Paid Family and Medical Leave Policy: An Investment in Minnesota\u27s Families

The current policy Minnesota, the federal Family and Medical Leave Act (FMLA), is unpaid and simply insufficient to meet the needs of Minnesotans. In 2016, only 1 in 7 U. S. civilian workers had access to paid family and medical leave (PFML) as an employee benefit. Ten percent of Minnesotans will take family or medical leave (FML) in any given year. While almost three-quarters of Minnesota workers receive at least some pay when they are out of work for family or medical reasons; access to pay during leave is not equally distributed. Low-wage (46%); part-time (38%); less educated (38%); black (42%) or Hispanic (39%); and younger (39%) workers are much more likely to receive no compensation during leave. 90% of companies surveyed in California, the first state to enact guaranteed paid leave, say the law had either a “positive effect or no effect on productivity, profit, morale, and costs.” If paid leave programs in California, New Jersey and Rhode Island can effectively deliver paid leave insurance programs for a small payroll tax of around 1% or less; Minnesota can do the same. Debra Fitzpatrick from the Humphrey School of Public Affairs has laid out six models for how guaranteed paid leave can be achieved, with each a step in the right direction. Model 6 provides the best approach to meeting the needs of all Minnesotans: Up to 12 Weeks of Paid Family and Medical Leave using a Progressive Replacement Rate Structure (80% to 55%) and Maximum Weekly Benefit of $1,000

Metabolic activation pathway for the formation of DNA adducts of the carcinogen 2-amino-l-methyl-6-phenyumidazo[4,5-b]pyridine (PhIP) in rat extrahepatic tissues

The food-borne mutagen 2-amino-l-methyl-6-phenylimidazo[ 4,5-b]pyridine (PhIP) induces tumors in colon of male rats and has been implicated in the etiology of human cancers, particularly colorectal cancer. This study was conducted to examine: (1) the biliary and/or circulatory transport of N-hydroxy- PhIP and its N-glucuronides, N-sulfonyloxy-PhIP and N-acetoxy-PhIP; (2) their role as proximate and ultimate carcinogenic metabolites of PhIP; (3) the potential role of glutathione in modulating PhIP-DNA adduct formation. PhIP-DNA adducts, measured by the P-postlabeling method, were highest in the pancreas (361 adducts/10 nucleotides or 100%), followed by colon (56%), lung (28%), heart (27%) and liver (2%), at 24 h after a single oral dose of PhIP (220 μmol/kg) to male rats. In each tissue examined, we observed two major adducts, each of which accounted for 35-45% of the total, and one minor adduct, which represented about 10-20% of the total. One of the major adducts was identified as N-(deoxyguanosin-8-yl)-2-amino-l-methyl- 6-phenylimidazo[4,5-b]pyridine by chromatographic comparisons with an authentic standard. The major urinary metabolites of PhIP in these rats were 4'-hydroxy-PhIP and its glucuronide and sulfate conjugates, followed by N-hydroxy-PhIP N3-glucuronide, N-hydroxy-PhIP N-glucuronide and unchanged PhIP. In bile duct-ligated rats, the urinary excretion of the N-OH-PhIP N3-glucuronide was increased two-fold, but there was no effect on PhIP-DNA adduct formation in the colon, heart, lung, pancreas or liver. 2,6-Dichloro-4-nitrophenol, which strongly inhibits arylsulfo-transferase-mediated DNA binding in vivo, had no effect on PhIP-DNA adduct levels in liver or in extrahepatic tissues. Pretreatment of rats with buthionine sulfoximine, which results in hepatic glutathione depletion, caused a five-fold increase in adduct formation in the liver. Intravenous administration (10 μmol/kg) of N-hydroxy-PhIP and N-acetoxy-PhIP each led to high levels of PhIP-DNA adducts in each of the extrahepatic tissues examined. Adduct levels ranged from two- to six-fold higher (for N-hydroxy-PhIP) and four- to 28-fold higher (for N-acetoxy-PhIP) as compared to that after an i.v. dose of the parent compound, indicating that these two bioactivated derivatives of PhIP are sufficiently stable to be transported through the circulation to extrahepatic tissues. Analyses of whole blood obtained at 2-8 h after oral administration of [H]PhIP failed to detect N-hydroxy-PhIP