PubMed · 7674785
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P S Myles, I Ryder. 1995-09-23. Pulse oximetry.. https://doi.org/10.1016/s0140-6736(95)91671-7
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Mechanical skin irritation creates vasodilatation in the line of a stroke and in the surrounding tissue. To obtain further insight on underlying physiological mechanisms we developed a model of the vascular network comprised of three layers, where the first and the last one have a tree structure. They represent the arterial and the venous system, respectively. Both are connected via an intermediate zone representing the core of the microcirculation, which is described by means of a compliant compartment model. Irritation induces change in compliance of vessels situated at the entrance of the intermediate zone. Thus the model describes flow and pressure behavior due to mechanical skin irritation.
We prospectively assessed whether metabolic and menstrual benefits of metformin-diet were equally realized in women with polycystic ovary syndrome (PCOS), categorized by pretreatment top (n = 32) and bottom (n = 35) quintile homeostasis model assessment insulin resistance (IR). Effects of metformin (2.55 g/d) and diet (6300-8400 J/d [1500-2000 cal/d], 26% protein, 44% carbohydrate) were prospectively assessed for 12 months. Pretreatment, the bottom and top insulin-resistant quintile groups differed by median weight (84 vs 121 kg), insulin (7.8 vs 40.5 I(1/4) U/mL), IR (1.62 vs 9.28), homeostasis model assessment insulin secretion (131 vs 416), glucose (82 vs 98 mg/dL), sex hormone-binding globulin (40 vs 15 nmol/L), (all P < .0001), free androgen index (2.76 vs 10.8) ( P < .001), triglyceride (92 vs 131 mg/dL), high-density lipoprotein (46 vs 39 mg/dL), systolic blood pressure (116 vs 128 mm Hg), and diastolic blood pressure (76 vs 84 mm Hg), (all P < .01). After 12 months on metformin-diet, weight fell by 7% in both insulin-resistant groups (P < .0001), insulin, IR, and insulin secretion fell in the top insulin-resistant group by 60%, 64%, and 39% (all P < .0001), with smaller reductions in the bottom insulin-resistant group of 18%, 13% (P > .05 for both), and 22% (P < .01), respectively. The free androgen index fell 39% (P > .01) in the top insulin-resistant group. The pretreatment percentage of expected menses in the top insulin-resistant quintile (26 +/- 39%) was 1.6 times less than in the bottom insulin-resistant quintile (41 +/- 38%) (P = .026). Over the 12-month treatment period, the percentage of spontaneous regular normal menses increased to 72 +/- 27% in the top insulin-resistant quintile group (P < .0001) and to 77 +/- 31% in the bottom quintile group (P < .0001), with no group difference (P = .33). Metformin-diet metabolic effects were much more marked in women in the top vs the bottom quintile for IR. Women with PCOS in the bottom insulin-resistant quintile, conventionally thought not to respond optimally to metformin-diet, nevertheless experience significant metabolic and menstrual benefits. Metformin-diet should benefit most women with PCOS, even those with normal serum insulin, without IR.
PURPOSE OF REVIEW: The serum and glucocorticoid inducible kinase 1 (SGK1) is induced in the aldosterone sensitive distal nephron (ASDN) where it may stimulate Na reabsorption, partly by inhibiting ubiquitin ligase Nedd4-2-mediated retrieval of epithelial Na+ channel ENaC from the luminal membrane. We describe recent advances in our understanding of SGK1 function in the regulation of renal function and blood pressure. RECENT FINDINGS: Thiazolidinediones, i.e. activators of peroxisome proliferator-activated receptor gamma (PPAR gamma), upregulate SGK1 and ENaC mRNA expression and increase cell-surface expression of ENaC alpha in a human cortical-collecting-duct cell line. cAMP/protein kinase A can induce phosphorylation and inhibition of Nedd4-2-independent of SGK1. Part of ENaC stimulation by SGK1 appears dependent on a SGK1 consensus motif in ENaC alpha and independent of Nedd4-2. SGK1-dependent upregulation of Na+ reabsorption in ASDN contributes to upregulation of renal K+ excretion. In oocytes, SGK1 activates various renal transport proteins including Na+/glucose cotransporter SGLT1, Na+-coupled dicarboxylate transporter NaDC-1, epithelial Ca+ channel TRPV5, renal outer medullary K+ channel ROMK and voltage gated K+ channels KCNE1/KCNQ1 and Kv1.3. A variant of the SGK1 gene associates with increased blood pressure and body mass index. SUMMARY: PPAR gamma activators may increase renal Na reabsorption by stimulating SGK1 and ENaC. Nedd4-2 integrates influences of cAMP/protein kinase A and SGK1. SGK1 can activate ENaC in part directly and independent of Nedd4-2. K+ homeostasis requires SGK1-dependent Na+ reabsorption in ASDN. SGK1 may affect renal transport mechanisms beyond Na+ reabsorption and K+ secretion in ASDN. Polymorphisms of SGK1 may be relevant to the pathophysiology of hypertension and other diseases.