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THIS RESTAURANT IS CLOSED Chef Eugene's Restaurant
428 Franklin Ave. (Brown St.) Send to Phone
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OpenLunch Mon.-Fri., Dinner nightly
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- Dress code: Casual
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- Kid-friendly
- Reservations suggested
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THIS RESTAURANT IS CLOSED Chef Eugene's Restaurant Restaurant Review: The atmosphere at Chef Eugene's on Franklin Avenue in Hartford is laid-back and as family-friendly as the prices. Yet the fare's pretty serious: the kitchen turns out some of the tastiest traditional Italian plates around. Try the calamari and the veal Eugene.
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July 31, 2012
YOLO COUNTY OFFICE OF EDUCATION, PLAINTIFF,v.STATE OF CALIFORNIA DEPARTMENT OF EDUCATION AND DOES 1-25, INCLUSIVE, DEFENDANTS.
The opinion of the court was delivered by: Morrison C. England, Jr. United States District Judge
Before the Court is Defendant California Department of Education's Motion to Dismiss ("MTD") (ECF No. 9). For the reasons that follow, the Motion to Dismiss is GRANTED without leave to amend.
Plaintiff, Yolo County Office of Education ("YCOE"), brings suit against Defendant California Department of Education ("CDE"), pursuant to provisions 20 U.S.C. §§ 1415(b)(6) and 1415(i)(2)(B) of the Individuals with Disabilities Education Act ("IDEA"), 20 U.S.C. §§ 1400 et seq. (Complaint ("Compl.") ECF No. 2, at 1.) YCOE is aggrieved by what it views as an abuse of discretion by the CDE -- and by failures in the CDE's informal dispute resolution proceedings -- in a dispute that arose between YCOE and a student regarding the use of American Sign Language. In this action, YCOE brings suit against CDE seeking a declaration of the rights and obligations of both parties under the IDEA. (Id.) Before turning to the factual allegations and the parties' contentions, the Court briefly discusses the IDEA, its implementation in California and, of particular relevance here, the dispute resolution process.
A. IDEA Framework, California's Implementation and Dispute
Resolution Process
The IDEA provides that all children with disabilities receive a free appropriate public education ("FAPE") through individualized education programs ("IEP"). Lake Washington School District No. 414 v. Office of Superintendent of Public Instruction, 634 F.3d 1065, 1066 (9th Cir. 2011) (citing 20 U.S.C. §§ 1400(d)(1)(A)) and 1415(a)). "The IDEA conditioned federal funding upon state compliance with the statute's 'extensive substantive and procedural requirements.'"
Id. (quoting Hoeft v. Tucson Unified Sch. Dist., 967 F.2d 1298, 1300 (9th Cir. 1992). Under California law, the county office of education of the child's residence is obligated "to identify disabled children, to assess suspected disability, to determine educational placements and related services through an IEP, and to provide needed education and related services." S.A. ex rel.
L.A. v. Tulare County Office of Educ., 2009 WL 30298, at *4 (E.D. Cal. Jan. 6, 2009) (citing Cal. Educ. Code, §§ 56300, 56302, 56340, and 56344(b)).
The IDEA provides a framework for dispute resolution that includes both a formal process and an informal one. See 20 U.S.C. § 1415; 34 C.F.R. § 300.151. As part of this process, the State and local agencies must provide students with procedures that allow a parent or a public agency to present a complaint with respect to "any matter relating to the identification, evaluation, or educational placement of the child, or the provision of a free appropriate public education to such child." 20 U.S.C. § 1415(b)(6)(A), see also § 1415(b)(7)(A); 34 C.F.R. § 300.507(a)(1). The implementing provisions call for the State Education Agency to address failures to provide appropriate services, and "appropriate future provision of services for all children with disabilities." See 34 C.F.R. § 300.151. The regulations also provide "the public agency with the opportunity to respond to the complaint."
34 C.F.R. § 300.152. The statute provides for either a formal impartial due process hearing under § 1415(f) or an informal voluntary mediation pursuant to § 1415(e).
The formal prong of the IDEA's dispute resolution process is the due process hearing. When a party makes a complaint under § 1415(b)(6), "the parents or the local educational agency involved in such complaint shall have an opportunity for an impartial due process hearing, which shall be conducted by the State educational agency..., as determined by State law..."
20 U.S.C. § 1415(f)(1)(A); see also 34 C.F.R. § 300.506. In California, the "CDE is required to enter into an interagency agreement with another state agency or contract with a nonprofit organization to provide the independent and impartial process." S.A., 2009 WL 30298 at *4 (citing Cal. Educ. Code § 56504.5). The due process hearing's formal procedural features include, inter alia, the right to counsel, the right to present evidence, and the right to cross-examine witnesses. See, e.g., Pedrazza v. Alameda Unified Sch. Dist., 2011 WL 4507111, at *5 (N.D. Cal. 2011) (citing 20 U.S.C. §§ 1415(f),(h); 34 C.F.R. §§ 300.511, 300.512); R.K. v. Hayward Unified Sch. Dist., 2007 WL 4169111, at *3 (N.D. Cal. 2007). Any party to a due process hearing who is aggrieved by the State Education Agency shall "have the right to bring a civil action with respect to the complaint presented pursuant to this section, which action may be brought in any State court of competent jurisdiction or in a district court..."
20 U.S.C. § 1415(i)(2)(A).
The alternative procedural safeguard provided for by the IDEA is the voluntary, informal mediation Complaint Resolution Procedure, available pursuant to § 1415(e).
That provision provides that any State Education Agency or Local Education Agency must "ensure that procedures are established and implemented to allow parties to disputes involving any matter, including matters arising prior to the filing of a complaint pursuant to subsection (b)(6), to resolve such disputes through a voluntary mediation process." 20 ...
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- November 25, 2013, 1:41 PM
Like those in the U.S., European airlines are rolling out guidelines to allow passengers to use portable electronic devices (PED) during all phases of flight. The European Aviation Safety Agency is also looking for a long-term solution that will allow passengers to make telephone calls from their mobile devices as well. If approved, the ability to make cellphone calls would be allowed only on European carriers. The FCC is also considering a mobile call option in the U.S.


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Joseph Phelps Cabernet Sauvignon 2010, Napa Valley
Cabernet Sauvignon
California, Usa
$106.95 (189795)
91 pts
September 28, 2013
Critic Reviews (2)
Julian Hitner
In magnum format (as tasted here), the 2010 Cabernet Sauvignon is both soothing and decadent. Opaque ruby in colour,...Sign In to see Critic Reviews. Not a Member? Please Sign Up.
David Lawrason
This is dark, dense, rich and full fruited young cabernet that shows off some class and generosity now (for those who...Sign In to see Critic Reviews. Not a Member? Please Sign Up.


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The Farmers' Market is held from 9 am to 2 pm at The Pantry at Loewen Gardens. The main idea behind the Farmers' Market is to capture a piece of home – the simple pleasure of people chatting about food and being passionate about produce. Find gourmet meats, wines, organic vegetables, cheeses, breads, and homemade baked goods. The Markets are held once a month on a Saturday. Mark these dates on your calendar for our upcoming Farmers' Markets
- Saturday 10th June
- Saturday 1st July
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- Saturday 9th September


