Between the rock and a hard place rolling stones

Competencies create an effortless experience At Challenger, we advocate moving to a competency-based QA model. Rather than a checklist, you should choose the select competencies that matter the most to your organization and define the type of service that you want your reps delivering in every service interaction — but leave the details for them to determine. This causes a certain degree of discomfort for customer service leaders.

Checklists are easy. Subjective approaches appear more complex and scary. There are a few common root causes where we typically see this discomfort, but the good news is that we can partner with you to ease those concerns. For example, those concerns may sound like: Too much autonomy is terrifying. With each competency comes a set of mastery levels to help you and your leadership team determine what novice looks like, what expert looks like, and everything in-between. Many of our clients might already be sold on the value in moving to a competency-based model, but worried that one Quality Analyst will hear aptitude while another hears incompetence.

During our Quality Transformation Engagement, we hold a working session where we calibrate together across 10 calls for one core performing rep. Participants evaluate two calls, then we summarize the evaluations and project the results for everyone to see.

Nearly all of our clients find that they are far more aligned than they thought they would be, even after two calls. This process is designed to focus on trends rather than one-off mistakes. We need a pulse on overall performance, and the score gives us that. Many of our clients find themselves still assigning a value to each mastery level so they can calculate their progress e.

If it is properly nurtured, if it is properly handled and respected and managed, if we take care of our forests, they will take care of us. So, how do those three compare with each other? They fed off of each other, they respected each other, they listened to each other, and they learned from each other. It was certainly true of Duane and Eric when Duane was alive.

I knew Stevie fairly well through my association with the Fabulous T-Birds, as he would come out and sit in with his brother. If you had to compare styles, I guess Eric and Stevie Ray would have been a little closer in style with the heavy emphasis on the blues.

Rock place rolling hard and between a stones the fanduel sportsbook footprint center

With you world cup 2022 predictor game apologise

Extra-axial The most common extra-axial aetiologies of brain stones include meningiomas, dural osteomas, calcifying tumours e. Calcified meningiomas can be associated with focal thickening of the overlying skull bones or with dilatation of the adjacent air-containing sinus of the skull base [ 20 ].

Dural osteomas are believed to be a result of new bone formation arising from the dura and falx; conversely, intra-axial intracerebral osteomas are postulated to originate from primitive mesenchymal cells that have migrated from connective tissue Fig. Unique to these rare ossified tumours is the fact that they do not possess a laminated bony architecture, but present as a solid mass of calcification [ 21 , 22 ].

Craniopharyngiomas are frequently located in the suprasellar region and usually present with haemorrhage and calcification mainly in an amorphous and sometimes lobulated pattern [ 8 , 23 ]. Calcifying pseudoneoplasms of the neuraxis CAPNON are extremely rare fibro-osseous lesions that can be extra- or intra-axial. Histologically, these benign lesions are composed of a pathognomonic chondromyxoid matrix in an amorphous or nodular pattern as well as palisading spindle or epithelioid cells and varying proportions of fibrous stroma [ 24 — 26 ].

When present in the skull base, they are known to symptomatically encase cranial nerves. Lastly, exaggerated physiological calcifications can theoretically lead to identification of brain stones in radiological examinations. Structures known to calcify include the pineal gland, choroid plexus, habenula, dura and arachnoid, falx cerebri, tentorium cerebelli, superior sagittal sinus, petroclinoid and interclinoid ligaments, arachnoid granulations and intra-axially the basal ganglia and cerebellum [ 9 , 27 ].

Although physiological calcifications are usually considered of no clinical significance, the presence of pathology may be suspected in cases of abnormal increase in their usual size [e. The faint calcification seen at the lateral skull x-ray a was confirmed on non-contrast-enhanced CT NCECT to be a calcified meningioma overlying the right frontal cortex b , better visualised on the 3D reconstruction c.

A year-old female who presented with a headache and distant history of head trauma. Subsequent NCECT c and 3D reconstruction d revealed a solid calcified lesion black arrow adherent to the squamous part of the temporal bone. Note the cortical buckling a , which suggests an extra-axial location. The homogeneously solid calcification c suggests a dural osteoma instead of a dural ossification Full size image Fig.

They generally do not have any clinical significance and are often incidental findings during CT scans of the brain [ 28 ]. Dural calcifications, which are a result of calcium salt deposition, should not be confused with dural ossifications, which actually involves new bone formation [ 29 ]. As the falx is derived from multipotential mesenchymal cells, they may become osteogenic after exposure to friction, haemorrhage or trauma [ 29 , 30 ]. Ossifications in the falx cerebri are considered to be a rare phenomenon [ 9 , 31 , 32 ].

However, their incidence may be underestimated as it has been shown that a percentage of previously identified dense calcification on conventional radiography and CT may actually possess an outer shell of cortical bone surrounding an inner core of fatty bone marrow using modern high-resolution CT and MR imaging [ 28 , 31 , 32 ].

