Canadian broadcast network CTV has picked up four new U.S. comedies and nine dramas from this years Los Angeles Screenings for the 2017-18 season.

They are comedies The Big Bang Theory spinoff Young Sheldon, Me, Myself & I from CBSandRoseanne revival and The Mayor from ABC. Dramas include Shondalands untitled Greys Anatomy spinoff, which will premiere midseason, and new legal drama For the People. Also on the list are new ABC dramas The Good Doctor, Ten Days in the Valley, The Crossing, Deception, The Gospel of Kevin and Marvels Inhumansalong with Foxs The Gifted.

CTV and CTV Twos 2017-18 primetime schedules will be unveiled at the CTV Upfront on June 7 in Toronto.

CTVs strategically curated mix of the years most-buzzed about sitcoms and compelling dramas sets the stage for viewers to root for both heroes, families and even misfits with heart, said Mike Cosentino, SVP Content and Programming atCTV parent company Bell Media. We cant wait to share our powerful new slate with advertisers and viewers next week.

More:
'Young Sheldon', 'Grey's Anatomy' Spinoff Among 13 U.S. Series Picked Up By CTV LA Screenings - Deadline

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John Knight is senior lecturer in biomedical science; Yamni Nigam is associate professor in biomedical science, both at the College of Human Health and Science, Swansea University.

The nervous system controls the activities of all body organs and tissues, receiving input from sensory organs and responding via effector organs. With around 100billion interconnected neurons, the brain is an extremely complex, and still poorly understood, organ. However we do understand, to some degree, how age affects it, as well as the nervous system as a whole. This fifth article in our series on the anatomy and physiology of ageing describes the age-related changes occurring in the brain, spinal cord and peripheral nerves. These changes lead to a gradual decline in cognitive function and a range of other issues, such as reduced bladder control or postural hypotension, but in health the brain normally continues to function adequately throughout life.

Knight J, Nigam Y (2017) Anatomy and physiology of ageing 5: the nervous system. Nursing Times [online]; 113: 6, 55-58.

The nervous system, along with the endocrine system, controls and integrates the activities of all the bodys organs and tissues. It receives and processes sensory input from organs such as the eyes, ears and skin, and responds through a variety of effector organs.

The main organ of the nervous system is the brain, which, with around 100billion interconnected neurons, is extremely complex; despite decades of research, its function remains poorly understood. Ageing leads to a progressive loss of neurons and depletion of neurotransmitters (Mather, 2016), these changes are usually associated with a gradual decline in cognitive function and influenced by environmental, genetic and lifestyle factors (Nyberg et al, 2012).

The ageing brain gradually loses neurons and supporting neuroglial cells (Fig 1). Between the ages of 20 and 60, the brain loses around 0.1% of neurons per year, after which the process speeds up (Esiri, 2007). By the age of 90, brain mass will have decreased by around 11% compared with individuals in their 50s, which equates to a loss of about 150g of neural tissue (Wyss-Coray, 2016). The remaining tissues harbour an increased concentration of potentially harmful materials such as iron, aluminium and free radicals.

Aged neural tissues also show increasing pigmentation, largely due to the deposition of two pigments: one brown, lipofuscin (Ottis et al, 2012), and one black, neuromelanin (Clewett et al, 2016). Lipofuscin is linked to amyloid

protein deposition and the formation of neurofibrillary tangles. These abnormal areas of neural tissue are often present at low densities in aged brain tissue, even in the absence of disease (Wyss-Coray, 2016); however, where Alzheimers disease is present, these are at high densities.

The loss of neurons is most apparent in the cerebral cortex. The grooves (sulci) that mark the surface convolutions (gyri) of the cerebral cortex are visibly deeper in brains of older people (Fig 1). It was originally thought that the frontal lobes were particularly vulnerable to neural loss, but similar losses have been observed in other cortical regions such as the parietal lobes (Fjell et al, 2014).

Fig 1. Three age-related changes in the brain

Fig 1. Three age-related changes in the brain

Structural changes in the frontal and parietal lobes are related to poor memory. Many people in their 80s have modest levels of amyloid protein deposition and retain their memory, while individuals with higher levels typically have a poorer working (short-term) memory (Nyberg et al, 2012). However, the role of amyloid deposition in impairing memory has recently been questioned and other factors, such as accumulation of tau proteins, may play a more important role (Brier et al, 2016).

