A Time Series Model for Assessing the Trend and Forecasting the Road Traffic Accident Mortality

Background: Road traffic accident (RTA) is one of the main causes of trauma and known as a growing public health concern worldwide, especially in developing countries. Assessing the trend of fatalities in the past years and forecasting it enables us to make the appropriate planning for prevention and control. Objectives: This study aimed to assess the trend of RTAs and forecast it in the next years by using time series modeling. Materials and Methods: In this historical analytical study, the RTA mortalities in Zanjan Province, Iran, were evaluated during 2007 - 2013. The time series analyses including Box-Jenkins models were used to assess the trend of accident fatalities in previous years and forecast it for the next 4 years. Results: The mean age of the victims was 37.22 years (SD = 20.01). From a total of 2571 deaths, 77.5% (n = 1992) were males and 22.5% (n = 579) were females. The study models showed a descending trend of fatalities in the study years. The SARIMA (1, 1, 3) (0, 1, 0) 12 model was recognized as a best fit model in forecasting the trend of fatalities. Forecasting model also showed a descending trend of traffic accident mortalities in the next 4 years. Conclusions: There was a decreasing trend in the study and the future years. It seems that implementation of some interventions in the recent decade has had a positive effect on the decline of RTA fatalities. Nevertheless, there is still a need to pay more attention in order to prevent the occurrence and the mortalities related to traffic accidents

A Cost-Minimization Analysis of Day-Care Versus in-Patient Surgery for Five Most Common General Surgical Procedures

Objective: This study aimed to compare costs of Day-care versus in-patient surgery for five most common general surgical proce-dures in a general hospital in Iran. Methods: In this retrospective study the records of all patients who underwent five most common general surgical operations (in-cluding Hernia, Hemorrhoid, Fistula, Pilonidal Sinus and Varicocele) between March 2011 and March 2013 were reviewed. The data about costs of these procedures was collected by a checklist, designed by the authors, one year before and one year after establishing the Day-Care ward in the hospital. The checklist was designed on the basis of 14 financial items related to surgical patients. All costs were measured from the provider's perspective. Results: The results of this study showed that after implementing day-care surgery ward, inpatient care costs, such as medi-cine/drugs, physician visits, medical consumable, personnel and hotel, reduced significantly per each procedure. However, the costs directly associated with each surgery, such as drugs and consumable, surgeon's wage and anesthesia costs, between these two periods was not significantly different. The highest amount of savings was related to the personnel costs, with 997,000 IRR reductions. On average, total cost of each procedure was reduced by 2,031,358 IRR after implementation of day-care ward. Conclusion: The findings from this study demonstrate that day-care surgery is a cost saving method compared to in-patient surgery for five most common general surgical procedures. It is recommended that hospital managers consider establishing day-care ward and conducting surgical procedures, in particular elective general surgical procedures, in this regimen, to decrease hospital costs and to make hospital beds free, for other patients who are more in need of specialized medical and nursing skills

Phylogenetic relationships of Pterocarya (Juglandaceae) with an emphasis on the taxonomic status of Iranian populations using ITS and trnH-psbA sequence data

Pterocarya fraxinifolia (Lam.) Spach., a relict tree species of the Juglandaceae family, is native to the Great Caucasus, Anatolia, and to the Hyrcanian forests of the southern Azerbaijan and Northern Iran. In this study, the phylogenetic relationship of the species, sampled in selected Iranian populations, and the global biogeography of the genus Pterocarya were addressed. Leaves were collected from 8 to 10 trees from three geographically isolated habitats. The samples were analyzed with nuclear (internal transcribed spacer [ITS] regions) and chloroplast (trnH-psbA) DNA markers. The obtained results were compared and analyzed with the data registered in NCBI GenBank. It is reported that the ITS regions varied from 644 to 652 for Pterocarya genus, but we did not observe polymorphisms for Iranian Pterocarya. The phylogenetic tree divided the Pterocarya genus in three clades: clade 1 grouping exclusively the samples P. fraxinifolia, clearly separated from the East Asiatic taxa; clade 2 that includes the species P. hupehensis and P. macroptera; clade 3 clustering P. stenoptera and P. tonkinensis. Although the Iranian Pterocarya samples and P. fraxinifolia from the Caucasus were in the same clade, they presented two different secondary structures. The Iranian populations showed the maximum genetic distance with P. stenoptera and P. tonkinensis. Our analysis demonstrates that the traditional division of all the six species sampled throughout their distribution area as well as the phylogeny of the genus Pterocarya needs to be reviewed

