Please don't forget the Grand Opening of the Fairfield County Real Estate Investors Association. The Reia meeting will be held at Liedles Caterers on the 3rd Wednesday of each month. This is the ultimate investors meet up.

Anyone who is anyone wants to be at our reia meeting. Our guest speaker, Attorney Gary Seymour, will be discussing how to legally stop a foreclosure. Real estate agents and mortgage brokers should want to be in the front row for this one.

We will have a cash bar on site so you can unwind and relax after a long days work. We look forward to hosting your meetings in the future.

If you know anyone who may be available, please let them know that they no longer have to drive to Cromwell, CT to go to a REIA. I know that has been a problem for many people who live in lower and middle fairfield county.

We are putting our list together for future speakers as we speak. Come on out and have a great time. Lets make some money in this great real estate market for buyers.

Until next time

Keep God 1st, Invest in People

CL

IMAGING IN CEREBRAL VASCULAR PATHOLOGIES:

EVOLUTION OF INTRACRANIAL HEMATOMA

1. Immediate

- liquid with 95% O2 saturated Hb, T2 hyper, T1 iso within seconds platelets thrombi form & cells aggregate

 2. Hyper acute stage -

4-6 hrs, fluid serum begins to disperse

Protein clot retracts, red cells become spherical, oxy

Early peripheral edema begins, T2 iso, T1 iso

OxyHb is diamagnetic with no unpaired electrons,

CT - isodense for 1-3hrs, then becomes dense, 60-100HU
3. Acute stage

- 7-72 hrs, red cells begin to compact, deoxyhb

Central portion T2 hypo, T1 iso

DeoxyHb is paramagnetic with 4 unpaired electrons, T2 shortening

Sheilded from H2O by globin, prevents T1 shortening

No proton-electron relaxation enhancement can occur

Edema pronounced in periphery

Dense on CT, window width of 150-250 best

4. Subacute stage -

1-4 wks, methemoglobin starts day 4

Begins at periphery & progresses towards anoxic center

Cells begin to lyse at 1 week releasing metHb, decrease in edema

Perivascular inflammatory reaction begins with macrophage at periphery

Ring Enhancement caused by this process

T1 BRIGHT due to 5 unpaired electrons exposed by globin change

Proton-electron relaxation enhancement does occur

Periphery affected 1st, middle remains iso initially

T2 HYPO early when methemoglobin still in RBC

BRIGHT once the cell breaks down & Hb diluted in water

CT attenuation decreases approx 1.5HU per day

CT is NOT an accurate indicator of age, due to variable Hb etc

5. Early Chronic stage

- >4wks, edema & inflammatory reaction subside

Vascular proliferation encroaches on haematoma decreasing its size

Dilute uniform pool of extracellular metHb with vascular walls

Macrophage contain ferritin & hemosiderin at periphery

T2 hypo due to strong magnetic susceptibility

T1 iso due to fact that hemosiderin is water insoluble

Hypodense on CT unless rebleeding has occurred

6. Late Chronic stage -

cystic or collapsed with dense capsule

Vascular proliferation gradually forms fibrotic matrix with macrophage

Infants may resolve completely

Ferritin laden scar persists for years in adults

10% calc with residual hypodense focus in 40%

Gradient echo is helpful in detecting Haem in low field MRI's

OVERVIEW OF HEMORRHAGE CAUSES

Underlying cause often hidden by the bleed. Intraventricular extension associated with 10% mortality

1. Neonatal Hemorrhage - germinal matrix hemorrhage secondary to prematurity

thin walled, proliferating vessels in subependyma of lateral caudothalamic groove

involution occurs at 34 wks when all cells have migrated

No hemorrhage in utero or beyond first 28 days post birth

Grade I - Hemorrhage confined to germinal matrix, can be bilateral

Grade II - rupture into normal size ventricles

Grade III - intraventricular hemorrhage with Hydrocephalus

Grade IV - extension to adjacent hemispheric white matter

Can be seen by US in acute & subacute, lucent if chronic

Term Infants - Hemorrhage usually secondary to trauma, subdural mostly

Asphyxia & infarction most commonly in non-traumatic cases

Posterolateral lentiform nuclei & ventral thalamus most susceptible

2. Hypertension – Most common cause of nontraumatic bleed in adult

Lenticulostriate & Pontine vasculatures mostly involved, penetrating branches of MCA

Usually spontaneous in elderly patients, basal ganglia mostly

Vessels often abnormal, ruptured microanuerysms etc

50% have hemorrhage dissection into ventricles, poor prognosis

Lobar white matter hemorrhage in 20%, cerebellum 10%, midbrain & brainstem rare

Originates along perforating branches near dentate nuclei

Active bleeding usually lasts <1hr

Edema progresses for 24-48hrs, 25% die in this period

Hypertensive Encephalopathy - occurs secondary to elevated BP

Toxemia (Most common) - autoregulation overwhelmed especially in posterior aspect

Overdistention of arteriole leads to BBB breakdown

Reversible vasogenic edema results, frank hemorrhage rare

Cortical petechia & subcortical hemorrhage possible, especially in occipital regions

