The Sample Scientific Poster - Using Microsoft Office Power Point Template

1
The Sample Scientific Poster - Using Microsoft
Office Power Point Template
T. Farra1, M. Jacisin21Brigham and Womens
Hospital, 2New England College of Optometry,
Boston, MA
Results - cont
Methods
Introduction
Results - cont

• The sample was selected from patients aged 40 and
  older who presented to the Division of
  Ophthalmology at Brigham and Womens Hospital
  from July 1998 to January 1999. Patients were
  required to have electronic medical records
  dating back to at least 1996.
• All patients were examined by a single observer.
• Each patient was questioned about their past
  ocular, medical and surgical history, as well as
  current use of medications. An extensive history
  of past and present steroid use was obtained
  which included name of the steroid, dose,
  frequency of administration, duration, and time
  period of use.
• Subsequently, all patients underwent a complete
  eye examination.
• Any patient suspected of having glaucomatous
  optic neuropathy based on the appearance of the
  optic nerve and nerve fiber layer underwent
  visual field testing with either the Humphrey or
  Goldmann perimeters. Patients with unreliable
  visual fields or no reproducible visual field
  loss were excluded.
• Ophthalmic information regarding ocular
  conditions, surgeries and maximum IOP was
  corroborated from the patients eye records.
• Non-ophthalmic information was confirmed by a
  review of the patients electronic medical
  record. These records contained information
  regarding the patients medical conditions, as
  well as the date of first and filled prescription
  for all medications.
• Steroid exposure was defined as a dichotomous
  variable in three ways relative to July 1, 1997
  (1 year prior to the onset of the study).
• Steroid use for a period of 1 month at any given
  time in the past.
• Steroid use prior to July 1, 1997 for at least 1
  month.
• Steroid use after July 1, 1997 for at least 1
  month.
• The Odds ratio for steroid use was calculated
  using logistic regression analysis for each
  definition of steroid use. The results were
  adjusted for age, race, gender, hypertension,
  diabetes and diseases that were indications for
  steroid use.

• The NTG group used significantly less steroids
  then the control group for all definitions of
  steroid exposure. Fig. 1 and 2 show the
  proportion of people taking steroids in the NTG
  and Control group for total steroid use and
  steroid use excluding anterior segment surgery
  respectively. indicates a statistically
  significant difference between the NTG and
  Control groups using ?2.

Table 2 Conditions/Procedures Included in the
Allergic, Inflammatory and Ant Seg surg
Categories.
Retinal ganglion cells (RGC) die by apoptosis in
both high tension1 and low tension2 glaucoma.
Ischemia and neuronal compression may deprive the
RGCs of essential trophic factors necessary for
their survival3. When apoptosis occurs, the RGC
cytoplasmic volume decreases and the cell
membrane ruptures, while the nucleus condenses4.
RGC membrane lysis is mediated by phospholipases
and oxidative enzymes. Leaky RGC may release
other toxic substances such as excitatory amino
acids, which further damages neighboring cells3.
Glutamate, an excitatory amino acid, has been
found in elevated concentrations in the vitreous
body of glaucomatous eyes5. Steroids are known
to be nonspecific blockers of cell membrane
lipases6 which may inhibit apoptosis in this
setting. Furthermore, certain glucocorticoids
are thought to intercalate into the cell membrane
and decrease neuronal and vascular membrane
fluidity by inhibiting oxygen free
radical-induced lipid peroxidation7. Studies have
shown that RGC survival in vitro is dependent on
the addition of steroids to the culture8.
Finally there is data suggesting an immune
deviation in patients with NTG2 where serum
antibodies directed to retinal elements have been
found. Exogenous steroids could prevent NTG by
nonspecifically blunting this aberrant response.
Fig 2 Steroid Use excluding ocular surgery in
NTG and Control groups

• Fig. 6 shows the proportion of different types of
  steroids used for systemic conditions by patients
  in the NTG and Control groups respectively. Table
  3 indicates the specific steroids included in the
  Inhaler, Topical and Oral categories.

Fig 1 Steroid Use in NTG and Control groups
Table 3 Specific steroids included in the
Inhaler, Topical and Oral categories.
Fig 6 Type of Steroids Used for systemic
conditions in NTG and Control groups.
Control
NTG

• Logistic regression predicted the Odds ratio to
  be 0.517 Model A (p0.07), 0.408 Model B
  (p0.02), and 0.81 Model C (pgt0.05) for the
  development of NTG. The Odds ratios are plotted
  in Fig. 3 for the 3 Models. Models A, B, and C
  are described in Table 2.

