The renal medulla: life at the edge of anoxia.
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Animals↗
Biomedical subjects
S Rosen
Publications and source records attributed to S Rosen.
The seasonal occurrence of ticks (Acari: Ixodidae) on sheep and in the field in the Judean area of Israel.
A 2 year survey of ixodid ticks in the Judean area of Israel between 1983 and 1985 showed that sheep were parasitized by the following species: Rhipicephalus sanguineus group (30.6%), Rhipicephalus bursa (25.3%), Haemaphysalis cretica (20.5%), Haemaphysalis otophila (20.1%) and Hyalomma anatolicum excavatum (3.1%). Three other species, Hyalomma marginatum rufipes, Boophilus annulatus and Amblyomma lepidum were also present but in very low numbers. A total of 50,816 specimens (78.1% adult ticks) were collected from the sheep. In the field, a total of 4780 ticks (8.7% adults) were collected and 64.3% consisted of R. bursa. Other species found were H. cretica (14.5%), H. a. excavatum (13.7%), H. otophila (3.4%), R. sanguineus group (1.9%) and 1.7% was Ixodes eldaricus. The number of ticks collected varied from year to year and seasonal activity was observed in all species except for H. a. excavatum. In all species, males outnumbered females, with the exception of H. cretica. The seasonal occurrence, tick ecology and disease relationship is discussed for each species.
Acari↗
Resistance to activated protein C, the FV:Q506 allele, and venous thrombosis.
Vitamin K-dependent protein C is an important regulator of blood coagulation. After its activation on the endothelial cell surface by thrombin bound to thrombomodulin, it cleaves and inactivates procoagulant cofactors Va and VIIIa, protein S and intact factor V working as cofactors. Until recently, genetic defects of protein C or protein S were, together with antithrombin III deficiency, the established major causes of familial venous thromboembolism, but they were found in fewer than 5-10% of patients with thrombosis. In 1993, inherited resistance to activated protein C (APC) was described as a major risk factor for venous thrombosis. It is found in up to 60% of patients with venous thrombosis. In more than 90% of cases, the molecular background for the APC resistance is a single point mutation in the factor V gene, which predicts substitution of an arginine (R) at position 506 by a glutamine (Q). Mutated factor V (FV:Q506) is activated by thrombin or factor Xa in normal way, but impaired inactivation of mutated factor Va by APC results in life-long hypercoagulability. The prevalence of the FV:Q506 allele in the general population of Western countries varies between 2 and 15%, whereas it is not found in several other populations with different ethnic backgrounds. Owing to the high prevalence of FV:Q506 in Western populations, it occasionally occurs in patients with deficiency of protein S, protein C, or antithrombin III. Individuals with combined defects suffer more severely from thrombosis, and often at a younger age, than those with single defects, suggesting severe thrombophilia to be a multigenetic disease.
Alleles↗
Autoimmune interstitial nephritis and hepatitis in polyglandular autoimmune syndrome.
A 6-year-old female with polyglandular autoimmune syndrome type I, chronic active hepatitis, and renal failure is described. The renal biopsy demonstrated advanced tubulointerstitial disease with antibodies directed against tubular basement membranes. The patient's serum contained circulating antibodies directed against both renal and hepatic parenchyma. Renal disease culminating in renal failure and anti-tubular basement membrane disease have not been previously reported in association with polyglandular autoimmune disease. We describe for the first time a patient with polyglandular autoimmune syndrome, chronic active hepatitis, circulating antibodies directed against both renal and hepatic parenchyma, and primary tubulointerstitial disease culminating in renal failure.
Child↗
Ctenocephalides felis flea infestation in horses.
The horses were in two stables: in the first stable they were kept together with sheep and in the second stable they were kept together with goats. All horses in both stables were diagnosed as being infested with the cat flea Ctenocephalides felis felis. Foals were severely infested, whereas adult horses were only moderately infested.
Aging↗
Pseudo-mycosis fungoides in a patient taking clonazepam and fluoxetine.
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Antidepressive Agents, Second-Generation↗
Temporal discounting in choice between delayed rewards: the role of age and income.
This study examined the effects of age and income temporal discounting (i.e. the decrease in the subjective value of a reward as the delay to its receipt increases). The value of delayed hypothetical monetary rewards was discounted at similar rates by adults of different ages but similar income levels, but at different rates by adults of similar age but different income levels. Specifically, lower income older adults showed a greater degree of temporal discounting than did either upper income older adults or upper income younger adults, but there were no age differences in discounting between the upper income groups. Comparison of these findings with those of a previous study (Green, Fry, & Myerson, 1994) suggests that impulsivity in decision making declines rapidly in young adulthood, reaching stable levels in the 30s. Further, age and income appear to interact in determining the impulsivity of decision making by adults.
