Mineral established lubricant oils used for internal combustion (IC) engines, and it is not ecological and dangerous to the environment. Biobased lubricant (BBL) is ecological and environmentally ...friendly. In this paper, cottonseed oil chemically modified by trimethylolpropane (TMP) ester is used as lubricants for compression ignition engines, and its performance and emission characteristics are studied. Mineral lubricants and cottonseeds are compared for emission gases like hydrocarbon (HC), carbon dioxide (CO
2
), nitrogen oxides (NOx), and carbon monoxide (CO). The performance of brake thermal efficiency (BTE) and brake-specific fuel consumption (BSFC) is found to be similar for comparing CSTE lubricant and mineral-based oil. Hence, the recorded BSFC is 0.6 kg/KW-h, the recorded maximum HC emission is 45 ppm, NOx emission is 590 ppm, CO
2
emission is 2.99 ppm, and maximum CO emission is 0.16ppm. Hence, the main contribution of this proposed article is emission reduction.
Background: The voltage gated K + channel Kv1.5 participates in the repolarization of a wide variety of cell types. Kv1.5 is downregulated during hypoxia, which is known to stimulate the ...energy-sensing AMP-activated serine/threonine protein kinase (AMPK). AMPK is a powerful regulator of nutrient transport and metabolism. Moreover, AMPK is known to downregulate several ion channels, an effect at least in part due to stimulation of the ubiquitin ligase Nedd4- 2. The present study explored whether AMPK regulates Kv1.5. Methods: cRNA encoding Kv1.5 was injected into Xenopus oocytes with and without additional injection of wild-type AMPK (α1 β 1γ1), of constitutively active γR70Q AMPK (α1 β 1γ1(R70Q)), of inactive mutant αK45R AMPK (α1(K45R)β1γ1), or of Nedd4-2. Kv1.5 activity was determined by two-electrode voltage-clamp. Moreover, Kv1.5 protein abundance in the cell membrane was determined by chemiluminescence and immunostaining with subsequent confocal microscopy. Results: Coexpression of wild-type AMPK WT and constitutively active AMPK γR70Q , but not of inactive AMPK αK45R significantly reduced Kv1.5-mediated currents. Coexpression of constitutively active AMPKγR70Q further reduced Kv1.5 K + channel protein abundance in the cell membrane. Co-expression of Nedd4-2 similarly downregulated Kv1.5-mediated currents. Conclusion: AMPK is a potent regulator of Kv1.5. AMPK inhibits Kv1.5 presumably in part by activation of Nedd4- 2 with subsequent clearance of channel protein from the cell membrane.
The 5′-adenosine monophosphate-activated serine/threonine protein kinase (AMPK) is stimulated by energy depletion, increase in cytosolic Ca
2+
activity, oxidative stress, and nitric oxide. AMPK ...participates in the regulation of the epithelial Na
+
channel ENaC and the voltage-gated K
+
channel KCNE1/KCNQ1. It is partially effective by decreasing PIP
2
formation through the PI3K pathway. The present study explored whether AMPK regulates the renal outer medullary K
+
channel ROMK. To this end, cRNA encoding ROMK was injected into
Xenopus
oocytes with and without additional injection of constitutively active AMPK
γR70Q
(AMPK
α1
-HA+AMPK
β1
-Flag+AMPKγ1
R70Q
), or of inactive AMPK
αK45R
(AMPK
α1K45R
+AMPK
β1
-Flag+AMPK
γ1
-HA), and the current determined utilizing two-electrode voltage-clamp and single channel patch clamp. ROMK protein abundance was measured utilizing chemiluminescence in
Xenopus
oocytes and western blot in whole kidney tissue. Moreover, renal Na
+
and K
+
excretion were determined in AMPK
α1
-deficient mice (
ampk
−/−
) and wild-type mice (
ampk
+/+
) prior to and following an acute K
+
load (111 mM KCl, 30 mM NaHCO
3
, 4.7 mM NaCl, and 2.25 g/dl BSA) at a rate of 500 μl/h. As a result, coexpression of AMPK
γR70Q
but not of AMPK
αK45R
significantly decreased the current in ROMK1-expressing
Xenopus
oocytes. Injection of phosphatidylinositol PI
(4,5)
P
2
significantly increased the current in ROMK1-expressing
Xenopus
oocytes, an effect reversed in the presence of AMPK
γR70Q
. Under control conditions, no significant differences between
ampk
−/−
and
ampk
+/+
mice were observed in glomerular filtration rate (GFR), urinary flow rate, serum aldosterone, plasma Na
+
, and K
+
concentrations as well as absolute and fractional Na
+
and K
+
excretion. Following an acute K
+
load, GFR, urinary flow rate, serum aldosterone, plasma Na
+
, and K
+
concentration were again similar in both genotypes, but renal absolute and fractional Na
+
and K
+
excretion were higher in
ampk
−/−
than in
ampk
+/+
mice. According to micropuncture following a K
+
load, delivery of Na
+
to the early distal tubule but not delivery of K
+
to late proximal and early distal tubules was increased in
ampk
−/−
mice. The upregulation of renal ROMK1 protein expression by acute K
+
load was more pronounced in
ampk
−/−
than in
ampk
+/+
mice. In conclusion, AMPK downregulates ROMK, an effect compromising the ability of the kidney to excrete K
+
following an acute K
+
load.