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In chronic renal failure (CRF), reduction in renal mass leads to an increase in the filtration rates of the remaining nephrons and increased excretion of sodium per nephron. To address the mechanisms involved in the increased sodium excretion, we determined the total kidney levels and the densities per nephron of the major renal NaCl transporters in rats with experimental CRF. Two weeks after 5/6 nephrectomy (reducing the total number of nephrons to ∼24 ± 8%), the rats were azotemic and displayed increased Na excretion. Semiquantitative immunoblotting revealed significant reduction in the total kidney levels of the proximal tubule Na transporters NHE-3 (48% of control), NaPi-II (13%), and Na-K-ATPase (30%). However, the densities per nephron of NHE-3, NaPi-II, and Na-K-ATPase were not significantly altered in remnant kidneys, despite the extensive hypertrophy of remaining nephrons. Immunocytochemistry confirmed the reduction in NHE-3 and Na-K-ATPase labeling densities in the proximal tubule. In contrast, there was no significant reduction in the total kidney levels of the thick ascending limb and distal convoluted tubule NaCl transporters BSC-1 and TSC, respectively. This corresponded to a 3.6 and 2.5-fold increase in densities per nephron, respectively (confirmed by immunocytochemistry). In conclusion, in this rat CRF model: 1) increased fractional sodium excretion is associated with altered expression of proximal tubule Na transporter expression (NHE-3, NaPi-II, and Na-K-ATPase), consistent with glomerulotubular imbalance in the face of increased single-nephron glomerular filtration rate; and2) compensatory increases in BSC-1 and TSC expression per nephron occur in distal segments.
- fractional excretion of sodium
- renal hypertrophy
- glomerulotubular imbalance
as the population of surviving nephrons is reduced in chronic renal failure (CRF), the remaining tissue undergoes hypertrophy and the function is dramatically altered. It is well documented that when total renal mass is reduced, single-nephron glomerular filtration rate (SNGFR) in the remaining nephrons markedly increases (19). The elevated filtration rate leads to an increased reabsorptive burden on the residual nephrons. This together with the compensatory renal hypertrophy is associated with marked alterations in tubular reabsorptive capacities of sodium and water (8, 14, 20, 45).
In CRF, there is an adaptive increase in sodium excretion by each residually functioning nephron (21, 44, 46). In this way, sodium balance can be maintained despite a diminishing GFR when intake of salt and water is unaltered in CRF. The mechanisms responsible for the increased fractional sodium excretion and marked natriuresis per nephron in remnant kidney have been investigated (8, 14, 21, 45, 49,53). However, the tubular sites for the markedly altered renal transport of sodium in CRF have not been clearly elucidated, and the results, especially concerning the proximal tubule, have been conflicting (4, 8, 21, 32, 45, 53). Several investigators have suggested that increased excretion of sodium per nephron in CRF was achieved through a reduction in proximal tubular reabsorption (32, 45), whereas others reported no changes in the proximal tubule (21). Since the type 3 Na/H exchanger (NHE-3) is a major sodium transport pathway in the renal proximal tubule (3), we speculate that the altered levels of apically expressed NHE-3 (2, 6) and basolaterally expressed Na-K-ATPase in the kidney tubules (23, 25) in response to the marked increase in SNGFR may account for the marked changes in proximal tubule sodium and hence water reabsorption in remnant kidney. Furthermore, in renal proximal tubules, transport of phosphate (Pi) through the proximal apical membrane is largely performed by the type II Na-Pi cotransporter (NaPi-II) (5,38). Thus we speculate that NaPi-II may also be dysregulated together with other proximal tubule transporters.
Another characteristic urinary manifestation of CRF is that the urinary concentrating ability decreases in response to a reduction of functioning renal mass (13, 30, 47). In contrast, the ability to dilute urine has been demonstrated to be well maintained long after impairment of the concentrating ability has taken place (28). Concentration of the urine requires establishment and maintenance of a hypertonic medullary interstitium. The loop of Henle generates a high osmolality in renal medulla by driving the countercurrent multiplication, which is dependent on the NaCl absorption by the thick ascending limb (TAL) (29). Furthermore, urinary dilution is also mediated by NaCl absorption in the TAL and distal convoluted tubule (DCT) (29). The apically expressed Na-K-2Cl cotransporter (rat type 1 bumetanide-sensitive cotransporter: BSC-1 or NKCC2) (10, 15, 24, 26, 39, 56) and type 3 Na/H exchanger (NHE-3) (2, 3, 6), as well as basolaterally expressed Na-K-ATPase, are key components responsible for sodium reabsorption by the TAL.
In the rat model of CRF induced by 5/6 nephrectomy, delivery of sodium and water to the TAL and DCT has been demonstrated to be significantly increased (8). This is caused by an increase in filtered load and a decrease in the fractional reabsorption of water and sodium in proximal tubule (8). Thus, in the remaining functioning nephrons where single nephron filtered load of fluid and solute is very high, we hypothesize that changes in the expression of NaCl transporters may play a critical role in the altered sodium handling and the urinary concentration and diluting ability in CRF. Interestingly, adriamycin-induced nephrotic syndrome in rats has been demonstrated to be associated with a marked decrease in the abundance of Na-K-2Cl cotransporter (BSC-1), NHE-3, and Na-K-ATPase, in association with a marked decrease in urinary concentrating ability and derangement of urinary sodium excretion (12). Thus it can be hypothesized that changes in the expression of NaCl transporters may play a critical role in the development of altered sodium handling in experimental CRF. Furthermore, a change in the expression of these NaCl transporters may play a role in the impairment of the urinary concentrating ability seen in response to a reduction of functioning renal mass.
In the present study, we performed semiquantitative immunoblotting and immunocytochemistry with the following purposes:1) to examine whether there are changes in the total kidney levels or densities per nephron of major proximal tubule sodium transporters and major distal tubule sodium transporters in rats with CRF induced by 5/6 nephrectomy; and2) to examine whether these changes are associated with changes in the urinary sodium excretion in rats with CRF.
Experimental animals. The studies were performed on 54 adult Munich-Wistar rats initially weighing 265 ± 8 g (Møllegard Breeding Centre). The rats were maintained on a standard rodent diet (Altromin, Lage, Germany) with free access to water.
Induction of CRF by surgical reduction of renal mass. Experimental CRF was induced by excision of about two-thirds of the left kidney and right total nephrectomy, using the so-called excision remnant kidney model (18). The protocols used in this study are depicted in Fig. 1.
The rats were anesthetized with halothane (Christian Friis, Copenhagen, Denmark) and during surgery, the rats were placed on a heated table to maintain rectal temperature at 37–38°C. The left kidney was exposed through left flank incision and gently dissected free from the adrenal gland, and approximately two-thirds of the left kidney including the upper and lower pole was excised (consistently ∼50% of the kidney mass was removed; seeresults section). One week later, these rats were again anesthetized with halothane, and the right kidney was removed through right flank incision after dissecting it free from the adrenal gland. The wound was closed with 4-0 Mersilene and metal clamps. Immediately after each surgical procedure, buprenorphium 0.2 mg/kg sc (Temgesic, Reckitt and Colman) was injected to relieve pain for 1 day, and during this time rats were allowed to recover from anesthesia and surgery in cages with free access to water and standard rat chow.
As a control group, rats were subjected to sham operations identical to those used for CRF rats except that kidneys or poles of kidney were not removed. Sham-operated rats were monitored for 2 wk in parallel with 5/6 nephrectomized rats. All rats were killed under light halothane anesthesia, and kidneys were rapidly removed and processed for membrane fractionation and immunoblotting at the same day.
We have chosen 2-wk followup after induction of 5/6 nephrectomy to1) produce severe chronic renal insufficiency, 2) to allow significant hypertrophy of the remnant kidney, and3) to minimize interstitial fibrosis. The functional data revealed marked chronic renal insufficiency, and the light microscopical evaluation confirmed a very mild fibrosis (see results).
Clearance studies. The rats were maintained in the metabolic cages, allowing quantitative urine collections and measurements of water intake (Fig. 1). Urine volume, osmolality, creatinine, and sodium and potassium concentration were measured. Plasma was collected from tail vein at the time of right nephrectomy, and from abdominal aorta at the time of death for measurement of sodium and potassium concentration, creatinine, and osmolality.
Experimental protocol. The following protocols were followed (Fig. 1). For protocol 1, CRF was induced in rats by excision remnant kidney model (n = 17). Forprotocol 2, rats were subjected to sham operation (n = 11). Forprotocol 3, CRF rats were treated with 1-deamino-[8-d-arginine]vasopressin (DDAVP, Sigma V1005) using implantable osmotic minipumps (model 2002; Alzet, Palo Alto, CA) for 7 days (n = 6). For protocol 4, sham-operated rats were treated with 0.9% NaCl solution using implantable osmotic minipumps for 7 days (n = 6). Forprotocol 5, in normal rats, both poles of left kidney were excised (n = 6). For protocol 6, for immunocytochemistry, kidneys of rats with CRF (n = 4, protocol identical toprotocol 1) and of sham-operated rats (n = 4, protocol identical toprotocol 2) were perfusion fixed (see below).
Implantation of osmotic minipumps. To examine whether the changes in expression of NaCl transporters in response to CRF are altered by long-term exogenous DDAVP treatment, osmotic minipumps were implanted in CRF (n = 6) and sham-operated (n = 6) rats (protocols 5 and6). For implantation, minipumps were filled with DDAVP in a carrier solution containing 5% dextrose and 0.05% acetic acid for CRF rats or 0.9% NaCl solution for sham-operated rats. The pumps were equilibrated with normal saline for 4 h before insertion (35). Rats were anesthetized with inhalation of halothane, and the minipumps were inserted into the subcutaneous tissue under the skin of the back. Under these conditions, the pumps delivered 0.1 μg/h (0.5 μl/h) of DDAVP to CRF rats or 0.5 μl/h of 0.9% NaCl solution to sham-operated rats for 7 days.
Induction of chronic metabolic acidosis. To examine whether there are changes in the expression of NHE-3 levels in response to chronic metabolic acidosis (CMA) per se, Munich-Wistar rats were treated orally with 0.28 M NH4Cl in the drinking tap water for 2 wk ad libitum (n = 8) (1, 34). Control rats were received tap water ad libitum (n = 6).
Membrane fractionation for immunoblotting. The kidneys were homogenized (0.3 M sucrose, 25 mM imidazole, 1 mM EDTA, pH 7.2, containing 8.5 μM leupeptin, 1 mM phenylmethylsulfonyl fluoride) using an Ultra-Turrax T8 homogenizer (IKA Labortechnik), at maximum speed for 10 s and the homogenate was centrifuged in an Eppendorf centrifuge at 4,000g for 15 min at 4°C to remove whole cells, nuclei, and mitochondria. The supernatant was then centrifuged at 200,000 g for 1 h to produce a pellet containing membrane fractions enriched for both plasma membranes and intracellular vesicles (36). Gel samples (Laemmli sample buffer containing 2% SDS) were made of this pellet.
Primary antibodies. For semiquantitative immunoblotting and immunocytochemistry, we used previously characterized monoclonal and polyclonal antibodies summarized in the following. 1) For NHE-3 (L546), an affinity-purified polyclonal antibody to NHE-3 was previously characterized (12). 2) For NaPi-II (L696), we prepared an affinity-purified polyclonal antibody to NaPi-II using a synthetic peptide corresponding to the final 24 amino acids of the COOH-terminal tail. A similar antibody was previously characterized by Biber et al. (5).3) For Na-K-ATPase, a monoclonal antibody against the α1-subunit of Na-K-ATPase was previously characterized (25). 4) For BSC-1 (L320), an affinity-purified polyclonal antibody to the apical Na-K-2Cl cotransporter of the TAL was characterized by Kim et al. (26).5) For the thiazide-sensitive Na-Cl cotransporter, TSC (L573), an affinity-purified polyclonal antibody to the apical Na-Cl cotransporter of the DCT was characterized by Kim et al. (27). 6) For Tamm-Horsfall protein, an affinity-purified polyclonal antibody to Tamm-Horsfall protein has been characterized (22).
Electrophoresis and immunoblotting. Samples of membrane fractions from total kidney were run on 6–16% gradient polyacrylamide minigels (Bio-Rad Mini Protean II) for Na-K-ATPase, BSC-1, TSC, or 12% polyacrylamide minigels for NHE-3, NaPi-II, and Tamm-Horsfall protein. For each gel, an identical gel was run in parallel and subjected to Coomassie staining to assure identical loading (48). The other gel was subjected to immunoblotting. After transfer by electroelution to nitrocellulose membranes, blots were blocked with 5% milk in PBS-T (80 mM Na2HPO4, 20 mM NaH2PO4, 100 mM NaCl, and 0.1% Tween 20, pH 7.5) for 1 h and incubated overnight at 4°C with affinity-purified primary antibodies (see above). The labeling was visualized with horseradish peroxidase (HRP)-conjugated secondary antibodies (P447 or P448, diluted 1:3,000; DAKO, Glostrup, Denmark) using an enhanced chemiluminescence system (ECL, Amersham International).