Measuring equity in household's health care payments (Tehran-Iran 2013): Technical points for health policy decision makers

Background: Households' financial protection against health payments and expenditures and equity in utilization of health care services are of the most important tasks of governments. This study aims to measuring equity in household's health care payments according to fairness in financial contribution (FFC) and Kakwani indices in Tehran-Iran, 2013. Methods: This cross-sectional study was conducted in 2014.The study sample size was estimated to be 2200 households. Households were selected using stratified-cluster sampling including typical families who reside in the city of Tehran. The data were analyzed through Excel and Stata v.11software. Recall period for the inpatient care was 1 year and for outpatient1 month. Results: The indicator of FFC for households in health financing was estimated to be 0.68 and the trend of the indicator was ascending by the rise in the ranking of households' financial level. The Kakwani index was estimated to be a negative number (-0.00125) which indicated the descending trend of health financing system. By redistribution of incomes or the exempt of the poorest quintiles from health payments, Kakwani index was estimated to be a positive number (0.090555) which indicated the ascending trend of health financing system. Conclusion: According to this study, the equity indices in health care financing denote injustice and a descending trend in the health care financing system. This finding clearly shows that deliberate policy making in health financing by national health authorities and protecting low-income households against health expenditures are required to improve the equity in health

Small Cell Carcinoma of Bladder; Still A Diagnostic and Therapeutic Challenge: Seven Years of Experience and Follow-up in A Referral Center

PURPOSE: To report clinical, histopathological, and treatment features of small cell carcinoma of (SmccB) bladder during 7 years in a referral center. METHODS: The clinical, histopathological features, treatment modalities, and outcome of all patients with bladder SmccB treated between 2009 and 2016 who were managed in Hasheminejad Kidney Center (HKC) were retrospectively collected. RESULTS: Thirteen patients were diagnosed and managed with SmccB. The average age of patients was 64.92 years. For each patient, 8 markers were used for IHC staining on average. Neuroendocrine markers such as CD 56, Neuron Specific Enolase, Synaptophysin, and Chromogranin were found in a significant percentage of patients (69, 38, 54, and 31 respectively). Patients were managed with TURBT alone (N=3), chemotherapy after TURBT (N=4), chemotherapy plus radical surgery (N=4) and radical surgery alone (N=2). The best clinical result was seen in chemotherapy received patients with or without radical surgery. The mean(SE) of survival rate in patients who received only chemotherapy alone was 42.4 (10.0) months, while in those who were managed with chemotherapy plus radical surgery it was 47.7 (10.1) months. CONCLUSION: In our center immunohistochemistry was needed for definitive diagnosis in 17/19 samples. Misdiagnosis happened in two samples without IHC request. We think that use of immunohistochemistry should be mandatory for diagnosis of SmccB to exclude misdiagnosis. Chemotherapy is the most important part of treatment and the addition of radical surgery can slightly improve patients' survival

Quantitative analysis of regional distribution of tau pathology with 11C-PBB3-PET in a clinical setting.

