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

Translated by: Ronald A. Bergman, PhD and Adel K. Afifi, MD, MSPeer 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 H-

bonds 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.html

BackgroundDermatitis 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 Days

20 Days 22 Days 24 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&EThe 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 finger-like 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. First-degree 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 Image reconstruction reveals the complex molecular organization of adenovirus

Genus Aviadenovirus

fowl adenovirus 1

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 Click on Image to Enlarge it

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 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 adrenalGeneral Gross Description

• May be cortical or medullary, tan with or without hemorrhage or necrosis.General Microscopic Description

• Resembles primary siteClinical 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