The anterior surface of the (left) outer ear cartilage and outer ear

muscles.
Translated by: Ronald A. Bergman, PhD and Adel K. Afifi, MD, MS
Peer Review Status: Internally Peer Reviewed

a) Helix.
b) Spina helices.
c) Cruraanthelicis.
d) Crus superiusanthelicis.
e) Crus inferiusanthelicis.
f) Fossa triangularis (s. fossa innominata).
g) Scapha (s. fossa navicularis).
h) Tragus.
i) Antitragus.
k) Incisuraintertragica (s. incisuraauriculae).
l) m. Concha auris.
m) External auditory meatus.
n) m. Auricularis superior (s. m. attolens).
o) m. Auricularis anterior (s. m. attrahans).
p) m. Auricularis posterior s. m. retrahentes).
q) m. Helicis major.
r) m. Helicis minor.
s) m. Tragicus.
t) m. Antitragicus.

http://www.anatomyatlases.org/atlasofanatomy/plate31/01antouterear.shtml

Figure: Lipid Rafts enriched in SM and Cholesterol

(screen capture from: http://multimedia.mcb.harvard.edu/anim_innerlife.html )

Lipid Conformational Transitions

If a liposome preparation is placed in a sensitive calorimeter and the temperature slowly increased, it
is observed that the liposome preparation absorbs a significant amount of heat at a temperature
characteristic of the PL which compose the liposome. This is analogous to what would happen if
solid water was heated. At the melting point of water, an increment of heat is required, the heat of
fusion, to break H-bonds and cause melting. Likewise the heat of vaporization is measured when Hbonds are broken on the liquid-gas transition. These transition are associated with non-covalent
processes, namely, breaking H-bonds. Graphs of heat absorbed (Q) as a function of temperature, or
heat absorbed/T (i.e. the heat capacity) vs temperature are shown below for the melting and
evaporation of water, and for liposome transitions.

http://employees.csbsju.edu/hjakubowski/classes/ch331/lipidstruct/oldynamicves.ht
ml

Background
Dermatitis herpetiformis (DH) is an autoimmune blistering disorder associated with a gluten-sensitive
enteropathy (GSE). The disease was described and named in 1884 by Dr. Louis Duhring at the University of
Pennsylvania.1Dermatitis herpetiformis is characterized by grouped excoriations; erythematous, urticarial
plaques; and papules with vesicles. The classic location for dermatitis herpetiformis lesions is on the extensor
surfaces of the elbows, knees, buttocks, and back. Dermatitis herpetiformis is exquisitely pruritic, and the
vesicles are often excoriated to erosions by the time of physical examination, as shown in the image below.

Classic vesicles of dermatitis herpetiformis.

Diagnosis requires direct immunofluorescence of a skin biopsy specimen showing deposition of

immunoglobulin A (IgA) in a granular pattern in the upper papillary dermis. Although most patients are
asymptomatic, greater than 90% have an associated gluten-sensitive enteropathy upon endoscopic
examination. Among patients with celiac disease, 15-25% develop dermatitis herpetiformis. The mainstays of
treatment are dapsone and a gluten-free diet.

http://emedicine.medscape.com/article/1062640-overview

Neural Tube Development:

Formation and Closure (Page 1 of 4)

16
20
22 Days 24 Days
Days Days
Prior to implantation early in the 2nd week the inner cell mass converts to an epiblast
(primitive ectoderm) and a hypoblast (primitive endoderm). Beginning at the third week,
gastrulation begins and mesoderm appears (also originating from epiblast). Gastrulation
begins with the formation of the primitive streak at the posterior (caudal) end of the
embryo; the streak is a linear thickening on the dorsal surface of the epiblast in which cells
of the epiblast form endoderm and mesoderm. A collection of cells at the end of the
primitive streak is the primitive node (Hensen's node) - epiblastic cells migrate anteriorly
through the node to become the longitudinally running cellular rod called the notochord.

Under the influence of the underlying is seen lying notochord, which develops from the axial
mesoderm, the dorsal ectodermal surface of the early embryo thickens and elongates to
form neural plate. Subsequent changes convert the plate into a neural tube which will give
rise to the CNS.

http://isc.temple.edu/neuroanatomy/lab/embryo_new/nt/1/

Introduction
Over the past 30 years, the methods available for the removal or improvement of acne scars and for the
correction of wrinkle lines increased exponentially with the advent of new skin filler substances, improved

techniques for elevating existing scars, and technology for abrading and resurfacing facial contours. Seemingly
every month, a new and improved filling agent or laser, which will be the best of all available methods,
becomes available. In the midst of these technological breakthroughs, the basic mechanisms remain the same.
Three categories of techniques are presently available to improve acne scars: (1) scar removal and revision;
(2) filling depressed scars; and (3) contouring the surface of scars.
Before and after images are below.

Photograph before collagen injection.