The hippocampus has a key role in memory and the acquisition of new skills. With age, it loses a significant amount of neural tissue (Burke and Barns, 2006), which may explain why activities such as learning a new language become more difficult with advancing age. Recent research indicated that navigating a computer-generated virtual environment improved spatial awareness and reduced the shrinkage of the hippocampus, both in younger and older people (Lvdn et al, 2012). Virtual reality computer programs could therefore potentially be used to reduce shrinkage in this vital brain area.

Around 35% of people over the age of 70years have gait problems; while there are many contributing factors, including age-related changes to muscles and joints, the nervous system is also implicated. The somatic motor cortex located in the frontal lobes of the brain controls the movement of muscles involved in walking. From middle age onwards the neurons in this region show signs of atrophy (Manini et al, 2013), which can contribute to gait problems, potentially reducing mobility in older people (Rosso et al, 2013).

Ageing is associated with a gradual increase in the size of the ventricles (fluid-filled chambers) in the brain (Fig 1). This is likely to result from a progressive loss of the cells that line the ventricles. Enlarged ventricles fill with more cerebrospinal fluid, and are readily observable using techniques such as magnetic resonance imaging. On average, the volume of the ventricular system increases by around 2.9% per year; this expansion appears to accelerate with age, with people over the age of 70 having a median rate of expansion of 4.25% per year (Raz and Rodrigue, 2006). Although ventricular expansion is seen in most older people, the cognitive impact of this remains unclear.

The medulla oblongata and other areas of the brainstem lose fewer neurons than other regions of the brain. The brainstem is probably the best preserved region of the brain, which probably reflects its essential role in supporting life: it controls breathing, peristalsis, heart rate and blood pressure. However, the autonomic function of the brain does decline with age and this can compromise the bodys ability to respond quickly to internal and external environmental changes (Hotta and Uchida, 2010). Both branches of the autonomic nervous system (ANS) the parasympathetic and sympathetic branches are compromised with age (Parashar et al, 2016).

These changes can negatively affect older people. For example, the blunting of baroreceptor responses increases the risk of postural hypotension, so standing up suddenly can lead to falls and injury. Another negative consequence is the gradual loss of bladder control. To control micturition, the body relies on the interplay of sensory stretch receptors and the ANS (which together monitor bladder filling) and the conscious areas of the cerebral cortex (which signals when the bladder is full). To initiate micturition, the body needs motor control of the urinary sphincter. All these elements function less well with age, and these age-related changes combine with those in other body systems such as prostate enlargement in men and weakened pelvic floor muscles in women to reduce bladder sensitivity and control (Hotta and Uchida, 2010), which can lead to continence problems.

Cerebral blood flow decreases by around 0.38% per year, equating to a 27% decline over 70years of life (Chen et al, 2011). This is a direct consequence of the age-related changes in the cardiovascular system, and may be exacerbated in patients with atherosclerotic occlusion of the carotid arteries.

The blood-brain barrier (BBB) is formed primarily of tight junctions between adjacent endothelial cells within the blood vessels in the brain. Additionally, specialised neuroglial cells called astrocytes wrap around the cerebral vessels, forming a further physical barrier between the blood and neural tissues. The BBB is essential to prevent most pathogens and many toxic materials crossing into the neural networks and pathways of the brain, but its integrity appears to diminish with ag
e. A recent study indicates that, during normal ageing, the BBB is first weakened in the hippocampus, thereby allowing harmful substances and pro-inflammatory mediators to cross into this vital region of learning and memory. This breaching of the BBB may contribute to hippocampal shrinkage, and therefore to cognitive decline (Montagne et al, 2015).

Ageing is associated with a declining production of many neurotransmitters, including noradrenaline, glutamate, dopamine and serotonin. The decline in dopamine appears to be particularly important: dopamine modulates motor function and the acquisition of new skills, while also acting as one of the brains reward chemicals (Mather, 2016). The number of dopamine-producing neurons decreases as part of the normal ageing process, and this can adversely affect the ability to learn from past experiences. Recent studies show that many older people who boosted their levels of dopamine by taking L-DOPA (a drug normally used to treat Parkinsons disease) were learning as quickly as young adults again (Chowdhury et al, 2013).