Increased T2 in external capsule & basal ganglia more common

Chronic renal Diseases, TTP, & Hemolytic-Uremic syndrome other causes

3. Hemorrhagic Infarction

Arterial Infarction - hemorrhage when endothelium reperfused

Occurs in 50%, but only seen in 10%, sensitivity: MRI>CT

Cortex & basal ganglia from MCA distribution most commonly, 24-48hrs later

Pseudolaminar Cortical Necrosis - generalized hypoxia

Middle layers usually effected, gyriform hemorrhage

Nonhemorrhagic ischemic changes can occur, gyri calcification possible

Venous Infarction - usually associated with dural sinus thrombosis

Dura around sinus will enhance, clot stays hypodense (empty delta sign)

More likely to effect white matter than cortex

4. Aneurysms - 90% of nontraumatic subarachnoid hemorrhage

Headache common presenting sign for aneurysm, CT best for acute SAH

Blood usually fills ambient cisterns & sylvian first

90% of blood cleared from CSF in 1wk

MRI better for subacute or chronic SAH, dirty CSF

Superficial siderosis - hemosiderin deposit on meninges

Cerebellum brainstem & cranial nerves also coated - neurological dysfunction

Giant aneurysms >2.5cm often have intramural hemorrhage

most from carotid, cavernous portion most common, all ages

75% have calc if thrombosed, none otherwise

Charcot-Bushard Aneurysm - secondary to HTN

5. Vascular Malformations -

AVM & Cavernous Angioma commonly

Most bleed into parenchyma rather than subarachnoid space

Arteriovenous Malformation - pial, dural or mixed, No cap bed

Pial AVM's - hemorrhage @ 2% per year, often in previously normal young pts

70% bleed by 1st exam, repeated hemorrhage can simulate neoplasm

Central nidus with gliosis & encephalomalacia

Dural AVM's - no central nidus, SAH or subdural

hemorrhage rare unless drainage through cortical veins

Cavernous Angioma - bleed @ .5% per year, freq repeated bleeds

Popcorn like with mixed signal foci & hemosiderin ring

Venous Angiomas - bleed rare, similar hematoma of other malformations

Medusa like collection of dilated medullary veins

Capillary Telangiectasias - usually small & clinically silent

may see multiple small foci of hemosiderin on T2

INTRACRANIAL ANEURYSMS & VASCULAR MALFORMATIONS

Charcot-Bushard Aneurysm - secondary to Hypertension

20% multiple, higher incidence in females.

Look for familial causes such as Polycystic Kid Disease

SACCULAR ANEURYSMS

Berrylike out pouching from arterial bifurcation

Include intima & adventitia, media ends with normal vessel

1. Etiology - hemodynamic induced injury, abnormal shear forces most commonly

Trauma, infection, tumor, drug abuse & AV malformations

Berry Aneurysms - associated with polycystic kidney Diseases & aortic coarctation

2. Incidence - 1% of angios & 5% of postmortems

Multiple in 20%, esp in females & polycystic kidney Diseases

Bilateral in 20%, esp at cavernous sinus, Pcom & MCA trifurcation

Occur age 40-60 unless traumatic or mycotic,

3. Associated Conditions - occur at anomalous vessels & AVM

Inc pressure ie HTN & aortic coarctation

Systemic Diseases - Marfan’s, fibromuscular dysplasia, polycystic kidney diaeases

4. Location - 30% at anterior communicating, 30% at posterior communicating, 20% MCA origin

10% in post circulation especially basilar artery bifurcation

traumatic or mycotic occur anywhere

5. Clinical Presentation - asymptomatic until rupture or giant >2.5cm

1-2% risk of rupture per year, 3.5% risk of surg

No different risk with HTN, age, sex or multiplicity

All should be repaired if >3yr life expectancy

Subarachnoid Hem - clinical grade by Hunt & Hess scale I-V

Vasospasm most common cause of morbidity, 30% die

highest bleed rate in 1st 24hrs, 50% rebleed in 2wk

CT - shows SAH in >80% of ruptured aneurysms

Cavernous sinus aneurysms can compress Nerves III-VI

TIA, Seizures & embolic ischaemia less common

Giant Aneurysms - most from supraclinoid carotid, all ages

Fibrous vascular walls, rarely rupture, Symptoms secondary to mass effect

Partially Thrombosed Aneurysms - 75% have curvilinear calcification

CT most specific for these with target seen

NO calc if not thrombosed

D/D - Meningioma, both erode sella & lat sphenoid

aneurysm has no associated hyperostosis or atherosclerosis

6. Appearance of Saccular Type - catheter angiography definitive

asses for relation to vessel, adjacent branches & vasospasm

essential in assessment of nontraumatic SAH

Thrombosed aneurysm will have no finding, 15%

may see mass effect if large

irregularity or local vasospasm can indicate rupture

D/D vascular loops & infundibuli (embryonic funnel <2mm)