Quantitation of total kidney levels of NaCl transporters and Tamm-Horsfall protein. ECL films with bands within the linear range were scanned (36) using an AGFA scanner (ARCUS II) and Corel Photopaint Software to control the scanner. The labeling density was determined of blots where samples from CRF kidneys were run on each gel with samples from control kidneys from sham-operated animals (36). The labeling density was corrected by densitometry of Coomassie-stained gels. The total kidney levels of NaCl transporters in the experimental animals were calculated as a fraction of the mean sham control value for that gel after correction for the fraction which was loaded of the total kidney mass. The loading fraction of total kidney mass was calculated by using the loading volumes of the gel samples to get identical densities of the Coomassie-stained lanes and by correction for body weight and kidney weight as follows: Loading fraction of total kidney mass = (loading volume of gel sample to get identical Coomassie staining)/(total volume of entire gel sample) × (the volume fraction that the entire gel sample constitute out of total kidney homogenate used for preparation of gel sample) × (total kidney weight per 100 g body wt corresponding to the left remnant kidney in CRF and the left plus right kidneys in sham-operated rats)/(numbers of kidney being 1 in CRF and 2 in sham-operated rats).1
Quantitation of densities per nephron of NaCl transporters and Tamm-Horsfall protein. To estimate the changes in the expression of NaCl transporters per single nephron to the increased SNGFR in remnant kidneys, total kidney levels of NaCl transporters and Tamm-Horsfall protein were divided by the fraction of the total kidney mass that remained immediately after 5/6 nephrectomy. Since the reduction in the number of nephrons in the remaining kidney should be roughly proportional to the initial reduction in renal mass, this provides an estimation of the changes in final protein expression per nephron of NaCl transporters in remnant kidney. Since there is no way to determine exactly the weight of the remaining tissue after polectomy, we used an additional protocol to estimate this. The fraction of the total kidney mass remaining immediately after 5/6 nephrectomy in protocol 1 (rats with CRF) was estimated from protocol 5(normal rats with left 2/3 nephrectomy). This appeared to be a reasonable approach, since the weight of the surgically removed renal tissue from the left kidney in protocol 5 was nearly identical to that removed in rats fromprotocol 1 (0.176 ± 0.008 vs. 0.172 ± 0.008 g/100 g body wt inprotocols 5 and1, respectively).2
Statistical analyses. Values were presented in the text as means ± SE. Comparisons between groups were made by unpaired t-test.P < 0.05 was considered significant.
Preparation of tissue for immunocytochemistry. The kidneys from four CRF rats and four sham-operated rats were fixed by retrograde perfusion via the aorta with periodate-lysine-paraformaldehyde (PLP: 0.01 M NaIO4, 0.075 M lysine, and 2% paraformaldehyde, in 0.0375 M Na2HPO4buffer, pH 6.2). In a separate experiment, 0.1% glutaraldehyde was added. Tissue blocks prepared from the cortex, outer stripe of outer medulla, inner stripe of outer medulla, and inner medulla were infiltrated for 30 min with 2.3 M sucrose containing 2% paraformaldehyde, mounted on holders, and rapidly frozen in liquid nitrogen (40). For light microscopy, the frozen tissue blocks were cryosectioned (0.8–1 μm, Reichert Ultracut S Cryoultramicrotome), sections were incubated with primary antibodies, and the labeling was visualized with HRP-conjugated secondary antibodies (P447 or P448, 1:100; DAKO), followed by incubation with diaminobenzidine. For fluorescence microscopy, the label was visualized using goat-anti-rabbit IgG (Z0421, 1:50; DAKO) and FITC-conjugated rabbit-anti-goat antibody (F250, 1:50, DAKO).
Freeze-substitution of kidney tissue. The frozen samples were freeze-substituted (model AFS; Reichert, Vienna, Austria) (30, 39). Briefly, the samples were sequentially equilibrated over 3 days in methanol containing 0.5% uranyl acetate at temperatures gradually increasing from −80 to −70°C, and then rinsed in pure methanol for 24 h while increasing the temperature from −70 to −45°C. At −45°C, the samples were infiltrated with Lowicryl HM20 and methanol 1:1, 2:1, and, finally, pure Lowicryl HM20 before ultraviolet polymerization for 2 days at −45°C and 2 days at 0°C. For electron microscopy, immunolabeling was performed on ultrathin Lowicryl HM20 sections (60–80 nm), which were incubated overnight at 4°C with primary antibodies diluted in PBS with 0.1% BSA or 0.1% skimmed milk. The labeling was visualized with goat-anti-rabbit IgG conjugated to 10-nm colloidal gold particles (GAR.EM10; BioCell Research Laboratories, Cardiff, UK) diluted 1:50 in PBS with 0.1% BSA. The sections were stained with uranyl acetate and lead citrate before examination in Philips CM100 or Philips 208 electron microscopes.
Five-sixths nephrectomy is associated with significant renal insufficiency and renal hypertrophy. As shown in Table 1, the levels of plasma urea nitrogen in CRF rats (24 ± 4 mmol/l, n = 17) were significantly higher (P < 0.05) than in sham-operated rats (6 ± 0.5 mmol/l,n = 11). Furthermore, the levels of plasma creatinine in CRF rats (136 ± 15 μmol/l) were significantly higher (P < 0.05) than in sham-operated rats (34 ± 1 μmol/l). Consistent with this, the creatinine clearance was significantly reduced in rats with CRF: 0.21 ± 0.03 in CRF vs. 0.81 ± 0.05 ml ⋅ min−1 ⋅ 100 g body wt−1 in sham-operated rats (P < 0.05), consistent with chronic renal insufficiency.
Another known feature following 5/6 nephrectomy is renal hypertrophy of the remnant kidney (19). The weight of kidneys where both poles have been removed (i.e., corresponding to the initial 2/3 left nephrectomy) is only 0.18 ± 0.01 g/100 g body wt (protocol 5). Two weeks after induction of 5/6 nephrectomy, remnant kidneys in CRF rats were significantly hypertrophied and weighed 0.41 ± 0.02 g/100 g body wt compared with 0.31 ± 0.02 g/100 g body wt of left kidney of sham-operated rats (P < 0.05). Despite the hypertrophy, the total renal mass of the remnant kidney was only 65 ± 3% of total renal mass in sham-operated rats (P < 0.05).
Light microscopical examination revealed extensive hypertrophy of all the nephron and collecting duct segments with the marked dilatation. Very mild interstitial fibrosis with few fibroblasts was only observed in the inner medulla but not in cortex and outer medulla of remnant kidneys at the light and electron microscopic level (not shown).
Quantity of sodium excreted in urine increases progressively as the creatinine clearance is reduced in rats with CRF. As shown in Fig. 2, the urinary sodium excretion rate increased markedly after induction of CRF established by 5/6 nephrectomy compared with sham-operated rats [0.50 ± 0.03 in rats with CRF (n = 17) vs. 0.39 ± 0.02 μmol ⋅ min−1 ⋅ 100 g body wt−1 in sham-operated controls (n = 11),P < 0.05]. Fractional excretion of sodium (FENa) after 2 wk of induction of 5/6 nephrectomy was also significantly increased (2.7 ± 0.6% in CRF rats vs. 0.4 ± 0.1% in sham controls,P < 0.05; Table 1). Furthermore, the fractional excretion of potassium (FEK) was much higher in rats with CRF (132 ± 9% in CRF vs. 39 ± 2% in sham controls,P < 0.05; Table 1). As shown in Fig.3, A andB, the fractional excretion of sodium and potassium significantly increased progressively as the creatinine clearance was reduced in experimental rats, suggesting the quantity of sodium and potassium excreted per nephron progressively increases as the renal functions were reduced during development of CRF.
Urine production is increased and urinary concentrating ability is decreased in rats with CRF.During the period of acclimation, daily urine production averaged 40 ± 2 μl ⋅ min−1 ⋅ kg−1in rats with CRF (n = 17). As reported earlier (30), this rose to 111 ± 3 μl ⋅ min−1 ⋅ kg−1after induction of 5/6 nephrectomy (P< 0.05). There was a parallel increase in water intake, from 94 ± 4 to 155 ± 5 μl ⋅ min−1 ⋅ kg−1per day (P < 0.05). In contrast, urine production and urine osmolalities were unchanged in sham-operated rats (n = 11). Thus the urine output of a single remnant kidney was approximately four times that of one kidney of sham control rats. This marked increase in urine output was associated with significant impairment of urinary concentrating ability in CRF rats: urine osmolality was 494 ± 16 in CRF vs. 1,326 ± 56 mosmol/kgH2O in sham-operated rats (P < 0.05). Consistent with changes in urine output and urine osmolalities, the urine-to-plasma osmolality ratio [(U/P)osm] was 1.6 ± 0.1 in CRF vs. 4.6 ± 0.4 in sham-operated controls, and the solute-free water reabsorption (TcH2O) was 65 ± 12 in CRF vs. 141 ± 13 μl ⋅ min−1 ⋅ kg−1in sham-operated rats, respectively (P< 0.05, Table 1).
Total kidney levels of NHE-3 are decreased in rats with CRF. In renal proximal tubules, apical Na/H exchange mediates most of the transcellular NaCl transport and two-thirds of the transcellular NaHCO3 (43), and NHE-3 plays a major role in this (3). The affinity-purified anti-NHE-3 antibody recognized an ∼87-kDa band in membrane preparations from the whole kidney, consistent with studies from other investigators (2, 6, 12). As shown in Fig. 4, densitometric analysis of all samples from CRF and sham-operated rats revealed a marked decrease in total kidney NHE-3 levels to 48 ± 14% in rats with CRF (n = 13) of levels in sham-operated rats (100 ± 19%, n = 11,P < 0.05; Table2).3The density of NHE-3 per nephron in remnant kidney was estimated to 199 ± 58% of levels in sham-operated rats (100 ± 19%,P > 0.05, Table 3).
CMA often accompanies CRF, and rats with 5/6 nephrectomy are often acidotic (33). To examine whether acidosis per se would affect NHE-3 levels, we have investigated this directly using an additional protocol where rats were treated with NH4Cl for 2 wk to induce CMA (1, 34). Chronic acid loading produced reduced plasma HCO3 levels in rats with CMA, consistent with CMA (18.7 ± 1 in CMA vs. 30.5 ± 0.4 mmol/l in controls, P < 0.05). Compared with controls, densitometric analysis of all samples from CMA and control rats revealed a significant increase in NHE-3 levels in rats with CMA to 143 ± 12% (n = 8) of levels in control rats (100 ± 12%,n = 6,P < 0.05, not shown), consistent with previous observations (1). Thus acidosis per se appears not to be the cause of the reduced expression of NHE-3 in CRF.
Total kidney levels of NaPi-II are decreased in rats with CRF. In renal proximal tubules, transport of Pi through the proximal apical membrane is largely performed by the NaPi-II cotransporter. To confirm whether apical proximal tubule NaCl transporter expression other than NHE-3 can also be altered in the remnant kidneys, we examined the changes in density and total kidney levels of NaPi-II. The affinity-purified anti-NaPi-II antibody recognized an ∼85-kDa main band in membrane preparations from the whole kidney, consistent with previous studies (5). As shown in Fig. 5, densitometric analysis of 85-kDa bands in all samples from CRF and sham-operated rats revealed a marked decrease in total kidney NaPi-II levels in rats with CRF to 13 ± 4% (n = 13) of levels in sham-operated rats (100 ± 6%,n = 11,P < 0.05; Table 2). The density of NaPi-II per nephron in remnant kidney was estimated to 56 ± 20% of levels in sham-operated rats (100 ± 10%,P > 0.05; Table 3).
Total kidney levels of Na-K-ATPase are decreased in rats with CRF. The renal tubule is rich in Na-K-ATPase, an important transport protein capable of coupling hydrolysis of ATP to the active translocation of sodium and potassium across the cell membrane and secondary active transport of other solutes. Figure6 shows an immunoblot of Na-K-ATPase, using membrane preparations from the whole kidney of rats with CRF and sham-operated rats. The α1-isoform-specific monoclonal antibody recognized a band migrating at ∼96 kDa (25). Densitometric analysis of all samples from CRF and sham-operated rats revealed a marked decrease in total kidney Na-K-ATPase levels in CRF rats to 30 ± 9% (n = 13) of levels in sham-operated rats (100 ± 8%, n = 11,P < 0.05; Table 2). Density per nephron in remnant kidney was estimated to 124 ± 37% in rats with CRF of levels in sham-operated rats (100 ± 8%,P > 0.05; Table 3).
Total kidney levels of two major absorptive Na-K-Cl cotransporters (BSC-1 in the TAL and TSC in the DCT) are not decreased in rats with CRF. Figure 7,A andC, shows immunoblots of the BSC-1 and TSC, using membrane preparations from whole kidney of rats with CRF and sham-operated rats. Affinity-purified anti-BSC-1 antibody recognized a broad band of molecular mass 146–176 kDa centered at ∼161 kDa, consistent with previous observations (10, 26, 39). Affinity-purified anti-TSC antibody recognized a broad band centered at ∼165 kDa (27). In contrast to the significant reductions in total kidney levels of NHE-3, NaPi-II, and Na-K-ATPase in rats with CRF, densitometric analysis revealed unchanged levels of total kidney BSC-1 in rats with CRF corresponding to 88 ± 15% of levels in sham-operated rats (100 ± 21%; Fig. 7 B and Table 2) and TSC corresponding to 61 ± 15% of levels in sham-operated rats (100 ± 18%; Fig. 7 D and Table 2) Furthermore, significant increases in densities per nephron of BSC-1 (365 ± 62% of sham levels, P < 0.05) and TSC (253 ± 62%, P < 0.05) were estimated (Table 3), consistent with the observed absence of a reduction in total kidney levels despite reduction in renal mass.
Total kidney levels of Tamm-Horsfall protein is decreased in rats with CRF. We examined the abundance of Tamm-Horsfall protein, a glycosyl-phosphatidylinositol-linked protein expressed predominantly in the apical plasma membrane of TAL cells. This was performed as a control to assess whether changes in the BSC-1 expression are accompanied by changes in other TAL proteins. In contrast to the significant increase in density of BSC-1 in the TAL cells of rats with CRF as well as unchanged total kidney levels, there was a marked decrease in total kidney Tamm-Horsfall protein levels in rats with CRF: 34 ± 8% in rats with CRF (n = 13,P < 0.05; Fig. 8) compared with 100 ± 7% in sham-operated controls (n = 11; Table 2). Density per nephron in remnant kidney was estimated to 141 ± 33% in rats with CRF of levels in sham-operated rats (100 ± 7%; Table3).
