulinemic glucose clamp procedure on FBF and to relate the increase to the glucose disposal rate (GDR), i.e. insulin sensitivity. Borderline hypertensive young men were examined with the clamp technique or received saline infusion, and FBF was measured using plethysmography. It is of particular interest to study this group of subjects because their GDR correlates to a number of metabolic and hemodynamic variables, and these subjects hyperreact to stressful stimuli. There was no correlation between deltaFBF during clamp and GDR (r = -0.002, p = 0.99, n = 28). While serum insulin increased from 107 +/- 5 to 628 +/- 31 pmol/l in the hyperinsulinemic group and remained unchanged (135 +/- 11 vs 116 +/- 11 pmol/l) in the saline group, FBF increased from 3.5 +/- 0.3 to a maximum of 5.1 +/- 0.4 ml/min/100 ml (p < 0.001, n = 28) and from 2.8 +/- 0.5 to a maximum of 4.5 +/- 0.5 ml/min/100 ml (p = 0.01, n = 8), respectively. The increase in FBF (delta%) was similar in the two groups (p = 0.9). Thus, we could not demonstrate any relationship between insulin sensitivity and increments in FBF during hyperinsulinemic glucose clamp in borderline hypertensive young men. The moderate increases in FBF during insulin infusion with serum concentrations within the physiological range seem to be time-dependent and not caused by hyperinsulinemia.     

Cardiopulmonary bypass copolymer surface modification reduces neither blood loss nor transfusions in coronary artery surgery

OBJECTIVE: Surface-modifying additives (SMA) have been suggested for improving cardiopulmonary bypass (CPB) circuit biocompatibility, potentially minimizing inflammatory complications and bleeding associated with CPB. The purpose of this prospective, randomized clinical study was to compare a novel copolymer surface-modified CPB circuit (SMARXT; COBE Cardiovascular) against the unmodified circuit. METHODS: We randomized 122 patients with isolated coronary artery disease subjected to first-time surgery on CPB into either the SMA (n = 62) or the control group (n = 60). Exclusion criteria included renal insufficiency, liver disease, coagulopathy, anticoagulation therapy < 6 days preop, carotid artery stenosis > 70 %, and a history of stroke. We collected perioperative clinical data including drainage blood loss, transfusion requirements, duration of mechanical ventilation, and ICU stay. Platelet function was determined pre- and post-CPB. RESULTS: SMA patients received 3.2 +/- 0.9 (SD) grafts during 48 +/- 16 min of aortic cross clamp and 91 +/- 30 min CPB (Control: 3.0 +/- 0.9 grafts; p = 0.33, 46 +/- 14 min AXC; p = 0.36, and 84 +/- 23 min CPB; p = 0.14). In the SMA group, 23 patients (37 %) received red blood-cell transfusions, 9 patients (15 %) fresh frozen plasma, and 3 patients (5 %) received platelets (control: n = 27 [46 %], p = 0.44; n = 10 [17 %], p = 0.91; and n=4 [7 %], p = 0.71, respectively). Platelet count on CPB fell to the same level in both groups. In SMA patients, platelet function decreased from 94.2 +/- 24.9 % pre-CPB to 79.5 +/- 32.8 % post-CPB (p = 0.043) (control: from 87.7 +/- 25.6 % to 69.4 +/- 34.7 %; p = 0.001). Postoperative drainage blood loss, mechanical ventilation duration, and ICU stay were similar in both groups (p > 0.3). One patient of the control group was excluded due to surgical bleeding, and one SMA patient died. CONCLUSIONS: Our results show that the surface-modified CPB circuit decreased neither blood loss nor transfusions despite slightly better platelet function preservation compared to the unmodified circuit. This type of CPB circuit surface modification does not appear to improve clinical outcome in low-risk coronary artery surgery patients.     

IL-6 deficiency in mice neither impairs induction of metabolic genes in the liver nor affects blood glucose levels during fasting and moderately intense exercise

Aims/hypothesis  

Fasting and exercise are strong physiological stimuli for hepatic glucose production. IL-6 has been implicated in the regulation of gluconeogenic genes, but the results are contradictory and the relevance of IL-6 for fasting- and exercise-induced hepatic glucose production is not clear.     

The appropriate goals of antihypertensive therapy: neither too much nor too little.

