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Biomedical subjects

M W Miller

Publications and source records attributed to M W Miller.

At least 19 recordsLinked to original sources

Biomechanics of the porcine basilar artery in hypertension.

Hypertension is a significant risk factor for diverse cerebrovascular diseases ranging from stroke to arteriovenous malformations and saccular aneurysms. Our increasing understanding of vascular mechanobiology reveals that changes in mechanical stimuli, such as increased blood pressure, alter basic cellular functions including the production and degradation of extracellular matrix as well as proliferation, migration, and apoptosis. Understanding changes in the biomechanical properties of the vascular wall is fundamental to correlating mechanobiological responses with the altered loads. In this paper, we present the first biomechanical data on a large cerebral artery in terms of the time of development of hypertension in maturity. Specifically, we report rapid changes in both the structural and the material stiffness of the passive basilar artery in a novel aortic-coarctation model of hypertension in the mini-pig. Histological measurements reveal associated increases in fibrillar collagens in the media and adventitia as well as increased smooth muscle in the media. That such dramatic changes occur within 2 weeks of the initiation of hypertension in maturity necessitates a detailed study of the early changes as well as the potential to reverse these changes at later times.

Animals↗

Effect of prenatal exposure to ethanol on glutamate and GABA immunoreactivity in macaque somatosensory and motor cortices: critical timing of exposure.

The present study explored the effects of gestational ethanol exposure on enduring changes in the distribution of projection neurons and local circuit neurons in somatosensory/motor cortex. Critical events in corticogenesis occur during macaque gestation: the first six weeks of gestation include the period of primary stem cell production and the next 18 weeks are marked by the birth, migration, early differentiation, and death of cortical neurons. Monkeys were exposed to ethanol (or saline) one day per week during the first six or during the entire 24 weeks of gestation. Offspring were killed as adolescents. Projection neurons and local circuit neurons were identified immunohistochemically with antibodies directed against glutamate and anti-GABA, respectively. In all animals, both projection neurons and local circuit neurons were distributed in all laminae of both somatosensory and motor cortices. Ethanol did not affect the size of Cresyl Violet-stained, glutamate-positive, or GABA-immunolabeled somata, however, it did decrease neuronal density. The total density of Cresyl Violet-stained neurons was reduced in monkeys treated with ethanol (or saline) one day per week during the first six weeks of gestation and during the entire 24 weeks of gestation. Similar reductions were detected for glutamate- and GABA-positive neurons. The densities of Cresyl Violet-stained and of glutamate- and GABA-expressing neurons were reduced in all cortical layers. The only exception was layer V which was unaffected in monkeys treated with ethanol (or saline) one day per week during the first six weeks of gestation and during the entire 24 weeks of gestation. Thus, the parallel effects on both neuronal subpopulations suggest that ethanol targets a population of undetermined neuronal precursors.

Animals↗

Transarterial coil embolization for canine patent ductus arteriosus occlusion.

Left to right shunting patent ductus arteriosus (PDA) is the most common canine congenital heart defect. If not occluded PDA is associated with high morbidity and mortality. Historically, surgical ligation has been the standard method of correction. Although highly successful, surgical ligation is associated with some operative morbidity and mortality. More recently, minimally invasive transcatheter techniques have been employed for PDA occlusion. Transarterial PDA coil embolization is a safe, cost effective, less invasive alternative offered by many specialty centers for PDA occlusion. This procedure involves catheterization of the femoral artery under general anesthesia. An angiogram is then performed to delineate PDA morphology and facilitate coil selection. Coils are commercially available and composed of surgical stainless steel with prothrombotic poly-Dacron fibers. Coils are advanced through a catheter into the PDA under fluoroscopic guidance until satisfactory angiographic occlusion is documented. Patients are then recovered and released the following day. This procedure requires substantial technical expertise and specialized equipment.

Animals↗

Chronic wasting disease of cervids.

