Behavioral change and public attitudes toward public health

One hundred patients suffering from recurrent acute tonsillitis were studied. One hundred tonsils were cultured. Surface bacteria were compared to deep bacteria. In 48 per cent of the cases a different pathogen was cultured from the interior of the tonsil as compared to the surface culture. This fact may explain recurrence of tonsillitis and makes the reliability of the conventional tonsillar culture questionable. Surgical extirpation of the tonsils seems to be the only treatment since deep bacteria remain unidentified and resist the antibiotic therapy that may affect only the surface microflora.     

Reduction of central nervous system reperfusion injury in rabbits using doxycycline treatment

BACKGROUND AND PURPOSE: Activated leukocytes appear to potentiate central nervous system reperfusion injury, and agents that block leukocyte adhesion have shown neuroprotective efficacy in experimental models. Doxycycline, a tetracycline antibiotic, inhibits leukocyte function in vitro, presumably through divalent cation binding. We used a model of focal central nervous system reperfusion injury to determine the efficacy of doxycycline treatment in preserving neurological function. METHODS: Rabbits randomly received 10 mg/kg i.v. doxycycline 30 minutes before ischemia (pretreatment group) or 45 minutes after ischemia (posttreatment group) or received phosphate-buffered saline vehicle (control group) followed by 10 mg/kg q 8 hours times two. The average length of reversible spinal cord ischemia required to produce paraplegia (P50) at 18 hours was calculated for each group. RESULTS: For the control group (n = 13), the P50 was 22.8 +/- 2.2 minutes; for the pretreatment group (n = 14), 35.5 +/- 2.4 minutes (P < .01; t = 3.8); and for the posttreatment group (n = 13), 31.4 +/- 4.2 minutes (not significant; t = 1.6). Doxycycline also attenuated postischemic decreases in vivo leukocyte counts and inhibited in vitro leukocyte adhesion. Therapeutic doxycycline levels at 24 hours were confirmed in the plasma and spinal cord. CONCLUSIONS: This significant protective effect suggests that doxycycline, a safe and readily available agent, may play a role in reducing clinical central nervous system reperfusion injury.     

Ureteropelvic junction injuries secondary to blunt abdominal trauma

PURPOSE: To describe the clinical and imaging findings of ureteropelvic junction (UPJ) injuries caused by blunt trauma. MATERIALS AND METHODS: In two children (aged 10 and 16 years) and eight adults (aged 23-82 years) with UPJ injuries, findings at computed tomography (CT) (n = 10), excretory urography (n = 6), and retrograde pyelography (n = 8) were retrospectively reviewed to identify the location and extent of contrast material extravasation. Clinical and follow-up data were correlated with radiologic findings. RESULTS: CT and urography played complementary roles in diagnosis. UPJ avulsion, defined as complete transection of the ureter with no filling of the ipsilateral ureter below the level of the UPJ, was diagnosed in four patients. UPJ laceration, defined as contrast material extravasation from the UPJ with contrast material in the ipsilateral ureter distal to the point of injury, was diagnosed in six patients. Medial perirenal contrast extravasation was seen in all 10 patients but failed to help differentiate UPJ avulsion from laceration. A distinctive pattern of contrast material extravasation at CT termed "circumrenal urinoma" was present in five patients and was found to be specific for UPJ injury. CONCLUSION: Medial perinephric contrast material extravasation was highly suggestive of UPJ injury. Demonstration of ureteral filling differentiated UPJ laceration from avulsion.     

Aldosterone in obesity

Plasma aldosterone levels were measured in adults whose body mass index ranged from lean to obese. Blood was drawn while subjects rested supine for 30-90 minutes. Aldosterone was higher in obese subjects, but could not be explained by renin or K+. The best predictors of plasma aldosterone were abdominal obesity measured as waist/hip ratio or by CT scan, and insulin resistance measured by insulin or oral glucose tolerance tests, or euglycemic clamp. In one cohort, these correlations were limited to women; in the other, they were also found in men. In the women with a strong correlation between aldosterone and visceral fat, aldosterone also correlated with cortisol and DHEA-S. The data are consistent with an effect of visceral fat on adrenal steroidogenesis. Visceral adipocytes have a high rate of triglyceride turnover, and their circulation drains directly to the liver. In an experiment based on these characteristics, rat hepatocytes responded to fatty acids by releasing an unidentified secretagogue that stimulated aldosterone production by rat adrenal glomerulosa cells. The clinical data suggest that aldosterone participates in hypertension associated with the "Insulin Resistance Syndrome". The adrenal in viscerally obese subjects may be driven by a secretagogue released from the liver by fatty acids from abdominal adipocytes.     