CT may show bone erosion in long standing case

Patent aneurysms enhance intensely w contrast

Location of SAH can be prognostic indicator

Ambient cisterns anterior to brainstem probably just venous rupture

No repeat angio needed

Suprasellar cistern to lateral sylvian fissure

more aneurysmal pattern, must do F/U angio

MRI dependent on pattern of flow, turbulence & clot

may have wall enhancement with gadodiamide, laminated with thrombosis

7. Traumatic Aneurysm -

nonpenetrating usually occur at skull base, or shear

hyperextention stretches ICA over lat C1

8. Mycotic Aneurysms - Secondary to infection of arterial wall, rare <10%

adventitia & muscularis disrupted, thoracic aorta commonly

Angio - occur dist to usual location, 2nd branch MCA commonly

most common cause of multiple MCA aneurysms

usually small, staph & strep most common, inc in child

bleed into parenchyma or SAH equal incidence

Medical Treatment usually sufficient to control, surgery if enlarge on angio

Mucor & Aspergilla invade direct from nasopharynx cause thrombosis & infarct more often than aneurysm

9. Oncotic Aneurysms - usually extra cranial, exsanguinate freq

tumor may implant or cause emboli, primary or metastatic

10. Flow-Related Aneurysms - seen with AVM's in 30%

distal ones most likely to hemorrhage

11. Vasculopathies - rare but seen with SLE, infarct & TIA commonly

Takayasu's Arteritis - 9:1 female, inflammation & stenosis most commonly

prox arch vessels, L subclavian commonly, often occludes

Fibromuscular Dysplasia - up to 50%, dissection & A-V fistula, 65% bilateral

Cocaine - 50% with CNS symptoms have SAH, may be secondary to HTN treatment

several drugs cause vasculitis .