Chronic wasting disease (CWD) has recently emerged in North America as an important prion disease of captive and free-ranging cervids (species in the deer family). CWD is the only recognized transmissible spongiform encephalopathy (TSE) affecting free-ranging species. Three cervid species, mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and Rocky Mountain elk (Cervus elaphus nelsoni), are the only known natural hosts of CWD. Endemic CWD is well established in southern Wyoming and northern Colorado, and has been present in this 'core area' for two decades or more. Apparently CWD has also infected farmed cervids in numerous jurisdictions, and has probably been endemic in North America's farmed deer and elk for well over a decade. Several free-ranging foci distant to the Colorado-Wyoming core area have been discovered since 2000, and new or intensified surveillance may well identify even more foci of infection. Whether all of the identified captive and free-ranging foci are connected via a common original exposure source remains undetermined. Some of this recently observed 'spread' may be attributable to improved detection or natural movements of infected deer and elk, but more distant range extensions are more likely caused by movements of infected captive deer and elk in commerce, or by some yet unidentified exposure risk factor. Research on CWD over the last 5 years has resulted in a more complete understanding of its pathogenesis and epidemiology. CWD is infectious, transmitting horizontally from infected to susceptible cervids. Early accumulation of PrP(CWD) in alimentary tract-associated lymphoid tissues during incubation suggests agent shedding in feces or saliva as plausible transmission routes. Residual infectivity in contaminated environments also appears to be important in sustaining epidemics. Improved tests allow CWD to be reliably diagnosed long before clinical signs appear. Implications of CWD are not entirely clear at this time. Natural transmission to humans or traditional domestic livestock seems relatively unlikely, but the possibility still evokes public concerns; impacts on wildlife resources have not been determined. Consequently, where CWD is not known to occur surveillance programs and regulations that prevent or reduce the likelihood that CWD will be introduced into these jurisdictions should be encouraged. Where CWD is known to occur, affected jurisdictions are conducting surveillance to estimate and monitor trends in geographic distribution and prevalence, managing deer and elk populations in attempts to limit spread, and developing and evaluating techniques for further controlling and perhaps eradicating CWD. Programs for addressing the challenges of CWD management will require interagency cooperation, commitment of funds and personnel, and applied research. Chronic wasting disease (CWD) is perhaps the most enigmatic of the naturally occurring prion diseases. Although recognized as a transmissible spongiform encephalopathy (TSE) since the late 1970s (Williams and Young 1980, 1982), interest in and concern about CWD has only recently emerged. CWD most closely resembles scrapie in sheep in most respects, but recent media and public reaction to CWD has been more reminiscent of that afforded to bovine spongiform encephalopathy (BSE) less than a decade ago. Yet, with the exception of transmissible mink encephalopathy (TME), CWD is the rarest of the known animal TSEs: fewer than 1,000 cases have been diagnosed worldwide, and all but two of these occurred in North America. CWD is unique among the TSEs in that it affects free-living species (Spraker et al. 1997; Miller et al. 2000). The three natural host species for CWD, mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and Rocky Mountain elk (Cervus elaphus nelsoni), are all in the family Cervidae and native to North America. Like scrapie, CWD is contagious: epidemics are self-sustaining in both captive and free-ranging cervid populations (Miller et al. 1998, 2000). The geographic extent of endemic CWD in free-ranging wildlife was initially thought to be quite limited and its natural rate of expansion slow; however, recent investigations have revealed that CWD has been inadvertently spread much more widely via market-driven movements of infected, farmed elk and deer. Both the ecological and economic consequences of CWD and its spread remain to be determined; moreover, public health implications remain a question of intense interest. Here, we review current understanding of CWD, its implications, and its management.

Animals↗

Proliferation and death of conditionally immortalized neural cells from murine neocortex: p53 alters the ability of neuron-like cells to re-enter the cell cycle.

