Spasticity, resulting in involuntary and sustained contractions of muscles, may evolve in patients with stroke, cerebral palsy, multiple sclerosis, brain injury, and spinal cord injury (SCI). The authors critically review the neural mechanisms that may contribute to spasticity after SCI and assess their likely degree of involvement and relative significance to its pathophysiology. Experimental data from patients and animal models of spasticity as well as computer simulations are evaluated. The current clinical methods used for the management of spasticity and the pharmacological actions of drugs are discussed in relation to their effects on spinal mechanisms. Critical assessment of experimental findings indicates that increased excitability of both motoneurons and interneurons plays a crucial role in pathophysiology of spasticity. New interventions, including forms of spinal electrical stimulation to suppress increased neuronal excitability, may reduce the severity of spasticity and its complications.

We previously showed that genetic inactivation of malonyl-CoA decarboxylase (MCD), which regulates fatty acid oxidation, protects mice against high-fat diet-induced insulin resistance. Development of insulin resistance has been associated with activation of the inflammatory response. Therefore, we hypothesized that the protective effect of MCD inhibition might be caused by a favorable effect on the inflammatory response. We examined if pharmacological inhibition of MCD protects neonatal cardiomyocytes and peritoneal macrophages against inflammatory-induced metabolic perturbations. Cardiomyocytes and macrophages were treated with LPS to induce an inflammatory response, in the presence or absence of an MCD inhibitor (CBM-301106, 10 M). Inhibition of MCD attenuated the LPS-induced inflammatory response in cardiomyocytes and macrophages. MCD inhibition also prevented LPS impairment of insulin-stimulated glucose uptake in cardiomyocytes and increased phosphorylation of Akt. Additionally, inhibition of MCD strongly diminished LPS-induced activation of palmitate oxidation. We also found that treatment with an MCD inhibitor prevented LPS-induced collapse of total cellular antioxidant capacity. Interestingly, treatment with LPS or an MCD inhibitor did not alter intracellular triacylglycerol content. Furthermore, inhibition of MCD prevented LPS-induced increases in the level of ceramide in cardiomyocytes and macrophages while also ameliorating LPS-initiated decreases in PPAR binding. This suggests that the anti-inflammatory effect of MCD inhibition is mediated via accumulation of long-chain acyl-CoA, which in turn stimulates PPAR binding. Our results also demonstrate that pharmacological inhibition of MCD is a novel and promising approach to treat insulin resistance and its associated metabolic complications.

The continued use of ASA during AMI and PUD bleeding was variable. However, patients with low-risk ulcers and those who received coronary intervention were more likely to have ASA continued during PUD bleeding. Further studies evaluating the gastrointestinal risk of immediate ASA use in AMI with acute PUD bleeding are required.

анал л кування 320 д тей в ком в д 3 до 18 рок в с астичними ормами дитячого церебрального арал чу. тям було роведено о еративне л кування. о о ерац д ти отримували ре арат сирдалуд, сля о ерац-сирдалуд, маса , л кувальну культуру. Пре арат мен у с астичний стан м'я в, чинить небол вальну д. Ключові слова: дитячий церебральний арал ч, с рдалуд, л кувальна культура. ЛЕЧЕНИЕ СПАСТИЧЕСКИХ ФОРМ ДЕТСКОГО ЦЕРЕБРАЛЬНОГО ПАРАЛИЧА У ДЕТЕЙ НА ЭТАПАХ ОПЕРАТИВНОГО ВМЕШАТЕЛЬСТВА Summary. Analysis of examination of 320 children with the spastic forms of cerebral palsy from 3 to 18 years old was carried out. All children were treated by surgical therapy. Children received sirdalud before the operation, after the operation they received sirdalud, massage and therapeutic gymnastics. This remedy reduces muscular tonus and pain.

ДУ «Національний науковий центр «Інститут кардіології ім. акад. М.Д. Стражеска» НАМН України», м. Київ Резюме. У роботі досліджується зв'язок між психоемоційним станом пацієнта із серцево-судинною патологією та оцінкою якості життя. Акцентується увага на цілісному підході в наданні медичної допомоги соматичному пацієнту з урахуванням фізичних, психологічних та соціальних аспектів його життя. Інтегро-ваний підхід передбачає залучення психотерапевта та/або медичного психолога до лікування соматичної патології.Ключові слова: якість життя, тривога, депресія, серцево-судинна патологія. ВЛИЯНИЕ ТРЕВОГИ И ДЕПРЕССИИ НА КАЧЕСТВО ЖИЗНИ ПАЦИЕНТА С СЕРДЕЧНО-СОСУДИСТОЙ ПАТОЛОГИЕЙ В.М. Корнацкий, Д.Н. МорозРезюме. В работе исследуется связь между психоэмоциональным состоянием пациента с сердечно-сосудистой патологией и оценкой качества жизни. Акцентируется внимание на целостном подходе в предоставлении медицинской помощи соматическому пациенту с учетом физических, психологических и социальных аспектов его жизни. Интегрированный подход предусматривает привлечение психотерапевта и/или медицинского психолога к лечению соматической патологии.