Adult↗
Characterization of a radula opener neuromuscular system in Aplysia.
1. Several lines of evidence suggest that the I7-I10 muscle group contributes to the radula opening phase of behavior in Aplysia; 1) extracellular stimulation of these muscles in reduced preparations causes the halves of the radula to separate, 2) synaptic activity can be recorded from muscles I7-I10 in intact animals when the radula is opening, and 3) motor neurons innervating I7-I10 are activated out of phase with retractor/closer motor neurons during cycles of buccal activity driven by the cerebral-to-buccal interneuron 2 (CBI-2). 2. All of the opener muscles are innervated by the B48 neurons, a bilaterally symmetrical pair of cholinergic motor neurons. B48 neurons produce excitatory junction potentials (EJPs) in opener muscle fibers that summate to produce muscle contractions. Contraction size is determined by the size of depolarization in muscle fibers and/or by action potentials that are triggered by summation of B48-evoked EJPs. 3. In addition to input from B48 neurons, opener muscles also receive excitatory input from the cholinergic multiaction neurons B4/B5. EJPs evoked by stimulation of neurons B4/B5 are 1/10 the size of B48-evoked EJPs. Consequently, changes in muscle tension produced by B4/B5 activity are relatively small. In contrast to B48 neurons, neurons B4/B5 are likely to be active during the closing/retraction phase of behavior. During cycles of buccal activity driven by neuron CBI-2, neurons B4/B5 fire in phase with closer/retractor motor neurons. Thus opener muscles may develop a modest amount of tension during the closing/retraction phase of behavior as a result of synaptic input from neurons B4/B5. 4. Opener muscles may also develop tension during closing/retraction simply by virtue of the fact that they have been stretched. When isolated opener muscles are lengthened, depolarizations are recorded from individual muscle fibers, and muscle tension increases. With sufficient changes in fiber length, action potentials are elicited. These action potentials produce twitchlike muscle contractions that become rhythmic with maintained stretch. Stretch-activated depolarizations are generally first apparent when muscle length is increased by 1 mm. Length changes of 4-5 mm are generally necessary to elicit twitchlike muscle contractions. Changes of 1-2 mm in muscle length are observed when the opener muscle's antagonist, the accessory radula closer, is activated in reduced preparations. 5. Stretch may also modulate B48-induced contractions of the opener muscles. When muscle length is increased, B48-elicited contractions of the I7 muscle are larger. These increases in contraction amplitude are accompanied by decreases in contraction latency. 6. We conclude that muscles I7-I10 contract vigorously in response to strong excitatory input from neuron B48 and contribute to radula opening. Stretch may potentiate this activity. Thus, if radula closer muscles contract vigorously and pull on the opener muscles, the opener muscles will respond by contracting more vigorously themselves. This may be a mechanism for maintaining amplitude relationships between antagonistic muscles. Additionally, it is likely that the opener muscles will develop at least a modest amount of tension during closure/retraction of the radula. Part of this activation may derive from the weak excitatory input that the muscles receive from neurons B4/B5. Another part may derive from the stretch. One function of this co-contraction may be to act as a brake on closure, bringing this phase of feeding behavior to a smooth halt.
Action Potentials↗
Expression of vascular permeability factor (VPF/VEGF) is altered in many glomerular diseases.
Vascular permeability factor (VPF), also known as vascular endothelial growth factor (VEGF), is a potent enhancer of microvascular permeability and a selective endothelial cell growth factor. In normal human kidney, VPF/VEGF mRNA and protein are strongly expressed by visceral glomerular epithelial cells, and VPF/VEGF may be an important regulator of glomerular endothelial cell function. This study examined 47 renal biopsies from patients with a variety of glomerular diseases for expression of VPF/VEGF mRNA and protein by in situ hybridization and immunohisto-chemistry. In many glomerular diseases, VPF/VEGF-expressing cells were decreased in number or absent in areas of focal or global glomerular sclerosis. Decreased numbers of VPF/VEGF-expressing cells in glomeruli were also noted in amyloidosis, diabetes, crescentic glomerulonephritis, and diffuse endocapillary proliferative glomerulonephritis associated with systemic lupus erythematosus. Normally, release of VPF/ VEGF must be under strict control because it is some 50,000 times more potent than histamine as an inducer of microvascular permeability. Damage to visceral epithelial cells in a variety of glomerular diseases has the potential for releasing relatively large amounts of VPF/VEGF locally, leading to increased glomerular permeability. In addition, because VPF/ VEGF is also an endothelial growth factor, the loss of normal, controlled secretion of VPF/VEGF after damage to visceral epithelial cells could lead to important alterations in glomerular endothelial cell function.
Capillary Permeability↗
Myoglobinuric acute renal failure in the rat: a role for medullary hypoperfusion, hypoxia, and tubular obstruction.