Total kidney levels of BSC-1 and Tamm-Horsfall protein: modification of CRF response by long-term administration of DDAVP. We examined whether changes in densities or total kidney levels of NaCl transporters and Tamm-Horsfall protein seen in CRF rats are modified in response to long-term exogenous DDAVP administration (Table 4). A densitometric analysis revealed that the total kidney BSC-1 levels in DDAVP-treated rats with CRF (n = 6, 0.1 μg/h sc for 7 days) increased to 202 ± 38% of levels in sham-operated rats (Fig. 9), a substantially higher level of BSC-1 expression than seen in response to CRF without DDAVP infusion. The upregulation appeared to be rather specific, since total kidney Tamm-Horsfall protein levels remained significantly decreased despite DDAVP treatment, corresponding to 21 ± 4% of sham levels (100 ± 11%, P < 0.05; Table 4), comparable to the levels seen without DDAVP infusion.
Immunocytochemical analysis of NaCl transporter expression. In sham-operated rats, anti-NHE-3 antibody labeled the apical plasma membrane domains of S1 and S2 segments of proximal convoluted tubule with a weaker staining of the late S2 and S3 segments of proximal tubule (Fig.10 A, arrows), as previously described (2). The labeling was exclusively confined to the apical domains and intermicrovillar cleft of the proximal tubule cells (arrows), whereas the apical brush border (arrowhead) and basolateral plasma membranes were consistently unlabeled (Fig. 10 A). Furthermore, an intense labeling was also seen of the apical plasma membrane domains of medullary TALs (MTALs) in sham-operated rats (not shown). In contrast, immunocytochemistry showed that the labeling of NHE-3 in the hypertrophied proximal tubules in the remnant kidneys (Fig.10 B, arrows) as well as of MTAL (not shown) were much weaker. The NHE-3 labeling patterns were confirmed by immunoelectron microscopy (not shown).
The proximal tubules exhibited strong Na-K-ATPase labeling of basolateral plasma membranes (Fig. 10,C andD). No or little labeling was detected in the thin descending limb of the loop of Henle (not shown), whereas significant basolateral labeling was observed of collecting duct principal cells, and very intense basolateral labeling was present in the TAL cells in the inner stripe of the outer medulla. This strong labeling also extended into the cortical portions of the TAL and of DCT (not shown). This is consistent with previous evidence (25). In rats with CRF, the labeling of the proximal tubule was much weaker (Fig.10 D), consistent with a significant decrease in total kidney levels determined by immunoblotting. In contrast, no major differences in the labeling density were seen in the MTAL cells from rats with CRF compared with sham-operated rats (Fig.11,E andF). This together with the observed increase in TSC in the DCT (Fig.11 B) and of BSC-1 in the TAL (Fig.11 D) suggests that the NaCl transporters in these segments are not decreased, despite a significant reduction of renal mass in rats with CRF.
The TSC is expressed in the DCT and is responsible for a large fraction of the net sodium and chloride reabsorption in the distal portion of the mammalian renal tubule (9, 11, 27, 41, 50). In sham-operated rats, immunocytochemistry confirmed that TSC immunolabeling was seen in DCT in the apical and subapical regions (Fig.11 A). Importantly, a strong labeling of TSC was noted in DCT cells in rats with CRF (Fig.11 B), which was confirmed by electron microscopy (not shown). This is consistent with the increased TSC density determined by immunoblotting (Fig.7 C).
In sham-operated rats, an intense BSC-1 labeling was seen in apical and subapical domains of MTAL (Fig. 11 C) and cortical TAL cells (not shown) as previously shown (10, 24, 26, 39,56). Rats with CRF also exhibited strong labeling of TAL cells (Fig.11 D), consistent with the increased BSC-1 density observed by immunoblotting (Fig.7 A).
The microscopy also confirmed that the cells of proximal tubules (Fig.10), descending thin limbs, MTAL, DCT (Fig. 11), and collecting ducts all underwent a marked hypertrophy with increased tubular diameters in rats with CRF.
Consistent with previous evidence, rats with CRF induced by 5/6 nephrectomy had 1) extensive hypertrophy and dilatation of remaining nephrons,2) significant azotemia,3) significant increases in urinary sodium excretion, and 4) marked increase in urine output with an impairment in urinary concentrating ability. In association with this, we report that there is a significant decrease in total kidney levels of the major proximal tubule sodium transporter NHE-3, NaPi-II, and Na-K-ATPase in rats with CRF. Immunocytochemistry confirmed that NHE-3 and Na-K-ATPase levels in the proximal tubule are reduced. Consistent with this, densities per nephron of NHE-3, NaPi-II, and Na-K-ATPase did not increase proportionately to the extensive nephron hypertrophy, associated with the hyperfiltration in remnant nephrons. This is likely to play a significant role for the increased sodium excretion in CRF. In contrast, we report that total kidney levels of the TAL and DCT sodium transporters BSC-1 and TSC are not decreased in rats with CRF. Consistent with this, the densities per nephron of both BSC-1 and TSC are significantly increased, as also demonstrated by immunocytochemistry. Also, there was no decrease in Na-K-ATPase labeling in TAL and DCT. Thus expression of sodium transporters in the loop of Henle and DCT is not decreased in remnant kidneys, indicating that the altered tubular handling of sodium in CRF may be caused primarily by changes in proximal tubule NaCl transporter expression levels and that there appears to be a compensatory increase in NaCl transporter expression in the distal nephron.
The proximal tubule is the site of reabsorption of approximately two-thirds of the NaCl that enters the tubular fluid by glomerular filtration (3) and therefore is the main energy-expending compartment of kidney. Thus it is evident that structural and functional adaptation of the proximal tubule in response to increased SNGFR and tubular fluid flow rate, which are known to occur in remnant kidney, may play a critical role in the changes of reabsorption and excretion of sodium and water. It has been demonstrated that the absolute sodium reabsorption in the proximal tubule is increased in parallel with the rise in SNGFR in the remnant kidney (8, 14, 49), whereas the fraction of the filtered sodium and water reabsorbed in the proximal tubule was significantly reduced (8, 32, 45, 55).
In the "remnant kidney model," SNGFR increases uniformly to values that are two- to threefold greater than normal (8, 52). However, if the fraction of the filtered sodium load reclaimed by the proximal tubule is significantly decreased as suggested by many investigators (8, 32, 45, 55), then it appears that changes in sodium excretion are modulated by proximal nephron segments. Indeed, we have demonstrated a significant decrease in total kidney NHE-3, NaPi-II, and Na-K-ATPase levels associated with reduced labeling density of NHE-3 and Na-K-ATPase in the proximal tubule in rats with CRF. Moreover, estimated densities of NHE-3 and Na-K-ATPase per nephron in remnant kidneys revealed a modest increase, but this was not significant. The hypertrophy, manifested by an increase in tubular diameter and length of the proximal tubule in remnant kidneys, appears to offer an explanation for this modest increase in densities per nephron of NHE-3 and Na-K-ATPase. This may provide an explanation for the previously observed increase in absolute sodium reabsorption in the proximal tubule from CRF animals (14, 49). However, at the same time, the inability to increase the densities per nephron of these NaCl transporters proportionately to the increased SNGFR and tubular fluid flow rate may provide an explanation for1) the previously observed reduced fractional reabsorption of sodium in proximal tubule,2) the glomerulotubular imbalance, and 3) the increased urinary excretion of sodium in CRF.
The NaPi-II cotransporters are also expressed in the proximal tubule and contribute to the sodium and phosphate reabsorption in this segment. Especially, NaPi-II is known to be the rate-limiting and physiologically regulated step in proximal tubular phosphate reabsorption (5). CRF is well known to be associated with elevated serum parathyroid hormone (PTH) levels and changes in mineral ion homeostasis including secondary hyperparathyroidism (37). Since PTH is a potent inhibitor of proximal tubular NaPi-II by inducing the retrieval from the brush-border membrane and the lysosomal degradation (38), we speculate that the decreased density and total kidney levels of NaPi-II in rats with CRF in the present study may be at least partly attributed to the increased levels of serum PTH.
The delivery of sodium and water to the distal end of the proximal tubule of superficial nephrons and to the bend of Henle's loop of juxtamedullary nephrons is known to be increased in remnant kidneys due to an increase in the filtered load and a decrease in the fractional reabsorption of sodium and water in the proximal tubule (8). This condition may be similar to acute and chronic loading with isotonic saline in normal rats. A large amount of evidence indicates that isotonic saline loading is associated with an elevation of SNGFR rate as well as a decrease in fractional proximal NaCl reabsorption (54). Furthermore, Landwehr et al. (31) demonstrated that the increase in delivery to the loop of Henle is associated with a marked increase in NaCl absorption by the loop of Henle, presumably due in part to an increase in TAL NaCl absorption (31). Consistent with this, Ecelbarger et al. (10) demonstrated that chronic oral saline loading in rats markedly increased BSC-1 abundance in the TAL of rats. Our data showing increased densities of BSC-1 in CRF rats is also consistent with this view. Moreover, it was observed that long-term oral NaCl loading results in an increase in the Na-K-ATPase activity of the MTAL of rats (51). This is also consistent with our observation that the Na-K-ATPase labeling density of the TAL cells of remnant kidney was similar to the sham-operated controls, which contrasts the significant reduction in the labeling density of the proximal tubule. This also supports the view that a marked increase in the delivery of NaCl and water to the loop of Henle may partly upregulate several NaCl transporters across the TAL and DCT. Thus we speculate that the increase in density of BSC-1 seen following 2 wk after induction of 5/6 nephrectomy could at least partly be a consequence of a prolonged increase in the NaCl load delivered to the TAL partly due to both hyperfiltration and altered expression in the proximal sodium transporters in remnant kidneys. Other factors may also play an important role, including potential increases in plasma vasopressin levels, which have previously been found to be associated with CRF induced by surgical reduction in kidney mass (7). Consistent with this, we demonstrated that DDAVP treatment for 7 days of rats with CRF resulted in a greater increase in BSC-1 levels than seen in response to CRF alone, indicating that DDAVP can induce an increase in BSC-1 expression in CRF rats as demonstrated previously in normal rats (26). The TSC is expressed in the DCT of the kidney (41) and is responsible for a large fraction of the net sodium and chloride reabsorption that occurs in the distal portion of the mammalian renal tubule (9, 11, 42, 50). Micropuncture studies of superficial nephron segments of the rat have demonstrated that the distal tubule of the rat is responsible for reabsorption of 6–8% of the filtered load of sodium, whereas the collecting duct system normally reabsorbs 1% or less of the filtered load (16). Recently, it was demonstrated that the DCT is an important site of action of mineralocorticoids, and that aldosterone upregulates the expression of TSC significantly (27, 50). Since plasma aldosterone levels are known to be elevated significantly (17), this is likely to play a role in increasing TSC expression in 5/6 nephrectomized rats.
In summary, the reduction in total kidney levels of NHE-3, NaPi-II, and Na-K-ATPase with altered expression per nephron of these transporters in response to the increased SNGFR and tubular fluid flow rate may provide cellular and molecular mechanisms for the increase in urinary sodium excretion in remnant nephrons. In contrast, there are compensatory increases in BSC-1 and TSC densities and maintained Na-K-ATPase expression in TAL and DCT. This indicates a compensatory increase, which may be partly due to increased blood vasopressin and aldosterone levels and increased delivery of NaCl to the distal nephron in CRF. Additional studies will be required to determine whether NaCl transporters elsewhere along the renal tubule of remaining nephrons in CRF are regulated or altered.
We thank Annette Blak Rasmussen, Zhila Nikrozi, Mette Vistisen, Inger-Merete Paulsen, and Gitte Christensen for expert technical assistance.
Address for reprint requests and other correspondence: S. Nielsen, Dept. of Cell Biology, Institute of Anatomy, Univ. of Aarhus, DK-8000 Aarhus C, Denmark (E-mail: sn{at}ana.au.dk).
Support for this study was provided by the Karen Elise Jensen Foundation, Novo Nordic Foundation, Danish Medical Research Council, University of Aarhus Research Foundation, the University of Aarhus, and the intramural budget of the National Heart, Lung, and Blood Institute.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
↵1 Sample calculation:1) Loading volume of gel sample which gave identical Coomassie staining compared with other chronic renal failure (CRF) and sham samples: 2.0 μl.2) Total volume of entire gel sample: 333 μl. 3) The volume fraction that the entire gel sample constitute out of total kidney homogenate used for preparation of gel sample: 18.75%.4) Total kidney weight per 100 g body wt: 0.48 g. 5) Number of kidneys: 1 (CRF). This loading corresponds to (2.0/333) × 18.75% × 1 = 0.113% of total kidney mass.
↵2 Sample calculation of density per nephron in Na-K-ATPase. 1) Total kidney levels of Na-K-ATPase in rats with CRF: 30 ± 9% of sham levels.2) Estimated fraction of total kidney mass which was remained immediately after 5/6 nephrectomy: 24.1%. 3) Density per nephron in remnant kidney 2 wk after induction of CRF was calculated by dividing the value obtained in 1) by that obtained in 2). This correspond to 124 ± 37% compared with sham-operated control rats.
3 These values were obtained after correction for the fraction of total kidney mass loaded and after densitometry of Coomassie-stained gels to correct for minor changes in loading.
- Copyright © 1999 the American Physiological Society