PURPOSE The recent developments of tau-positron emission tomography (tau-PET) enable in vivo assessment of neuropathological tau aggregates. Among the tau-specific tracers, the application of 11C-pyridinyl-butadienyl-benzothiazole 3 (11C-PBB3) in PET shows high sensitivity to Alzheimer disease (AD)-related tau deposition. The current study investigates the regional tau load in patients within the AD continuum, biomarker-negative individuals (BN) and patients with suspected non-AD pathophysiology (SNAP) using 11C-PBB3-PET. MATERIALS AND METHODS A total of 23 memory clinic outpatients with recent decline of episodic memory were examined using 11C-PBB3-PET. Pittsburg compound B (11C-PIB) PET was available for 17, 18F-flurodeoxyglucose (18F-FDG) PET for 16, and cerebrospinal fluid (CSF) protein levels for 11 patients. CSF biomarkers were considered abnormal based on Aβ42 ( 450 ng/L). The PET biomarkers were classified as positive or negative using statistical parametric mapping (SPM) analysis and visual assessment. Using the amyloid/tau/neurodegeneration (A/T/N) scheme, patients were grouped as within the AD continuum, SNAP, and BN based on amyloid and neurodegeneration status. The 11C-PBB3 load detected by PET was compared among the groups using both atlas-based and voxel-wise analyses. RESULTS Seven patients were identified as within the AD continuum, 10 SNAP and 6 BN. In voxel-wise analysis, significantly higher 11C-PBB3 binding was observed in the AD continuum group compared to the BN patients in the cingulate gyrus, tempo-parieto-occipital junction and frontal lobe. Compared to the SNAP group, patients within the AD continuum had a considerably increased 11C-PBB3 uptake in the posterior cingulate cortex. There was no significant difference between SNAP and BN groups. The atlas-based analysis supported the outcome of the voxel-wise quantification analysis. CONCLUSION Our results suggest that 11C-PBB3-PET can effectively analyze regional tau load and has the potential to differentiate patients in the AD continuum group from the BN and SNAP group

Failure to repair endogenous DNA damage in β-cells causes adult-onset diabetes in mice

Age is the greatest risk factor for the development of type 2 diabetes mellitus (T2DM). Age-related decline in organ function is attributed to the accumulation of stochastic damage, including damage to the nuclear genome. Islets of T2DM patients display increased levels of DNA damage. However, whether this is a cause or consequence of the disease has not been elucidated. Here, we asked if spontaneous, endogenous DNA damage in β-cells can drive β-cell dysfunction and diabetes, via deletion of Ercc1, a key DNA repair gene, in β-cells. Mice harboring Ercc1-deficient β-cells developed adult-onset diabetes as demonstrated by increased random and fasted blood glucose levels, impaired glucose tolerance, and reduced insulin secretion. The inability to repair endogenous DNA damage led to an increase in oxidative DNA damage and apoptosis in β-cells and a significant loss of β-cell mass. Using electron microscopy, we identified β-cells in clear distress that showed an increased cell size, enlarged nuclear size, reduced number of mature insulin granules, and decreased number of mitochondria. Some β-cells were more affected than others consistent with the stochastic nature of spontaneous DNA damage. Ercc1-deficiency in β-cells also resulted in loss of β-cell function as glucose-stimulated insulin secretion and mitochondrial function were impaired in islets isolated from mice harboring Ercc1-deficient β-cells. These data reveal that unrepaired endogenous DNA damage is sufficient to drive β-cell dysfunction and provide a mechanism by which age increases the risk of T2DM. </p

Drosophila DNA polymerase theta utilizes both helicase-like and polymerase domains during microhomology-mediated end joining and interstrand crosslink repair