They can range in size from small islands of bone to large bony structures, can involve the entire falx [ 29 , 33 ] and can be associated with certain endocrine and congenital disorders [ 30 , 33 ]. Neoplastic Various intracranial tumours are associated with haemorrhage because of a combination of neovascularisation, intralesional arteriovenous shunt formation and rapid enlargement that outgrows the tumour blood supply resulting in necrosis, especially in those with high tumour grades.

This condition then promotes disruption of intracellular calcium regulation, resulting in calcium deposition [ 23 , 34 , 35 ]. In some cases, the calcification can be punctate, ribbon-like or even peripherally located, and can extend into adjacent brain parenchyma. Low-grade astrocytomas are by far the most common glial neoplasms. However, only a small fraction of these tumours are known to calcify, with patterns ranging from linear, diffuse to punctate. Other brain tumours may calcify to various degrees such as pineal gland tumours, germ cell tumours, primitive neuroectodermal tumours PNET , dysembryonic neuroectodermal tumours DNET , gangliogliomas and pilocytic astrocytomas.

Although rare, metastasic tumours to the brain can also calcify, often in the setting of treatment [ 37 ]. Combined with other imaging features, the presence, but not the pattern of calcification can narrow down the differential diagnosis of intracranial neoplasms. In the same context, the presence of calcification in tumours is not associated with the pathological grade of malignancy, but the eventual development thereof may suggest a favourable response to therapy [ 5 , 38 ].

Axial a , sagittal b and 3D reconstruction c show a calcified lesion black arrows in the left post central gyrus. The entire lesion was surgically removed and was found to be a glioblastoma with an extensive oligodendroglioma component. Ninety percent of oligodendrogliomas are known to form dense, clump-like calcifications Full size image Vascular Ever since Shafey first reported brain stones due to angiomatous cavernous malformations, vascular pathologies have been recognised as important causes of intracranial calcification in general [ 2 ].

Other vascular lesions that may result in the formation of intracranial calcifications and brain stones include arteriovenous malformations, dystrophic calcification in chronic infarction, chronic vasculitis and aneurysms Fig. In most situations, radiological features as well as location allow differentiation between these entities.

Pathophysiological mechanisms leading to calcification include chronic venous ischaemia and the formation of dystrophic calcification as a result of haemorrhage. Vasculitis leading to microinfarctions and subsequent dystrophic calcifications can be seen in a number of pathologies, such as in systemic lupus erythematosus [ 41 ].

The presence of a round or lobulated densely calcified mass in the suprasellar or parasellar regions is highly suggestive of the presence of a calcified brain aneurysm. The calcification in this case involves the vessel wall, usually in larger aneurysms, and their presence can correlate with the extent of intraluminal thrombosis [ 42 ].

There is also an intraventricular drain present white arrows. The subsequent appearance of calcifications in known post-traumatic or post-ischaemic areas of the brain is largely attributed to dystrophic calcification Full size image Fig. The large amorphous calcification seen at the base of the left temporal lobe in this NCECT represents a known case of an embolised AV malformation. As with vascular pathologies, the mechanism of calcification involved in these infections is dystrophic calcification.

With congenital toxoplasmosis and cytomegalovirus infections, these calcifications are usually seen in the basal ganglia and periventricular areas, whereas with herpes simplex infections, the calcifications are located in the thalamic, periventricular and gyral regions [ 16 ]. The dense calcifications seen in patients with congenital toxoplasmosis can also have a random distribution, with lesion sizes that correlate with the duration of infection.

I was not under the influence of any mood-altering substance. I paid for the ticket. I realise how this experience has exposed me as possessing a deep character flaw. Not even nostalgia can be cited as a defence. In fact, there is no logical reason — not on the face of it anyway — why I would subject myself to an evening in Croker watching four men with a combined age of do their thing as if they still had time on their side. Curiosity got the better of me though.

I had to check out whether the past really can be recreated. Other performing artists mature and adapt. The Stones are different. They are the past. Would the mythic rock gods of yesteryear take the stage, or would it be a cartoonish incarnation, like an exhibition wheeled out of a museum for the day? The omens for the gig were poor from way out. Then a few weeks back, the ultimate indignity. Could this be happening? Jumping Jack Flash himself had to descend from the gilded pantheon of rock and roll immortality to rustle up a bit of interest in the gig.

Is he that stuck for a few bob? Anyway, curiosity got the better of me and I toddled off to Croker to see whether the glory had faded or turned to black. The result was just on the right side of decent. The songs have aged well, but remain rooted in their time. It could have been the Rolling Stones taking off a tribute band for the Rolling Stones up there.

From the speakers came the sounds of the guitar riffs and the Jagger snarl that has long been embedded in popular culture.