FUSIFORM ANUERYSMS

Etiology - atherosclerosis, exaggerated arterial ectasia

media damaged, stretches & elongates, frequent mural thrombus

Vertebrobasilar Dolichoectasia - Common site, older patient

often thrombus producing brainstem infarcts

can also compress local stem causing nerve palsies

Imaging - enhances if patent, hyperintense if thrombosed

curvilinear calcification pathognomonic, may cause skull base erosion

DISSECTING ANEURYSMS

Etiology - intramural blood from tear in intima

may narrow or occlude lumen, may distend subadventitia

do not confuse with Pseudoaneurysm, a encapsulated hematoma

Presentation - usually extracranial unless severe trauma

Commonly in midcervical ICA & vertebral from C2 to skull base

Catheter angio remains procedure of choice for assesment

INTRACRANIAL VASCULAR MALFORMATIONS

1. Parenchymal AVM - congenital, dilated arteries & veins without capillary bed

98% solitary, multiple in Osler-Weber-Rendu & Wyburn-Mason

Incidence - 85% supratentorial, peak 20-40y, 25% children

Hemorrhage in 85% with 3% per year risk, seizure 25%, deficit 25%

Size not predictive, deeper & smaller ones bleed more

Parenchymal commonly, also common cause of SAH if

Vascular Steal - atrophy due to vasculopathy of feeding vessel

atrophic low density regions & hematoma with high density

Overlying meninges thick & hemosiderin stained

Angio - shows feeding arteries & tortuous veins

often wedge shaped, possible to appear Normal if thrombosed

GBM may simulate but usually has tissue between vessels

10% have aneurysms in feeding arteries, can bleed

Cryptic AVM's - not seen by angio, 10%

CT - often absent w/o contrast, 25% have mild curvilinear calcification

mixed increased & decreased density if seen, Mild mass effect possible

Enlarged post venous sinuses but not cavernous sinus

Calcification seen in

MRI - honeycomb of flow voids, increased signal if thrombosed

hemorrhage in different stages often present

No significant intervening brain tissue, D/D : GBM

TX - resection if unruptured, must be completely removed

Aneurysms must be treated separately, increased risk for bleed

2. Dural AVM's & Fistulae - form within a venous sinus

no discrete nidus, multiple microfistulae, occluding sinus frequent

Follow recanulation of thrombosed sinus, 10% of all AVM's

Transverse or Sigmoid sinus commonly, Bruits & headache most common

Cavernous sinus AVM - proptosis, retro orbital pain, proptosis

SAH common if reflux flow forced into cortical veins

Carotid-Cavernous fistula related, follow trauma

Occipital & Meningeal branch of ext carotid #1 feeders

CT often N, MRI may show dilated cortical veins

3. Mixed - 15%, if parenchymal AVM recruits arteries from dural supply

4. Capillary Telangiectasias - multiple nests of dilated capillaries

Common in pons & Cerebellum, usually incidental

Gliosis of adjacent brain & hemosiderin staining from hem possibly

Cavernous Angiomas assoc or simply the extreme form

Osler-Weber-Rendu - hereditary hemorrhagic Telangiectasias

25% have brain abnormalities, most are true AVM's

Visceral angio dysplasia with scalp & mucous membrane telangiectasia

2nd most common lesion to venous angioma at autopsy

Not visualized by angio, may present with epistaxis

CT may faintly enhance, faint on MRI

5. Cavernous Angiomas - Hemangioma or cavernoma

Circumscribed nodule of honeycomb sinusoidal vascular spaces

separated by fibrous bands but no intervening neural tissue

frequently MULTIPLE HEMATOMAS at different stages, reticulated core of vessels

Supratentorial 80% but can occur anywhere, 50% multiple

Most Common vascular lesion identified, 20-40y/o

Seizure, deficits & bleed most common presenting features

Angio does NOT visualize, possible faint blush in early venous

CT shows freq Calc, variable enhancement, can simulate neoplasm

MRI - popcorn like appearance on T2 due to multiple hem

multiple areas of signal drop-out due to hemosiderin

VENOUS MALFORMATIONS

1. Venous Angioma - dilated anomalous veins converge on central vein

Etiology - remnant embryonic venous system, usually solitary

assoc with migrational abnormalities & cavernous Angiomas in 30%

Asymptomatic, Hemorrhage very rare unless from associated cavernous angioma

CT - may show linear tuft of vessels post contrast

located in deep White Matter of cortex or Cerebellum, commonly adjacent to frontal horn

MRI - shows stellate tributary veins into prominent collector vein

gliosis or hemorrhage seen in only 15%

Angio - the only vascular malformation with a single draining vein

Medusa head appearance on venous phase of angio

2. Vein of Galen Aneurysm - enlargement of Galenic system

Secondary to arteriovenous fistulae from choroidal arteries

AVM in thalmus or midbrain can also cause this

Present at birth with high-out put cardiac failure, cranial bruit +

Macrocephaly with obstructive hydrocephalus, deficits & ocular symptoms

US shows bi-directional flow in vein of Galen

Angio demonstrates either choroidal artery or thalmoperforating feeder

dilation to venous varix with or without distal stenosis

if stenosed distally will often thrombose

CT - large enhancing midline mass posterior to 3rd ventricle

Hydrocephalus frequent but hemorrhage rare

enhancing serpentine vessels in thalamic region

3. Venous varix - assoc with several intracranial vascular abnormalities

Enlarged & thin veins resulting in SAH, hydrocephalus & increased ICP

Sinus Pericranii - venous haemangioma adherent to outer skull, deep to galea

supplied from intracranial sinus & blood returns to sinus

present with enlarging fluctuant soft tissue mass, enlarge with crying

often secondary to trauma, often resolved with prolonged compression

Frontal commonly, parietal next, most near sagittal sinus, can be very lateral

Skull Film - usually sharp margins, vascular honeycombs possible

CT - shows strong uniform enhancement

MRI - well delineated ovoid or fusiform areas variable signal

Venous Cavernoma - subcutaneous lesions of scalp

blood supply from external carotid, drain to external jugular

4. Orbital Venous Varix - rare vascular malformation in orbit

Causes intermittent proptosis & diplopia with valsalva & bending over

Disappear completely with axial views, use tourniquet on jugular vein

NEONATAL HEMORRAGE

Caudothalamic groove - between head of caudate & thalamus

both make up lateral wall of lateral ventricle, terminates in Monroe

Foramen of Monroe - divides frontal & body portions of ventricles

thalmus entirely posterior, caudate head anterior, choroid enters it

1. Subependymal Hemorrhage - preterm infants <32wks

Correlates with size of germinal matrix at birth, largest 24-32wks

involutes & is absent by 40wks, last in inferior lateral wall of frontal

lies inferior to ependyma, superior to head of caudate & anterior to thalmus

Usually occurs in first 3 days, always by 7-8 days

Grade 0 – Normal

Grade I - Subependymal alone

Grade II - intraventricular with no ventriculomegaly

Grade III - Hydrocephalus,

Grade IV - intraparenchymal

grade does not predict ultimate outcome, may progress

Serial studies required, only applies to germinal matrix hemorrhage

2. Parenchymal Hemorrhage - extends farther lateral than germinal matrix

can be "grade IV", but not all secondary to germinal matrix bleed

most extend from SHE (Subependymal haemorrhage) to frontal or parietal lobes

Hypoxia & Hypercapnia implicated as etiology

stress causes vessels to dilate & burst

Phase 1 - echogenic like SEH for 1-2wks

Phase 2 - central Hypoechoic, bright peripheral rim 2-4wks

Phase 3 - retracts & settles into dependent position

Phase 4 - necrosis & phagocytosis complete, encephalomalacia

Cerebellar hematoma best scaned in coronal behind ear

assoc with mortality of 50%.