The effects of morphine, nicotine and epibatidine on lymphocyte activity and hypothalamic-pituitary-adrenal axis responses

Acute administration of morphine alters various neuroendocrine and immune parameters via opioid receptors located within the central nervous system. Similar effects have been reported after systemic nicotine treatment. To examine the possible relationship between opioid and nicotinic receptor activation on the immune system, we compared the effects of morphine with both nicotine and the highly selective nicotinic agonist, epibatidine. Male Sprague-Dawley rats were treated with either morphine (10 mg/kg, s.c.), nicotine (2.85 mg/kg, s.c. = 1 mg/kg freebase), or epibatidine (5 microg/kg, s.c.) and sacrificed 2 hours later. Each drug increased plasma corticosterone levels and decreased the magnitude of the peripheral blood lymphocyte proliferation response to the T cell mitogen concanavalin A. None of the treatments had a significant effect on splenic or thymic lymphocyte responses. The effects of nicotine treatment were dose-dependent. Pretreatment with the quaternary ganglionic antagonist chlorisondamine (0.5 mg/kg, i.p.), completely blocked the effect of epibatidine on blood lymphocytes without altering the elevation of corticosterone levels. Although naltrexone (10 mg/kg, s.c.) blocked all effects of morphine, the effects of epibatidine were not blocked by the opioid receptor antagonist. Furthermore, in contrast to morphine (), central injection of neither nicotine (30 or 240 nmol) nor epibatidine (5, 50, or 500 ng) altered blood lymphocyte responses. These results suggest that, like morphine, nicotinic agonists decrease blood lymphocyte proliferation responses, apparently independent of elevated corticosterone. However, unlike morphine, nicotinic agonists appear to act predominantly at peripheral receptors, suggesting that nicotinic receptors are downstream of opioid receptors in a centrally mediated opioid-induced immunomodulatory pathway.     

Solid-phase assay for luteinizing hormone in mouse plasma

A solid-phase tube assay for measuring LH levels in mouse plasma is described. The assay utilizes an antiserum to ovine LH and ovine LH standards and it measures LH levels in 20 mul of plasma with a sensitivity of less than 0.6 ng/ml. Various parameters affecting the sensitivity and specificity of the assay were investigated. Serial dilutions of plasma from pregnant mice, a pituitary homogenate from mice and plasma from hypophysectomized mice, injected subcutaneously with ovine LH, ran parallel with ovine LH standards in plasma from hypophysectomized mice and plasma with low LH levels from intact mice. Ovine TSH showed about 12% cross reaction in the assay system, whilst rat FSH and prolactin and also ovine FSH, prolactin and GH showed practically no cross reaction. Measurements of plasma LH levels have been made in hypophysectomzied mice after injection with different vehicles containing 10 or 50 mug LH or 50 mug FSH per animal. Daily measurements of LH levels throughout pregnancy in the mouse show a rise in LH level prior to implantationand a further rise around mid-pregnancy which drops off sharply to levels which remain fairly constant until parturition when there is another rise.     

On the susceptibility of human platelets to aggregation by concanavalin A and the effect of this lectin on their response to ADP

Concanavalin A aggregated gel-filtered platelets in 0.9% NaCl solution signifying cross-bridging by the lectin. Aggregation of these platelets by concanavalin A was temperature dependent; it did not occur at 0-4 degrees C unless the platelets were previously trypsinized. The level of aggregation of trypsinized platelets by concanavalin A at 0-4 degrees C was similar to that of untreated platelets at 37 degrees C. It is suggested that trypsin facilitates platelet aggregation by concanavalin A at 0-4 degrees C by causing a configurational change in membrane glycoproteins which orientates concanavalin A receptor sites into positions that favour lectin cross-bridging. Concanavalin A failed to aggregate platelets in plasma. Radioisotope studies showed that the amount of [3H]concanavalin A which combined with platelets in plasma was extremely low compared with gel-filtered platelets in saline. The aggregation of Ehrlich ascites cells by concanavalin A was considerably reduced when platelet-free plasma was added to the medium suggesting that it was due to the presence of concanavalin A-reactive components in the plasma. Concanavalin A inhibited the ADP-induced aggregation of platelets suspended in plasma or in a salts solution supplemented with calcium and fibrinogen, although the inhibitory effect was more conspicuous in the latter case. The results suggests that concanavalin A produces its inhibitory effect on ADP-induced platelet aggregation by interacting with membrane glycoproteins, and this further suggests their involvement in aggregation.