BackgroundPeptic ulcer disease (PUD) is a major public health burden significantly impacting the cost of hospitalization in the United States (US). We examined the trends, characteristics, complications, cost, and seasonality of PUD-related hospitalizations from 2000 to 2011.MethodsWith the use of the Nationwide Inpatient Sample from 2000 through 2011, we identified PUD-related hospitalizations using the International Classification of Diseases (ICD-9), 9th Revision, and the Clinical Modification code 531.00 to 534.91 as the principal discharge diagnosis. The total number of hospitalizations for each calendar month of the year were added over a 12-year period, and this number was divided by the number of days in that particular month to obtain the mean hospitalizations per day for each month.ResultsThe study found that 351,921 hospitalizations with the primary discharge diagnosis of peptic ulcer disease (PUD) occurred in the US between 2000 and 2011. This number dropped significantly from 49,524 to 17,499 between 2000 and 2011, and the rate of PUD-related mortality decreased from 4.3% to 3.1%. The mean age of the study population was 66.2 ± 17.4 years; 52.3% were males, and 56.8% were white. The number of hospitalizations in the US peaked in the spring season (916/day), and reached a nadir in the fall season (861/day). The mean cost of PUD hospitalization increased significantly from $11,755 in 2001 to $13,803 in 2011 (relative increase of 17%; p <0.001).ConclusionThe incidence of PUD and its mortality has decreased significantly in the last decade, but its economic burden on the healthcare system remains high. A seasonal pattern of PUD hospitalization showed a peak in PUD-related admissions in the spring season and a trough in the fall season.

Health and environmental problems arising from metals present in the aquatic ecosystem are very well known. The present study investigated toxicological effects of LC15 of metals such as copper, chromium, and lead for 24, 48, 72, and 96 h on hematological indices, RBC nucleus and cell morphology, and gill and muscle tissues of grass carp (Ctenopharyngodon idella). Experimental dose concentrations of copper were 1.5, 1.4, 1.2, and 1 mgL−1. Similarly, dose concentrations of chromium were 25.5, 22.5, 20, and 18 mgL−1 while those of lead were 250, 235, 225, and 216 mgL−1, respectively. Maximum decrease in the concentration of Hb, RBCs, and monocytes was observed against chromium, while maximum increase in the concentration of lymphocytes was reported against lead. Abnormalities such as single and double micronuclei, deformed nucleus, nuclear shift, irregular nucleus, deformed cells, microcyte cells, and vacuolated and swollen cells were observed. Gill tissues absorbed maximum concentration of lead followed by chromium and copper. Muscle tissues also absorbed maximum concentration of lead followed by chromium and copper, respectively. Histological alterations such as epithelial lifting, interlamellar spaces, club gill filaments, gill bridging, curling filaments, swelling and fusion of cells, irregular cells, destruction of epithelial cells, cellular necrosis, and inflammatory cells were observed in gill tissues while inflammation and necrosis of muscle fibers, degeneration of muscle fibers, edema of muscle bundles, zig-zag of muscle fibers, and lesions were observed in muscle tissues of fish exposed with different doses of these heavy metals, indicating the toxicity of metals to aquatic fauna as well as to human being via food chain.

The main purpose of this study is to provide essential information regarding the molecular basis of insecticide resistance and to report candidate genes which are responsible for resistance in insects/pests. There are two basic resistance mechanisms existing in pests, i.e., target site resistance and metabolic resistance. During resistance of target site, the specific binding site of an insecticide is modified (mutated) and/or lost, which makes the target site incompatible for activation. Mutation occurs in most common pest (Myzus persicae, Musca domestica and Drosophila melanogaster) target regions, i.e., subunits like nicotinic acetylene choline receptors (nAChRs), knock-down resistance (KDR) etc. Due to these mutations, insecticides are unable to bind into the target region, resulting in loss of binding affinity. Furthermore, in metabolic resistance over production of enzymes occurs which break down (detoxify) insecticides and resulting resistance of pests. The amplification of metabolic enzymes, i.e., Cytochromes p450 monooxygenase, hydrolyses, and Glutathione S-transferase play a central role in evolving metabolic resistance. Various successful approaches are used to combat pests resistance such as insecticides, bio-pesticides and biological control agents. However, some of these strategies have certain limitations such as contamination of the environment, while others possess a low capacity in management of pests. Recent studies have highlighted some novel mechanisms of insecticide resistance that are part of the ongoing efforts to define the molecular basis of insecticide resistance in insect species.

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Ebola virus (EBOV) was discovered for the first time in 1976. It belongs to the family Filoviridae, which causes hemorrhagic fever that could lead to death in a few days. West Africa faced a major outbreak where symptoms appeared in the form of chills, myalgia, fever, diarrhea, and vomiting, and the disease finally reached a severe state as a result of hemorrhagic complications and failure of multiple organs. EBOV spreads by contact with body fluids of an infected person such as blood, saliva, urine, and seminal fluid, and also spreads by a contact with contaminated surfaces. Viral infection depends on the virus and host defenses. When the virus invades the body, the immune system becomes activated in an attempt to neutralize it. However, if this fails, EBOV viral infection spreads and leads to impaired innate and adaptive immune responses and uncontrollable viral replication. Consequently, the symptomatic patient is isolated and various medicinal regimens such as BCX-4430n TKM- EBOV are used, to cure EBOV, though, a specific treatment is not available. Accordingly, the aim of the present review is to survey and summarize the recent literature pertaining to the outbreak of EBOV, systematic infection of the human body, along with transmission and treatment. In addition, the review also aims to identify areas that need more research and development in combatting this dangerous virus. In the meantime, it should be noted that there is no fully FDA approved drug to treat infections by this virus. Therefore, there is a pressing need to focus on drug discovery along with public awareness to effectively manage any outbreaks in the future.