Integrating quantitative and qualitative approaches to assess wintertime illness-related absenteeism and its direct and indirect costs among the private sector in Ulaanbaatar.

Causes for employee absenteeism vary. The commonest cause of work absenteeism is "illness-related." Mongolia's capital city, Ulaanbaatar, experiences high employee absenteeism during the winter than during other seasons due to the combination of extreme cold and extreme air pollution. We identified direct and indirect costs of absenteeism attributed to air pollution among private-sector employees in Ulaanbaatar. Using a purposive sampling design, we obtained questionnaire data for 1,330 employees working for private-sector companies spanning six economic sectors. We conducted 26 employee focus groups and 20 individual employer in-depth interviews. We used both quantitative and qualitative instruments to characterize the direct and indirect costs of absence due to illnesses attributed to severe air pollution during wintertime. Female employees and employees with a young child at home were more likely to be absent. Respiratory diseases accounted for the majority of reported air pollution-related illnesses. All participants perceived that air pollution adversely affected their health. Individual employee direct costs related to absence totaled 875,000 MNT ($307.10) for an average of three instances of three-day illness-related absences during the winter. This sum included diagnostic and doctor visit-related, medication costs and hospitalization costs. Non-healthcare-related direct cost (transportation) per absence was 50,000₮ ($17.60). Individual indirect costs included the value of lost wages for the typical 3-day absence, amounting to 120,000₮ ($42.10). These total costs to employees, therefore, may amount to as much as 10% of annual income. The majority of sick absences were unpaid. Overall, the cost of wintertime absences is substantial and fell disproportionately on female employees with young children.

Impact of Seasonal Winter Air Pollution on Health across the Lifespan in Mongolia and Some Putative Solutions.

Environmental pollution of the air, water, and soil comprise an increasingly urgent challenge to global health, well-being, and productivity. The impact of environmental pollution arguably has its greatest impact across the lifespan on children, women of childbearing age, and pregnant women and their unborn children, not only because of their vulnerability during development, but also because of their subsequent longevity. Ulaanbaatar, Mongolia, is a highly instructive, perhaps extreme, example of what happens with recent, rapid urbanization. It is the coldest capital city on Earth, where average ambient temperatures routinely fall below -40°C/F between November and February. During the cold winter period, more than 200,000 "Gers" (traditional felt-lined dwellings) in the "Ger district" burn over 600,000 tons of coal for domestic heating (>3 tons each). Thus, outdoor ambient particulate levels frequently exceed 100 times the WHO-recommended safety level for sustained periods of time, and drive the majority of personal particulate matter exposure. Indoor levels of exposure are somewhat lower in this setting because Gers are equipped with chimneys. Major adverse health impacts that we have documented in the Ger districts include the following: respiratory diseases among those between 1 and 59 years of age and cardiac diseases in those over 60; alarming increases in lung cancer rates in females are also beginning to emerge; and fertility and subsequent successful completion of term pregnancy falls by up to half during the winter pollution season, while early fetal death rises by fourfold. However, the World Bank has intervened with a Ger stove replacement project that has progressively reduced winter pollution by about 30% over the past 5 years, and this has been accompanied by an increase in mean term birth weight of up to 100g. Each incremental decrement in air pollution clearly has beneficial effects on pregnancy, which are likely to have the greatest positive health and macroeconomic impact across the lifespan. However, innovative policies and solutions are clearly needed to eliminate coal heating in Gers and thus further reduce the markedly negative health impact of this practice.

Tissue engineering of the intestine in a murine model.

Tissue-engineered small intestine (TESI) has successfully been used to rescue Lewis rats after massive small bowel resection, resulting in return to preoperative weights within 40 days.(1) In humans, massive small bowel resection can result in short bowel syndrome, a functional malabsorptive state that confers significant morbidity, mortality, and healthcare costs including parenteral nutrition dependence, liver failure and cirrhosis, and the need for multivisceral organ transplantation.(2) In this paper, we describe and document our protocol for creating tissue-engineered intestine in a mouse model with a multicellular organoid units-on-scaffold approach. Organoid units are multicellular aggregates derived from the intestine that contain both mucosal and mesenchymal elements,(3) the relationship between which preserves the intestinal stem cell niche.(4) In ongoing and future research, the transition of our technique into the mouse will allow for investigation of the processes involved during TESI formation by utilizing the transgenic tools available in this species.(5)The availability of immunocompromised mouse strains will also permit us to apply the technique to human intestinal tissue and optimize the formation of human TESI as a mouse xenograft before its transition into humans. Our method employs good manufacturing practice (GMP) reagents and materials that have already been approved for use in human patients, and therefore offers a significant advantage over approaches that rely upon decellularized animal tissues. The ultimate goal of this method is its translation to humans as a regenerative medicine therapeutic strategy for short bowel syndrome.

Fibroblast growth factor 10 plays a causative role in the tracheal cartilage defects in a mouse model of Apert syndrome.

Patients with Apert syndrome (AS) display a wide range of congenital malformations including tracheal stenosis, which is a disease characterized by a uniform cartilaginous sleeve in place of a normally ribbed cartilagenous trachea. We have studied the cellular and molecular basis of this phenotype in a mouse model of AS (Fgfr2c(+/Delta) mice), which shows ectopic expression of Fgfr2b in mesenchymal tissues. Here we report that tracheal stenosis is associated with increased proliferation of mesenchymal cells, where the expression of Fgf10 and its upstream regulators Tbx4 and Tbx5 are abnormally elevated. We show that Fgf10 has a critical inductive role in tracheal stenosis, as genetic knockdown of Fgf10 in Fgfr2c(+/Delta) mice rescues this phenotype. These novel findings demonstrate a regulatory role for Fgf10 in tracheal development and shed more light on the underlying cause of tracheal defects in AS.