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5 : From Death To Morning _HOT_

The incident began around 10:30 a.m. and authorities declared a mass casualty incident 30 minutes later. The southbound lanes of the interstate were closed from the Highridge Park Road exit (119) and the northbound lanes were closed from the Hegins exit (112).

5 : From Death to Morning

When Burrous graduated Chapman University in 1997, he became the main news anchor at KEVN-LD in Rapid City, South Dakota. In January 1999, he moved south to KGET-TV in Bakersfield, California to become the station's morning news anchor. While there, he met Mai Do, a journalist, who became his wife.[4]

His next move was as the morning news anchor at KGPE-TV in Fresno, California,[5] and KMAX-TV/KOVR-TV Sacramento, California.[6] At the latter, Burrous became anchor for the newly launched Good Day Sacramento weekend morning show that aired on the two affiliated stations.[7]

According to a Los Angeles County coroner's report, Burrous died from methamphetamine toxicity, complicated by hypertensive and atherosclerotic cardiovascular disease on December 27, 2018. He was found unresponsive at a Glendale, California Days Inn. [11] It was reported that Burrous was in the company of a male companion, and had been engaged in a sexual encounter and using crystal meth at the time of his death, which he had inserted into his anus. His death was ruled an accident.[9]

"This is a tragedy for our department," Garcia said. "Here is an officer driving to work to protect our city in full uniform when his life was taken. He was reporting to work -- in his morning roll call Officer Arellano's name was called like it always is at the start of his shift and Officer Arellano didn't answer."

At about 11:15 a.m. Wednesday, before the department publicly confirmed Arellano's death, officers gathering outside of Methodist Medical Center in Dallas were seen placing black mourning bands across their badges, a common practice to recognize the death of a fellow officer.

This week, we have some of the first polls on how Americans feel about the death of George Floyd, a black man who was killed by a police officer in Minneapolis, and the protests that have cropped up across the U.S. in response.

SIDS is not only a traumatic and devastating event for parents and medical examiners, it is also a cause of death that continues to thwart the efforts of scientists and physicians to prevent it, or at least to identify those children who are at risk. Indeed, the term SIDS was coined to provide a convenient diagnosis for a medical examiner to label an otherwise unexplainable death.

SIDS is a combination of genetic, metabolic and environmental factors that culminate in the death of an infant. Not surprisingly, the literature abounds with many proposed mechanisms, theories and scientific concepts, which are rapidly changing. Nonetheless, researchers have been able to identify various prenatal and postnatal factors that increase the risk of SIDS (see Sidebar A).

Another documented cause of death is the compromising of an infant's airway by a sleeping parent or sibling when bed sharing; in recent years such deaths have increased as bed sharing has become more popular and could explain as many as 50% of sudden unexpected infant deaths (Unger et al, 2003; Blair et al, 2006). The presumed mechanism of death is accidental suffocation by close contact with a co-sleeper. However, the actual cause of death in this situation is usually very difficult to prove.

As mentioned above, educational campaigns with the aim of preventing both prone sleeping and bed sharing have led to a significant decrease in the number of infants dying from suffocation. Nevertheless, SIDS still occurs in seemingly healthy children, even if they sleep on their backs. The main focus of research is therefore to identify other risk factors and to investigate possible pathophysiological mechanisms, as well as theories of how various factors contribute to and cause SIDS. A plausible mechanistic theory is essential to develop diagnostic tests to accurately identify children at risk and, eventually, to develop preventive or therapeutic measures (Leiter & Böhm, 2007).

However, several observations argue against heat stress as being a major cause of SIDS. As dangerous asphyxia can occur very soon after an infant turns its face into the bedding, it would seem that this might cause death before the heat stress could take effect. This, of course, does not eliminate the possibility that a combination of elevated body temperature and re-breathing might be more lethal than either factor alone. In the USA, SIDS rates do not increase during summer heat waves when the country witnesses a marked increase in heat-related deaths (Scheers-Masters et al, 2003), which indicates that heat stress is not a main cause of SIDS, at least in the USA. Finally, perhaps the greatest problem with the heat stress theory is that there has been no pathophysiological mechanism identified so far that could cause sudden death.

