| J TN Academy Sci., Volume
73, Number 3-4, pgs 115-120 July-October 1998. Union University.
1.
DOES NITRIC OXIDE PRODUCTION LOWER
MEAN ARTERIAL BLOOD PRESSURE DURING PREGNANCY? Swanette Anderson1
and Robert A. Ahokas2, PhD. 1Dept. of Biology, Christian Brothers University,
Memphis, TN; 2Dept. of Obstetrics and Gynecology, and Physiology / Biophysics,
University of Tennessee at Memphis.
Pregnancy is normally associated
with vasodilation, and in hypertensive animals, such as the spontaneously
hypertensive rat (SHR), causes a profound decrease in blood pressure. To
test the possibility that enhanced basal vascular nitric oxide (NO) activity
has a role in the vasodilation of pregnancy, we measured the changes in
mean arterial blood pressure (MAP) induced by NG-nitro-L-arginine methyl
ester, a specific inhibitor of NO synthesis, in conscious postganglionic
c blocked non-pregnant and pregnant SHR's. In the pregnant rats, litter
size was adjusted to 1-12 on day 7 of pregnancy. On days 14 and 21 of pregnancy,
MAP was measured before and 30 minutes after Hexamethonium (20 mg/kg, IV).
MAP of the day 21, but not 14 day pregnant rats was significantly lower
than that of the non-pregnant rats. Hexamethonium decreased MAP 50-60 mm
Hg in all rats. NG-nitro-L-arginine methyl ester (10 mg/kg, IV) increased
MAP greater in the non-pregnant than in the 21 day pregnant rats. These
results suggest that vascular NO activity is not increased in pregnancy,
and is not responsible for the decrease in MAP. Rather, vasodilation is
due to a late pregnant decrease in sympathetic neurogenic vascular tone
which is modulated by some unknown mechanism by the fetoplacental unit.
Supported by: the Department of Obstetrics
and Gynecology, UT Memphis
2.
INFLUENCE OF THE NORTH HOLLYWOOD DUMP
ON WOLF RIVER SEDIMENT METALS CONCENTRATIONS. T. Briggs1, C. J. Leppanen2,
and K. J. Maier2 1Dept. of Biology, Christian Brothers Univ.,
Memphis, TN; 2Dept. of Biology, Univ. Memphis, Memphis TN.
The North Hollywood Dump in
Memphis, TN is a closed municipal/industrial landfill and federally listed
superfund site. We examined core Wolf River sediments for metal concentrations
upstream, adjacent to, and downstream of the dump to determine the influence
of the dump on Wolf River sediment toxicity. Metal concentrations were
determined using graphite furnace atomic absorption for Pb, and flame atomic
absorption for Al, Ba, Cu, Fe, Mn, and Zn. Aluminum, iron, and zinc
concentrations were highest along side of the dump. Copper and lead
concentrations peaked at the downstream site. Manganese concentrations
were greatest upstream and Barium was not present in any sediment. More
frequent sampling, as well as taking a greater number of samples will aid
in pinpointing the source(s) of contamination.
3.
DEXAMETHASONE INHIBITION OF INDUCIBLE
NITRIC OXIDE SYNTHASE PRODUCTION IN MACROPHAGES STIMULATED WITH GENITAL
MYCOPLASMAS. Karima T. Causey 1, Dennis T. Crouse2, 3, B. Keith English2,
3, Cindy Newman2, 3, Elizabeth Meals 2,3, Lisa Livingston 2,3. 1Christian
Bro. Univ., Depart. of Biol, Memphis, TN. 2 UT, Memphis, TN., Dept. Pediatrics
& OBGYN, & 3Crippled Children's Foundation Research Center, LeBonheur
Children's Medical Center.
In preterm infants, mycoplasmas
are associated with the chronic lung disease, Bronchopulmonary Dysplasia.