Few studies have examined age-related changes to the spinal cord. A recent animal-model study shows an increase of cholesterol content in the ageing spinal cord, and the authors suggest this may potentially impair cord function (Parkinson et al, 2016).

Age-related changes to neurons and neuroglial cells appear to have little effect on spinal cord function. However, age-related changes to the vertebrae and intervertebral discs may increase pressure on the spinal cord and its branching nerve roots. This can slow down the conduction of nerve impulses along motor neurons, contributing to reduced muscular strength (Manini et al, 2013). Reduced sensory and motor conduction will increase the risk of injury due to poor coordination, poor balance and poor fine motor control.

With age, some peripheral neurons show a dying back (shrinkage of axonal length), loss of mitochondria and a degeneration of their insulatory myelin sheaths. Some of this damage may be caused by a rise in the concentrations of pro-inflammatory mediators in the body. The ageing body becomes less effective in clearing toxic metabolites and, as peripheral nerves are not afforded the protection of the BBB, this may contribute to peripheral nerve damage (Manini et al, 2013).

The loss of myelin slows the conduction of peripheral nerve impulses by around 5-10% (Joynt, 2000). In health, this reduction in conductivity causes few problems, but in older people with diabetes it may contribute to, and exacerbate, diabetic neuropathy. Damaged peripheral nerves are not repaired as efficiently in older people as in their younger counterparts, and some of these nerves are never repaired. This can contribute to reduced sensation and motor control.

In the absence of disease, intellectual ability can be retained throughout life. However, the gradual loss of neurons, depletion of neurotransmitters and slowing of nerve conduction may act together to slow down the processing of information. As a result, older people may take longer to complete certain tasks, and commonly experience the functional brain changes described below.

The loss of short-term and episodic memory is probably the earliest indication of age-related changes in the brain. Unlike what happens in dementia, the loss of short-term memory in the absence of disease does not affect life skills (such asthe ability to cook), but manifests as inconveniences (such as forgetting an item from the shopping list). Episodic memory (that is, remembering autobiographical events and their timings and sequence) also gradually declines in many older people (Fjell et al, 2014).

Verbal communication skills generally remain strong throughout life (Park and Reuter-Lorenz, 2009), but people over the age of 70years may have increasing problems using or recalling words. The ability to quickly name a common object usually remains stable up to the age of 70, but then declines with advancing years (Harada et al, 2013).

The progressive loss of neurons, reduction in impulse velocity and minor changes in the spinal cord lead to a slowing down of reaction times (Spirduso, 1995). This can create problems, particularly when a fast reaction is essential (for example, to step out of the way of oncoming traffic).

In England, around 22% of men and 28% of women over the age of 65 are affected by depression; in care homes, the figures are even greater, with around 40% of residents affected (Age UK, 2017).

It is almost impossible to determine whether depression in older people occurs as a normal consequence of ageing or as a result of chemical imbalances seen in types of depression that also affect younger people. Concentrations of neurotransmitters involved in lifting mood (particularly serotonin) diminish with age and this can contribute to symptoms of depression (Fidalgo et al, 2013). The Royal College of Psychiatrists estimates that >85% of depressed older people receive no help from the NHS (Age UK, 2017). Depression can often produce symptoms that mimic dementia (pseudo-dementia) and this often causes great anxiety.

On the whole, older people are less prone to emotional outbursts than younger people. This may be related to the relative structural stability of some of the brain regions linked to emotions. Most studies of the amygdalae which are heavily involved in impulsive behaviours and emotional reactions reveal little evidence of atrophy or shrinkage at a much slower rate than in other brain regions. Additionally, the amygdalae also appear to retain most of their functional activity in older age (Mather, 2016).

Because the overall neural mass reduces with age, neuroactive drugs such as antidepressants and neuroleptics can be more potent in older people. Doses normally prescribed to adults may induce confusion or delirium, and may therefore need to be adjusted.