Although the treatment of hypertension has increased markedly during the last decade, many patients have been left undertreated, including many of the disadvantaged, the elderly, and those at relatively high overall risk for cardiovascular disease. A rapidly growing number of patients, however, are being exposed to overtreatment with resultant interference with their quality of life and potential hazards to their health. These include patients who are diagnosed and treated without adequate documentation of the presence of persistent hypertension, patients who are not appropriately managed with nondrug therapies, and patients who are given inappropriate and overly aggressive drug therapies. Better recognition of the frequency and potential hazards of overtreatment is needed so that more appropriate goals of antihypertensive therapy can be established and maintained.     

Low glucose relates to greater aggression in married couples

Intimate partner violence affects millions of people globally. One possible contributing factor is poor self-control. Self-control requires energy, part of which is provided by glucose. For 21 days, glucose levels were measured in 107 married couples. To measure aggressive impulses, each evening participants stuck between 0 and 51 pins into a voodoo doll that represented their spouse, depending how angry they were with their spouse. To measure aggression, participants competed against their spouse on a 25-trial task in which the winner blasted the loser with loud noise through headphones. As expected, the lower the level of glucose in the blood, the greater number of pins participants stuck into the voodoo doll, and the higher intensity and longer duration of noise participants set for their spouse.

Quarrel not at all. No man resolved to make the most of himself can spare time for personal contention. Still less can he afford to take all the consequences, including the vitiating of his temper and loss of self control.Abraham Lincoln

As former US President Abraham Lincoln notes, quarrels and contentions not only waste time, they can also produce harmful consequences, such as damaging relationships. It is somewhat ironic that such quarrels and contentions often occur between people who are closest to each other: intimate partners. Sometimes these “lovers’ quarrels” can escalate beyond hurtful words to physical acts of aggression and violence. Intimate partner violence refers to physical, sexual, or psychological harm caused by a partner or spouse (1). Intimate partner violence affects millions of people around the world (2). As Lincoln suggests, loss of self-control may help explain why people quarrel and contend with others, even their intimate partners.     

Mould exposure at home relates to inflammatory markers in blood.

Living in damp buildings has been associated with airway symptoms, suspected to be due to inflammatory reactions. The relationship between home exposure to mould and signs of inflammation was, therefore, studied. Nonsmoking subjects with a high (G-high, > 4.0 ng x m(-3), n = 17) or low (G-low, < 2.0 ng x m(-3), n = 18) amount of airborne beta(1 --> 3)-D-glucan, an indicator of mould biomass, in the home were recruited. Blood samples were analysed for granulocytic enzymes, T-cell subsets and the secretion of cytokines from in vitro incubated peripheral blood mononuclear cells (PBMCs). In the G-high group, the proportion of cytotoxic T-cells (CD8+S6F1+) was lower and secretion of tumour necrosis factor-alpha from PBMCs higher than in the G-low group. There were no significant differences in secretion of interferon gamma and interleukin (IL)-4 from PBMCs between the two groups. Among nonatopic subjects, the ratio between interferon gamma and IL-4 was significantly higher in the G-high group than in the G-low group and was related to the amount of beta(1 --> 3)-D-glucan in the home. No significant differences were found regarding secretion of IL-10 or IL-Ibeta from PBMCs, eosinophil cationic protein or myeloperoxidase in serum, or differential cell counts in blood. The effects found on inflammatory markers in relation to beta(1 --> 3)-D-glucan in the home suggest upregulation of some parts of the inflammatory/immunological system due to mould exposure.     

Angiotensin-converting enzyme gene DD genotype neither increases susceptibility to acute pancreatitis nor influences disease severity

Background

The renin-angiotensin system (RAS) has been implied in the pathogenesis of various diseases including acute and chronic pancreatitis. Angiotensin-converting enzyme (ACE) is the key enzyme in activating the RAS. Deletion (D)-type polymorphism in the 16th intron of the ACE gene has been associated with higher serum levels of the enzyme. Inhibition of ACE was found to ameliorate acute pancreatitis in animal models suggesting that ACE plays a role in pathogenesis and progression of acute pancreatitis. Objectives were to investigate the occurrence of the ACE insertion/deletion (I/D) polymorphism in acute pancreatitis patients and its association with the severity of the disease.