Dexamethasone is a corticosteroid often administered to these infants to
suppress inflammation. Nitric oxide (NO) formation, in macrophages
and increased intrinsically in humans during inflammation, is controlled
by an enzyme called inducible nitric oxide synthase (iNOS). Thus,
studying iNOS production could be used as a marker for inflammation that
occurs due to the stimulation of macrophages by mycoplasmas and the effect
of dexamethasone on this process. We hypothesized that dexamethasone
would decrease iNOS production in mycoplasmal-stimulated macrophages. Macrophage
cell cultures were incubated with sterile media alone, Lipopolysaccharide
(LPS) (1ng or 100ng), Mycoplasma hominis (Mh) (104, 105 and 106 colony
forming units (cfu)/ml, or Ureaplasma urealyticum (Uu) (104, 105, 106 cfu/ml)
for 16 hours. Immunoelectrophoresis was used to measure iNOS.
Incubation of the macrophages with 1U (unit) or 10U Interferon Gamma and
either LPS, or Uu, or Mh produced iNOS in a dose-dependent manner.
Dexamethasone reduced the production of iNOS in all experiments.
Thus, genital mycoplasmas stimulate iNOS in a dose-dependent fashion, which
can be inhibited by dexamethasone.
4.
LOW ANTIOXIDANT POTENTIAL AND PSYCHOLOGICAL
DISTRESS AMONG THE MORBIDLY OBESE. Michael E. Cole**, Cynthia K.
Buffington, Ph.D.+, Richie J. Feuers, Ph.D.*, Ronald W. Hart, Ph.D.*, and
George S.M. Cowan, M.D.+. **The Dept. of Biology, Christian Brothers
University, Memphis, TN, +The Dept. of Surgery, UT, Memphis, TN, and *The
National Center for Toxicological Research, Jefferson, AR.
Free radicals such as peroxides
cause irreversible damage to membranes, DNA, mitochondria, and other cellular
components. Glutathione plays an important role in the destruction
of organic peroxides and other free radicals through a reaction catalyzed
by Glutathione peroxidase (GPx). In our studies, we measured the
activities of GPx and enzymes important in the reduction of glutathione,
glucose-6-phosphate dehydrogenase (G6PDH) and glutathione reductase (GR),
in isolated red blood cells of morbidly obese (MO) and lean patients (LC).
We found that neither G6PDH nor GR activities (using student t-tests) significantly
differed (p>0.05) between the MO and LC groups, suggesting normal levels
of NADPH and reduced glutathione in our MO population. GPX activities
of the MO, however, were found to be significantly (p<0.001) below LC
values. As GPx is important in catalyzing the removal of hydrogen
peroxide, low activities of this enzyme would thus reduce antioxidant potential.
We therefore conclude that the ability to detoxify free radicals within
our morbidly obese population is impaired, producing a potential for the
accumulation of oxidative damage. This may contribute to the development
of degenerative diseases often associated with obesity such as arthritis,
diabetes, and artherosclerosis.
5.
NITRIC OXIDE SYNTHASE (NOS) ACTIVITY
IN THE RED BLOOD CELL: IS IT POSSIBLE? Kevin Ford1 and Ellen S. Kang2,
1Christian Brothers Univ. Memphis, TN; 2Dept. of Medicine, Univ. of Tennessee,
Memphis, TN.
Nitric oxide (NO) is a powerful
mediator of physiological processes in the vascular system. It is
tightly regulated by rapid inactivation to NO2 upon interaction with reducing
substances such as the iron in hemoglobin and cysteine and tyrosine as
amino acids or peptide residues. Each of these mechanisms for inactivation
is present in the RBC. We studied whether the RBC had NOS activity
by a direct assay, unlike two reports of NOS activity in RBC by increase
in NO2 which could result from nitrosothiol groups released from peptide
residues. Normal human RBCs recovered after washing with Tris buffer
(pH 7.2) were sonicated at 4oC, spun at 15,000g for 30 min., aliquoted
and kept at -70oC until analysis. NOS activity was measured with
mM NADPH by recovery of 3H L-citrulline from 3H L-arginine as substrate.
Time and protein (Lowry) were varied with incubated at 37oC, detected by
beta counting of 3H L-citrulline. NOS activity was detected in the
supernatant fraction but not in the pellet fraction. Optimum conditions
for NOS were 50 ug protein using 0.5 mM 3H L-arginine incubated for 5 min.
at 37oC. These findings with a more direct assay support the
eariler reports that the RBC does express NOS activity which is limited
to the cytoplasmic fraction and is not expressed by the membrane.