The eventual cause of death in SIDS infants is a failure to breathe. However, this should not happen: humans, as well as many animals, have evolved highly effective emergency reflexes to spontaneously recover from severe hypoxia (Thach et al, 1991). If hypoxia turns into coma, cortical activity in the central nervous system and most brainstem-mediated reflexes cease to function. This triggers a set of emergency reflexes that eventually reinstate normal respiration by intermittent hypoxic gasps that, in the absence of compromised lung or cardiovascular function, provide enough oxygen for the body to reinstate normal function.

Infants born prematurely are notoriously susceptible to episodes of apnea, which can be generally distinguished into two types. Awake apnea is attributed to acute hypoventilation associated with breath holding as a result of pain or emotional upset (Abu-Osba et al, 1982). Such spells can result in sudden severe hypoxia with secondary hypoxic apnea. However, once the body's emergency mechanisms kick in, the children autoresuscitate by gasping. Indeed, the hypoventilation associated with ordinary crying has many similarities to clinical breath holding, which is often preceded by crying. Breath holding during arousal from sleep is a common cause of oxygen desaturation in pre-term infants (Abu-Osba et al, 1982). Although SIDS is believed to occur when infants are sleeping, the potential role of brief arousal accompanied by breath holding with severe hypoxia and failed autoresuscitation cannot be excluded as a cause for some SIDS deaths.

The second main type of apnea occurs primarily during sleep. The most important of these are obstructive sleep apnea (OSA) and reflex apnea caused by laryngeal chemoreflexes (LCRs; Pickens et al, 1988; Davies et al, 1988). As the muscle tone of the body ordinarily relaxes during sleep, the soft tissues that make up the walls of the human throat can collapse, thereby causing OSA, which, in a mild form, is quite common. LCRs are stimulated by hypochloride or acid solutions from the stomach content that contact mucosal nerve endings at the entrance to the larynx. They consist of apnea, swallowing, laryngeal closure and coughing. Unlike OSA, apnea in premature infants predominantly consists of respiratory pauses associated with sporadic obstructed breaths. It is usually associated with swallowing during the spell, a characteristic of LCR apnea, but it is not known to happen during OSA (Pickens et al, 1988).

Studies of sleeping human infants, stimulated with water infused into the pharynx, have shown that repeated swallowing, apnea and airway obstruction occurs more often in pre-term infants (Pickens et al, 1988; Davies et al, 1988). Furthermore, several studies have found that apnea and bradycardia associated with swallowing and intermittent airway obstruction occur spontaneously during sleep in pre-term infants, even in the absence of any detectable stimulus (Pickens et al, 1988; Miller & DiFiore, 1995). Apnea can also occur through regurgitation of the stomach content. This suggests that endogenous stimuli from accumulated pharyngeal secretions or regurgitated gastric fluid can elicit LCR responses in pre-term infants (Pickens et al, 1989). Apnea therefore remains a viable hypothesis for sudden death in infants. In fact, a few of the home recordings of SIDS cases indicate that apnea preceded death (Poets et al, 1999; Sridhar et al, 2003; Meny et al, 1994). The apnea hypothesis is also strengthened by the observation that its persistence is much stronger in pre-term infants who are at an especially high risk for SIDS (Hunt et al, 2004).

In support of the argument that viral infection could be a precursor for at least some cases of SIDS, Vege & Rognum (2004) reported increased levels of interleukins in the cerebrospinal fluid of many SIDS victims. Other studies associated RSV infection with increased LCR reflexes and an increase in inflammatory interleukin in the laryngeal mucosa. It remains to be seen how increased interleukin in the brainstem might cause sudden death, but these observations support the theory of subtle infections as an initial cause of apnea and eventually SIDS. There is also epidemiological support for this theory: seasonal outbreaks of RSV during the winter months coincide with a peak of SIDS cases. Together, this would make a strong but circumstantial case for upper-airway infections that cause LCR apnea as the mechanism for the increased SIDS incidence in the winter.

Some have speculated that OSA could also cause sudden death in infants because the vast majority of SIDS infants are presumed to die during their sleep and OSA is entirely a sleep-dependent disorder (White, 1995). Indeed, the severity of OSA increases with viral infections of the upper airway, which increase nasal resistance. Moreover, epidemiological studies found that a family history of OSA is a risk factor for SIDS (Tishler et al, 1996) and that brief episodes of OSA were more common in infants who ultimately died of SIDS (Kahn et al, 1992). 041b061a72


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