3. Choroidal Hemorrhage - usually grade II or III

Second cause of intraventricular hemorrhage not caused by SEH

Difficult to discern from normal choroid on US

asym scanning can show marked asym in choroid size

isolated choroid hematoma simulates ventricular hematoma with no hydrocephalus

Myelomeningocele assoc with pedunculated choroid

CT more reliable than US for Dx

D/D - Choroid Papilloma, very rare, consider if CSF clear on tap

all assoc with hydrocephalus, enhance intensely on CT

HEMORRHAGIC NEOPLASMS & CYSTS

1. Malignancy Related Coagulopathy - esp with leukemia & chemotherapy

systemic neoplasms can be assoc with term coagulopathy

2. Intratumoral Hematomas - 10%, malignant , Astrocytoma’s are most common.

Neovascularity, central necrosis, plasminogen activators etc contribute

Heterogeneous, incomplete hemosiderin ring, edema persist

multiple lesions & min edema suggests nonneoplastic cause

Cysts & slow growing cystic neoplasm like cranio rarely bleed

Oligodendroglioma, neuroectodermal & teratoma hemorrhage frequently

Ependymoma & choroid tumors - frequent SAH & hemosiderosis

Pituitary Adenoma - may bleed more frequently than astrocytoma

Lymphoma rarely bleed unless with AIDS

Renal cell Ca, chorio Ca, melanoma, thyroid & lung mets, 15%

3. Nonneoplastic Hemorrhagic Cysts -rare, colloid cysts never bleed

Rathke cleft cysts & Arachnoid cysts more commonly bleed

Arachnoid cysts bleed secondary to trauma, bridging vessels rupture

sometimes assoc with subdural hematoma

MISCELLANEOUS CAUSES OF BENIGN INTRACRANIAL HEMORRHAGE

1. Amyloid Angiopathy – Most common cause of bleed in elderly patient with no HTN

nonbranching fibrillar protiens form beta-pleated sheets

Deposit is Cortical & leptomeningeal vessels

extend from small vessels to brain parenchyma

Contractile elements replaced by the crystals

Multiple hematomas frequent & occurs at cortico medullary junction

basal ganglia & brainstem not affected

2. Infection & vasculitis - rare, increased chance if immuncompromised

septic emboli - mycotic aneurysms & hemorrhagic infarct

10% of Infective endocarditis have SAH or parenchymal

Aspergillosis & other fungi directly invade vessel

Thrombosis, infarction & hem result

Herpes Simplex II - the only encephalitis assoc with hematoma

3. Recreational Drugs - 50% have preexisting AVM or aneurysm

Cocaine can induce an acute hypertensive episode, vasospasm

also enhances platelet aggregation, dural sinus thrombosis

amphetamine & PCP also associated with hemorrhage

endothelial damage & necrotizing vasculitis

4. Blood Dyscrasias & Coagulopathies - iatrogenic or acquired

Vit K deficiency, hepatocellular diseases, antibody against clot, DIC

Anticoagulants, thrombolytics, aspirin, Etoh abuse, chemo

15% of all intracranial hemorrhage on anticoagulants

Supratentorial, intraparenchymal bleeds most common

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L'Italia si conferma incapace di vincere in Bulgaria. A Sofia finisce 0-0 il match valevole per le qualificazioni ai Mondiali del 2010. Lippi sceglie Gilardino al posto di Toni e schiera dall'inizio il debuttante Pepe. I padroni di casa si affidano alla stella Berbatov, ma la partita non decolla. A metà ripresa il ct inserisce prima Perrotta e Giuseppe Rossi, poi Toni, ma il risultato non cambia. Italia sempre prima nel Gruppo 8, con 7 punti.

La prima e unica parata di Amelia è arrivata al 43esimo della ripresa. Quanto basta per dire che l'Italia è stata capace per 90 minuti di controllare la partita, senza però riuscire a trovare il modo di perforare il muro bulgaro. Bene Pepe e Dossena sulle fasce, meno brillante Di Natale. Ma nel complesso la manovra azzurra non ha prodotto reali pericoli alla porta di Ivankov. Giuseppe Rossi ci ha messo un pizzico di vivacità in più, anche se nel finale le occasioni migliori sono venute su conclusioni dalla distanza del solito De Rossi, già decisivo con la Georgia (che con Cipro non è andata oltre l'1-1). Mercoledì a Lecce arriva il Montenegro di Vucinic. Non ci sarà Luca Toni, che - già diffidato - s'è fatto ammonire a pochi minuti dal fischio finale.

Bulgaria : Ivankov 6, Milanov 6,5, Iliev 5, Tunchev 5,5, Wagner 5 (37' Ivanov 6), Dimitrov 6, St. Petrov 6,5, Yankov 5,5, M. Petrov 6,5 (90' Popov s.v.), Georgiev 6, Berbatov 6.

Italia : Amelia 6, Zambrotta 5,5, Cannavaro 6, Chiellini 6, Dossena 6,5, Gattuso 6,5, De Rossi 7, Montolivo 6(68' Perrotta 6); Pepe 7,5, Gilardino 6 (73' Toni 5,5), Di Natale 6 (68' Rossi 6,5).

MP3 File

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Jesus Was A Democrat by Everclear (Free mp3 download)

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In a vote of 4-3, the Connecticut Supreme Court ruled today that Civil Unions are not equal to Marriage. The court ruled that all families must have the right to Civil Marriage.

Please go to the link below for the actual rulling!!!