Neurons are distinctive in that they are generally considered to be permanently post-mitotic cells. The oncoprotein p53 is a key regulator in neuronal development, notably in cell proliferation and neuronal death. We hypothesize that p53 maintains the post-mitotic characteristic of differentiated neurons. New lines of conditionally immortalized cortical cells were generated to test this hypothesis. Populations of cells were obtained from the neocortices of dual transgenic mice that were null for p53 and expressed a temperature-sensitive SV40 large T antigen. At a permissive temperature (32 degrees C), the cells continued to proliferate and most expressed nestin and proteins associated with glia. At a non-permissive temperature (39 degrees C), the cells expressed cytoskeletal proteins associated with differentiated neurons such as microtubule associated protein 2 and neurofilament 200. Under permissive conditions, both p53(+/-) and p53(-/-) cells exhibited similar cycling behaviors; the length of the cell cycle was 13-15 h and >85% of the cells were actively cycling. In non-permissive conditions, most p53(+/-) cells stopped dividing, whereas the p53(-/-) cells continued to proliferate. The survival of the cells also differed. In the non-permissive conditions, many p53(+/-) cells died following treatment with a neurotoxin (ethanol, 400 mg/dl), whereas the p53(-/-) cells did not. After re-introduction to the permissive conditions, both cell lines expressed neuron-like characteristics, but only the p53(-/-) cells retained their ability to cycle. Therefore, p53-mediated activities appear to be involved in the proliferation, survival, and post-mitotic nature of neuron-like cells.

Animals↗

Transmissible spongiform encephalopathies in non-domestic animals: origin, transmission and risk factors.

The transmissible spongiform encephalopathies (TSEs), scrapie and bovine spongiform encephalopathy (BSE), are serious diseases of domestic animals. Although not as significant in terms of numbers of animals affected or geographical distribution, TSEs also affect non-domestic animals. Transmissible mink encephalopathy (TME) was the first TSE to be identified in non-domestic animals. This disease of captive mink (Mustela vison) is very rare and is associated with exposure through feed contaminated by a TSE agent. The second TSE to be identified in non-domestic animals was chronic wasting disease (CWD) of deer and elk. This disease is not known to be associated with feedstuffs contaminated with the agent of CWD, but the natural route of exposure appears to be oral, possibly through direct interaction between animals or through environmental contamination. Over the last five years, the known distribution of CWD across North America has expanded, increasing concerns over the impact of this disease on populations of free-ranging cervids and the viability of game farming industries. Concurrent with the epidemic of BSE, a variety of non-domestic ruminants and felid species were also affected in the United Kingdom, presumably through exposure to the agent in contaminated feed. These examples illustrate that when non-domestic animals are held in captivity, they depend upon feeds supplied by their caretakers and may show degrees of susceptibility to infectious agents in feeds which vary from those of domestic species. Although humans have less influence over exposure of free-ranging species to infectious agents, monitoring these populations for diseases may be important for managing the health of these animals. It is important to institute or continue surveillance for an entire range of infectious diseases, including TSEs, in free-ranging and captive non-domestic species. Study of diseases in these species may provide important information about infectious agents of concern for domestic animals and humans.

Animals↗

Validation of monoclonal antibody F99/97.6.1 for immunohistochemical staining of brain and tonsil in mule deer (Odocoileus hemionus) with chronic wasting disease.

A new monoclonal antibody (MAb), F99/97.6.1, that has been used to demonstrate scrapie-associated prion protein PrP(Sc) in brain and lymphoid tissues of domestic sheep with scrapie was used in an immunohistochemistry assay for diagnosis of chronic wasting disease (CWD) in mule deer (Odocoileus hemionus). The MAb F99/97.6.1 immunohistochemistry assay was evaluated in brain and tonsil tissue from 100 mule deer that had spongiform encephalopathy compatible with CWD and from 1,050 mule deer outside the CWD-endemic area. This MAb demonstrated abnormal protease-resistant prion protein (PrP(res)) in brains of all of the 100 mule deer and in 99 of the 100 tonsil samples. No immunostaining was seen in samples collected from deer outside the endemic area. MAb F99/97.6.1 demonstrated excellent properties for detection of PrP(res) in fresh, frozen, or mildly to moderately autolytic samples of brain and tonsil. This immunohistochemistry assay is a sensitive, specific, readily standardized diagnostic test for CWD in deer.