Material and Methods

Seventy-nine acute pancreatitis patients and 95 healthy controls were evaluated. Acute pancreatitis cases were grouped as mild or severe according to the Atlanta criteria. Main outcome measure: The presence of the ACE I/D polymorphism.

Results

ACE gene I and D allele frequency of patients (44% and 56%) were similar to controls (45% and 55%, respectively). There were no significant differences in severity of pancreatitis between patients with the ACE-insertion or ACE-insertion/deletion versus ACE-deletion genotypes.

Conclusions

The ACE gene deletion polymorphism is neither a risk factor for development of acute pancreatitis nor contributes to the severity of disease or development of complications.     

Eosinophils are neither migrated nor activated in the skin lesions of atopic dermatitis in infants.

Eosinophils and eosinophil cationic protein (ECP) were examined in the skin lesions of 10 infants with atopic dermatitis (aged 4 months to 7 years). In all 10 patients, neutrophils and eosinophils were rarely seen in these lesions. Moreover, in the immunohistochemical study, ECP was scarcely detected in any of them. Our results suggest that eosinophils are neither migrated nor activated in the skin in atopic dermatitis in infants.     

In vitro adrenocorticotropin/beta-endorphin-releasing activity of vasopressin analogs is related neither to pressor nor to antidiuretic activity

Cells of the 7315c tumor released immunoreactive PRL (IR-PRL). Cholera toxin enhanced this release. Morphine and other opiate agonists inhibited IR-PRL release from both untreated and cholera toxin-treated tumor cells. The opiate-induced inhibition of IR-PRL release was concentration dependent and naloxone sensitive. Cholera toxin also enhanced the adenylate cyclase activity of 7315c tumor tissue. Opiates inhibited enzyme activity in both untreated and cholera toxin-treated 7315c tissue in a concentration-dependent and naloxone-sensitive manner. FK 33824 was more potent than [D-Ala2,D-Leu5]enkephalin in inhibiting IR-PRL release and adenylate cyclase activity. In cholera toxin-treated 7315c tumor tissue, GTP was required for opiate-induced inhibition of adenylate cyclase activity. Nonhydrolyzable analogs of GTP inhibited toxin-stimulated cyclase activity in the absence of an opiate. These results suggest that the 7315c tumor possesses a mu-opiate receptor; stimulation of this receptor inhibits both IR-PRL release and adenylate cyclase activity. An inhibitory guanyl nucleotide component may link the mu-opiate receptor to adenylate cyclase.     

Platelet count and platelet parameters in hemoglobin E carriers.

Hemoglobinopathies are an important inherited disorder with a high prevalence in Thailand. Of several hemoglobinopathies, hemoglobin E (Hb) disorder (beta 26, GAG-AAG, Glu-Lys) is the most common. Coagulation disorders in these patients have also been proposed. Even though thrombotic risks in the patients with hemoglobin disorders from standpoints of platelet dysfunction and coagulation factors are controversial, they are in favor of thrombosis due to thrombocytosis. A study was performed in 57 healthy subjects to evaluate platelet count and platelet parameters in hemoglobin E carriers compared to values in healthy subjects. Classified by standard hemoglobin electrophoresis, there were 46 healthy subjects and 11 hemoglobin E carriers. There are no significant differences in platelet count and platelet parameters between the two groups (p > 0.05). Although there are reports that indicate the change in the quality of platelet in hemoglobin E disorders, no quantitative disorder was detected. There was no trend toward increased platelet count in the HbE carriers.     

The complete blood count and leukocyte differential count. An approach to their rational application

The complete blood count and leukocyte differential count have no value in screening asymptomatic members of the general population. The complete blood count may be useful for screening infants in the first year of life, institutionalized elderly persons, pregnant women, and recent immigrants from Third World countries, if poor nutrition or inadequate iron intake is suspected. These tests are not useful for hospitalized patients, unless an abnormality is suspected or surgery with major blood loss is anticipated. It is appropriate to obtain the tests when a hematologic or infectious disorder is suspected, but they may not affect decision making if the diagnosis is clinically evident. The leukocyte differential count is unnecessary to confirm an infection in most cases in which leukocytosis is present. Repeat tests should be limited to situations where the clinical course is unclear, and at intervals long enough such that the results might affect clinical decision making.