We speculate that this capability gives the RBC a vital role in the regulation
of processes controlled by NO. Supported by: a grant from LeBonheur
Childern’s Hospital
6.
CARNITINE LEVELS IN RAT RED BLOOD
CELLS, WHITE BLOOD CELLS, AND BLOOD SERUM. N. Koenigsknecht1, M.
Volk2, M.S., and M. Banschbach3, Ph.D) 1Dept. Of Biology, Christian
Brothers Univ. Memphis, TN; 2,3 Dept of Microbiology and Biochemistry,
Oklahoma State Univ. College of Osteopathic Medicine, Tulsa, OK.
Carnitine is an essential carrier
molecule of fatty acids that plays a key role in the human body by serving
as an accessory for burning fat energy. When the levels of carnitine
are low, the body exclusively depends on glucose as the energy source.
Severe carnitine deficiency can result in muscular dysfunction with serious
clinical implications. The purpose of this study was to determine
if carnitine could be measured in either red blood cells or white blood
cells using a new coupled enzyme spectrophotometric assay that we developed.
Serum and washed red or white blood cell fractions were prepared from rat
blood. The spectrophotometric assay using alpha-ketoglutarate dehydrogenase,
carnitine acetyl transferase, and diaphorase was used to determine free
carnitine (in untreated samples) and total carnitine (in base hydrolyzed
samples). While carnitine was easily detected in serum, no carnitine
was detected in red or white blood cell extracts. If future experiments
to improve extraction of the carnitine from the red and white blood cells
do not yield satisfactory results, one of the more costly but more sensitive
carnitine assays will need to be used to assay these samples.
7.
THE DISLOCATED KNEE. Trent A.
Gullett, Dept. of Biology, Christian Brothers Univ., Memphis, TN; Fred
Azar, M. D., Campbell’s Clinic, Memphis, TN; Scott Sharp, M.D., Campbell’s
Clinic, Memphis, TN; Marc Mihalko, Univ. Tennessee, Memphis, TN.
Dislocation of the knee is a traumatic
injury that involves ligament damage. In this retrospective study,
the charts of 38 knee dislocation patients over the last twelve years (the
Med, Memphis TN) were reviewed. The purpose of this research was
to determine if one form of treatment (surgery and/or physical therapy)
was more beneficial to the healing of the knee than another type of treatment
(physical therapy without surgery). Background, associated injuries,
and treatment were recorded for each patient. This research revealed
two interesting aspects. The first was the comparison between associated
injuries (arterial and/or nerve damage) and the velocity of the knee dislocation
(high velocity or low velocity). There was a higher incidence of
associated injuries with low velocity dislocations as compared high velocity
injuries. Also, research revealed that the range of motion of patientís
knees that received surgery was less than those who did not receive surgery.
This study revealed that low velocity knee dislocations can be very traumatic,
and that a follow-up of at least two years is needed for determining the
health and the progress of a re-cooperating dislocated knee.
8.
DIFFERENTIAL DIAGNOSIS FOR PATIENTS
WITH PRE-SYNCOPE SYMPTOMS ((F. A. Hayes, H. Rashed)) Dept. of Biology,
Christian Brothers Univ. Memphis, TN; Dept. of Autonomic Function, Univ.
Tennessee, Memphis, TN. Syncope or fainting is a common clinical
disorder whose main etiology is deficient cerebral blood flow resulting
from peripheral circulatory failure. Using tilt table testing, a
non-invasive method, subjects with histories of frequent fainting and dizziness
were studied. Two other groups were also studied; those with pre-syncope
and age-matched control groups were compared. Because syncope is
mainly a peripheral autonomic dysfunction, monitoring brachial blood pressure
alone during tilt table testing was often insufficient in diagnosing syncope.