Animals↗

Comparison of histological lesions and immunohistochemical staining of proteinase-resistant prion protein in a naturally occurring spongiform encephalopathy of free-ranging mule deer (Odocoileus hemionus) with those of chronic wasting disease of captive mule deer.

In this investigation, the nature and distribution of histologic lesions and immunohistochemical staining (IHC) of a proteinase-resistant prion protein were compared in free-ranging mule deer (Odocoileus hemionus) dying of a naturally occurring spongiform encephalopathy (SE) and captive mule deer dying of chronic wasting disease (CWD). Sixteen free-ranging deer with SE, 12 free-ranging deer without SE, and 10 captive deer with CWD were examined at necropsy. Tissue sections were stained with hematoxylin and eosin, and duplicate sections were stained with a monoclonal antibody (F89/160.1.5). Histological lesions in the free-ranging deer with SE and captive deer with CWD were found throughout the brain and spinal cord but were especially prominent in the myelencephalon, diencephalon, and rhinencephalon. The lesions were characterized by spongiform degeneration of gray matter neuropil, intracytoplasmic vacuolation and degeneration of neurons, and astrocytosis. IHC was found throughout the brain and retina of deer with SE and CWD. Positive IHC was found in lymphoid tissue of deer with SE and CWD. Histologic lesions and IHC were not found in multiple sections of integument, digestive, respiratory, cardiovascular, endocrine, musculoskeletal, and urogenital systems of deer with SE or CWD. Comparison of histologic lesions and IHC in tissues of free-ranging deer with those of captive deer provides strong evidence that these two diseases are indistinguishable morphologically.

Animals↗

Distribution of protease-resistant prion protein and spongiform encephalopathy in free-ranging mule deer (Odocoileus hemionus) with chronic wasting disease.

Serial sections of brain and palatine tonsil were examined by immunohistochemical staining (IHC) using monoclonal antibody F89/160.1.5 for detecting protease-resistant prion protein (PrP(res)) in 35 hunter-killed mule deer (Odocoileus hemionus) with chronic wasting disease. Serial sections of brain were stained with hematoxylin and eosin and examined for spongiform encephalopathy (SE). Clinical signs of disease were not observed in any of these deer. On the basis of the location and abundance of IHC and the location and severity of SE, deer were placed into four categories. Category 1 (n = 8) was characterized by IHC in the palatine tonsil with no evidence of IHC or SE in the brain. Category 2 (n = 13) was characterized by IHC in the palatine tonsil and IHC with or without SE in the dorsal motor nucleus of the vagus nerve (DMNV). Category 3 (n = 2) was characterized by IHC in the palatine tonsil, IHC with SE in the myelencephalon, and IHC without SE in the hypothalamus. Category 4 (n = 12) was characterized by IHC in the palatine tonsil and IHC with SE throughout the brain. Category I may represent early lymphoid tissue localization of PrP(res). The DMNV appears to be the most consistent single neuroanatomic site of detectable PrP(res). Categories 2-4 may represent a progression of spread of PrP(res) and SE throughout the brain. IHC in tonsil and brain and SE in brain were not detected in 208 control deer.

Animals↗

Chronic wasting disease in deer and elk in North America.