How normal age-related changes to the brain can be distinguished from pathological changes associated with dementia (for example, Alzheimers disease) is hotly debated. The problem is that three of the main clinical features of Alzheimers disease loss of episodic memory, loss of brain tissue and amyloid deposition are also seen in apparently healthy older people with little or no evidence of dementia. However, it is generally recognised that the main risk factor for developing dementia is advancing age (Fjell et al, 2014).

Unlike cells in many other parts of the human body, most neurons do not undergo cell division so, when they dieas a result of age or injury, they are generally not replaced. Fortunately, the brain contains over 100billion interconnected neurons (the connectome) and many researchers agree that it has an in-built redundancy, known as the brain reserve. This is defined as the physical resources of the brain in terms of brain mass and number of neurons; a larger brain reserve is often associated with better outcomes after brain injury and in various neurological diseases (Tucker and Stern, 2011).

The brain reserve is not necessarily a good predictor of cognitive function (many people with normal cognition have significant brain atrophy), so the concept of cognitive reserve has emerged. People with a high cognitive reserve are able to use their brain reserve more efficiently to perform tasks, and this seems to happen through increased efficiency of functional connections between neurons (Marques et al, 2016).

Good predictors of a high cognitive reserve include high education level, high IQ, highly complex occupation and large amount of social interaction. Recent research indicates that cognitive ability may also be maintained by neural compensation, a process in which new circuits of neurons are recruited to perform tasks that were once carried out by aged ordamaged neural pathways (Steffener and Stern, 2012). In normal ageing, the brain reserve does decline but cognition ismaintained thanks to the brains in-built redundancy.

Keeping mentally active throughout life can reduce the effects of age on th
e nervous system (Mahncke et al, 2006), and engaging in social, sporting and mentally challenging activities can slow downthe decline in cognitive performance (Nyberg et al, 2012). It appears the more intellectually demanding and complex an individuals occupation, the better their cognitive performance in later years; however, in retirement, when the mental challenges of work are removed, this effect appears to decline.

Older people should be encouraged to engage in stimulating activities such as socialising, reading and games, which are thought to improve cognitive function and memory, as well as reduce the riskof depression. It is a common misconception that ageing naturally leads to conditions such as confusion, dementia and delirium. The human brains in-built redundancy allows it to adequately cope with the physical changes associated with ageing. Indeed, in the absence of disease, adequate mental function can be retained throughout life.

Age UK (2017)Later Life in the United Kingdom, January 2017.London: Age UK.

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Chen JJ et al (2011) Age-associated reductions in cerebral blood flow are independent from regional atrophy.Neuroimage;55: 2, 468-478.

Chowdhury R et al (2013) Dopamine restores reward prediction errors in old age.Nature Neuroscience;16: 5, 648-653.

Clewett DV et al (2016) Neuromelanin marks the spot: identifying a locus coeruleus biomarker of cognitive reserve in healthy aging. Neurobiology of Aging; 37: 117-126.

Esiri MM (2007) Ageing and the brain. Journal of Pathology; 211: 2, 181-187.

Fidalgo S et al (2013) Serotonin: from top to bottom. Biogerontology; 14: 1, 21-45.

Fjell AM et al (2014) What is normal in normal aging? Effects of aging, amyloid and Alzheimers disease on the cerebral cortex and the hippocampus. Progress in Neurobiology; 117: 20-40.

Harada CN et al (2013) Normal cognitive aging; Clinics in Geriatric Medicine; 29: 4, 737-752.

Hotta H, Uchida S (2010) Aging of the autonomic nervous system and possible improvements in autonomic activity using somatic afferent stimulation. Geriatrics and Gerontology International; 10: Suppl 1, S127-S136.

Joynt RJ (2000) Aging and the nervous system. In: The Merck Manual of Geriatrics. West Point PA: Merck & Co.

Lvdn M et al (2012) Spatial navigation training protects the hippocampus against age-related changes during early and late adulthood. Neurobiology of Aging; 33: 3, 620.e9-620.e22.

Mahncke HW et al (2006) Memory enhancement in healthy older adults using a brain plasticity-based training program: a randomized, controlled study. Proceedings of the National Academy of Sciences of the United States of America; 103: 33, 12523-12528.

