The City of Brockton's "Champion Plan": The Role of Police Departments in Facilitating Access to Treatment.

The City of Brockton (Massachusetts) initiated The Champion Plan (TCP) in February 2016 as part of a community-wide effort to redefine the public safety sector's approach to policing the drug crisis. TCP program model allows those suffering from addiction to walk into a police station and ask for treatment. Early evidence suggests substantial successes for this approach to addressing addiction. Data show 523 individuals walked into the Brockton Police Department 818 times looking for help during the first 24 months of operation. Program staff were able to secure placement beds, on average, within 90 minutes of making contact with clients. Program clients report high levels of satisfaction with the program model, and early data indicate that a substantial number of clients retain engagement with services beyond intake. Findings from this study indicate police-centered treatment-on-demand programs may be viable strategies for getting those suffering from the disease of addiction into treatment.

Angiotensin-II is a putative neurotransmitter in lactate-induced panic-like responses in rats with disruption of GABAergic inhibition in the dorsomedial hypothalamus.

Intravenous sodium lactate infusions or the noradrenergic agent yohimbine reliably induce panic attacks in humans with panic disorder but not in healthy controls. However, the exact mechanism of lactate eliciting a panic attack is still unknown. In rats with chronic disruption of GABA-mediated inhibition in the dorsomedial hypothalamus (DMH), achieved by chronic microinfusion of the glutamic acid decarboxylase inhibitor L-allylglycine, sodium lactate infusions or yohimbine elicits panic-like responses (i.e., anxiety, tachycardia, hypertension, and tachypnea). In the present study, previous injections of the angiotensin-II (A-II) type 1 receptor antagonist losartan and the nonspecific A-II receptor antagonist saralasin into the DMH of "panic-prone" rats blocked the anxiety-like and physiological components of lactate-induced panic-like responses. In addition, direct injections of A-II into the DMH of these panic-prone rats also elicited panic-like responses that were blocked by pretreatment with saralasin. Microinjections of saralasin into the DMH did not block the panic-like responses elicited by intravenous infusions of the noradrenergic agent yohimbine or by direct injections of NMDA into the DMH. The presence of the A-II type 1 receptors in the region of the DMH was demonstrated using immunohistochemistry. Thus, these results implicate A-II pathways and the A-II receptors in the hypothalamus as putative substrates for sodium lactate-induced panic-like responses in vulnerable subjects.

Myostatin inhibition slows muscle atrophy in rodent models of amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease leading to motor neuron cell death, but recent studies suggest that non-neuronal cells may contribute to the pathological mechanisms involved. Myostatin is a negative regulator of muscle growth whose function can be inhibited using neutralizing antibodies. In this study, we used transgenic mouse and rat models of ALS to test whether treatment with anti-myostatin antibody slows muscle atrophy, motor neuron loss, or disease onset and progression. Significant increases in muscle mass and strength were observed in myostatin-antibody-treated SOD1(G93A) mice and rats prior to disease onset and during early-stage disease. By late stage disease, only diaphragm muscle remained significantly different in treated animals in comparison to untreated controls. Myostatin inhibition did not delay disease onset nor extend survival in either the SOD1(G93A) mouse or rat. Together, these results indicate that inhibition of myostatin does not protect against the onset and progression of motor neuron degenerative disease. However, the preservation of skeletal muscle during early-stage disease and improved diaphragm morphology and function maintained through late stage disease suggest that anti-myostatin therapy may promote some improved muscle function in ALS.

Use of magnesium sulfate for pediatric patients with acute asthma exacerbations.

The number of children with a diagnosis of asthma has increased significantly over the years, and asthma currently is the most common pediatric chronic disease. Asthma continues to take the lives of children at an alarming rate. Proper diagnosis, education, and appropriate management are essential for decreasing morbidity and mortality. Asthma can be diagnosed with a thorough medical history, family history, and physical examination. Diagnostic and assessment tools such as pulmonary function tests and pediatric asthma scores are valuable for determining the severity of asthma. Immediate assessment and initiation of appropriate medications and management are essential for a positive outcome. The use of bronchodilator therapy with corticosteroids is the gold standard for acute asthma exacerbation, but it may not be effective for certain moderate to severe exacerbations. This article discusses the prevalence, pathophysiology, and diagnosis and treatment of asthma, including the role of magnesium sulfate for acute asthma exacerbations.

Inhibition of myostatin in adult mice increases skeletal muscle mass and strength.

A human therapeutic that specifically modulates skeletal muscle growth would potentially provide a benefit for a variety of conditions including sarcopenia, cachexia, and muscular dystrophy. Myostatin, a member of the TGF-beta family of growth factors, is a known negative regulator of muscle mass, as mice lacking the myostatin gene have increased muscle mass. Thus, an inhibitor of myostatin may be useful therapeutically as an anabolic agent for muscle. However, since myostatin is expressed in both developing and adult muscles, it is not clear whether it regulates muscle mass during development or in adults. In order to test the hypothesis that myostatin regulates muscle mass in adults, we generated an inhibitory antibody to myostatin and administered it to adult mice. Here we show that mice treated pharmacologically with an antibody to myostatin have increased skeletal muscle mass and increased grip strength. These data show for the first time that myostatin acts postnatally as a negative regulator of skeletal muscle growth and suggest that myostatin inhibitors could provide a therapeutic benefit in diseases for which muscle mass is limiting.