Double strand breaks (DSBs) and interstrand crosslinks (ICLs) are toxic DNA lesions that can be repaired through multiple pathways, some of which involve shared proteins. One of these proteins, DNA Polymerase theta (Pol theta), coordinates a mutagenic DSB repair pathway named microhomology-mediated end joining (MMEJ) and is also a critical component for bypass or repair of ICLs in several organisms. Pol theta contains both polymerase and helicase-like domains that are tethered by an unstructured central region. While the role of the polymerase domain in promoting MMEJ has been studied extensively both in vitro and in vivo, a function for the helicase-like domain, which possesses DNA-dependent ATPase activity, remains unclear. Here, we utilize genetic and biochemical analyses to examine the roles of the helicase-like and polymerase domains of Drosophila Pol theta. We demonstrate an absolute requirement for both polymerase and ATPase activities during ICL repair in vivo. However, similar to mammalian systems, polymerase activity, but not ATPase activity, is required for ionizing radiation-induced DSB repair. Using a site-specific break repair assay, we show that overall end-joining efficiency is not affected in ATPase-dead mutants, but there is a significant decrease in templated insertion events. In vitro, Pol theta can efficiently bypass a model unhooked nitrogen mustard crosslink and promote DNA synthesis following microhomology annealing, although ATPase activity is not required for these functions. Together, our data illustrate the functional importance of the helicase-like domain of Pol theta and suggest that its tethering to the polymerase domain is important for its multiple functions in DNA repair and damage tolerance

Spontaneous DNA damage to the nuclear genome promotes senescence,redox imbalance and aging

Accumulation of senescent cells over time contributes to aging and age-related diseases. However, what drives senescence in vivo is not clear. Here we used a genetic approach to determine if spontaneous nuclear DNA damage is sufficient to initiate senescence in mammals. Ercc1-/Δ mice with reduced expression of ERCC1-XPF endonuclease have impaired capacity to repair the nuclear genome. Ercc1-/Δ mice accumulated spontaneous, oxidative DNA damage more rapidly than wild-type (WT) mice. As a consequence, senescent cells accumulated more rapidly in Ercc1-/Δ mice compared to repair-competent animals. However, the levels of DNA damage and senescent cells in Ercc1-/Δ mice never exceeded that observed in old WT mice. Surprisingly, levels of reactive oxygen species (ROS) were increased in tissues of Ercc1-/Δ mice to an extent identical to naturally-aged WT mice. Increased enzymatic production of ROS and decreased antioxidants contributed to the elevation in oxidative stress in both Ercc1-/Δ and aged WT mice. Chronic treatment of Ercc1-/Δ mice with the mitochondrial-targeted radical scavenger XJB-5–131 attenuated oxidative DNA damage, senescence and age-related pathology. Our findings indicate that nuclear genotoxic stress arises, at least in part, due to mitochondrial-derived ROS, and this spontaneous DNA damage is sufficient to drive increased levels of ROS, cellular senescence, and the consequent age-related physiological decline

Spontaneous DNA damage to the nuclear genome promotes senescence, T redox imbalance and aging

Accumulation of senescent cells over time contributes to aging and age-related diseases. However, what drives senescence in vivo is not clear. Here we used a genetic approach to determine if spontaneous nuclear DNA damage is sufficient to initiate senescence in mammals. Ercc1-/Δ mice with reduced expression of ERCC1-XPF endonuclease have impaired capacity to repair the nuclear genome. Ercc1-/Δ mice accumulated spontaneous, oxidative DNA damage more rapidly than wild-type (WT) mice. As a consequence, senescent cells accumulated more rapidly in Ercc1-/Δ mice compared to repair-competent animals. However, the levels of DNA damage and senescent cells in Ercc1-/Δ mice never exceeded that observed in old WT mice. Surprisingly, levels of reactive oxygen species (ROS) were increased in tissues of Ercc1-/Δ mice to an extent identical to naturally-aged WT mice. Increased enzymatic production of ROS and decreased antioxidants contributed to the elevation in oxidative stress in both Ercc1-/Δ and aged WT mice. Chronic treatment of Ercc1-/Δ mice with the mitochondrial-targeted radical scavenger XJB-5–131 attenuated oxidative DNA damage, senescence and age-related pathology. Our findings indicate that nuclear genotoxic stress arises, at least in part, due to mitochondrial-derived ROS, and this spontaneous DNA damage is sufficient to drive increased levels of ROS, cellular senescence, and the consequent age-related physiological decline