Link to ruling: http://www.jud.state.ct.us/external/supapp/Cases/AROcr/CR289/289CR152.pdf

I don't watch the news that much, but today I received several text messages and e-mails letting me know the Big Gay News, that I can get married in Connecticut now! The first text messages I got was from Matty in Texas and from Jaded City, luv him! I even got a text proposal from my virtual boyfriend Brad from the 773Podcast asking when we were getting hitched ;) I told him when he moves over to CT (which is now the third state in the US to grant equal rights to same-sex unions as men/women marriages.) Now all I need is to find a man first to marry... Hey guys! I'm single want to go on a date and if we find out we are Mr. Right for each other and decide to spend the rest of lives together, well we can now become official and equal by CT law :)

Now that the gays can get married it has inspired many people from other states to make it possible in their state. See prthecrazyone's reaction below:

To continue the fight for equal marriage rights for same-sex couples in NY Click Out what you can do at:

www.MarriageEqualityNY.org and the rest of the USA Click Out www.MarriageEquality.org

Cranston – Rhode Island is now surrounded by states that allow same-sex couples access to civil marriage. Left out are gay and lesbian citizens living in the Ocean State.

“Marriage Equality Rhode Island is very excited to see that our gay and lesbian neighbors in Connecticut now have access to all of the rights and responsibilities of civil marriage. We remain saddened for our own gay and lesbian citizens who do not have that civil right here at home,” said Susan Heroux, chairperson of the Marriage Equality Rhode Island Education Fund Board of Directors (MERI).

“Rhode Island has become an island of inequality surrounded by states that treat their gay and lesbian citizens with dignity and respect by affording them an equal right to marry. Marriage is a significant social status and provides security that gay and lesbian Rhode Islanders deserve to have as human beings. It’s time for Rhode Island to catch up to its neighbors in this important civil rights area. We call on Rhode Island’s Legislators and the Governor to change the law to allow us civil marriage and keep Rhode Island on the forefront of civil rights,” she said.

The ruling comes from a suit (Kerrigan & Mock et all v. Connecticut Department of Public Health) filed by Gay & Lesbian Advocates & Defenders (GLAD) on behalf of seven gay and lesbian Connecticut couples who were denied marriage licenses in Madison, CT. Connecticut is the second state in New England—and the third in the United States—to swing open the doors to true equality for lesbian and gay couples.

“Today’s victory fulfills the hopes and dreams of gay and lesbian families to live as full and equal citizens in Connecticut,” says GLAD attorney Bennett Klein. “Marriage is unparalleled in the dignity, respect and protection it gives families.”

Plaintiffs Beth Kerrigan and Jodie Mock expressed their joy at hearing the decision: “We are overjoyed to tell our twin boys that we will be married, just like their friends’ parents. We are profoundly grateful to live in a state which recognizes our equality.”

Connecticut's Supreme Court ruled Friday that gay couples have the right to marry, making the state the third behind Massachusetts and California to legalize such unions through the courts.

The ruling comes just weeks before Californians go to the polls on a historic gay-marriage ballot question, the first time the issue will be put before voters.Connecticut's court ruled 4-3 that gay and lesbian couples cannot be denied the freedom to marry under the state constitution. It was a logical next step for a state that was the first to voluntarily pass laws affirming and protecting civil unions.

Good for them!  It is about time these people had a right to the same privledges everyone else does.  The government has no right deciding what people do in their personal lives, or how they choose to live it.

And hell, it doesn't change my life one bit... what the hell do I care?

Harold R. Cummings, Chairman

VERNON REPUBLICAN TOWN COMMITTEE

32 Ravenscroft, Vernon, CT 06066

 (860)871-1185

October 7, 2008

LETTER TO THE EDITOR

ReminderNews

130 Old Town Road

P. O. Box 210

Vernon, CT  06066

RE:     "McCAIN PALIN" TICKET A "SHOO-IN"

Contrary to recent polls, the "McCain Palin" ticket will be victorious in Connecticut, or at least in Vernon.  This prediction is based upon the extraordinary demand for "McCann Palin" yard signs in our town.  In just the last two weeks, twenty-six "McCain Palin" yard signs have disappeared off of  the front lawns of Vernon homeowners.  The demand is so great, that some signs have disappeared within hours of being placed.  These "McCain Palin" supporters are agile and fast on their feet.  They were able to remove signs placed as far away as forty feet from the road, in broad daylight, without being seen. 

These "McCain Palin" supporters are also adroit.  In one instance, a vehicle (subsequently identified, from the tire marks left in the lawn, as a pink Prius) managed to maneuver through three other signs, leaving them unscathed, in order to run over the McCain/Palin sign. 

We are very disappointed that these ardent followers of "McCain Palin" have not come forward and identified themselves.  Since we are always on the lookout for persons supporting our candidates, we have placed security cameras at two locations to assist us in identifying these folks, so that, we can personally welcome them to our fold. 

I have to confess, however, that several members of the Vernon Republican Town Committee have chastised me for being naive.  They tell me that the persons taking these signs are not supporters of "McCann Palin", but rather, supporters of Barack Obama.  Frankly, I refuse to believe, given Senator Obama's nice appearance, that he would attract thieves and trespassers.              

