Detection and Molecular Characterization of Staphylococci from Eggs of Household Chickens.

Eggs are a healthy and nutritious food source, but may be contaminated by bacteria. Previous studies have reported the presence of staphylococci in eggs of farmed chickens, but no study has evaluated the staphylococcal population of eggs from household chickens. In this study, staphylococci from eggs (n = 275) of household chickens collected from November 2016 to March 2017 from different villages of Khyber Pakhtunkhwa province, Pakistan, were characterized. Seven species of staphylococci were identified from 65 eggs, including the predominant species, Staphylococcus xylosus (49/275; 17.8%). S. xylosus isolates (n = 73) were tested for antimicrobial susceptibility, presence of resistance genes, genetic relatedness, and inhibitory activity against other bacteria. The majority of isolates were resistant to oxacillin (83.6%) and tetracycline (24.7%), but also exhibited resistance to daptomycin and linezolid (5.5% each). Of the 10 resistance genes tested, isolates were only positive for mecA (35.6%; 26/73), mecC/C1 (2.7%; 2/73), and tet(K) (14/73; 19%). Using pulsed-field gel electrophoresis (PFGE), nine clusters had identical PFGE patterns. Isolates produced inhibitory activity against a broad spectrum of bacteria; 20.5%, 19.2%, 17.8%, and 16.4% of S. xylosus were able to inhibit growth of Salmonella enterica serotype Typhi, methicillin-susceptible Staphylococcus aureus, Escherichia coli, and methicillin-resistant Staphylococcus aureus, respectively. This study demonstrated the presence of genetically related antimicrobial-resistant S. xylosus from eggs from household chickens. Like table eggs, eggs of household chickens also contain staphylococci that may be resistant to antimicrobials used to treat human infections. These data will allow comparison between staphylococci from eggs from different sources and may indicate the relative safety of eggs from household chickens. Further study of these egg types and their microbial composition is warranted.

Calcium Regulation in Alzheimer's Disease: Mechanistic Understanding.

This study is systematic review of the research, focused on all possible pathways involved in calcium (Ca2+) regulation in order to utilize them in the control and remediation of Alzheimer's disease (AD), because Ca2+ plays important role in pathogenesis of AD. Electronic databases, Science Direct and PubMed/Medline, for relevant publications between 2000April 2017, were searched. Ca2+ ions are very important in cell signaling in body, specially the neuronal signaling. Many pathways are involved in normal neuronal Ca2+ signaling. AD is one of the most commonly known neurodegenerative disorders, causing dementia and some other neuropathological signs in mostly elderly people reaching a rate of 44 million until now. Depending upon certain possibilities, many hypothesis were proposed related to AD; out of which, one is Ca2+ hypothesis. According to this hypothesis, disturbance in Ca2+ signaling pathway due to certain reasons, such as accumulation of beta-amyloid proteins, ER stress, cytochrome c activation etc., causes AD. Due to less clinical research, only few FDAapproved pharmaceuticals are available for treatment of AD. Reviewed studies suggest that Ca2+ channel blocker and initiator may play an important role in cure of AD.

Prenatal cigarette smoke exposure and postnatal respiratory responses to hypoxia and hypercapnia.

Prenatal cigarette smoke (CS) exposure, in combination with hypoxia and/or hyperthermia can lead to gasping and attenuated recovery from hypoxia in 7 days old rat pups. We studied 95 unanesthetized spontaneously breathing 14 days old rat pups to investigate if the destabilizing effects of increased ambient temperature and prenatal CS exposure on respiratory control observed in 7 days old rats were still evident at day 14. This postnatal age was selected as it is beyond the analogous risk period for SIDS in human. Furthermore, we investigated if the breathing responses to hypercapnia are affected by prenatal CS exposure. Since high ambient (HA) temperature can lead to gasping and aberrant respiratory control, we recorded respiratory patterns at low (24-25°C) and high (29-30°C) ambient temperatures, and under hypoxic or hypercapnic states. No gasping was observed in 14 days old rat pups. During hypoxia, breathing frequency increased in the CS-exposed group under low and HA temperatures. Rectal temperature decreased only in the sham group in response to low ambient temperature hypoxia. At HA temperature, breathing frequency increased in both sham and CS-exposed groups during hypercapnia, however, it remained elevated during washout period only in the sham group. We demonstrate that prenatal CS exposure continues to have profound effects on respiratory and thermoregulatory responses to hypoxia and hypercapnia at day 14. The attenuated respiratory and thermoregulatory responses to acute hypoxia and hypercapnia on day 14 demonstrate a strong interaction between CS exposure, respiratory control, and thermoregulation during postnatal maturation.

Respiratory control in neonatal rats exposed to prenatal cigarette smoke.

RATIONALE: Prenatal cigarette smoke (CS) exposure, increased environmental temperature, and hypoxic episodes have been postulated as major risk factors for sudden infant death syndrome. OBJECTIVES: To test the hypothesis that maternal CS exposure disrupts eupneic breathing and depresses breathing responses of neonatal rats to thermal and hypoxic challenges. METHODS: Experiments were performed on 1-week-old rat pups exposed prenatally to CS (n = 39) or room air (sham; n = 30). Breathing patterns were recorded by whole-body plethysmography during thermoneutral or hyperthermic states under normoxic and hypoxic conditions. MEASUREMENTS AND MAIN RESULTS: Mean pup weight, breaths per minute, and gasping respiratory patterns were measured for both smoke- and sham-exposed groups during thermoneutral and hyperthermic states under normoxic and hypoxic conditions. Under thermoneutral conditions, hypoxia caused gasping in CS-exposed animals but not in sham-exposed animals. Furthermore, under hyperthermic conditions, whereas hypoxia induced gasping in both groups, only CS-exposed animals exhibited a pronounced and longer lasting respiratory depression after the termination of hypoxia. CONCLUSIONS: We show that prenatal CS exposure increases the likelihood of gasplike respiration and provide the first experimental evidence that the combined effects of prenatal CS exposure and hyperthermia dramatically prolong the time required for neonates to return to eupneic breathing after hypoxia. These observations provide important evidence of how prenatal CS exposure, hypoxic episodes, and hyperthermia might place infants at higher risk for sudden infant death syndrome.