Chronic wasting disease (CWD) has emerged as an important disease of wildlife in North America. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs) or prion diseases, which naturally affect only a few species. Of the TSEs, CWD is the only one found in free-ranging species. However, interest in CWD has recently grown, by association with the better-known TSEs such as variant Creutzfeldt-Jakob disease of humans and bovine spongiform encephalopathy. Knowledge of the geographic distribution of CWD, though still limited, has greatly improved since the mid-1990s as a result of surveillance in free-ranging deer and elk and in commercially owned Rocky Mountain elk (Cervus elaphus nelsoni), and the disease has now been found in multiple areas of the plains and Rocky Mountain foothills of western North America. Studies of the biology and natural history of CWD over recent years have resulted in a better understanding of the pathogenesis and epidemiology of the disease. Early involvement of the lymphoid tissues of the alimentary tract during the incubation period of CWD suggests plausible routes for agent exit from an infected individual, such as in faeces or saliva. Chronic wasting disease is laterally transmitted and environmental contamination may play an important role in local maintenance of the disease. Studies on the epidemiology of CWD have led to the development of models to help explain the history of CWD and to simulate future impacts on deer and elk populations. Diagnostic tests have been improved, allowing diagnosis early in the incubation period, long before the appearance of clinical disease. Surveillance techniques and programmes have been developed and instituted by wildlife management agencies for free-ranging deer and elk and by state and federal agricultural agencies for privately-owned elk. During the 1990s, perceptions of TSEs have altered dramatically; perhaps most remarkably, the goal of global eradication of all prion diseases is now being discussed.

Animals↗

Deficient neurogenesis in forebrain-specific presenilin-1 knockout mice is associated with reduced clearance of hippocampal memory traces.

To examine the in vivo function of presenilin-1 (PS1), we selectively deleted the PS1 gene in excitatory neurons of the adult mouse forebrain. These conditional knockout mice were viable and grew normally, but they exhibited a pronounced deficiency in enrichment-induced neurogenesis in the dentate gyrus. This reduction in neurogenesis did not result in appreciable learning deficits, indicating that addition of new neurons is not required for memory formation. However, our postlearning enrichment experiments lead us to postulate that adult dentate neurogenesis may play a role in the periodic clearance of outdated hippocampal memory traces after cortical memory consolidation, thereby ensuring that the hippocampus is continuously available to process new memories. A chronic, abnormal clearance process in the hippocampus may conceivably lead to memory disorders in the mammalian brain.

Alzheimer Disease↗

Effects of prenatal exposure to ethanol on the expression of bcl-2, bax and caspase 3 in the developing rat cerebral cortex and thalamus.

Prenatal exposure to ethanol causes neuronal death in somatosensory cortex, but apparently not in the ventrobasal nucleus of the thalamus. Effectors such as bcl-2, bax, and caspase 3 can determine whether a neuron survives or dies. We hypothesize that ethanol differentially affects the expression of these proteins in the cortex and thalamus during the periods of naturally occurring and ethanol-induced neuronal death. Pregnant rats were fed ad libitum with an ethanol-containing liquid diet (Et) or pair-fed an isocaloric non-alcoholic diet (Ct). Samples were collected from fetuses (gestational day (G) 16 and G19) and pups (postnatal day (P) 0 through P30) and examined for bcl-2, bax, or caspase 3 expression using a quantitative immunoblotting procedure. Prenatal exposure to ethanol reduced cortical bcl-2 expression, but not bax expression on P6. Hence, the bcl-2/bax ratio was lower in Et-treated rats than in controls. In contrast, thalamic expression of neither bcl-2 nor bax was significantly different in the two groups of rats. Thus, the thalamic bcl-2/bax ratio was unaffected by exposure to ethanol. During the period of naturally occurring neuronal death, the expression of the active (20 kDa) and inactive isoforms (32 kDa) of caspase 3 was altered in the cortices of Et-treated rats, but not in their thalami. Thus, prenatal exposure to ethanol affected the early postnatal expression of death-related proteins in the cortex, but not in the thalamus. These biochemical changes concur with anatomical data on the spatial and temporal selectivity of ethanol toxicity in the developing CNS.

Aging↗

Dichotomy in phasic-tonic neuromuscular structure of crayfish inhibitory axons.