                                    Harold R. Cummings

                                    Chairman

                                    Vernon Republican Town Committee

11000

Sit back.

Enjoy the computervoice audio version of Joe Kinnear press conference...

http://www.guardian.co.uk/football/audio/2008/oct/03/joe.kinnear

Wenn du neu in Marburg bist oder so Bock hast, gibt es jetzt bald im CT eine Welcome-Party und ich lasse mich als billiges Blogflitchen natürlich gerne zur Werbung missbrauchen. Mehr Infos hier oder wenn ihr auf den Flyer an der Seitenleiste klickt.

Rick Allen and his wife Lauren Monroe devote a good deal of their time to their (non-profit) charity Raven Drum Foundation.

The foundation provides free educational programs to inspire personal growth during times of adversity.

Basically, they help those in need. Please visit Raven Drum for more information.

Short video clip (from the RI show, not this one) here.

Check out Phil's other endeavor, ManRaze!

In his interview Mr. Sweeney makes some interesting points about the next generation of graphics hardware & software architectures:

1. 3D APIs as we know them are a thing of the past and will soon die, replaced by more flexible software rendering pipelines implemented with CUDA/Compute Shaders/OpenCL or other languages.
2. (Some) fixed function/not programmable hardware units will still make sense for the foreseeable future.
3. DirectX 9 has been the last important revolution in 3D APIs, everything that followed or that will come next won't have such a dramatic impact on computer graphics engineers and researchers' life.
4. A good auto-vectorizing C++ compiler on all next gen platforms is perhaps all we need, developers will take care of the rest.
5. Next gen consoles might be based on a single massively parallel IC with general purpose computing capabilities plus some fixed function hardware units to speed up certain graphics related tasks such as texture mapping or rasterization.

3D APIs

Regarding the first point I believe Tim Sweeney's view is quite optimistic, many developers will neither be able nor interested in implementing their own rendering pipeline. 3D APIs, as we know them, will perhaps slowly lose their relevance, though I don't think their premature death is going to happen anytime soon.

There is some chance that all present and future big players in the market (namely NVIDIA, AMD, Intel and Microsoft) will agree on a common way to 'hijack' the current 3D pipeline, allowing developers to add new stages and to bypass old ones. This might sound like a good option for whoever wants to be creative without having to entirely lose the benefits of something which is proven, works well and can be efficiently re-used. It might even open a whole new world of possibilities for middle-ware developers.

Fixed Function What?

For all those skilled in the arts point number two is a no brainer. For example TMUs' dedicated logic performs tasks such as texture addressing, fetching, de-compression and filtering; If you have ever written a software renderer then you have experienced first hand how most of these operations are not amenable to be easily and efficiently implemented in software.

Custom rasterization hardware won't likely disappear that soon either. Even Intel, that will not employ rasterization logic on Larrabee, agrees that "rasterization is unquestionably more efficient in dedicated logic than in software when running at peak rates". That's why fixed function hardware will likely stay with us for many years to come.

It's interesting to notice how with Larrabee Intel got rid of a long list of dedicated hardware blocks that have been part of GPUs for a long time. Here's a list of the most important ones:

• input assembly (already implemented in software on some GPUs).
• pre and post transformed vertex caches.
• primitive assembly, culling & setup.
• hierarchical z-buffer.
• rasterization.
• attributes interpolation (partially implemented in software on NVIDIA GPUs).
• all output merge stages: alpha/stencil/depth tests, blending, alpha to coverage, etc.
• color, z and stencil compression.
• a plethora of obscure and relatively small fifos and caches.

Intel has clearly made a bold move here. They are taking huge risks and only time (and competition from other companies) will tell whether they are right or not.

Their software renderer seems to be incredibly well architected and it's a pity we had to wait so many years to see a big player adopting a tile based deferred renderer. One of the few advantages of TBDRs over immediate mode renderers is that they can be more efficient at using programmable hardware and memory bandwidth, making some  dedicated logic unnecessary. Say goodbye to color and z compression, and don't forget to commemorate output merge stages (aka ROPs) for all the good work they have done over the last 15-20 years!

Unfortunately we all know that nothing is for free and increased flexibility will come at a certain cost (this kind of bills are usually paid in perf/mm2 and perf/watt). On the other hand, giving up a big chunk of often idle dedicated logic is a great way to have more & more programmable hardware on board, which is inherently less likely to be inactive at any given time. A simple picture of NVIDIA GT200 can give a rough idea of how much area is spent on fixed function units, as you can see at least a fourth of the chip area is devoted to non programmable hardware.

DirectX

DirectX 9 was a huge step in the right direction, and DirectX 10 is helping consolidating that step adopting new render states, driver and unified shading models. In contrast, for a variety of reasons that go from <what am I supposed to do with this?> to <it's not a very clean design> I am not exactly enamored with DX10's geometry shaders or DX11's three brand new tessellation stages. I think these recent developments show us that as we enter in partially uncharted territory we don't know yet which direction should be taken.

