Publications by authors named "H Shumaker"

Purpose Of Review: To review the status of antiabortion restrictions enacted over the last 5 years in the United States and their impact on abortion services.

Recent Findings: In recent years, there has been an alarming rise in the number of antiabortion laws enacted across the United States. In total, various states in the union enacted 334 abortion restrictions from 2011 to July 2016, accounting for 30% of all abortion restrictions since the legalization of abortion in 1973.

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The mechanism of the pancreatic ductal HCO secretion defect in cystic fibrosis (CF) is not well defined. However, a lack of apical Cl(-)/HCO exchange may exist in CF. To test this hypothesis, we examined the expression of Cl(-)/HCO exchangers in cultured pancreatic duct epithelial cells with physiological features prototypical of CF [CFPAC-1 cells lacking a functional CF transmembrane conductance regulator (CFTR)] or normal duct cells (CFPAC-1 cells transfected with functional wild-type CFTR, CFPAC-WT).

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The sodium--hydrogen (Na(+)/H(+)) exchanger is one of the few transporter proteins involved in the regulation and maintenance of intracellular pH and cell volume in most eukaryotic cell types. The current study investigates the expression of isoforms of the Na(+)/H(+) exchanger (NHE) in human skin and in cultured keratinocytes, melanocytes, and melanoma cells by reverse transcription-polymerase chain reaction (RT--PCR), immunohistochemical analysis and functional studies. Neonatal foreskins were used to isolate RNA from epidermis and dermis, and to initiate cultures of keratinocytes and melanocytes.

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Thickening of airway mucus and lung dysfunction in cystic fibrosis (CF) results, at least in part, from abnormal secretion of Cl(-) and HCO(3)(-) across the tracheal epithelium. The mechanism of the defect in HCO(3)(-) secretion is ill defined; however, a lack of apical Cl(-)/HCO(3)(-) exchange may exist in CF. To test this hypothesis, we examined the expression of Cl(-)/HCO(3)(-) exchangers in tracheal epithelial cells exhibiting physiological features prototypical of cystic fibrosis [CFT-1 cells, lacking a functional cystic fibrosis transmembrane conductance regulator (CFTR)] or normal trachea (CFT-1 cells transfected with functional wild-type CFTR, termed CFT-WT).

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