Manini TM et al (2013) Aging and muscle: a neurons perspective. Current Opinion in Clinical Nutrition and Metabolic Care; 16: 1, 21-26.

Marques P et al (2016) The functional connectome of cognitive reserve. Human Brain Mapping; 37: 9, 3310-3322.

Mather M (2016) The affective neuroscience of aging. Annual Review of Psychology; 67: 213-238.

Montagne A et al (2015) Blood-brain barrier breakdown in the aging human hippocampus. Neuron; 85: 2, 296-302.

Nyberg L et al (2012) Memory aging and brain maintenance. Trends in Cognitive Sciences; 16: 5, 292-305.

Ottis P et al (2012) Human and rat brainlipofuscin proteome. Proteomics; 12: 15-16, 2445-2454.

Parashar R et al (2016) Age related changes in autonomic functions. Journal of Clinical and Diagnostic Research; 10: 3, CC11-CC15.

Park DC, Reuter-Lorenz P (2009) The adaptive brain: aging and neurocognitive scaffolding. Annual Review of Psychology; 60: 173-196.

Parkinson GM et al (2016) Perturbed cholesterol homeostasis in aging spinal cord. Neurobiology of Aging; 45: 123-135.

Raz N, Rodrigue KM (2006) Differential aging of the brain: patterns, cognitive correlates and modifiers. Neuroscience and Biobehavioral Reviews; 30: 6, 730-748.

Rosso AL et al (2013) Aging, the central nervous system, and mobility. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences; 68: 11, 1379-1386.

Spirduso WW (1995) Physical Dimensions of Aging. Champaign, Il: Human Kinetics.

Steffener J, Stern Y (2012) Exploring the neural basis of cognitive reserve in aging. Biochimica et Biophysica Acta; 1822: 3, 467-473.

Tucker AM, Stern Y (2011) Cognitive reserve in aging. Current Alzheimer Research; 8: 4, 354-360.

Wyss-Coray T (2016) Ageing, neurodegeneration and brain rejuvenation. Nature; 539: 7628, 180-186.

More:
Anatomy and physiology of ageing 5: the nervous system - Nursing Times

It's lavish, multi-racial and a bit of a confusing mess.

And, apparently, being Shonda Rhimes will only get you so far. ABC ordered only seven episodes of "Still Star-Crossed," and it's airing them during the summer, with a debut on Memorial Day.

Elsewhere on TV

Stanley Cup Final (6 p.m., NBC/Ch. 5): Game 1 Nashville Predators at Pittsburgh Penguins

"Michael Jackson: Searching for Neverland" (6 p.m., Lifetime): Jackson life is recalled by his bodyguards. Really.

"Gotham" (7 p.m., Fox/Ch. 13): Gordon races to save the city from the Alice Tetch virus; some of Gotham's worst villains band together.

"The Bachelorette" (8 p.m., ABC/Ch. 4): Ashton Kutcher and Mila Kunis judge a contest; Kareem Abdul Jabbar plays basketball with the guys; one bachelor betrays Rachel.

"Lucifer" (8 p.m., Fox/Ch. 13): In the Season 2 finale, Charlotte accidentally burns a man to death and Lucifer has to keep Chloe from figuring out what happened.

"American Dad" (8 p.m. TBS): The town turns on Steve after he convinces the star quarterback of the arena-football team to quit playing.

"Angie Tribeca" (8:30 p.m., TBS): Holy 'Blindspot'! A naked woman emerges from a child's backpack and doesn't remember a thing.

National Memorial Day Concert (10 p.m, Ch. 11): Recorded on Sunday.

"Leah Remini: Scientology & the Aftermath" (10 p.m., A&E): In this two-hour special, Leah Remini and Mike Rinder explore the relationship between the Church of Scientology and its critics.

Read more here:
Monday on TV: 'Grey's Anatomy' producer tries to improve on ... - Salt Lake Tribune (blog)

Welcome to the Anatomy of a Goal, where each week we dissect one goal (or near goal) from Columbus Crew SCs previous match.

For match 14 of the 2017 MLS Season, we take a look at Toronto FC midfielder Justin Morrows 39th minute goal that put Toronto up 2-0 as part of the 5-0 win over Crew SC on Friday.