That's why as we move towards more flexible and open rendering pipelines computer graphics researchers and game developers will unleash their imagination and come up with new interesting ideas. We will certainly see old but high profile graphics research brought back to life again (A-buffer anyone?) and used in real-time applications such as video games. Perhaps in ten years or more, after long and fruitful experimentation, we will settle down for a new and specific rendering pipeline model and it will be "The Wheel of Reincarnation" all over again!

Is CUDA good enough?

We will soon have at least three different CUDA-like languages to play with: CUDA, OpenCL and DX11's compute shaders and each of them seem to be well versed in exploiting data level parallelism. Sweeney thinks we can fully implement a modern rendering pipeline with languages like C++ or CUDA, though I have a couple of concerns about CUDA-like languagues:

• CUDA memory model is complex and it's tied to NVIDIA hardware. Will it scale well on future hardware?
• Many algorithms map poorly to DLP.

Conversely I expect CUDA and its younger siblings to evolve quite rapidly and embrace other forms of parallelism (it seems OpenCL will support some sort of thread level parallelism..), and here lies my hope to see some major innovation in this area. Speaking of which Intel is also working on the Ct programming language that promises to breath new life into the nested data parallel programming paradigm. Notice how all these new languages are based on dynamic JIT-style compilers: a necessary step in order to abstract code from specific hardware quirks, to maintain compatibility across the board and ensure scalability over next hardware generations.

Tim Sweeney also advocates the use of auto-vectorizing compilers, which occurs to me tend to be effective only at exploiting DLP and not much else. That's perfect for pixel shaders et similia, not so good for all sort of tasks that don't need to work on a zillion entities or that need some sort of control on how threads are created, scheduled and destroyed (unless you are brave enough to manually manage dozens or even hundreds of threads).

Can One Chip Rule Them All?

Following Mr. Swenney's suggestion: how likely is to have in a few years a first game console entirely based on a single chip or at least on a single massively parallel architecture? I don't want to dig too much into this extremely interesting topic as I would like to discuss it at length in a future post, but let me say that what is in the realm of possibility is not always feasible (yet).

A Glimpse Of The Future

In this long post I have been talking extensively about a future where a rendering pipeline is more general, flexible and less tied to a specific hardware implementation, so it is perhaps time to show what this all means in terms of real change. I don't want to take in consideration particularly exotic and unproven stuff, as I believe there is a lot of cool work to be done without having to throw the metaphorical baby out with the water!

For instance, it occurred to me many times that there is nothing inherently special in a stencil buffer that diversifies it from a color buffer or a z-buffer, unless we take in consideration the status it assumes in the rendering pipeline thanks to the stencil test. While fifteen years ago made perfect sense to have such an hardwired capability, now it feels more like an old gimmick that was not improved over the years while the rest of the pipeline was getting more modern and flexible.

Since we are at it what about alpha test, alpha blending and alpha-to-coverage? Why is the stencil buffer just using 8 bit per pixel? Why is the set of operations it supports so limited? Why can't I have my own special alpha blending operations? And most of all do these old features still make sense?

Of course they do, I use them all the time! But as it happens to many other engineers and researchers I find myself fighting them on a daily basis while trying to bypass their awkward limitations. There is clear lack of generality and orthogonality with respect to the rest of the pipeline, and that's why I am convinced that the whole set of output merge stages need to be re-architect-ed. We know that as the hardware evolves it gets rid of fixed function units, but these changes won't automagically fix the software layers that go on top of it.

It would be nice if we could remove these features:

• stencil buffer & stencil test
• alpha blending, alpha test and alpha to coverage.

• can be invoked before and/or after fragment shading
• can read from and write to all render targets
• can kill a fragment and/or generate a coverage mask for it (to avoid aliasing..)

For example a stencil buffer would be just another render target (don't forget we had support for multiple render targets for years now) and these shaders could be automatically linked by the driver to the main fragment shader or kept separate and executed in multiple stages. I have to admit that while I'm writing these few lines I'm having something like Larrabee and its software renderer in mind, but I wouldn't be surprised if in two years from now the rest of the graphics hardware landscape ends up being much more similar to Larrabee than current GPUs.

Final Words

Even barring incidental display devices breakthroughs I believe no one knows for sure how we will do graphics in 10-15 years from now. That's why it is hard to disagree with Mr. Sweeney when he notes that the next few years are going to be very exciting for engineers and researchers!

the leaves are changing colors! and this is probably the first time in my entire life i have appreciated it.

(one of) my favorite thing in the world 

my childhood home living room!

it was really great to be able to visit for a short time. i got to see the cat and had dinner paid for all weekend. home is comforting.

Keep the Promise offers both the Essential of Legislative Advocacy and the Essential of Legislative Leadership trainings for FREE at the Legislative Office Building each year in October/November and December respectively. However, upon request, these trainings are available to 15 or more persons in a condensed version.

Please contact Cheri Bragg, Coordinator, if you are interested in holding a training at your office, clubhouse, or other local venue at 860-882-0236 or 1-800-215-3021.

Training Dates: Wednesday, December 3rd and Wednesday, December 10th 2008.