1. Flocks of migratory birds avoid crashing into each other upon landing by always landing in alignment with earth's magnetic field. Quote: "The latest research suggests that birds detect magnetic fields in two ways. One relies on small pieces of magnetite (a magnetic iron oxide) lodged in their beaks, or inner ears, or both. The other employs a magnetism-sensitive chemical reaction in their eyes, allowing them to “see” the Earth’s magnetic field, probably as bright and dark spots superimposed on their visual fields" (Economist)
2. Fascinating show from radiolab about Emergence, the property of order emerging spontaneously from a large group of disorganized individuals (i.e. acting without central leadership). Emergence is addressed in the context of swarm animals (ants, fireflies) and in neurons in the brain. A theory is proposed that brain cells of different senses firing at the same time/rate is the foundation for coherent, integrated ideas-- i.e. the smell, appearance, feel, taste of coffee are integrated to make the concept of "coffee" (Radiolab)
3. GDM leads to organomegaly as well as macrosomia: hepatosplenomegaly and enlargement of the interventricular septum. The latter reverses upon reduction of insulin levels. At birth, IDM will have hypoglycemia, as well as certain electrolyte abnormalities: hypomagnesemia and hypocalcemia (present 10-50% of the time, depending on the study, often associated with hyperphosphatemia-- possibly a function of polycythemia and cell lysis? possibly a function of decreased PTH from increased Ca in utero?). Finally, the polycythemia (hi glucose -> hi metabolism -> hypoxia -> polycythemia) leads to paradoxical iron deficiency elsewhere in the body as iron is shunted into RBC synthesis.
4. Ceftriaxone displaces bilirubin from albumin, increasing blood [UCB] and leading to gallstones and biliary sludging.
5. Red cell factors that will lead to increased hemolysis in a neonate, and thus more jaundice: 
-Structural: spherocytosis
-Enzyme: G6PD, pyruvate dehydrogenase def.
-Immune: ABO/Rh
6. GI factors that will lead to decreased excretion of UCB: meconium ileus, duodenal atresia
7. Physiological (i.e. nonpathological) causes of jaundice: 
-Race (see previous post)
-Physiologic: infants have b-glucoronidase, their RBCs have shorter lifespans, more ineffective hematopoesis takes place, liver function is not as good, UGT1A1 activity is not as good.
-Breastfeeding (early jaundice): the low amount of breastmilk/colostrum made in the first days post-partum mean that exclusively breastfed babies will be slightly food/drink deprived in the early days of life. Less albumin/protein, and increased hepato-GI cycling of GI contents, leading to increased b-glucorindase activity.
-Breastmilk: (later jaundice) some substance in the breast milk increases UCB in the blood. Perhaps there's something that inhibits UGT1A1, or has b-glucorinidase activity (or is b-glucoronidase)
7. Jaundice due to increased CB is rarer than UCB, and merits an extensive workup for biliary obstruction (choledochal cyst, progressive familial intrahepatic cholestasis, biliary atresia) or genetic diseases (dubin-johnson, rotor)
8. Catfact: cats can jump up to 5x their height in a leap.
9. Insects must beat their wings hundreds of times a second in order to stay aloft, which is far too fast to be explained by calcium-regulated myosin-actin mechanisms. A new paper out in Nature examining bumblebees flying by x-ray scattering found data to support a theory that bee muscles act via oscillatory stretch activation, where stretching of one muscle by a counterpoint/yoked muscle flexing leads to increased myosin head affinity, leading to reflexive contraction. This process is Ca independent. (Nature)
10. Significant steps were made in figuring out why anti-EGFR drugs cause those awful pruritic rashes, published this week in Science. From the abstract: "We established a parallel mouse model by ablating EGFR in the epidermis. These mice developed skin lesions similar to the human rash. Before lesion development, we detected increased mRNA expression of chemokines in the skin associated with early infiltration of macrophages and mast cells and later infiltration of eosinophils, T cells, and neutrophils. As the skin phenotype evolved, changes in blood counts and circulating chemokines reproduced those seen in the gefitinib-treated patients. Crossing the mutant mice with mice deficient for tumor necrosis factor–α (TNF-α) receptors, MyD88, NOS2, CCR2, T cells, or B cells failed to reverse the skin phenotype. However, local depletion of macrophages provided partial resolution..." (Science)