Heres a look at the finish from the Toronto FC midfielder.

It was hard to pick just one of Torontos five goals to break down, but Morrows goal is indicative of Torontos successful strategy in this match. When Columbus pushed up the field, Toronto looked to counter quickly, often playing a long pass into the Crew SC defense, looking to build off of a turnover or a win of possession by TFC.

During the first half, Crew SC lined up in what the official lineup called a 4-4-2, with Wil Trapp and Federico Higuain playing together in the midfield. This 4-4-2 sacrificed a defensive midfielder for an attacker, and left Trapp with much more ground to cover. As the lone defensive midfielder, Trapp was often the only player in the middle of the field, leaving acres of space for Toronto runners and creating chaos for the Crew SC defense.

Morrows goal begins with this Kekuta Manneh clearance. Manneh, lined up at forward, stuck to the left side of the field for much of the match. Here, Manneh has tracked back on defense, and seeing no other options, clears the ball up the field.

TFC center-back Eriq Zavaleta, pressured by Ola Kamara, heads the ball forward into the path of Michael Bradley.

Bradley immediately plays a risky pass back to Zavaleta, who is directed to clear the ball by fellow center-back Drew Moor. Notice here that Crew SC has 4 players in Toronto FCs defensive half. Wil Trapps midfield partner, Federico Higuain, provides the most pressure to Zavaletas clearance. By providing this pressure, Higuain leaves Trapp alone to cover much of the midfield.

Once Zavaleta clears the ball forward, Toronto immediately has a numerical advantage over Crew SC. Wil Trapp, highlighted near midfield, is almost totally alone in the midfield, because Higuain was pressuring the TFC center-backs. Jonathan Mensah is back the furthest on defense. Nicolai Naess is marking TFC striker Ben Spencer, while Harrison Afful doesnt seem to realize that Justin Morrow is totally unmarked right behind him.

As Waylon Francis receives the ball, he has two options: get the ball to Trapp, alone in the middle of the field, or send the ball up the sideline/out of bounds.

Francis opts to send the ball toward Trapp, but note the way the he heads the ball. Francis heads the ball with his momentum going away from the ball. Because his momentum is away from the ball, Francis slows the ball down, sending an incredibly weak and slow pass toward Trapp, who has to speed up to receive the ball.

Ben Spencer notices the weak pass, and immediately heads toward the ball.

Trapp and Spencer are in a footrace to the ball while the Crew SC defense drops into shape. Notice that Harrison Afful, just above the highlighted Ben Spender, is still unaware of Justin Morrow.

Trapp appears to be on track to win the ball, but has Ben Spencer bearing down on him. To make a successful pass, Trap would have to immediately play a first touch pass to one of the three Crew SC players near him: Nico Naess, Jonathan Mensah, or Waylon Francis.

However, as the above video shows, the ball takes a high bounce right before it gets to Trapp, and the Crew SC midfielder is unable to play a first touch pass. Forced to take an awkward touch on the ball, Trapp is dispossessed by the much larger Ben Spencer. Trapp is listed at 58 and Spencer is listed at 65 and Spencer easily knocks Trapp off the ball to spring the Toronto attack.

Having just dispossessed Trapp, Spencer has two options. Because Naess has shifted to cover him, Spencer will have to make a pass: a slotted ball to Tosaint Ricketts, who would be marked by Jonathan Mensah, or an easy pass to Justin Morrow, who is running at pace and will be just ahead of Harrison Afful. To Affuls credit, he finally noticed Morrow sprinting behind him, but will start his run too late to catch the TFC midfielder.

With Afful having pushed high up the field, notice now much space is open on the Crew SC defensive right flank.

Spencer opts to push the ball to the onrushing Morrow, who has already pushed ahead of Harrison Afful. As has happened a few times this year, Afful is forced to catch up with a midfielder who has built up pace while Afful was pushed up the field. This isnt necessarily Affuls fault, but the Crew SC right back, and the Crew SC managerial staff, have to realize that teams have punished Afful being pushed too far upfield multiple times this season. When Afful pushes that far up field, he does not have the luxury of being able to mentally switch off, and must be aware of his surroundings at all times. Afful was absolutely switched off until he noticed Morrow streaking over his left shoulder.