Myoglobin induces renal injury by mechanisms that remain incompletely defined. In this study, the effects of myoglobin upon renal microcirculation, oxygenation, morphology, and function were investigated in anesthetized rats, and the contribution of coexisting perturbations to myoglobin nephrotoxicity were evaluated. Myoglobin infusion (3.3 mg/min) reduced outer medullary blood flow and Po2, whereas renal blood flow and cortical Po2 were unaffected. Myoglobin infusion (38 mg/100 g weight over 45 min) induced renal failure associated with collecting duct and medullary thick ascending limb dilation and casts, with focal tubular damage, confined mainly to the superficial cortex. Preconditioning with indomethacin, I-N-monomethyl arginine, and theophylline reduced cortical superficial damage but enhanced injury within the inner stripe of the outer medulla and in medullary rays, the zones of lowest O2 supply. In preconditioned animals, tubulorrhexis was primarily observed in collecting ducts transversing the inner stripe, and was remarkably reminiscent of human descriptions (J. Oliver et al., J Clin Invest 1951; 30: 1307-1440). Deterioration in kidney function closely correlated with morphologic features of both tubular obstruction and necrosis. In conclusion, medullary vasoconstriction and intrarenal hypoxia may play a role in myoglobin-induced renal failure. The deterioration in kidney function appears to reflect the combined effects of cortical damage, medullary hypoxic injury, and tubular obstruction.
Acute Kidney Injury↗
Sarcoptic mange in wild ruminants in zoological gardens in Israel.
Sarcoptic mange (Sarcoptes scabiei) occurred among wild ruminant species in five zoological gardens in Israel, from 1984 to 1994. Infestation of five ruminants by S. scabiei is reported for the first time: mountain gazelles (Gazella gazella), Nubian ibexes (Capra ibex nubiana), a barbary sheep (Ammotragus lervia), elands (Taurotragus oryx), and an Arabian oryx (Oryx leucoryx). All animals in the herds were administered ivermectin orally at a dose of 200 micrograms/kg body weight daily for 3 consecutive days. This was repeated three times at 2-wk intervals. The disease was eradicated in four small zoos, whereas in the biggest zoo, only control was achieved. Mortality among animals < 4 mo and > 8-yr-old animals composed 65% of mortality among all age classes.
Administration, Oral↗
In vivo adenovirus-mediated gene transfer into normal and cystic rat kidneys.
Gene transfer into the mammalian kidney has proved difficult because of the structural complexity of the organ and its low mitotic index. This article describes the use of intra-arterially injected adenovirus to study gene transfer into the rat kidney in vivo. By pre-chilling the kidney, and incubating the virus with the kidney in the cold for extended periods of time, we were able to successfully transfer a beta-galactosidase (beta-gal) reporter gene into the vasculature without ischemic injury to the kidney. Transfer occurred largely in the cortex when cold was used alone, whereas with the use of cold and vasodilators, transfer was accomplished into the outer medulla in both the inner and outer stripes. In the Han:SPRD rat model of autosomal dominant polycystic kidney disease (ADPKD), gene transfer occurred into the vasculature, some epithelial cysts and interstitial cells. This is the first description of substantial in vivo gene transfer into both normal and cystic kidneys. The methodology could find application in the creation of new models of renal disease, for in vivo therapeutic intervention or for genetic modification of an allograft at the time of harvest.
Adenoviridae↗
Hypoxia of the renal medulla--its implications for disease.
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Acute Disease↗
Non-nephrotic children with membranoproliferative glomerulonephritis: are steroids indicated?
Alternate-day steroids are currently recommended to treat children with membranoproliferative glomerulonephritis (MPGN). This recommendation is based largely on uncontrolled studies demonstrating improved renal survival with steroid therapy. We reviewed the outcome of 39 children who presented with MPGN between 1968 and 1990; 27 children were treated with steroids and 12 children received no drug therapy. Life-table analysis comparing renal survival of treated versus untreated children demonstrated no difference by log rank analysis. Treated and untreated groups were compared on the basis of nine features at presentation: age, sex, type of MPGN, presence and type of hematuria, hypocomplementemia renal insufficiency, hypertension, and nephrosis. Treated children were likely to be female (P < 0.01) and nephrotic (P < 0.02). Actuarial survival analyses were performed comparing the nine features with renal survival through 10 years of follow-up. Normotensive (P < 0.025) and non-nephrotic (P < 0.05) children had improved renal survival. The 11 non-nephrotic children demonstrated 100% long-term renal survival, including 7 who received no steroid therapy. At last follow-up, all non-nephrotic children had normal renal function, serum albumin levels > 3 g/dl, and were normotensive. These data suggest that non-nephrotic children with MPGN may forego steroid treatment without compromising long-term renal function. The current common practice of treating all children with MPGN with steroids should be re-examined.