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Illuminate your night with this hot number, the 'Priestess' Dress in Red by Romance the Label. The Priestess Dress has a simple design yet a dramatic look due to its captivating red colour. The asymmetric neckline is modern yet softening for both narrow and broad shoulders. To add a touch of sexiness it's finished with a wrap over skirt, allowing a split effect when walking.
Style Tip: Pair up with strappy heels to break the block colour / statement drop earrings.
The Priestess Dress is perfect for your black tie events, as well as formals, weddings, masquerade parties.


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Holy Week -Tuesday
This week, we enter "Holy Week." This is the week that begins on Palm Sunday with the triumphant entry of Jesus into Jerusalem and ends on Easter Sunday with an empty tomb and a resurrected Savior. This week contains the heart of the Christian gospel. At its core, our message is the vicarious death, subsequent burial, and victorious resurrection of Jesus Christ from the dead. This is the message of first importance that we long to make unignorable in our community (1 Corinthians 15:1-4).
For the next few days, I will be posting a series of blogs that will take us on the journey of Jesus through Holy Week. My prayer is that our souls will find refuge, strength, hope, life, and resurrection in the story of our Great King Jesus. Also, as we prepare for the biggest Christian holiday (or holy day if you prefer), I pray that this blog series will help acclimate your heart to sing louder, pray deeper, laugh more, and celebrate with an abiding confidence this Easter Sunday. Our God is not dead, but HE IS RISEN!
At Providence, we have an ongoing blog series entitled "To the Glory of God." Periodically throughout the year, men and women of our church will author a blog post explaining how they are leveraging a season or focus in their life to God's glory. This is what Paul calls us to do in 1 Corinthians 10:31 and our biblical conviction is that everything in the universe is being done and proceeding forth with one ultimate goal and prize; the glory of God is the goal and the prize. We were made to glory in and glorify the God that made us.
As Jesus walked through Jerusalem after his triumphant entry on Palm Sunday, the Bible records an encounter with some of the crowds. Jesus seems to be single-minded this week. He sees the looming cross and begins to speak about it:
"Now is my soul troubled. And what shall I say? Father, save me from this hour? But for this purpose I have come to this hour. Father, glorify your name." Then a voice came from heaven: "I have glorified it, and I will glorify it again." The crowd that stood there and heard it said that it had thundered. Others said, "An angel spoke to him." Jesus answered and said "This voice has come for your sake, not mine. Now is the judgment of this world; now will the ruler of this world be cast out. And I, when I am lifted up from the earth, will draw all people to myself." John 12:27-32
Jesus says his soul is troubled because he knows the cross is coming. Yet, he claims that this is the purpose for which he entered the world. What a comment right? Jesus was born to die. He knew his whole life that this day was coming, through childhood, feasts of celebration, choosing the twelve, healing the masses, and even mundane things like weddings, birthdays, family get-togethers, and more, he knew the cross was at hand. And now, the week of his death has come.
But what does Jesus ask God to do in this hour of turmoil.
"Glorify your name" Jesus says.
Here we get a glimpse into the core theology of our Savior. More than anything else, he desires the Father's name to be glorified and displayed to the world. He wants God to be seen, as He truly is, glorious and worthy of worship. Jesus wants to display the heart of his Father as he hangs on the sinner's cross.
The Father leaves nothing to imagination. He says emphatically; "I have glorified it, and I will glorify it again."
What does he mean? God has been glorifying his name by working majestically on behalf of his people for centuries. Through the plagues of Egypt, he glorified his name. Through the parting waters of the Red Sea, he glorified his name. Through the falling of Jericho's walls, he glorified his name. Through the death of deadly Goliath at David's hands, he glorified his name. And countless other times throughout history God attaches the glory of his name to doing good for his people. Don't take my word for it, go back and search these stories and find God's glory at the center of God's desire when he does good for the people. Take the famous Psalm 23:
"He leads me in paths of righteousness, for his names sake." Psalm 23:4
So here we have Jesus desiring God's glory, and we have the Father promising to fulfill that desire.
But doesn't that seem a little arrogant? I mean, when we think of Christ, we don't see a glory seeker do we? When we think of God, we don't think of someone whom needs the praise of billions do we? God is not pleased with us when we glorify ourselves, so wouldn't it follow that when he does the same thing that it is wrong?
Answer: absolutely not.
The unstoppable, unquenchable, unshakable, unquestionable glory of God is the very fountain of the universe itself. We are right to say that God does not need billions to praise his glory. He does not need anything. He stands alone as the only independent, self-sufficient being in the entire universe. Instead of creating us out of need, by creating he freely gives everything.
When Adam and Eve were created and invited into fellowship with God, it is his glory that they were enjoying in the garden. They were made to reflect the image of God and enjoy the glory of God. Everything they did pointed back to the magnificence of the artist who created them. And this was not only acceptable; it was good. It was good to God because he delighted in the delight of his children. They were made to enjoy him and it pleased his heart when they did. It was good to Adam because his everyday existence included the enjoyment of God and his glory in unfettered amounts. Adam and Eve were invited to feast on the glory of God with all their might and power, and as they did so the glory of God was magnified more and more. Like a snowball effect, the more they enjoyed God, the more he got the glory. We honor an artist by marveling at his work, and in that same way Adam and Eve honored God and glorified him by marveling and reveling in his work. Like a beautiful song that you never want to end, the song of God's glory got louder and louder and sweeter and sweeter as the children of God relished in his light and grace.
Then the serpent enters. He beguiles Eve into believing that she as missing out on something. If she was simply to disobey God she could find real life and be God herself. In other words, the serpent convinced her that she could defy the very fabric of her being. She and Adam had been made to enjoy God, but never could they be God. They were image bearers, but not the image itself. She was coerced that because she so enjoyed the glory of God, she might as well cut out the middleman and become God herself. Then she would always be able to have the same level of joy, but without God.
Ultimately the sin of Adam and Eve was not mere disobedience, it was a rejection of the God that made them.
Here we see that for God to be committed to his glory is for God to be committed to us. The two affections are the same pursuit. Or as John Piper so elegantly puts it:
"God is most glorified in us when we are most satisfied in Him."
Now back to John 12. So, what is Jesus getting at here. After the Father speaks from heaven, there is a disagreement about the author of the voice. Some say it thundered, others say it was an angel. Jesus doesn't try to convince them of the origin, but instead explains the purpose. He says, "This was for you, not me." He goes on to discuss judgment and a promise. He says that judgment has finally come to the world.
I don't know about you, but based on the story I just told about Adam and Eve, righteous judgment is the last thing I want to hear is coming for me. A righteous God would demolish the children of Adam and Eve. Yet, Jesus says something different. He says "Judgment is here and the ruler of this world is cast out." Then he says "And when I am lifted up, I will draw the world back to me."
Let's recap. Jesus looks to the cross and says "God, make it about your glory." God says, "I have always done that, and I will do it again." We know that God's glory is our ultimate source and our reason for being created in the first place. We were made to be wrapped up in the glory of God, enjoying him and magnifying him. But Satan tricked us, and we willingly staged a treasonous takeover resulting in our fallen condition.
So what is God's response?
Here is the judgment of God: Jesus will take our place.
It is as if the judge heard all the facts, saw the defendant was guilty and rather than asking the bailiff to take him away, stepped down from his chair, was stripped of his robe and led away in chains on his behalf.
Jesus will live the life that we could not live, Jesus will die the death that we deserved, and Jesus will rise again on Easter Sunday and begin to draw the world back to himself and relationship with the Father. He will begin to restore what was lost in Eden. We will be able to drink from the fountain of God's glory again. We will get to enjoy him again. And we will get to glorify him with our actions again.
What about the serpent? What does he get?
Jesus doesn't leave you in the dark there either. He had his season to rule. But when Jesus breathes his last breath on the cross, Satan is cast out. As the old hymns say "the Ole Deluder Satan" has been defeated! By one death, life has returned!
We were on our way to the gallows and Jesus beat us there and laid his neck on the wood. The nail pierced hands were meant for me, but my God would have none of it! My father Adam wanted a crown of glory, but he deserved a crown of thorns. But my King Jesus embraced my crown of thorns, so I could receive a crown of glory!
Oh how Holy this week truly is! Sinners like me get a saints reward. The outcast is brought near, the villain is celebrated, the criminal is forgiven, the dead are brought to life, and the slave is set free! These sinful stains that tarnish my heart are cleansed by a spotless life and a vicarious death! This is the crux of Holy Week! The glory of God wrapped in human flesh and then broken on a cross so that the whole world can see; our God loves us and desires us to be free.
But wait, its only Tuesday. Just wait for what tomorrow brings…


