Just the Facts: Ovarian torsion in the emergency department setting.

A 23-year-old female presents with right lower quadrant pain that has been intermittent for the past several days. The pain suddenly worsened 1 hour ago. She denies vaginal bleeding or discharge, dysuria, fever, and back pain, but she has had several episodes of nausea with nonbloody, nonbilious vomiting. On examination, she is tender in the right lower quadrant, but her abdomen is not rigid.

Just the Facts: Diagnosis and management of small bowel obstruction.

A 63-year-old female patient presents with abdominal pain, vomiting, and abdominal distention. She has previously had a cholecystectomy and hysterectomy. She has had no prior similar episodes, and denies fever, hematemesis, or diarrhea. She takes no medications. Vital signs include blood pressure 123/61 mm Hg, heart rate 97, oral temperature 37.2°C, respiratory rate 18, oxygen saturation 97% on room air. Her abdomen is diffusely tender and distended.

Just the Facts: Diagnosis and management of rhabdomyolysis.

A 32-year-old male presents with diffuse myalgias, weakness, and dark urine for 1 day. The patient states he recently started a new exercise program. He is hemodynamically stable, and his physical examination reveals diffuse muscle tenderness. His creatine kinase (CK) returns at 8,000 international units per liter (IU/L), and his urinalysis reveals blood but only three red blood cells (RBCs) on microscopy.

Thermally induced gelable polymer networks for living cell encapsulation.

We report the encapsulation of MIN6 cells, a pancreatic beta-cell line, using thermally induced gelable materials. This strategy uses aqueous solvent and mild temperatures during encapsulation, thereby minimizing adverse effects on cell function and viability. Using a 2:1 mixture of PNIPAAm-PEG-PNIPAAm tri-block copolymer and PNIPAAm homopolymer that exhibit reversible sol-to-gel transition at approximately 30 degrees C, gels were formed that exhibit mechanical integrity, and are stable in H(2)O, PBS and complete DMEM with negligible mass loss at 37 degrees C for 60 days. MTT assays showed undetectable cytotoxicity of the polymers towards MIN6 cells. A simple microencapsulation process was developed using vertical co-extrusion and a 37 degrees C capsule collection bath containing a paraffin layer above DMEM. Spherical capsules with diameters ranging from 500 to 900 microm were formed. SEM images of freeze-dried capsules with PBS as the core solution showed homogenous gel capsule membranes. Confocal microscopy revealed that the encapsulated cells tended to form small aggregates over 5 days, and staining for live and dead cells showed high viability post-encapsulation. A static glucose challenge with day-5 cultured microencapsulated cells exhibited glucose-dependent insulin secretion comparable to controls of free MIN6 cells grown in monolayers. These results demonstrate the potential use of these thermo-responsive polymers as cell encapsulation membranes.

Antagonism of rat beta-cell voltage-dependent K+ currents by exendin 4 requires dual activation of the cAMP/protein kinase A and phosphatidylinositol 3-kinase signaling pathways.

Antagonism of voltage-dependent K+ (Kv) currents in pancreatic beta-cells may contribute to the ability of glucagon-like peptide-1 (GLP-1) to stimulate insulin secretion. The mechanism and signaling pathway regulating these currents in rat beta-cells were investigated using the GLP-1 receptor agonist exendin 4. Inhibition of Kv currents resulted from a 20-mV leftward shift in the voltage dependence of steady-state inactivation. Blocking cAMP or protein kinase A (PKA) signaling (Rp-cAMP and H-89, respectively) prevented the inhibition of currents by exendin 4. However, direct activation of this pathway alone by intracellular dialysis of cAMP or the PKA catalytic subunit (cPKA) could not inhibit currents, implicating a role for alternative signaling pathways. A number of phosphorylation sites associated with phosphatidylinositol 3 (PI3)-kinase activation were up-regulated in GLP-1-treated MIN6 insulinoma cells, and the PI3 kinase inhibitor wortmannin could prevent antagonism of beta-cell currents by exendin 4. Antagonists of Src family kinases (PP1) and the epidermal growth factor (EGF) receptor (AG1478) also prevented current inhibition by exendin 4, demonstrating a role for Src kinase-mediated trans-activation of the EGF tyrosine kinase receptor. Accordingly, the EGF receptor agonist betacellulin could replicate the effects of exendin 4 in the presence of elevated intracellular cAMP. Downstream, the PKCzeta pseudosubstrate inhibitor could prevent current inhibition by exendin 4. Therefore, antagonism of beta-cell Kv currents by GLP-1 receptor activation requires both cAMP/PKA and PI3 kinase/PKCzeta signaling via trans-activation of the EGF receptor. This represents a novel dual pathway for the control of Kv currents by G protein-coupled receptors.