Photograph after collagen injection.

http://emedicine.medscape.com/article/1271282-overview

Oesophagus, human - H&E

The oesophagus is lined by a
stratified squamous epithelium
consisting of many cell layers.
Basal cells often form a well
defined layer at the border of the
epithelium to the underlying
connective tissue. The underlying
connective tissue forms fingerlike extensions towards the lumen
of the oesophagus, which are
called papillae. The border
between epithelium and
connective tissue may appear
quite irregular because of the
papillae. This irregular border
aids in anchoring of the
epithelium to the connective
tissue. If these extensions are not
cut exactly along their long axis,
they may look like isolated small
islands of connective tissue and
blood vessels within the
epithelium.
Draw the stratified squamous
epithelium of the oesophagus and
label your drawing. Try to draw a
little schematic illustration which
shows how the plane of section
would effect the appearance of the

connective tissue extensions.

http://www.lab.anhb.uwa.edu.au/mb140/

On an electrocardiogram (ECG), the PR interval is defined as the time interval between the initial deflection of
the P wave to the start of the QRS complex. Normally, this interval should be between 120 and 200 msec. Firstdegree heart block, or first-degree atrioventricular (AV) block, is defined as prolongation of the PR interval on
the ECG to more than 200 msec.1First-degree heart block is considered "marked" when the PR exceeds 300
msec.2While the conduction is slowed, there are no missed beats. ECG of a patient with first-degree heart block
is shown below.

ECG in a patient with first-degree heart block.

http://emedicine.medscape.com/article/758322-overview

an adenovirus

Genus Aviadenovirus
fowl
adenovirus 1

Image reconstruction reveals the complex

molecular organization of adenovirus

avian
adenovirus

From Milan Nermut from the UK's National

Institute for Biological Standards and
Control. The sample was freeze-dried and
shadowed with Pt/C.

animal
adenovirus

From Stewart McNulty at Veterinary

Sciences, Queen's University, Belfast.

Egg Drop
Syndrome
Virus

http://www.virology.net/Big_Virology/BVDNAadeno.html

Choroidal melanoma is the most common primary malignant intraocular tumor and the second most common
type of primary malignant melanoma in the body. It is nevertheless an infrequently found tumor.

Color photograph of a dome-shaped choroidal melanoma.

Choroidal melanoma is a subtype of uveal melanoma. Uveal melanomas can be classified in anterior uveal
melanomas, when the tumor arises in the iris, and in posterior uveal melanomas, when it arises in either the
choroid or the ciliary body. Intraocular melanomas simultaneously can involve more than one uveal structure.
The ocular tissue where these tumors arise, the uvea, is a densely pigmented layer that forms part of the wall
of the eye. The uvea is subdivided into iris, ciliary body, and choroid. The choroid underlies the retina and its
pigment epithelium throughout the ocular fundus. The main function of the uvea is to provide oxygen and other
nourishment to the highly metabolically demanding retinal photoreceptors. It is primarily a vascular tissue, with
fenestrated capillaries and stroma containing melanocytes.
http://emedicine.medscape.com/article/1190564-overview

Superficial bursitis should be suspected in patients with swelling or signs of inflammation over bursae. Deep bursitis is suspected in patients with
unexplained pain worsened by motion in a location compatible with bursitis. Usually, bursitis can be diagnosed clinically. Ultrasonography or MRI can
help confirm the diagnosis when deep bursae are not readily accessible for inspection, palpation, or aspiration. These tests are done to confirm or
exclude a suspected diagnosis. These imaging techniques increase the accuracy of identifying the involved structures.

If bursal swelling is particularly painful, red, or warm or if the olecranon or prepatellar bursa is affected, infection and crystal-induced disease should be
excluded by bursal aspiration. After a local anesthetic is injected, fluid is withdrawn from the bursa using sterile techniques; analysis includes cell count,
Gram stain and culture, and microscopic search for crystals. Gram stain, although helpful, may not be specific, and WBC counts in infected bursae are
usually lower than those in septic joints. Urate crystals are easily seen with polarized light, but the apatite crystals typical of calcific tendinitis appear
only as shiny chunks that are not birefringent. X-rays should be taken if bursitis is persistent or if calcification is suspected.

Prepatellar Bursitis

Acute bursitis should be distinguished from hemorrhage into a bursa, which can cause similar manifestations because blood is inflammatory. Fluid in
traumatic bursitis is serosanguinous. Cellulitis can cause signs of inflammation but does not normally cause bursal effusion; cellulitis overlying the
bursa is a relative contraindication to bursal puncture through the cellulitis, but if septic bursitis is strongly suspected, aspiration must occasionally be
done.

http://www.merck.com/mmpe/sec04/ch040/ch040b.html

Metastatic Adenocarcinoma
The gray white nodules which obliterate
normal architecture are metastatic
carcinoma.
Yellow tissue is normal cortex; brown gray
normal medulla.
(Description By:Melinda Sanders, M.D. )
(Image Contrib. by: UCHC )

Metastatic Adenocarcinoma
Click on Image to Enlarge it

Metastatic Adenocarcinoma
Etiology
Unknown.
Pathogenesis
Arrive via systemic circulation
Unknown why lung carcinoma has predilection for adrenals,
Epidemiology
Up to 25% of patients with metastatic carcinomas
Lung and breast predominate
Also GI tract, thyroid, kidney, other adrenal
General Gross Description
May be cortical or medullary, tan with or without hemorrhage or necrosis.
General Microscopic Description
Resembles primary site

Clinical Correlation
Requires chemotherapy to treat.
May be associated with mild adrenal failure.
References
Diagnostic Surgical Pathology, 2d edition, Sternberg SS (ed).
Philadelphia: Lippincott-Raven,1996, pp. 585-6.
Metastatic Adenocarcinoma
http://radiology.uchc.edu/eAtlas/Endo/299.htm