During the period 1990–1998, 99 cases of human cystic hydatidosis (12.4 cases per year) were surgically treated at the two main hospitals in Arbil province, northern Iraq, and from this the human occurence for the province was estimated to be 2 per 100,000 inhabitants. In the same area, 1270 sheep, 550 goats and 320 cattle were examined at slaughter for hydatid cysts and prevalence rates were found to be 15.0%, 6.2% and 10.9%, respectively. A decreasing tendency in livestock prevalences was found towards the end of the study period. As in humans, most of the hydatid cysts in livestock were located in the liver. Fertility of sheep cysts, i.e. those containing protoscoleces, was found to be significantly higher (64%) than that of goats (35.7%) and cattle (29.8%). The percentage of fertile cysts containing viable protoscoleces varied between 63 and 82% in the livers and between 72 and 79% in the lungs of the different animal species. A total of 97 stray dogs were examined post-mortem in the years 1991, 1992 and 1998, and Echinococcus granulosus worms were found in the intestines of 48 dogs (49.5%). High worm burdens (> 1000) were observed in 37% of the dogs, medium worm burdens (200–1000) in 41%, and low worm burdens (< 200) in 22%. In 1998, the prevalence of canine echinococcosis (24.3%) was found to be significantly lower than in 1991 (70.4%) and 1992 (60.6%). The prevalence of human hydatidosis did not differ significantly over the years, but the study confirmed that hydatidosis is endemic in northern Iraq, and that housewives, labourers and farmers appear to be at the greatest risk of infection.

The immunoglobulin (IgG, IgM, IgA) content of normal, reactive and migrated rat astrocytes was studied in lesioned adult rat cortex and after fetal cortex grafts. Implantation pockets were aspirated in the somatomotor cortex (under bregma) of adult Sprague-Dawley rats. A fetal (E14) rat hemicortex incubated in the plant lectin Phaseolus vulgaris leucoagglutinin (graft premarker) was placed in the aspiration pocket or the pocket left empty (control). Sections of brain were immunohistochemically double labeled for immunoglobulins-GFAP or Phaseolus vulgaris leucoagglutinin-GFAP 3-60 days postoperative. Mature or fetal astrocytes in situ did not contain immunoglobulins. In pocket-only animals, individual reactive astrocytes lining and subjacent to the pocket were positive for rat IgG, IgM and IgA (3-60 days). In grafted animals, graft derived astrocytes (Phaseolus vulgaris leucoagglutinin-GFAP positive) were intermingled with host reactive astrocytes (Phaseolus vulgaris leucoagglutinin negative) lining and subjacent to the pocket. Both classes of astrocytes contained immunoglobulins IgG, IgM and IgA. Immunoglobulin positive graft derived astrocytes migrated into the corpus callosum, cingulum and habenula. These results demonstrate that astrocytes sequester immunoglobulins and probably other serum proteins as a critical function in restoring homeostasis to the injured or diseased nervous system.

Nerve growth factor (NGF) immunoreactivity in the nucleus gracilis of the medulla was quantitated for 90 days after aspiration of the C3 spinal hindlimb dorsal columns of 36 adult rats. Half the lesioned animals were a lesion-only group. The remaining lesioned animals received an immediate graft of two 1.0-mm pieces of 14 day gestation fetal rat cervical spinal cord (prelabeled with Phaseolus vulgaris leucoagglutinin) into the aspiration pocket (graft group). There were 3 normal controls. Groups of animals were analyzed at 7, 14, 21, 30, 60, and 90 days. At 90 days, NGF immunoreactivity was significantly elevated in the nucleus gracilis of lesion-only animals. This increase in NGF immunoreactivity was augmented in glial end-feet surrounding neurons and was also observed in the cytoplasm of astrocytes and some neurons. Previous experiments have shown that the cluster neurons of the nucleus gracilis undergo atrophy at this time with a concomitant decrease in hindlimb placement. NGF immunoreactivity (90 days) in grafted animals, however, was significantly less than in lesion-only animals (P < 0.05) but remained significantly elevated above control animals (P < 0.05). Unlike in lesion-only animals, there were no NGF positive neurons in the nucleus gracilis of grafted animals. Previous experiments have shown that astrocytes from fetal spinal cord grafts migrate to the nucleus gracilis, maintain cluster neuron cell size, and improve hindlimb placement at 90 days. The present data indicate that modulation of detrimental increases in NGF appeared to be a mechanism by which migrated fetal astrocytes can be used as a system for cell therapy.