Actuarial Analysis↗
A study of an enzootic focus of sheep babesiosis (Babesia ovis, Babes, 1892).
Morbidity and mortality due to Babesia ovis in sheep flocks grazing in an enzootic area of Israel occur yearly, about 2 weeks after detection of adult Rhipicephalus bursa ticks on the animals. Disease incidence peaks in May, but lasts throughout the active period of the adult ticks in the spring-summer months of April-July. No clinical cases of babesiosis have been registered during the active period of the preimaginal stages of R. bursa, from October to February. Incidence of parasitaemia during the spring-summer months was variable, ranging between 2 and 25%. However, in the winter months the incidence of parasitaemia in hoggets increased considerably, reaching 4-60% of the animals. A positive serological response to B. ovis was found in 84.5% of the hoggets and 88.9% of the ewes. In ewes, the prevalence of the serological response showed no marked seasonal variations. Colostral sera of 67.5% and 75% of the ewes and hoggets, respectively, were serologically positive for B. ovis. No antibodies were detected in the sera of lambs less than 3-4 months of age. The epizootiology of sheep babesiosis appears to differ from that of bovine babesiosis.
Animals↗
Induction of heat-shock proteins does not prevent renal tubular injury following ischemia.
The possible protective effect of heat-shock proteins (HSPs) on ischemic injury to renal cells was assessed in two different experimental models: ischemia-reflow in intact rats and medullary hypoxic injury as seen in the isolated perfused rat kidney. Heat shock was induced by raising the core temperature of rats to 42 degrees C for 15 minutes. Following this, Northern blots showed enhanced gene expression of HSP70, HSP60 and ubiquitin at one hour and reaching a maximum by six hours after heat shock in all regions of the kidney, but most prominently in medulla and papilla. The HSP70 protein in the kidney, estimated by immunohistochemical means, was detectable 24 hours following heat shock and further increased at 48 hours following heat shock. In the first set of experiments, the animals underwent uninephrectomy followed by cross clamping of the remaining renal artery for 40 minutes prior to reflow. Serum creatinine and urea nitrogen rose to 3.15 +/- 0.98 and 126.4 +/- 62.5 mg/dl at 24 hours. No significant differences were observed at 24, 48 and 72 hours after reflow between these values in control rats and rats pretreated with heat shock 48 hours earlier. Severe morphological damage to proximal tubules of the renal cortex was observed to the same extent in both groups. In a second set of experiments, the right kidney was removed either 24 or 48 hours after heat shock and perfused in isolation for 90 minutes. Functional and morphological parameters were compared with those of isolated perfused kidneys obtained from animals that had not been subjected to heat shock.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Rapid DNA fragmentation from hypoxia along the thick ascending limb of rat kidneys.
Extensive DNA fragmentation, a marker for programmed cell death, was selectively and rapidly induced by hypoxia in the thick ascending limbs of rat kidneys. In isolated perfused kidneys, DNA breaks were present in medullary tubules as early as after 10 minutes of local hypoxia and were prevented by reduction of metabolic work. In a model of radiocontrast-induced acute renal failure, DNA breaks were detected selectively along thick ascending limbs as early as 15 minutes following insult, preceding overt morphological damage. Hypoxia induces rapid DNA fragmentation along thick ascending limbs, where programmed cell death could play an important role in nephron injury and kidney failure.
Acute Kidney Injury↗
Infections complicating tunneled intraspinal catheter systems used to treat chronic pain.
Tunneled intraspinal catheters and catheter-pump systems are increasingly common treatments for severe chronic pain, but these long-term catheters have caused meningitis, epidural abscesses, and other serious infections. At a cancer referral center, 81 catheters were placed in 72 patients over a 7-year period. There were seven catheter-associated infections: two were meningeal (one was accompanied by an epidural abscess and one by a pocket infection and bacteremia), four were associated with a pocket, and one was associated with a tunnel. The infection rate was 0.77 per 1,000 catheter-days. Pathogenic organisms that were isolated were primarily normal skin flora. By multivariate Cox analysis, the only factor significantly associated with catheter infection was prolonged catheter placement surgery, i.e., a procedure lasting at least 100 minutes (RR, 8.8; 95% CI, 1.6-50). Three patients were cured by removal of the catheter and treatment with antibiotics, and symptoms were satisfactorily suppressed in four patients with antibiotics alone. Considering the severity of illness in catheter recipients, the infection rate was relatively low. Removal of the catheter does not appear mandatory when the goal is suppression of infection-related symptoms, especially when the infection has not spread to the CNS, the infecting organism has an intrinsically low virulence, and the infected patient is terminally ill.
Abscess↗