Crustacean muscles are unique in their innervation by both excitatory and inhibitory neurons; therefore, they exhibit polyneuronal and multiterminal innervation. Because excitatory motoneurons are broadly divided into phasic and tonic types, we hypothesized that inhibitory neurons would follow a similar dichotomy. The abdominal extensor muscles in crayfish are separated into parallel deep and superficial bundles; the former has fast muscle fibers innervated by phasic excitatory motoneurons, and the latter has slow fibers supplied by tonic excitatory motoneurons. Each muscle also is innervated by a single, separate inhibitory neuron that uses gamma-aminobutyric acid (GABA) as the inhibitory neurotransmitter. The pattern of axonal branching by the separate inhibitory axons in phasic and tonic abdominal extensor muscles was visualized with confocal microscopy in preparations labeled for GABA-like immunoreactivity. Initial observations indicated that the phasic muscle was covered by extensive GABAergic, filiform axon terminals, whereas innervation of the tonic muscle was comprised of more localized and varicose terminals. With quantitative analyses, we found that the phasic axon has a more highly branched nature than the tonic in first- and second-order branches. The phasic axon branches also were significantly longer than the tonic branches in the second- and third-order branches. Synaptic varicosities in the phasic branches were smaller and less frequent than those in the tonic branches. The fine structure of the inhibitory nerve terminals near synaptic contacts examined with thin-serial-section electron microscopy revealed distinct differences between the phasic system and the tonic system. The phasic terminals were smaller in cross-sectional area than the tonic terminals, and they had smaller synapses and fewer mitochondria. The presynaptic active zone dense bodies were similar in length and number between phasic and tonic synapses. However, their number per synaptic area was two-fold higher in phasic synapses compared with tonic synapses because of the smaller size of the phasic synapses. Thus, within the same neuromuscular system, inhibitory synaptic terminals revealed unique phasic and tonic identities similar to those observed for the excitatory axons.

Animals↗

Clinical features of dilated cardiomyopathy in Great Danes and results of a pedigree analysis: 17 cases (1990-2000).

OBJECTIVE: To determine clinical features of dilated cardiomyopathy (DCM) in Great Danes and to determine whether DCM is familial in this breed. DESIGN: Retrospective study. ANIMALS: 17 Great Danes with DCM. PROCEDURE: Medical records of Great Danes in which DCM was diagnosed on the basis of results of echocardiography (fractional shortening < 25%, end-systolic volume index > 30 ml/m2 of body surface area) were reviewed. Pedigrees were obtained for affected animals, as well as for other Great Danes in which DCM had been diagnosed. RESULTS: Dilated cardiomyopathy appeared to be familial and was characterized by ventricular dilatation, congestive heart failure (left-sided or biventricular), and atrial fibrillation. Pedigree analysis suggested that DCM was inherited as an X-linked recessive trait, but the mode of inheritance could not be definitively identified. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that DCM may be an X-linked recessive trait in Great Danes. Thus, dogs with DCM probably should not be used for breeding, and female offspring of affected dogs should be used cautiously. Male offspring of affected females are at an increased risk of developing DCM and should be evaluated periodically for early signs of disease. Results of pedigree analysis were preliminary and should be used only as a guide for counseling breeders, rather than as a basis for making breeding decisions.

Animals↗

Use of galactosyltransferase to assess the biological function of O-linked N-acetyl-d-glucosamine: a potential role for O-GlcNAc during cell division.

Many cytosolic and nuclear proteins are modified by monomeric O-linked N-acetyl-d-glucosamine (O-GlcNAc). The biological functions of this form of glycosylation are unclear but evidence suggests that it heightens regulation of protein function. To assess the biological function of O-GlcNAc addition, we examined the biological effects of galactosyltransferase (GalT) microinjected into the cytoplasm of Xenopus ovarian oocytes. GalT, which catalyzes beta1-4-galactose addition to O-GlcNAc, should inhibit deglycosylation and lectin-like interactions requiring unmodified O-GlcNAc residues. Although GalT injection into diplotene-arrested oocytes has no detectable effects on cell viability, it is toxic to oocytes entering meiosis. Cell-cycle-specific toxicity is recapitulated in vitro as GalT inhibits formation of nuclei and microtubule asters from cell-free extracts of ovulated frog eggs. These observations suggest that regulation of O-GlcNAc is important for cell cycle progression and may be important in diseases in which O-GlcNAc metabolism is abnormal. The methods described here outline a viable experimental scheme for ascribing a biological function to this form of glycosylation.