Renal denervation decreases arterial pressure (AP) in hypertensive rats and humans. This procedure destroys both afferent and efferent nerves. Several investigators have proposed that renal afferent nerves contribute to the elevated AP. We developed a procedure to selectively remove renal afferent nerves with capsaicin (1-100 mM) both topically on the nerve and in the renal pelvis. We examined the effects of renal deafferentation on the development of genetic and renal hypertension. We studied spontaneously hypertensive rats (SHR), and a model of renal hypertension, two kidney-one clip (2K1C) in Sprague-Dawley rats. SHR were treated at 3-4 weeks of age with capsaicin. Mean arterial pressure was recorded by tail cuff through 16 weeks of age. On week 17, rats were cannulated, allowed 3 days to recover then had their AP measured directly for 3 days (3 hrs/day). Rats with renal deafferentation (n=11) had lower arterial pressure weeks 9-16 (average reduction AP=10.1±1.4 mmHg, ANOVA, p=0.0049) compared to control (saline treated, n=6) although the final direct recording was not significantly different on week 17 (control AP=184.1±3.4 mmHg vs deafferented AP=173.9±4.3 mmHg, p=0.07). Substance P levels from the kidneys were reduced in deafferented rats compared to control (6.9±1.0 vs 17.3±5.2 pg/g protein, p=0.0009). In contrast, renal NE levels were not altered (307±19 vs 313±20 pg/g protein, p=0.428). In the second study, the left kidney in weanling Sprague-Dawley rats was exposed to capsaicin or saline. Rats were allowed to mature (>250 g BW) then subjected to left renal artery clipping (0.2mm) or sham clip. AP was recorded by tail cuff during development of 2K1C for 6 weeks before direct cannulation to record AP on week 7. Renal deafferentation prevented the development of hypertension in 13 rats compared to 9 saline treated rats (average reduction AP=16.9±2.7 mmHg, ANOVA, p=0.0031). Saline treated rats had a higher AP 7 weeks after clipping (147.1±10.2 vs 130.5±4.2 mmHg direct recording, p=0.02). The left kidney contained 48% SP compared to the right kidney (p=0.04). These data suggest that increased afferent renal nerve activity contributes to the elevation in AP in hypertension and contributes to essential hypertension in humans. Supported by USPHS DA017371.

Acute alterations in fluid volume elicit complex neurohumoral responses including activation of the sympathetic nervous system (SNS), renin‐angiotensin system and the release of vasopressin (AVP). We hypothesized that increased plasma osmolality, reduced plasma volume or direct stimulation of angiotensin receptors would suppress the initial stress‐induced increase in systemic vascular resistance (SVR) that results from activation of the SNS. We instrumented rats to measure mean arterial pressure (MAP), cardiac output, and heart rate. After recovery, ice cold water (1 cm deep) was rapidly added to a waterproof cage to startle conscious rats. Hyperosmolality was induced by hypertonic saline (HTS, 20% NaCl, 1 ml/kg iv). Volume depletion was caused by furosemide (10 mg/kg, sc). In addition, angiotensin II was infused (20 μg/kg/min) to directly activate angiotensin receptors. After pretreatment with HTS, furosemide, or angiotensin II, the increase in SVR during the initial startle response was attenuated. In rats pretreated with HTS or angiotensin II, the increase in MAP during the initial startle response was also attenuated. Our results demonstrated that HTS, furosemide, and angiotensin II suppress vasoconstriction in response to startle. This may be due to direct inhibition of the SNS, indirect inhibition from an increase in AVP release, or a combination of these effects. Supported by USPHS DA13256.