As Morrow approaches the ball, Afful catches up to him. If Afful can get in front of Morrow, he can force the TFC midfielder to take a difficult shot or make a cross to one of the, well-defended, TFC players in the box.

As Morrow prepares to shoot or pass, notice the Crew SC defense. For some reason, Naess has totally abandoned Ben Spencer, the tallest player on the field, who is now making an undefended run into the box. Naess may be attempting to get in front of Morrow, but the TFC midfielder already has a difficult angle on goal. Naess should have stayed with Spencer in an attempt to prevent TFCs tall striker from being open for a chipped cross.

But, Naesss leaving Spencer doesnt matter. Morrow fires a left-footed rocket at the near post. Afful has recovered, and does a good job to cut off Morrows crossing angles, forcing that shot from a tough angle. Afful should expect his goal keeper to have the near post covered from that angle.

However, Zack Steffen is caught flat-footed and is beaten to his near post by Morrows shot. Morrows shot here is excellent and perfectly placed, but Steffen cannot afford to be beaten to his near post from that angle.

Findings:

Read more from the original source:
Anatomy of a Goal: Morrow Makes it 2 - Massive Report

In this post-truth era, it is becoming increasingly difficult to distinguish real scandals from bogus ones. Spotting the difference has become more important than ever, given the ease with which scandals are created, escalated and sent into orbit through social media.

In the parasitic relationship between social and conventional media, fake news is often used to generate outrage, and fake outrage, in turn, to generate news. Things that should generate outrage often pass unnoticed.

Outrage manufacturing becomes particularly marked in the months before political parties hold elective conferences for new leadership. During this period, internal jockeying for positions includes candidates raking as much muck on their opponents as possible.

Healthy scepticism is, therefore, a useful attitude with which to approach the many revelations that make their way into the media as South Africas major political parties approach their congress season.

It is fascinating to watch the links between some politicians and those journalists who are prepared to provide a public platform for their schemes. A few journalists even become pro-active agents in a partys internal battles and vendettas.

It was in this frame of mind that I read an article in last weeks Sunday Times headlined: Contractors paid for DA MECs bash.

The opening paragraph read, Acting DA provincial leader Bonginkosi Madikizela is facing allegations of impropriety after a swanky birthday bash in his honour was apparently partially funded by construction companies that benefit from projects financed by his department.

Despite the inclusion of a denial from Mr Madikizela himself, who is the provincial Minister of Human Settlements, the overwhelming impression left by the headline and the article is that contractors funded a party for the political head of a department that awards contracts and tenders worth billions annually. If that were true, it would (at the very least) be improper. At worst, it would indicate corruption.

So confident was the journalist of the latter that he publicly predicted the unfolding scandal would end Madikizelas career.

Before long, the lines were buzzing. Journalists wanted comment. The party hierarchy advised me to take urgent and immediate action.

The next day, the story escalated with a breathless front-page headline in the Cape Times screaming: Madikizela birthday party sleaze, followed by an article dripping in insinuations.

Experience, lifes best teacher, cautioned me to proceed carefully, gather as many facts as possible, and speak to the individuals involved before determining a course of action or making a public statement.

I knew at least two things:

So if it turned out that there were contractors who thought they could buy favours by sponsoring the event, they would end up sorely disappointed.

Nevertheless, if there had been such an attempt, it would have been wrong and action would be required. It was obviously important to establish the facts.

My first discussion was with Bonginkosi himself. I told him I was going to investigate the issue in as much detail as possible, so that I could determine an appropriate course of action. He welcomed my approach. He told me the party had been organised as a surprise for him. He thought he was going out to a birthday dinner with a group of friends, only to walk into a room full of guests shouting surprise.

What he knew about the background was as follows: He has, for years, been part of a 20-strong network of friends who support each other, specifically in times of celebration and bereavement, helping to raise money for events ranging from parties to funerals. This group (loosely based on the traditional stokvel saving model) meets on a regular basis. When Bonginkosi was elected the DAs interim Western Cape leader, they wanted to throw a celebration party for him.