Discussion

• The speculation that steroids may prevent
  apoptosis is plausible based on their ability to
  inhibit cell membrane lysis mediated by
  phospholipases and oxidative enzymes. In our
  study, univariate analysis suggests that steroid
  use was associated with a reduced odds of having
  NTG.
• Problems regarding confounding by indication make
  the univariate result of this study
  controversial. Larger scale prevalence studies
  confirming our univariate finding are necessary.
  In these studies, very careful estimate of
  steroid exposure would be indicated.

Purpose

• To study the association of steroid use and
  prevalence of NTG in a clinic-based population.

Sample
Conclusions
Fig 6 Type of Steroids Used for systemic
conditions in NTG and Control groups.
Fig 6 Type of Steroids Used for systemic
conditions in NTG and Control groups.

• The sample consisted of 154 patients
• 72 NTG (mean age 69.0 ? 10 44-85 25M, 47F)
• 82 controls (mean age 64.8 ? 11 44-86 31M, 51F)
• Definition of NTG Cases
• Patients with ONH or NFL appearance consistent
  with glaucoma.
• Maximum IOP less then 21mmHg.
• At least two reliable visual field examinations
  with reproducible defects consistent with the
  nerve fiber layer pathology.
• No evidence of exfoliation or trauma on slit lamp
  examination and no evidence of an occludable
  angle or angle recession on gonioscopy.
• Patients with pre-existing iridotomies were
  excluded form the study.
• Definition of Controls
• No evidence of glaucomatous optic neuropathy
• cup/disc ratios lt 0.6 OU
• cup/disc asymmetry lt 0.2
• unremarkable red-free ophthalmoscopic
  examinations.
• No family history of glaucoma.
• Maximum IOP less then 21mmHg.
• Controls did not undergo visual field testing.

Results

• Univariate logistic regression analysis
  demonstrates a reduced odds of NTG in steroid
  users.
• Controlling for age strengthens this association.
  Controlling by indication for steroid use
  produces a result that is not statistically
  significant.
• Larger numbers of cases and controls will be
  necessary to demonstrate the true relation
  between steroid use and NTG.

• Cataract extraction was significantly higher in
  the Control group compared to the NTG group. No
  difference was found in any systemic conditions
  between cases and controls. Fig. 4 and 5 show the
  breakdown of conditions requiring steroids in the
  NTG and Control group for systemic and ant. seg.
  ocular surgery respectively. Table 2 shows the
  conditions/procedures included in the Allergic,
  Inflammatory and Total Ant. Seg. surgery
  categories. indicates a statistically
  significant difference between the NTG and
  control groups using ?2.

• The demographic and clinical characteristics of
  NTG and Control groups is described in Table 1.

Table 1 Demographic and Clinical Characteristics
of NTG and Control groups.
References
Fig 5 Breakdown of Ant. Seg. surgeries requiring
steroids for NTG and Control groups.
Fig 4 Breakdown of systemic conditions requiring
steroids for NTG and Control groups.

• Quigley HA, Nickells RW, Kerrigan LA, Pease ME,
  Thibault DJ, Zack DJ. Retinal ganglion cell death
  in experimental glaucoma and after axotomy occurs
  by apoptosis. Invest Ophthalmol Vis Sci
  199536774-86.
• Wax MB, Tezel G, Edward PD. Clinical and ocular
  histopathological findings in a patient with
  normal-pressure glaucoma. Arch Ophthalmol 1998
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• Chew SJ, Ritch R. Neuroprotection the next
  breakthrough in glaucoma? Proceedings of the
  Third Annual Optic Nerve Rescue and Restoration
  Think Tank. J Glaucoma 1997 6263-6.
• Spaeth GL. Glaucoma, apoptosis, death, and life.
  Acta Ophthalmol Scand Suppl 1998 2279-15.
• Dreyer EB, Zurakowski D, Schumer RA, Podos SM,
  Lipton SA. Elevated glutamate levels in the
  vitreous body of humans and monkeys with
  glaucoma. Arch Ophthalmol 1996 114299-305.
• Lee HM, Weinstein JN, Meller ST, Hayashi N,
  Spratt KF, Gebhart GF. The role of steroids and
  their effects on phospholipase A2 in an animal
  model of radiculopathy. Spine 1998
  23(11)1191-6.
• Hall ED. Neuroprotective actions of
  glucocorticoid and nonglucocorticoid steroids in
  acute neuronal injury. Cell Mol Neurobiol 1993
  13415-32.
• Lindsey JD, Weinreb RN. Survival and
  differentiation of purified retinal ganglion
  cells in a chemically defined microenvironment.
  Invest Ophthalmol Vis Sci 1994 353640-8.45

? indicates pgt0.05