Ankle blood pressure, when expressed as the ankle/brachial ratio has been
shown helpful in the assessment of the peripheral circulatory dysfunction
during tilt table testing. When this ratio was used to investigate
patients during tilt table testing, significant differences were found
in the ankle/brachial ratios of control subjects, syncope patients, and
pre-syncope patients. Systolic blood pressure ratios of patients
with syncope and control patients were compared; they differed in both
supine and tilted positions. When the controls were compared to the
pre-syncope patients a significant difference was found in the systolic
ratio only in the tilted position. The observed results suggest that
using ankle blood pressure, in a ratio with brachial blood pressure, to
monitor the autonomically-controlled peripheral cardiovascular responses
to posture is a valuable method to diagnose, evaluate and predict peripheral
autonomic dysfunction in patients with syncope and pre-syncope.
9.
RELATIONSHIP OF ACOUSTICAL PROPERTIES
OF THE VOICE AND HEALTH STATUS IN OLDER ADULTS. Y.Q. Lin**, Veronica
F. Engle+, Barbara Fuller*, Marshall J. Graney+, Douglas Connor*, **Dept.
of Biology, Christian Brothers University, Memphis TN, + College of Nursing,
UT Memphis, and * University of Colorado.
The
purpose of this study was to identify the relationship between acoustical
properties of the voice and health status (HS) of older adults. Acoustical
properties of the voice (jitter, shimmer, tenseness) are non-invasive,
physiological measure of stress that are influenced by HS, but have not
been studied in older adults. Older adult volunteers from the community
(N = 28, 50% men) with a mean age of 73.46 years (SD= + 6.62years) and
average educatiion of 13.61 years (SD = + 3.44 years) were recruited from
a Senior Citizen Center. HS and demographic data were collected using a
questionnaire. Participants produced three sets of four phonations of the
vowel ‘a’ and ‘e’. A uniform five second segment of each vowel phonation
was digitized and processed using computerized speech laboratory (CSL)
and Horii computer programs. The mean of 12 samples for each subject were
calculated and used for statistical analysis. In the vowel ‘a’, jitter,
shimmer, and tenseness were significantly correlated with male gender,
while only jitter and shimmer were significantly correlated with age; and
no significant correlations were observed between HS and the voice acoustics.
For the vowel ‘e’ only shimmer was significantly correlated with male gender,
and only jitter was significantly correlated with smoking and surgery.
Results indicate that there is a differential effect of HS and demographic
characteristics of the participant on acoustical properties of the voice
for vowels ‘a’ and ‘e’ which should be considered when conducting future
research.
Supported by a grant from the University
of Tennessee, Memphis of College of Nursing.
10.
Mechanism of Potassium Chloride induced
release of arachidonic acid and contraction of bloodvessels: Selective
activation of lipoxygenase and inhibition of prostaglandin synthesis
Zachary Maxwell, Mubarack M. Muthalif,
Jason Harper, Nour Karzoun and Kafait U. Malik Dept. Biology, Christian
Brothers University, Memphis, TN 38104 and the Department of Pharmacology,
College of Medicine, The University of Tennessee , Memphis 38163.
This study was conducted to
elucidate the mechanism by which potassium chloride (KCl), which causes
depolarization and increases extracellular calcium (Ca2+) influx, promotes
arachidonic acid release for prostaglandin synthesis and their contribution
to vascular smooth muscle contraction. In cultured rabbit vascular
smooth muscle cells (VSMC), KCl (60 mM) increased the activity of Ca2+/calmodulin
dependent protein kinase II which was followed by an increase in mitogen
activated protein kinase activity, cytosolic phospholipase A2 activity,
and arachidonic acid release. However, KCl failed to increase prostaglandin
synthesis in VSMC or intact aortic rings. In both VSMC and aortic
rings, exogenous arachidonic acid was converted to prostaglandins, but
their production was inhibited during exposure to KCl. Interestingly,
in the presence of the lipoxygenase inhibitor, baicalein, KCl increased
prostaglandin production in both VSMC and aortic rings. KCl-induced
contraction of aortic rings was reduced by the prostaglandin endoperoxide
receptor antagonist, ifetroban. These data suggest that KCl promotes
arachidonic acid release by increasing cytosolic phospholipase A2
activity via activation of Ca2+/calmodulin dependent protein kinase II
and mitogen activated protein kinase. Moreover, the arachidonic acid
released by KCl is converted by lipoxygenase, and the products of lipoxygenase
inhibit production of prostaglandins and cause accumulation of prostaglandin
endoperoxides, which contribute to KCl induced contraction of rabbit aorta.
