Natural bioburden levels detected on rigid lumened medical devices before and after cleaning

Controversy exists concerning the degree of microbial contamination associated with the us of rigid lumened medical devices, the efficacy of standard cleaning techniques used to remove pathogenic microorganisms from lumen channels, and whether patients are placed at risk of cross infection because of microbial contamination. In this study the level and types of microorganisms found on rigid lumened medical devices before and after cleaning in a hospital environment were investigated. The bioburden level after clinical use was found to be relatively low, ranging from 10¹ to 10⁴ colony forming units (CFU) per device. After the instruments were cleaned, none of the devices studied contained bioburden levels greater than 10⁴ CFU and 83% had bioburden levels less than or equal to 10² CFU. The bioburden present before cleaning was comprised of organisms derived from the handling of the device, from the hospital environment, and from the patient. The bioburden present after cleaning was comprised of organisms typically derived from the handling of the device and from the hospital environment. The level of bioburden per device was also related to the anatomic site where the device was used, with lower numbers of organisms found on devices exposed to sterile body sites and the respiratory tract.     

No quiet surrender: molecular guardians in multiple sclerosis brain

The brain under immunological attack does not surrender quietly. Investigation of brain lesions in multiple sclerosis (MS) reveals a coordinated molecular response involving various proteins and small molecules ranging from heat shock proteins to small lipids, neurotransmitters, and even gases, which provide protection and foster repair. Reduction of inflammation serves as a necessary prerequisite for effective recovery and regeneration. Remarkably, many lesion-resident molecules activate pathways leading to both suppression of inflammation and promotion of repair mechanisms. These guardian molecules and their corresponding physiologic pathways could potentially be exploited to silence inflammation and repair the injured and degenerating brain and spinal cord in both relapsing-remitting and progressive forms of MS and may be beneficial in other neurologic and psychiatric conditions.It is difficult to say a favorable word about a terrible disease, but one of the positive features of multiple sclerosis (MS) is the remarkable capacity for patients to spontaneously recover from neurologic deficits that are attributed to inflammatory attacks on the CNS. About 80% of patients initially present with a decade or more of relapsing attacks in various areas of the CNS. Most of the neurologic deficits in these recurrent acute attacks, known as relapses after the initial episode, resolve nearly completely over a few days to a few weeks (1). For example, an attack on the optic nerve can leave an individual unable to read for a few days or weeks, but in many cases, there is full recovery of visual acuity after the initial neurologic insult. An attack within the pyramidal system in the brain or spinal cord may cause paralysis of a limb, but often there is recovery from this deficit over days and weeks in the early stages of MS. Despite these remissions, the course of disease advances over a decade or more in about a quarter of individuals. In these unfortunate individuals, relapsing-remitting disease transitions to secondary progressive MS, which is characterized by a large burden of disability and a lack of distinct relapses (1).The substantial and remarkable recovery (remission) from an inflammatory insult (relapse) is a well-known phenomenon; however, more attention has been given to analyzing the inflammation that produces clinical deficits than to the processes that account for remission. The brain in MS frequently responds to immune damage with an array of molecules that serve to protect it from further damage and to foster recovery. This beneficial response to injury may be coordinated. Both cells extrinsic and intrinsic to the CNS are involved in the production of these guardian molecules. Some guardian molecules enter the somewhat privileged site of the brain via infiltrating immune cells (1–6), still others are present at the blood-brain barrier that forms an interface between the immune system and the brain (7–11), while others are produced within the CNS itself (12–35).This Review will describe these guardian molecules including protective cytokines like type 1 interferon, IL-10, and IL-27; the neurotrophins; neurotransmitters like GABA; antioxidants; small lipids present in the normal myelin sheath; nuclear hormone receptors; amyloid-forming molecules; and serpins and other inhibitory proteins. All these molecules may serve as platforms for novel restorative therapies, provided they can be delivered to the brain structures under attack.     

Exploiting PI3K/mTOR signaling to accelerate epithelial wound healing

The molecular circuitries controlling the process of skin wound healing have gained new significant insights in recent years. This knowledge is built on landmark studies on skin embryogenesis, maturation, and differentiation. Furthermore, the identification, characterization, and elucidation of the biological roles of adult skin epithelial stem cells and their influence in tissue homeostasis have provided the foundation for the overall understanding of the process of skin wound healing and tissue repair. Among numerous signaling pathways associated with epithelial functions, the PI3K/Akt/mTOR signaling route has gained substantial attention with the generation of animal models capable of dissecting individual components of the pathway, thereby providing a novel insight into the molecular framework underlying skin homeostasis and tissue regeneration. In this review, we focus on recent findings regarding the mechanisms involved in wound healing associated with the upregulation of the activity of the PI3K/Akt/mTOR circuitry. This review highlights critical findings on the molecular mechanisms controlling the activation of mTOR, a downstream component of the PI3K–PTEN pathway, which is directly involved in epithelial migration and proliferation. We discuss how this emerging information can be exploited for the development of novel pharmacological intervention strategies to accelerate the healing of critical size wounds.     

Protective effects of Mentha piperita Linn on benzo[a]pyrene-induced lung carcinogenicity and mutagenicity in Swiss albino mice

The Editor-in-Chief has retracted the published paper "ProtectiveEffects of     

Heme oxygenase-1 and carbon monoxide suppress autoimmune neuroinflammation

Heme oxygenase-1 (HO-1, encoded by HMOX1) dampens inflammatory reactions via the catabolism of heme into CO, Fe, and biliverdin. We report that expression of HO-1 dictates the pathologic outcome of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). Induction of EAE in Hmox1(-/- )C57BL/6 mice led to enhanced CNS demyelination, paralysis, and mortality, as compared with Hmox1(+/+) mice. Induction of HO-1 by cobalt protoporphyrin IX (CoPPIX) administration after EAE onset reversed paralysis in C57BL/6 and SJL/J mice and disease relapse in SJL/J mice. These effects were not observed using zinc protoporphyrin IX, which does not induce HO-1. CoPPIX protection was abrogated in Hmox1(-/-) C57BL/6 mice, indicating that CoPPIX acts via HO-1 to suppress EAE progression. The protective effect of HO-1 was associated with inhibition of MHC class II expression by APCs and inhibition of Th and CD8 T cell accumulation, proliferation, and effector function within the CNS. Exogenous CO mimicked these effects, suggesting that CO contributes to the protective action of HO-1. In conclusion, HO-1 or exposure to its end product CO counters autoimmune neuroinflammation and thus might be used therapeutically to treat MS.