Many researchers have been working on bio-based lubricant which is complete or partial replacement for mineralbased lubricant. Mineral-based lubricant is highly pollutant and possesses environmental ...threat as it is not biodegradable, in the initial days of the industrial revolution bio-based lubricants were widely used, later it was replaced by more sustainable and easily available but environmental polluting mineral oils, currently due to environmental concerns and scarcity of mineral oils, bio-based lubricant has gained importance. Bio-based lubricants are now a day’s used for various applications such as transformer oil and processes where there is complete loss of lubricants. They possess very good properties in such applications, whereas bio-based lubricants are also used internal combustion engines, pure biobased lubricant may not be suitable for long-duration, but genetically and chemically modified bio-based lubricants will be suitable for IC engine. Though bio-based lubricant possesses many good properties as a lubricant for IC engine and various other application, it is still at large to become commercial, more study is required for checking performance of such pure and modified bio-based lubricants oils, in this paper such study of cotton seed Trimethylolpropane (TMP) ester oil and its effects on performance of brake specific fuel consumption (BSFC), brake thermal efficiency (BTh) and emission of gases like hydrocarbon (HC), carbon monoxide (CO), carbon dioxide (CO2 ) nitrogen oxides (NOx ) are studied, bio-based have poor cold flow properties and oxidation stability to improve these additives are added. The experimental study shows that Cottonseed Trimethylolpropane Ester (CSTE) displays similar characteristics of thermal efficiency, brake specific fuel consumption and emission of gases as compared to mineralbased lubricating oil hence can be used in the IC engine instead of mineral-based lubricants.
► The glucose carrier SGLT1 is expressed in HPV-positive HELA carcinoma cells. ► Coexpression of the HPV18 E6 protein upregulates SGLT1. ► Coexpression of E6 increases SGLT1 protein abundance in the ...cell membrane. ► E6 stimulates insertion rather than retrieval and degradation of the carrier. ► SGLT1 thus contributes to excessive glucose uptake into HPV18 infected tumor cells.
Tumor cells utilize preferably glucose for energy production. They accomplish cellular glucose uptake in part through Na
+-coupled glucose transport mediated by SGLT1 (SLC5A1). This study explored the possibility that the human papillomavirus 18 E6 protein HPV18 E6 (E6) participates in the stimulation of SGLT1 activity. E6 is one of the two major oncoproteins of high-risk human papillomaviruses, which are the causative agent for cervical carcinoma. According to Western blotting, SGLT1 is expressed in the HPV18-positive cervical carcinoma cell line HeLa. To explore whether E6 affects SGLT1 activity, SGLT1 was expressed in
Xenopus oocytes with and without E6 and electrogenic glucose transport determined by dual electrode voltage clamp. In SGLT1-expressing oocytes, but not in oocytes injected with water or expressing E6 alone, glucose triggered a current (
I
g).
I
g was significantly increased by coexpression of E6 but not by coexpression of E2. According to chemiluminescence and confocal microscopy, coexpression of E6 significantly increased the SGLT1 protein abundance in the cell membrane. The decay of
I
g following inhibition of carrier insertion by Brefeldine A (5
μM) was not significantly affected E6 coexpression. Accrodingly, E6 was not effective by increasing carrier protein stability in the membrane. In conclusion, HPV18 E6 oncoprotein participates in the upregulation of SGLT1.