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I am a professional photographer from Florida and I have stayed at the Chimuri cottages 3 times in the last couple of years. I have always had a nice comfortable place to stay and I have taken some of my best photos right there on the property. If you like nature and the beach Chimuri is the place for you. I also like how the owners Mauricio and Colocha try to protecct all the animals and plants on the property. I saw anteaters,sloths,humming birds, many other birds Jesus Christ lizards, posssums, 3 different kinds of hawks and poison dart frogs. A true nature Paradise. Sincerely: Angel
- Official Description (provided by the hotel):
- Chimuri Beach Retreat offers three affordable, simple, self-catering, Caribbean style one- or two person equipped cottages in a tropical garden in front of a quiet beach for your personal retreat, either self-directed or supported. Meditation and introspection, Yoga, Universal Energy healing, holistic therapies and guided nature walks for your personal time away. ... more less
- Also Known As:
- Chimuri Beach Retreat Costa Rica/Limon


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Introduction to Watercolor Painting
Sold Out
Sunday, May 7th, 12-2pm.
Sunday, June 11th, 3-5pm
Instructor: Chelsea Dipman of Glitteracy
Class Fee: $30 (all materials included)
Want to create a personal masterpiece? Learn watercolor with local artist and art teacher Chelsea of Glitteracy! In this workshop, you'll learn drawing techniques, watercolor application techniques, and texture techniques with watercolor. After practicing watercolor techniques, you'll learn to transfer an image and fill it in with watercolor. Lots of fun images to choose from – this is a perfect class for beginners who love the look of watercolor art!


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Allen Poe - Pocket Full of Ohms
Posted 3 years ago
Tags: Allen Poe, Free Downloads
Kentucky rhymesayer Allen Poe has come together with The DJBooth to bring fans his second solo street release, Pocket Full of Ohms.
The project features a total of 13 original jams from the Basement Up member, which includes previously-featured singles "Gina" and "Know What I Got."
Basement Up, D Eazy, DJ Calcutta, Emma Shaheen, Jay Elly, Phorensicz, Sheisty Khrist, Unique Legrand, Von Pea and yU make guest appearances throughout the set, which packs production by Brock Berrigan, Cody Jordan, DJ Hellblazer, Foreign Allegiance, ILL CLINTON, J57, Jaze Baqti, Lofidel, Manifest Beats, Melodrama, Nemo Achida, Pawcut and Twigg.
Written by richard
Posted 3 years ago
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Allen Poe - Know What I Got
By richard | 3 years ago
Allen Poe ft. Basement Up & Von Pea - Gina
By richard | 4 years ago
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Let . Find the Galois group of the splitting field of f(x) over the field of rational numbers. (Deadline April 14.)
Month: March 2017
HW11, due Wed 4/5/17
- D&F, Section 13.3 #1, #2
- D&F, Section 13.4 #1, #2, #5, #6
HW10, due Wed 3/29
- D&F, Section 13.1, #1, #3
- D&F, Section 13.2, #4, #7, #11a, #16, #21
No office hours, 3/21-3/31
There will be no office hours 3/21-3/31. Bill Rau is available in the MAC at the usual times: 10-12, 4-5 Mondays.
HW9, due Wed Mar 22
- Let F(A) and F'(A) both satisfy the universal property of a free group on a set A. Show that there is a unique isomorphism from F(A) to F'(A) that is compatible with the canonical maps A -> F(A) and A -> F'(A). Hint: consider the universal property for all possible combinations, taking both F(A) and F'(A) to be the free group and the supplementary group.
- Can you see how a similar argument could be used to show quite generally that objects that satisfy universal properties are unique up to isomorphism?
- DF 5.5 #23-a
HW8, due Friday March 17
Do the following calculations in Sage (not GAP). You may use Sage Cell for the calculations and cut and paste the answers that you submit. You are welcome to improve the code.
- compute 77+31 (no semicolon!)
- compute the set of divisors of 60: divisors(60)
- compute the greatest common divisor: gcd(33,770)
- compute 17 mod 3: mod(17,3)
- compute a and b such that a*64+b*33 = 1, using xgcd(64,33) and check your answer in Sage
- find factor(2^126-1)
- check the largest factor is prime: is_prime(77158673929)
- compute the square of the permutation
- G = SymmetricGroup(7)
- a = G("(1,2,3,4)(6,5,7)")
- a^2
- compute the "left to right" (warning!) product of the cycles
- G = SymmetricGroup(3)
- a = G("(1,2,3)")
- b= G("(2,3)")
- a*b
- make a list of elements of the permutation group generated by (1,2,3,4,5) and (2,5)(3,4):
- G = SymmetricGroup(5)
- g1 = G("(1,2,3,4,5)")
- g2 =G("(2,5)(3,4)")
- H = G.subgroup([g1,g2])
- H.list()
- Calculate the conjugacy classes of A5:
- G = AlternatingGroup(5)
- G.conjugacy_classes_representatives()
- Find the derived subgroup of A4:
- G=AlternatingGroup(4)
- G.commutator()
- Calculate a 2-Sylow subgroup of S4: SymmetricGroup(4).sylow_subgroup(2)
- Show that the subgroup of S4 generated by (1,2,3) and (2,3,4) is A4:
- G=SymmetricGroup(4)
- g1=G("(1,2,3)")
- g2=G("(2,3,4)")
- H=G.subgroup([g1,g2])
- H.is_isomorphic(AlternatingGroup(4))
- Calculate a composition series for S4: SymmetricGroup(4).composition_series()
Schedule, Monday March 20-Friday March 31
- Monday 3/20, Hales, review of rings, ideals, fields, and extensions
- Wednesday 3/22, Fedorov, D&F Section 13.1, basic theory of field extensions
- Friday 3/24, Fedorov, D&F Section 13.2, algebraic extensions
- Monday 3/27, Xu, D&F, Section 13.3, classical straightedge and compass constructions
- Wednesday 3/29, Yarosh, D&F, Section 13.4 splitting fields
- Friday 3/29, Yarosh, D&F, Section 13.4, algebraic closures
HW 7, due Wednesday March 25, 2017
Perform the following calculations in GAP. You can use Sage Cell and choose GAP in the language menu at the bottom-right-hand corner of the input cell. You can cut and paste your answers into the submitted homework.
- compute 77+31;
- compute the set of divisors of 60: DivisorsInt(60);
- compute the greatest common divisor Gcd(33,770);
- compute 17 mod 3;
- compute a and b such that a*64+b*33 = 1, using GcdRepresentation(64,33); check your answer in gap
- find Factors(2^126-1);
- check the largest factor is prime: IsPrime(77158673929);
- compute the square (a^2;) of the permutation a:=(1,2,3,4)(6,5,7);
- compute the "left to right" (warning!) product of the cycles a:= (1,2,3); b:=(2,3); a*b;
- make a list of representatives of the permutation group generated by (1,2,3,4,5) and (2,5)(3,4): g:= Group((1,2,3,4,5),(2,5)(3,4)); c:= ConjugacyClasses(g);
- Calculate the conjugacy classes of A5: g:= AlternatingGroup(5);
c:= ConjugacyClasses(g);
- Find the derived subgroup of A4: DerivedSubgroup(AlternatingGroup(4));
- Calculate the 2-Sylow subgroup of S4: SylowSubgroup(SymmetricGroup(4),2);
- Show that the subgroup of S4 generated by (1,2,3) and (2,3,4) is A4: StructureDescription(Group((1,2,3),(2,3,4)));
- Calculate a composition series for S4: DisplayCompositionSeries(SymmetricGroup(4));
Some material on Sage/Gap
The easiest way to use Sage is through Sage Cell .
Here are some resources for doing group theory in Sage.
- Here is a primer on group theory in Sage by Beezer.
- Or try this tutorial by Joyner and Kohel
- or this Sagemath doc on group theory


text:
ROSEMONT, IL—Hyatt Hotels & Resorts and First Hospitality Group, Inc. have opened Hyatt Place Champaign/Urbana, the first Hyatt-branded hotel to open in downtown Champaign.
The property, a choice for University of Illinois visitors, features 145 rooms with a swiveling 42-in. HD television, the Hyatt Grand Bed and Cozy Corner sectional sofa; free WiFi property-wide; complimentary breakfast with breakfast sandwiches, cereal, yogurt, breads and more; 3,200 sq. ft. of high-tech meeting/function space; a 24/7 Gallery Menu serving made-to-order entrees and appetizers; and a Coffee to Cocktails bar with specialty coffees, premium beers, wines and cocktails.
Robert Habeeb, president of First Hospitality Group, stated, "We are excited to be bringing the Hyatt Place brand to such a thriving and vibrant community like Champaign. We are confident that Hyatt Place Champaign/Urbana will bring a new standard to the area and will provide a perfect mix of style, service and amenities that will exceed guest expectations."
"The Hyatt Place brand was designed for a lifestyle, not a demographic, and as a result, we are confident that everyone from business travelers to students' parents will appreciate the open, intuitive design, casual atmosphere and practical amenities, such as free WiFi and 24-hr. food offerings," said GM Victor Patterson.


text:
Separate names with a comma.
Join the leading DJI Inspire community for free!
Discussion in 'General Discussion' started by kdownard, Mar 24, 2016.
DJI has updated new Firmware on the OSMO today and took away the 1.5.2
V220.127.116.11 is supposed to fix the internal mic sound recording problem
The sound is a little better but it won't blow your socks off
========== 2014.01.01 00:00:08 remo-con disconnect======
Packet: OSMO_FW_V01.06.02.10.bin
Upgrading ...
Result: Success.
Due to the sound the mount makes it would be good if they used noise cancellation to reduce the recorded sound. And, since they will know where the sound is coming from it could be possible to more completely remove the sound through cancellation.
Thanks for the post, Brian. Even with the upgrade the sound of my voice at 2" sounds like I'm in the next door room with a pillow on my face. I honestly don't think I'll be using the Osmo to capture sound but might use it to sync to sound from my Zoom H5. The FlexiMic gives a much better result than the internal mic. My point was that the upgrade did not address the problem it was meant to.