Supported by grants from the NIH (USPHS-19134)
and the American Heart Association.
11.
IMMUNOASSAYS OF GLYCOPHORIN A: AN
ERYTHROCYTE MEMBRANE PROTEIN. L. Gregory Meriwether1, Dennis Carrigan2,
and Douglas P. Blackall2, 1Christian Brothers Univ., Memphis, TN, &
Dept. Pathology, 2UT Memphis, Memphis, TN.
Glycophorin A is an erythrocyte
integral membrane protein which carries the human MN blood group antigens.
This protein serves as a receptor for several pathogens, including reovirus
and Plasmodium falciparum, the causative agent of malaria. Recombinant
glycophorin A was expressed in a variety of eukaryotic cell lines through
transfection techniques. Chinese hamster ovary (CHO) cells were mainly
utilized for this purpose, and stable CHO cell lines were established expressing
either the M or the N allele of glycophorin A. Eight glycophorin
A-specific monoclonal antibodies were assessed for their ability to bind
with either red blood cell or recombinant glycophorin A through immunoblotting,
immunofluorescence, and immunomagnetic bead agglutination. These
monoclonal antibodies included three specific for the M allele of glycophorin
A (6A7, M2A1, AO9), four specific for the N allele of glycophorin A (N61,
NN3, N92, AH7), and one MN nondiscriminatory antibody (10F7). Immunoblotting
revealed that six of the eight antibodies were capable of binding normal
red blood cell glycophorin A, while only two antibodies bound recombinant
glycophorin A. Similarly, by immunofluorescence, only three antibodies
recognized recombinant glycophorin A in stable CHO cells, but six antibodies
recognized the glycoprotein when expressed transiently. Three of
the antibodies conjugated to immunomagnetic beads agglutinated CHO cells
expressing recombinant glycophorin A, while the other five failed.
These results suggest a fundamental difference between red blood cell and
recombinant glycophorin A. Future studies will be directed to expressing
a recombinant glycophorin A molecule more similar to the red blood cell
membrane version.
Supported in part by: the National
Blood Foundation.
12. THE ROLE OF SERUM EOSINOPHILIC
CATIONIC PROTEIN (ECP IN EXERCISE-INDUCED ASTHMA (EIA). B. Myers,
K.V. Leeper, J. Soberman, T.T. Mastin, & P. Jordan. Dept.
of Biology, Christian Brothers Univ. Memphis, TN; Dept. of
Pulmonary and Critical Care Medicine, UT, Memphis, TN; Dept. of Cardiology,
Heart Station, UT, Memphis, TN.
Asthma is
known to be a disease characterized by chronic inflammation. One
of the many key cells involved in the inflammatory process in the lung
is the eosinophil. Eosinophils and their mediators, specifically
eosinophilic cationic protein (ECP), are potential markers of the severity
of the inflammatory response. The aim of this work was to ascertain
whether patients with exercise-induced asthma (EIA) demonstrate not only
an immediate increase in ECP, but also one that is sustained up to 30 minutes
after exercise is ceased. We studied five asthma patients and seven
healthy nonasthmatics (controls) which were age, race, and sex matched.
Three different blood samples from each subject were obtained, one prior
to exercise (baseline), the next immediately after exercising at 1/2 predicted
VO2 max for five minutes (5 minutes), and a third after exercise was stopped
and the participant had rested for 30 minutes (35 minutes). A total
of 36 samples were analyzed using a RIA kit. Comparison of the EIA
group and the non-EIA group were done with the Kruskall-Wallis test.
In comparison with studies by Venge et.al., their results showed elevated
ECP levels in asthmatics. Therefore, it might be possible to determine
the severity of a disease based on ECP levels. Supported by: Dept.
of Pulmonary & Critical and Dept. of Cardiology, Univ. of TN, Memphis,
TN.