The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl
− channel critically important in Cl
− secreting epithelia. Mutations in the CFTR gene, such as
ΔF508CFTR leads ...to cystic fibrosis, a severe disease with defective Cl
− secretion. CFTR is stimulated by the serum and glucocorticoid-inducible kinase SGK1. The SGK1 dependent regulation of several carriers and channels involves the phosphatidylinositol-3-phosphate-5-kinase PIKfyve, which similarly mediates the regulation of glucose carriers by PKB/Akt. The present study was thus performed to elucidate whether PKB/Akt and PIKfyve are regulators of CFTR. To this end CFTR or
ΔF508CFTR were expressed in
Xenopus oocytes alone or together with PKB, PIKfyve or the SGK1/PKB resistant mutant
S318APIKfyve, and the current generated by cAMP upregulation with 10
μM forskolin
+
1
mM IBMX determined utilizing dual electrode voltage clamp. As a result, forskolin/IBMX treatment triggered a current (
I
cAMP) in CFTR-expressing
Xenopus oocytes, but not in oocytes expressing
ΔF508CFTR. Coexpression of PKB/Akt and PIKfyve, but not of
S318APIKfyve, stimulated
I
cAMP in CFTR-expressing (≈2- to 3-fold) but not in
ΔF508CFTR
-expressing or water injected
Xenopus oocytes. Immunohistochemistry revealed that the coexpression of PIKfyve, but not of
S318APIKfyve, enhanced the CFTR protein abundance but not the
ΔF508CFTR protein abundance in CFTR or
ΔF508CFTR-expressing oocytes. The present observations reveal a novel powerful regulator of intact but not of defective CFTR.
Akt/PKB stimulates the glucose carrier GLUT4. Here we explored whether Akt directly regulates Na+‐coupled transport of glucose (by SGLT1) or phosphate (by NaPiIIa). Immunohistochemistry showed that ...Akt2 is expressed in proximal renal tubules. According to dual electrode voltage clamp experiments the coexpression of Akt increased the glucose‐induced current in SGLT1‐expressing and the phosphate‐induced current in NapiIIa‐expressing Xenopus oocytes. Renal transport was further studied using Akt2 deficient (akt2−/−) and wild type mice (akt2+/+). akt2−/− mice suffered from glucosuria which was partially due to increased plasma glucose levels but was not observed in akt2+/+ mice made similarly hyperglycemic as akt2−/− mice by fructose feeding pointing to defective renal tubular glucose reabsorption. Glucose‐induced depolarization was significantly smaller in isolated perfused renal tubules from akt2−/− than from akt2+/+ mice. In addition, the phosphate clearance was higher in akt2−/− than in akt2+/+ mice despite a significantly decreased plasma PTH and enhanced 1,25‐dihydroxyvitamin D3 concentration and a tendency of lower plasma phosphate. Bone density was significantly reduced in akt2−/− mice. In conclusion, Akt plays a role in the regulation of renal glucose and phosphate transport contributing to the maintenance of phosphate balance and adequate mineralization of bone.
Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Nothing is known, however, of the role of Akt/PKB in the regulation of renal epithelial transport. To explore whether Akt2/PKBβ ...influences the Na(+)-coupled glucose cotransporter SGLT1, human SGLT1 was expressed in Xenopus laevis oocytes with or without Akt/PKB, and electrogenic glucose transport was determined by dual-electrode voltage clamp. The coexpression of Akt/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. To study the functional significance of Akt/PKB-sensitive renal glucose transport, further experiments were performed in gene-targeted mice lacking functional Akt2/PKBβ (akt2(-/-)) and in their wild-type littermates (akt2(+/+)). Plasma glucose concentration was significantly higher in akt2(-/-) mice than in akt2(+/+) mice but was virtually identical to the plasma glucose concentration in fructose-treated akt2(+/+) mice. Urinary glucose excretion was significantly higher in akt2(-/-) mice compared with akt2(+/+) mice with or without fructose treatment. Moreover, the glucose-induced depolarization of proximal tubular cells was significantly smaller in isolated, perfused renal tubules from akt2(-/-) mice than in those from akt2(+/+) mice. In conclusion, Akt2/PKBβ plays a role in the regulation of renal glucose transport.
Akt/PKB is known to regulate the facilitative glucose carrier GLUT4. Nothing is known, however, of the role of Akt/PKB in the regulation of renal epithelial transport. To explore whether Akt2/PKBb ...influences the Na...-coupled glucose cotransporter SGLT1, human SGLT1 was expressed in Xenopus laevis oocytes with or without Akt/PKB, and electrogenic glucose transport was determined by dual-electrode voltage clamp. The coexpression of Akt/PKB in SGLT1-expressing oocytes was followed by an increase in glucose-induced currents. To study the functional significance of Akt/PKB-sensitive renal glucose transport, further experiments were performed in gene-targeted mice lacking functional Akt2/PKBb (akt2...) and in their wild-type littermates (akt2...). Plasma glucose concentration was significantly higher in akt2... mice than in akt2... mice but was virtually identical to the plasma glucose concentration in fructose-treated akt2... mice. Urinary glucose excretion was significantly higher in akt2... mice compared with akt2... mice with or without fructose treatment. Moreover, the glucose-induced depolarization of proximal tubular cells was significantly smaller in isolated, perfused renal tubules from akt2... mice than in those from akt2... mice. In conclusion, Akt2/PKBb plays a role in the regulation of renal glucose transport. (ProQuest: ... denotes formulae/symbols omitted.)
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