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Marc Poirier Photographer
Reanna Lynn NixonModel Female Waterbury, Connecticut, US
My Website: FacebookMy MM URL: http://www.modelmayhem.com/ReannaLNixon
Mayhem # 2469963
About MeMy name is Reanna and I would really like to expand my portfolio.
I don't do nude nor topless don't ask ;)
Don't ask about web can modeling the answer is no.
I'm not shy and love taking directions.
I can do my own hair and makeup but wont argue if its provided.
Come off as a creep and you'll be shot down like one.
That being said...
Feel free to contact me to set something up.
Have you worked with Reanna Lynn Nixon? Add Credits for Reanna Lynn Nixon! >>
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text:
Traded for a .22 Rifle
I traded a FEG PA 63 and two boxes of Silver Bear ammo for this Norinco copy of a Browning ATD22. We'll do the swap in a couple of weeks. I think it would be great to stuff in a backpack or keep in a BOB.
CA357 You shoud be OK?
RON L here
Well,I have had one of the Norenco copys of the Browning, and you should be ok? It's No Browning Mind you, but if your carefull about assembly and re-assembly and don't mess with that alignment the rifle worked like a charm for me? They are not common any more and PA-63 are a good gun as well,so I see ya about even on that Trade? I'd insist on a Firing check before I'd except it or a Warranty on it's operability as you'd hate to trade a working gun for an Inop one? That's my call Good Luck and let ya know how it turns out, OK?
I've known the guy for quite a while, so if there was something wrong, he would have told me.
I had $150. in the FEG and the ammo was another twenty bucks or so. So I figure I've got about $175. tops in the trade.
I'd love to have the real Browning version, but this will work for now. I really like the idea of just keeping it in a BOB for just in case.
Nice trade. I sware you never hang onto anything, unless it becomes a project, for more than a month!! :D
Great, then you should be OK?
RON L here
Cool, then you should be fine then! While not made near as well as the Browning, these are Nice Little Rifles and were popular when they were imported here and as I said, as Long as your carefull about assembly and re-assembly they Lock up tight and work well! I do like how they break diown and all, I only got rid of mine as the Previous owner had goofed up the alignment of the barrel and receiver and it gave me fits till I shimmed the inside of the reciever! The Real Think Browning is a uge Collector item and way out of my Price range as well! Gopod Luck and give us a Range report when you get settled in and shoot it, OK?
Thanks for the tips Ron.
You're right Dune, it seems that I'm always looking for the "perfect" gun. However, my Sistema Colt will always stay with me.
Now that I'm (hopefully) on my way to a carry permit for this State, I'm on the hunt for a Commander size 1911. But, boy are they expensive. :eek:
Yes they are......... :eek:
I like it CA! Good idea, I might have to do the same with my breakdown Winnie M63.. How much do Colt commanders go for? I have a buddy selling one for what I think is cheap... (But more than I got right now..)
In this area, if you can find an actual Colt Commander, they're going for close to a grand.
Wow!! I really wish I had the funds right now.. :( The guy I know only asking $500 with a couple of holsters and a bunch of ammo (not sure how much).. and yes it is a Colt..
A buddy of mine just got a Sistema Colt, but his was turned into a target pistol and is all fancy....
|All times are GMT. The time now is 09:10 AM.
Copyright ©2000 - 2017, Jelsoft Enterprises Ltd.


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I spend a lot of time working on my 3D animation/modeling, cooking, restoring & using vintage cast iron pans, hanging with friends & looking to work on freelance art gigs. I like to take in Packers games but don't mind if you don't, breweing beer but not really drinking it, making sausages from old family recipes, and am about to dive deep into making cheese. Lately I snagged a decent DSLR camera and am getting back into photography, kinda a new old hobby/art avenue. I snagged a new digital drawing tablet so I feel like it's time to draw some Cowboys & Dinosaurs....cause that's cool. Since I know my way around a kitchen I'm all about checking out new restaurants around town for some inspirations and drinks. Someday I'd like to get a beat up old motorcycle and fix it, I'd like to build stuff like furniture, and I'd like to fix my own cars. I imagine once I get a house, that's when those things will happen.
I love the outdoors so I like to hike, camp, fish, canoe....and capsize canoes. I take pride in being a former Boyscout so there's a bit of dork in my outdoors. I want a cabin in the woods one day, on a lake, far away from the city(not that I'm not a fan of city life,) but the cabin still has to have the interwebs. Hopefully sooner than later I'm planning on squeezing in a bit of traveling, national and international as well. Don't know exactly where yet, the big national parks of the USA are kinda top priority and Japan.
I'm not too sure yet what I'm looking for other than someone who "gets" semi-eccentric artistic types, has a broad sense of humor that can boarder on blue, is pretty adventurous, can reign me in when needed in a charming way, and has their shit semi together or at least knows what they want in some aspects of their life.
I don't think I'm too set in ways so artistic like-minds, total mathematicians, and pretty much anything inbetween is certainly my cup of tea. I'm not really into the super self absorbed and if your profile ends up having a pic of you posing with duck lips unironically we might have some tension. I'm looking for a relationship with a solid base that can build towards long term with a lot of adventuring along way.
TV: Almost Everything HBO, Westworld, Game of Thrones, Star Trek TNG, True Detective (S1), Twin Peaks, Hannibal, Fargo(season 2 was the shit,) Adventure Time, Samurai Jack, Cowboy Bebop, and not really reality TV or Walking Dead(overrated)
Music: Radiohead, Air, Jim Guthrie, Royksopp, Led Zepplin, Bjork, Bob Dylan, OLD Country, Classical, tons more but usually not Top 40
Food:Everything.....well I suppose Cheese is my favorite food, a 5-10 year cheddar would be tops


text:
|Message view
|« Date » · « Thread »
|« Date » · « Thread »
|"William A. Rowe Jr." <wr...@rowe-clan.net>
|Re: svn commit: r885606 - /httpd/httpd/trunk/build/rpm/httpd.init
|Thu, 03 Dec 2009 20:15:07 GMT
Gregg L. Smith wrote: > Original Message ----------------------- >> Finally, I have yet to see any feedback on the pcre mandatory >> dependency issue. Comments? > > Personally, I thought your Monopoly metaphor was quite on target. > > libz, openssl, lua = batteries not included > apr, apu, pcre = drive train not included. > >> And what is passing for an excuse for a local PCRE install >> these days probably doesn't look like 7.8 or later, with >> various fixes we are vulnerable to. > > This does not leave me with a warm and fuzzy feeling. As a user, is the pcre 8.0 I've built going to expose me to risks that your maintained 7.8 does not? If yes, then I'd prefer your maintained one. After all, who knows better than you what will interact with your code to produce problems. Regardless of merit, who will ultimately get blamed in the end? Could your reputation be tarnished? Can you completely divorce yourself from something your software requires to run? I'm referring to pre v7 chaos. And mostly not referring to modern linux distros. > The 'Jump Ship' factor; > > To me, and I'm probably wrong, it sounds like Mr. Felt's comment was an ultimatum of sorts as 'indefinitely' is a pretty strong word. With this issue you have created a deal with it or jump ship ultimatum which could very well leave some people scrambling to get off. Each person is going to inevitably weigh the pain factor, the pain of dealing with it over the pain of jumping ship. I consider myself lucky that my second attempt to deal with it was successful, or so it seems so far anyway, but I never know from day to day. Agreed that ease-of-adoption is going to be the usual, first barrier to anyone jumping aboard 2.4 from 2.2, 2.0, or even still from 1.3. > I may be wrong but as an outsider looking in, I see you wanting to stop maintaining/including the gear box and are instead spending the time on adding more optional gadgets to choose from (some of the third party modules you've taken over). In the end, I'd prefer having a reverse gear over the rear window defogger. You are also loosing all control of a required piece of equipment, this has got to make some of you at least cringe a little. I'm not 100% sure I understand what you are saying here. Drop the gearbox and let them assemble their own transmission? Or distribute a most modern transmission that the user can ignore or swap out if they want to install their own? > Sorry for the outburst, but you opened the door for, and I've said what I've wanted to for some time now, thanks for listening. Corrections and daggers welcomed. No problems, thanks for chiming in.
|View raw message


text: Tomorrow I am going out with some friends. Included is a guy who when I last went out with kissed me. We were both drunk but I've liked him for years actually. This was a few days ago and apart from the text to invite me out, I Haven't seen him since. Any advice on what to say/ wear to really get his attention?


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221.661.01 Project Development for Primary Health Care in Developing Countries
- Department:
- International Health
- Term:
- 4th term
- Credits:
- 4 credits
- Academic Year:
- 2012 - 2013
- Location:
- East Baltimore
- Class Times:
- M W, 3:30 - 5:20pm
- Grading Restriction:
- Letter Grade or Pass/Fail
- Course Instructors:
- Resources:
- Prerequisite:
- Description:
Supplements 220.601 by focusing on the practical problems in the planning, design, implementation, and evaluation of primary health care programs in developing countries. Students design a primary health care program addressing community participation, needs assessment, training and supervision of CHWs, approaches to sustainability, logistics of service delivery, monitoring, and evaluation, and present them to the class.
- Learning Objectives:
Upon successfully completing this course, students will be able to:
- write realistic, appropriate and measurable project objectives
- develop an implementation strategy for a primary health care project
- create a health monitoring and evaluation component for the project
- write a budget and the narrative summary for the project you have designed
- conduct a 30-cluster household survey measuring child health indicators
- Methods of Assessment:
Student evaluation based on group assignments, class participation, a mid-term paper, and a review of a public health care proposal.
- Instructor Consent:
Consent required for all students
- For consent, contact:


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Whether you've just brought a spindly young Japanese maple tree (Acer palmatum) home from the nursery or are moving a large, established sugar maple (Acer saccharum) from the front yard to the backyard, transplanting is a serious undertaking that can make or break the future health of your tree. Young trees are more adaptable than established specimens and are more likely to transition easily.
When and Where
Transplant your maple tree in early spring, before tender new growth starts to emerge. Although you can transplant in fall, avoid transplanting in summer, when hot temperatures are more likely to stress the tree. Only plant where hardy: Japanese maple is hardy in U.S. Department of Agriculture plant hardiness zones 5 to 8, while sugar maple is hardy in USDA zones 3 to 8. Both trees prefer dappled sunlight or partial shade. Take the size of the tree into consideration when transplanting and space for mature growth; sugar maples can grow up to 80 feet tall and crowd power lines, houses and sidewalks.
Preparation is Prosperity
Maples require well-draining, slightly acidic soil and full sun to partial shade, depending on variety. Prepare the soil prior to transplanting by digging a hole that is three times the width of the root ball and just a little bit deeper. Digging a large hole improves the quality of the soil by introducing air and loosening it, which will make it easier for the roots to become established. Even if you're planting the tree right after digging, keep the tree in a shaded area with its roots moist and covered, so it doesn't dry out. If you're planting a bare root tree, soak the roots in water for about an hour before planting.
Hole New World
Place the maple in the planting hole so that it sits at the same depth as it was in the container or the ground. Fill about three-fourths of the hole with the soil you've just dug, without adding amendments. Water deeply to disperse air pockets, and fill the remaining quarter of the hole with soil. Mulch with about 3 inches of organic matter, keeping the mulch from touching the trunk, and water again. Do not tamp or press down on the soil, because this will compact it.
All About Aftercare
Most transplanted trees go through a period of shock and stress, known as transplant shock, in which they are more vulnerable to pests, diseases and other problems. Maple trees have thin bark, which makes them vulnerable to sunscald. Wrap the tree in late fall with a light-colored tree warp and remove it in spring, or paint the trunk up to the branches with white latex paint. Remove all grass and weeds, which compete for moisture, and provide about 1 inch of supplemental water a week throughout the growing season.
Related Searches
- University of California Cooperative Extension -- Napa County: Transplanting Shrubs and Trees
- Clemson Cooperative Extension: Maple
- Clemson Cooperative Extension: Newly Planted Trees -- Strategies for Survival
- Purdue University Cooperative Extension Service: Planting & Transplanting Landscape Trees and Shrubs
- Missouri Botanical Garden: Acer Saccharum
- Public Broadcasting Station: The Victory Garden: Ask: Trees and Shrubs
- Montana State University Extension: What's Wrong With This Tree?
- Photo Credit stockfotoart/iStock/Getty Images
You May Also Like
How to Transplant a Japanese Maple Tree
Japanese maples are notoriously delicate during a stressful move, making transplants difficult and risky. Despite its fragile state during a move, Japanese...