13.
THYROID HORMONE REGULATION OF UCP-2
AND THE ob GENE IN RAT ADIPOSE TISSUE. Linda Nguyen1 and Suleiman
Bahouth2. 1Dept. of Biology, Christian Brothers University, Memphis, TN;
2Dept. of Pharmacology, UT, Memphis, TN.
UCP-2 is an uncoupling protein
that has recently been discovered in white adipose as well as in extra
adipose tissue. UCP-2 belongs to the family of uncoupling proteins
which function to burn excess fat and to generate heat from ATP.
Another gene product produced in white adipocytes is the ob gene product
leptin which serves as a satiety signal. Therefore, we sought to
determine if UCP-2 and leptin expression could be regulated by thyroid
hormone since thyroid hormone controls much of the bodyís metabolic
functions. Twenty-five (g samples of RNA were obtained from epididymal
adipose tissue of euthyroid, hypothyroid, and hyperthyroid rats.
These samples along with markers and blanks, were then subjected to electrophoresis,
transferred onto nylon membranes, and probed by Northern blotting with
32P-labeled probes for UCP-2 and leptin. The blots were counted to
determine the influence of altered thyroid status on UCP-2 and leptin mRNA
levels. The Packard InstaimagerTM revealed that the radioactive count
in UCP-2 from hyperthyroid rats was 7, 386 cpm, the euthyroid cpm was 4,235,
and the hypothyroid count was 4,003 cpm. On the other hand, the cpm
in leptin mRNA were highest in hypothyroid RNA and lowest in hyperthyroid
conditions. These radioactive counts were representative of the levels
of UCP-2 and lepting mRNAs seen in altered thyroid states. Consequently,
the hyperthyroid condition resulted in much more UCP-2 than either of the
other two conditions tested while the reverse was true for leptin.
Therefore, in hyperthyroidism there is a decrease in satiety signaling
(increased food consumption) and an increase in fat utilization for heat
production. Supported by NIH grant HL-48169.
14.
LOCALIZATION OF D2 DOPAMINE RECEPTORS
IN AVIAN STRIATUM USING IMMUNOHISTOCHEMICAL LABELING. Rodney A. Paullus,
Dept. of Biology, Christian Brothers University, Memphis, TN.
The purpose of this research
was to provide evidence as to the neuronal location of the D2 subfamily
of dopamine receptors in avian (specifically pigeon) striatal projection
neurons in comparison with their mammalian counterparts (specifically rat).
The basal ganglia regulate motor output via dopamine connections from the
substantia nigra to the striatum. Neurodegeneration of part of the
basal ganglia occurs in Parkinson’s and Huntington’s Disease and impairs
the ability of the basal ganglia to originate movement within the striatum.
An Avidin Biotin Complex method of immunohistochemical labeling with antigen
retrieval in a sodium citrate buffer was used to localize the D2 receptors.
Examination of the immunohistochemical labeling showed that the LPO and
PA striatal regions possessed the greatest amount of labeling for D2 receptors.
The labeling appeared characteristic in labeling of cholinergic neurons.
These results are consistent with previous localization studies for D1
receptors in avain striatum using the phosphoprotein DARPP-32 in showing
that the striatium is enriched in D1 and D2 dopamine receptors. This
study also suggests a possible antigenic difference between rat D2 and
pigeon D2 receptors.
15.
PHOTORECEPTOR DAMAGE IN CULTURED ADULT
RABBIT RETINAL EXPLANTS M. Svadlenka, D.A. Johnson, M.E.C. Fitzgerald,
M.M. Jablonski, S. Ashraf, T.O. Woods, Center for Vision Research, U.T.
Memphis.
The purpose was development
of an explant culture system for utilization in establishing an in vitro
model of photoreceptor damage. To this end, sections of cornea were co-cultured
with retinal explants and/or retinal pigmented epithelial cells (RPE).
Morphology of processed tissue was assessed by light microscopy.