Acetylglucosamine↗

Use of echocardiography for the diagnosis of heartworm disease in cats: 43 cases (1985-1997).

OBJECTIVE: To determine the usefulness of echocardiography in the diagnosis of heartworm disease in cats and to compare this modality with other tests. DESIGN: Retrospective study. ANIMALS: 43 cats with heartworm infection that had echocardiographic examinations at 2 veterinary teaching hospitals between 1985 and 1997. Twenty-two of these 43 cats also underwent radiography of the thorax and heartworm antibody and heartworm antigen testing. PROCEDURE: Cats were determined to be infected with Dirofilaria immitis infection on the basis of 1 or more of the following findings: positive modified Knott or antigen test result, echocardiographic evidence of heartworm disease, or confirmation of the disease on postmortem examination. The percentage of echocardiographs in which heartworms were evident was compared with the percentage of radiographs in which pulmonary artery enlargement was evident and results of antigen or antibody tests in cats in which all tests were performed. RESULTS: Overall, heartworms were detectable by use of echocardiography in 17 of 43 cats, most often in the pulmonary arteries. In the 22 cats in which all tests were performed, antibody test results were positive in 18, antigen test results were positive in 12, and pulmonary artery enlargement was evident radiographically and heartworms were identifiable echocardiographically in 14. Heartworm infection was diagnosed exclusively by use of echocardiography in 5 cats in which the antigen test result was negative. CONCLUSIONS AND CLINICAL RELEVANCE: Although echocardiography was less sensitive than antigen testing, it was a useful adjunctive test in cats that had negative antigen test results in which there was a suspicion of heartworm disease. The pulmonary arteries should be evaluated carefully to increase the likelihood of detection of heartworms echocardiographically.

Animals↗

Comparative sensitivity of human fetal and adult erythrocytes to hemolysis by pulsed 1 MHz ultrasound.

Human fetal and adult erythrocytes differ significantly in mean corpuscular volume (MCV), the fetal cells being larger than adult cells and diminishing in MCV as gestational age (GA) increases. Previous studies have shown that the sensitivity of erythrocytes from different species to lysis by mechanically applied shear stress increases as MCV increases. The tested hypotheses in the present project were: 1. fetal erythrocytes would be more sensitive to sonolysis than adult erythrocytes because of the former's larger size, and 2. erythrocyte sonolytic sensitivity would scale with MCV. Fetal and adult erythrocytes were resuspended to 40% hematocrit in oxygenated isotonic saline solution and 500 microL aliquots were exposed for 60 s to 200 micros bursts of 1-MHz ultrasound (US) (peak pressures: approximately 4.8 MPa positive, approximately 2.7 MPa negative; duty factor = 0.01), either with or without 3.6 volume % Albunex (ALX) present. Background-corrected hemolysis was indistinguishable from zero in sham-exposed fetal or adult erythrocyte suspensions. Without ALX, mean background-corrected US-induced hemolysis was significantly greater than zero for fetal and adult cells (0.42 +/- 0.15% vs. 0.62 +/- 0.15), but fetal cell lysis was not significantly greater than adult cell lysis. With ALX, US-induced hemolytic yields increased approximately 80-fold (fetal: 50.53 +/- 2.14; adult: 46.40 +/- 1.85%), and were significantly higher for fetal than for adult cells. There was also a statistically significant correlation between MCV and US-induced background-corrected hemolysis. Thus, the two hypotheses were supported.

Adult↗