text:
Digital Account Manager Exciting Creative Agency
- Recruiter
- Web Recruit Ltd
- Location
- Exeter
- Salary
- £20,000 per annum Plus Benefits
- Posted
- 10 Aug 2017
- Expires
- 19 Aug 2017
- Sector
- Sales
Digital Account Manager – Exciting Creative Agency Exeter, Devon Are you looking to develop your career as a Digital Account Manager with a pioneering business? Want to utilise your creativity and deliver engaging social media and PPC campaigns for a diverse customer base? If so, we'd love to hear from you. The Company: Bigwave Media is a fun and growing creative agency with offices in Exeter, Plymouth and Torquay. Driven by our commitment to excellence, we provide a complete range of marketing, design and digital services. Now, we're looking for a social media savant to join our team as a Digital Account Manager in Exeter. The Benefits: - Salary of up to £20,000 DOE - Pension - Flexitime policy - Great location in the city centre - All the free tea and coffee you can drink - Full Christmas shutdown - 25 days' holiday plus Bank Holidays Fostering a friendly and highly collaborative environment, we offer excellent training and development opportunities to enable you to broaden your knowledge and remain at the top of your game. Working alongside a talented team, you'll have the chance to get involved with an array of interesting projects and put your creativity to the test. We're a sociable bunch here at Bigwave Media, so we hold plenty of events to ensure that we can hang out outside of work and blow off some steam. The Role: As a Digital Account Manager, you'll manage a range of PPC and social media campaigns for customers. In this exciting role, you will: - Develop and manage a range of digital projects and tasks, from creating and posting social media posts, to setting up and optimising PPC campaigns - Effectively manage resources to deliver projects and work within set timelines and budgets - Manage multiple work streams - Write engaging content, including blogs - Ensure that customer satisfaction is achieved - Share best practice with colleagues - Attend meetings with customers when required - Oversee a Digital Intern About You: To join the Bigwave Media team, you'll need: - Experience of Google Analytics and Google AdWords - Previous experience of managing Facebook advertising - Experience of social media management and channels - A good understanding of digital media and marketing channels - The ability to write briefs - Strong administrative, organisational and time-management skills Strong presentation skills would be beneficial to your application, as would experience of the following: website content management systems, managing staff or PPC platforms such as Twitter, LinkedIn or Bing. We're eager to hear from you if you've held the title of Digital Account Manager, Marketing Executive, Social Media Executive, Digital Marketing Account Manager or Account Manager. Other companies may call this role Customer Account Manager, Client Account Manager, PPC Campaign Manager, Social Media Campaign Manager or Digital Project Manager. Webrecruit and Bigwave Media are equal opportunities employers, value diversity and are strongly committed to providing equal employment opportunities for all employees and all applicants for employment. Equal opportunities are the only acceptable way to conduct business and we believe that the more inclusive our environments are, the better our work will be. So, if you're seeking your next challenge as a Digital Account Manager, please apply via the button shown. This vacancy is being advertised by Webrecruit. The services advertised by Webrecruit are those of an Employment Agency. Working hours: 40 hours per week This job was originally posted as www.totaljobs.com/job/75324780


text:
This property is no longer available.Search for Available Property.
2.68 acres in Hubbard County, Minnesota
Beautiful Little Sand Lake property features 2.68 AC, 165 ft of sand shoreline, energy efficient & quality craftsmanship, 4000 sq ft of living space, 3 br, 4 baths, master suite w/ walk in closets, jacuzzi tub & tiled walk in shower, fieldstone fireplace in living, formal dining + spacious kitchen w/ eat in dining, main floor laundry, sunroom w/ patio door to wrap around deck, full w/o bsmt, 2nd kitchen w/ storage, hobby room, attach heated gar, detach gar w/ workshop + steel storage building.
Hwy 71/34 in Park Rapids go E on Hwy 34 to left on County 226 (Dorset Corner) follow approx 3 miles to property #22954 on the right.
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NOTE: The information contained herein is provided as general information only and has been obtained from sources deemed reliable. It is provided without any guaranty, warranty or representation, expressed or implied, made by Lands of America, or any related entity, as to the accuracy or completeness of the information. The information is presented subject to errors, omissions, change of price or conditions, prior sale or withdrawal without notice. Prospective purchasers should make their own investigations, projections and conclusions concerning the information.


text:
Concertino Kolberg Oak Effect Laminate Flooring 1.48 m² Pack
This laminate flooring has an attractive Kolberg oak effect and 4 sided bevelled edge. Each plank uses a simple click system, so installation is simple and it's suitable for warm water underfloor heating systems under 28 degrees.
- Suitable for busy & splash areas including living rooms, hallways, bedrooms, studies, utility rooms & kitchens
- 20 years domestic guarantee
- No adhesive required
- Suitable for warm water underfloor heating systems under 28 degrees
- AC4 wear rating, ideal for residential use with high traffic, and commercial use with general traffic
- Delivery date confirmed at checkout
Product info
Tech specs
|Range :
|Finish :
|Kolberg oak effect
|Style :
|Coverage :
|1.48 m²
|Material :
|High density fibreboard (HDF)
|Thickness :
|Length (mm) :
|Width (mm) :
|Moisture resistance :
|Moisture resistant
|AC Rating :
|Pack quantity :
More information
- Made from responsibly sourced, Forest Friendly timber
- Made from responsibly sourced, Forest Friendly timber


text:
MIAMI -- New Orleans Saints defensive coordinator Gregg Williams was notified Wednesday that his youngest son, Chase, was named to the Super Prep All American Football Team.
Chase Williams, a linebacker, has committed to Virginia Tech, where he is currently enrolled and attending classes.
"We are proud of him," Gregg Williams said via text message Wednesday morning. "Let this be the start of good news to the Williams family during Super Bowl week!!"
Chase Williams, 6 feet 3 and 240 pounds, runs the 40 in 4.61 seconds and bench-pressed 225 pounds 25 times in the combine for college-bound players. During his senior season of high school, he had 173 tackles, 24 tackles for loss, 12 forced fumbles, 11 sacks and four interceptions. He finished his prep career with double-digit tackles in 27 straight games.
Adam Schefter is ESPN's NFL Insider.


text:
Real Touch Diamond Rose in Lavender 3.25" Bloom x 24" Tall
DetailsCheck out lifelike lavender wedding flowers like this beautiful real touch diamond rose in lavender with gorgeous petal structure. Add these romantic lavender real touch roses to your pastel color schemes to create soft DIY bouquets!
- 3.25" Wide x 2.25" Tall Bloom
- 24" Tall
Shop All Floral Supplies
Shipping & Returns
- Economy Shipping: 5-10 business days
- Ground Shipping: 1-5 business days
- Expedited, International, and SmartPost options available at checkout.
- More Shipping Information »
Return this item within 30 days for a full product refund. Return Policy »


text:
PHILADELPHIA - Track & field season just came to a close at the University of Pennsylvania, but that just means cross country season is right around the corner. Director of Track & Field/Cross Country Steve Dolan officially announced the 2015 cross country season on Monday.
Once again, the Quakers begin the season with the Big 5 Invitational on their home course at Belmont Plateau on Sept. 11. Last season, both the men and women took first place at the season-opening meet.
A week later, the Quakers take the short trip to Haverford, Pa., to compete in the Mainline Invitational before splitting up for the Notre Dame Invitational and Paul Short Invitational on Oct. 2. The Quakers wrap up the regular season on Oct. 17 with the Princeton Invitational.
The Heptagonal Championships return to Van Corlandt Park in New York City this year. The Quakers will race for the league title on Oct. 30. Two weeks later, Penn competes in the NCAA Regional Championships with the hopes of returning a few Quakers to the NCAA Championships on Nov. 21 in Louisville, Ky.
Full schedule is below. Start times are to be determined.
|2015 Cross Country
|Fri, Sep 11
|Big 5 Invitational
|at Philadelphia, Pa. (Belmont Plateau)
|Fri, Sep 18
|Mainline Invitational
|at Haverford, Pa.
|Fri, Oct 02
|Paul Short Invitational
|at Bethlehem, Pa.
|Fri, Oct 02
|Notre Dame Invitational
|at South Bend, Ind.
|Sat, Oct 17
|Princeton Invitational
|at Princeton, N.J.
|Fri, Oct 30
|Heptagonal Championships
|at Bronx, N.Y. (Van Cortlandt Park)
|Fri, Nov 13
|NCAA Regional Championships
|at Princeton, N.J.
|Sat, Nov 21
|NCAA Championships
|at Louisville, Ky.


text:
Full Circle
- Relax Your Mind
- The Color Of Love
- Ain't A Thang Wrong
- Oh Well
- Whatcha Need
- On The Road Again
- Makin' Love (Interlude)
- Roll Wit Me
- Right On Time
- Howz About It
- That's Why I Love You
- I'm OK, You're OK
- Luv N U
- I'll Show You
- Rádio interpreta
- Rok vydání: 2002
- Žánry: Boybandy, Ploužáky, R'n'B, Odpolední relax, Lovesongy
- Vydavatelství: Sony BMG
- Text písničky
(Hey, whassup, this is Michael.
Just call to see what you guys going on this weekend.
You know ever since I met you, I can't seem to let you go.
Make sure you call me back. OK?)
Ever since the day that we first met
Everything you do just seems to speak my interest
Girl you know you piss right through my soul
Make me want to tell you things nobody knows yeah
So here I am with heart in hand
Your life have a mission for both you and I in these demands
Wouldn't you like to take a trip with me
Heaven knows just where this thing to lead
So howz about it
You can just go away
Howz about it
We can leave today
Howz about it
No need to pack, I'll handle everything
We can take a private jet
Fly away
We can fly, fly away
Maybe you think it's a bit too soon
I realize it's only than a week or two but
Feels I know you all of my life
And I wouldn't be surprised if one day you were my wife
So howz about it
You can just go away
Howz about it
We can leave today
No need to pack, I'll handle everything
Take my jet, take my private jet
And we can fly away
Fly, fly away
Don't even give it too much thought
Just listen to your heart
We can go anywhere you want to go
All you gotta is
All you gotta is
Let me know
Howz about it
- Howz About It (04:01)