Bonginkosi vetoed the idea. He said it was not appropriate in the circumstances, and could potentially be interpreted as lauding it over other candidates. They accepted his reservations, and later hatched a plan to give him a surprise birthday party instead. It was a closely guarded secret. After the event, when he enquired who had paid for it, they told him that a fundraising subcommittee had called on people to make donations. He accepted their word and thought nothing further of it. This was normal in his friendship circle, he said.

He confirmed the newspapers claim that Ms Pumla Zantsi, a partner in a construction firm doing business with the province, had contributed a multilayered, multicoloured cake, worth R3,000. That was the only contractor involved as far as he was aware.

Bonginkosi told me that he and Pumla were part of the mutually supporting friendship circle. They had been friends for 20 years, from the time they were both activists in Khayelitsha and long before he had even thought of joining the DA. For her part, Pumla had been a contractor to the province long before Bonginkosi became provincial Minister of Human Settlements. She had never used her presence in their stokvel network to seek a business advantage or political favour.

In any event, said Bongikosi, do you think that I can be bought for a birthday cake?

I thought about our conversation. A long-standing friend buys you (an admittedly expensive) cake, from her own pocket, and it turns into a scandal because her company does work for the province, and has done for years prior to your arrival on the scene? This put a completely different spin on a story that had been touted as a career-ending scandal.

But of course, there could conceivably be more to the story than that, so I investigated further. A party at the One & Only hotel does not come cheap. I started by making contact with Pumla Zantsi. She immediately agreed to meet and was entirely forthcoming. She explained that the group of friends had met over many weeks to organise the party. They had nominated a fund-raising committee who had approached prospective donors. She gave me the full donor list, ranging from people who had contributed to the incidentals (such as tea and coffee at their planning meetings) to those who had paid for the big ticket items such as the hotels bar tab. I then submitted the donors names (and the companies with which they are associated) to the Chief Financial Officer of the Department of Human Settlements, to determine if any of them are contractors to the Department or the Province. None, he responded.

I managed to get the telephone number of the major donor, a Mr G, who is based in Durban, where Bonginkosis sisters live, and where he once lived himself. He still has a large friendship network there. Mr G confirmed that he had covered the lions share of the cost, and that he has no business interests in the Western Cape and none in construction, and that he had elicited further donations from his network in Durban. None did work for the Western Cape either, he assured me.

Next, I had to check whether the people who said they were donors were the ones that actually paid for the party, so I contacted the relevant hotel manager and asked to see copies of the invoices and receipts. He was unable to give them to me, due to client confidentiality, so I asked the party organisers to source the documents for me.

They promptly did, and my office undertook a reconciliation which showed the accuracy of the information we had been given.

Next I scoured some of the photographs from the party and, with the help of the Department of Human Settlements, identified two contractors who attended as guests: Mr M and Mr P. Neither had been on the donor list, but I called them nevertheless to find out whether they had been asked to contribute, and whether they had done so. I wasnt asked for a cent and I didnt pay a cent, replied Mr M. He had been invited to the party because he had known Bonginkosi through political circles from the time he was still a member of the ANC.

Mr P
told a similar story. He was a subcontractor to Mr M, who had phoned during the festivities to encourage him to pop into the party. Mr P did.

By then, I had followed all the leads open to me. And I am confident that, on the information available, there is no more to the story than that. Meanwhile, the impression has been indelibly created in the minds of the newspaper-reading public that the minister has been involved in shady dealings involving contractors to his department paying for a lavish birthday party. The ineluctable deduction is that he is corrupt.

The ANC has reported the allegations to the Public Protector who has powers to probe the matter even more deeply than I did. I will pass on everything I have to assist her. And if anything further emerges, I will study it very carefully.

The one question I have not answered to my satisfaction is where, from inside the DA, this allegation came from in the first place. The newspaper has kept its sources anonymous. I have said it before and I say so again: when it is established that informants have leaked fake news to the media, they (and their motives) should become the focus of the story, because they have not acted in the public interest, only in their own.

It is time that this becomes standard practice in the media. Too much damage is done by anonymous sources spreading fake news, aided and abetted by journalists who know, if they are honest, that their revelations have nothing to do with speaking truth to power. DM

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Helen Zille - Daily Maverick