Explant cultures, in the absence of RPE, were also subjected to complement-mediated
lysis of photoreceptors with B6-30N antiopsin. Retinas were examined
both light microscopically coupled with double labeling using indirect
immunolabeling with WGA(wheat germ agglutinin)/PNA (peanut lectin agglutinin)
followed by examination on the confocal microscope. WGA stains rods
green and PNA dyes cones red by binding to glycoproteins on the cell membranes.
The tissue co-cultures using cornea as a substrate did not remain in contact
with each other. The intrinsic qualities of the RPE were demonstrated
as it repeatedly formed a tight ball of cells away from the cornea substrate.
In retinas exposed to anti-opsin/complement, the structure of the photoreceptor
outer and inner segment complex was altered. Outer segments were
completely absent and the inner segments appeared to seep from the outer
nuclear layer. The lectin binding pattern was also modified and some
photoreceptor cell loss was noted. The cornea was determined a poor
substrate for RPE and retinal explant cultures. A model of photoreceptor
damage was successfully generated in a full thickness adult retinal explant.
This model will serve as a template in which potential photoreceptor rescue
factors can be tested. Funded by NIH grants EY01655, EY10853, Research
to Prevent Blindness.
16.
Up-regulation of Cadherins following
Central Nervous System injury in Rats
Félix Vázquez-Chona,1
and Eldon E. Geisert Jr.2 1Dept of Biology, Christian Brothers University,
Memphis TN, and 2Dept of Anatomy and Neurobiol., UT, Memphis, TN.
Following a lesion of the CNS,
astrocytes become reactive and in many cases form a scar. Defining
the molecular mechanisms governing glial scar formation is critical to
understanding how the CNS responds to injury. In the present study,
the role of cadherin at the glial scar was studied using immunohistochemistry
and western blotting. The expression of cadherin in astrocytes was
confirmed in cultures of rat astrocytes where it was expressed at regions
of cell-cell contact. Cadherin was consistently upregulated at the
site of gliosis following a stab wound in the CNS of the adult rat.
A quantitative analysis from injured and non-injured cortex revealed a
threefold increase of a cadherin, at 135 kDa band, in the injured tissue.
The location of this band is consistent with the electrophoretic mobility
of N-cadherin. Due to its crucial role in the intercellular adhesion
of most cell types, the high levels of cadherin at the site of CNS injury
indicate that cadherin may play a role in the response of astrocytes to
injury and in the formation and maintenance of the glial scar.
Supported by: University of
Tennessee Health Science Center.
17.
THE EFFECTS OF MANUAL LYMPHATIC STIMULATION
IN WOMEN SUFFERING FROM SECONDARY LYMPHEDEMA.
Lyndsay Woodward, Christian Brothers
University; Cathy Sanford, PT, Laurel Means, PT, Kris Valentine, PT, Tammy
Gibson, OT, Huntsville Hospital East, Huntsville, AL
Secondary lymphedema is a disease
that occurs due to some kind of external conditions, usually a result of
surgery that occurred in surrounding areas to lymphatic tissue. Patients
suffering from breast cancer are at high risk for lymphedema. These
studies were conducted on a cohort of twenty patients, female, suffering
from secondary lymphedema subsequent to breast cancer surgery. Manual
lymph drainage (MLD) is the main technique used for the treatment of this
disease. The treatment consisted of outpatients undergoing a series
of exercises and massages, in order to release some of the excess fluid
and proteins from the affected extremity. Measurements are taken
on both the affected and unaffected extremities at 5-cm increments.
The first 4-6 weeks, therapy was received three times a week. Once
positive results are seen, follow-up therapy is performed at 1 month, 3
months, 6 months and 12 months. The 20 patients were subdivided into
3 groups: 0-23 months, 24-59 months and 60-120 months, based on the onset
of lymphedema. Based on our results the percent edema was reduced
the most (89%) in patients who obtained treatment within two years of the
onset or in individuals that have been afflicted with the disease for at
least six years (79%) prior to the initiation of therapy. The least
percent of improvement (34%) was obtained from the group in which therapy
was initiated 3-5 years from the onset of the disease.
[end] |
Titles
CBU Biology Student Research Papers ~ TAS 1998