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Purpose: Occipital neuralgia (ON) is a disabling problem within the pediatric population. Many of these patients fail medical therapies and continue to suffer without further surgical management. Occipital nerve stimulation (ONS) is used to treat ON in the adult population leading to a 72–89% reduction in pain; however, there are limited studies regarding its use in the pediatric population. In this study, we examined the outcomes of ONS in pediatric patients with medically refractory ON. Methods: We performed a chart review of pediatric patients at our institution who have undergone ONS for the same indications. Results: We identified 3 patients at our institution who underwent ONS trial and/or permanent implantation for ON. One patient had complete pain relief after the trial and declined permanent implantation. The other patient had fewer attacks compared to his pre-trial baseline and controlled them by adjusting his permanent implant stimulation settings. The last patient had near complete relief of her symptoms and no longer required any pain medication. Conclusion: Our study highlights the paucity of studies evaluating the utility of ONS in the pediatric ON population. Limited data from both the literature and our institution's experience reveal that pediatric patients may benefit from trial and/or permanent implantation of ONS for medically refractory ON pain. [ABSTRACT FROM AUTHOR]

Endothelial cells possess multiple mechanisms for the control of Ca 2+ influx during agonist and mechanical stimulation. Increased intracellular Ca 2+ during such events is important in the production of vasoactive substances including NO, prostacyclin, and, possibly, endothelium-derived hyperpolarizing factor(s). The present studies examined the effect of arachidonic acid on cellular Ca 2+ entry and the underlying mechanisms by which this fatty acid regulates entry. Studies were conducted in cultured bovine aortic endothelial cells (passages 3 to 6) with changes in intracellular Ca 2+ determined using the fluorescent Ca 2+ -sensitive indicator fura 2. Arachidonic acid (1 to 50 μ M) stimulated Ca 2+ entry from the superfusate without affecting Ca 2+ release from intracellular stores. 2-aminoethoxydiphenyl borate (2APB) (100 μ M) added at the peak of Ca 2 + entry did not inhibit arachidonic acid–induced Ca 2+ entry but, in contrast, significantly inhibited entry stimulated by ATP (1 μ M). Arachidonic acid–induced Ca 2+ entry was inhibited by econazole (1 μ M), but not indomethacin (10 μ M) or nordihydroguairetic acid (10 μ M), suggesting the involvement of cytochrome P450 monooxygenase metabolite of arachidonic acid. Oleic acid (10 μ M) was ineffective in inducing Ca 2+ entry, whereas linoleic acid (10 μ M) stimulated Ca 2+ entry but by a mechanism insensitive to econazole. Collectively the data demonstrate that primary cultured aortic endothelial cells possess a Ca 2+ entry mechanism modulated by arachidonic acid. This mode of Ca 2+ entry appears to operate independently of store depletion–mediated mechanisms. [ABSTRACT FROM AUTHOR]

1 Agonists increase endothelial cell intracellular Ca[sup 2+], in part, by capacitative entry, which is triggered by the filling state of intraceltular Ca[sup 2+] stores. It has been suggested that depletion of endoplasmic reticulum (ER) Ca[sup 2+] stores either leads to a physical coupling between the ER and a plasma membrane channel, or results in production of an intracellular messenger which affects the gating of membrane channels. As an axis involving the IP[sub 3] receptor has been implicated in a physical coupling mechanism the aim of this study was to examine the effects of the putative IP[sub 3] receptor antagonists/modulators, 2 aminoethoxydiphenyl borate (2APB) and xestospongin C, on endothelial cell Ca[sup 2+] entry. 2 Studies were conducted in fura 2 loaded cultured bovine aortic endothelial cells and endothelial cells isolated from rat heart. 3 2APB (30-300 µM) inhibited Ca[sup 2+] entry induced by both agonists (ATP 1 µM, bradykinin 0.1 µM) and receptor-independent mechanisms (thapsigargin 1 µM, ionomycin 0.5 and 5 µM). 2APB did not diminish endothelial cell ATP-induced production of IP[sub 3] nor effect in vitro binding of [³H]IP[sub 3] to an adrenal cortex binding protein. Capacitative Ca[sup 2+] entry was also blocked by disruption of the actin cytoskeleton with cytochalasin (100 nM) while the initial Ca[sup 2+] release phase was unaffected. 4 Similarly to 2APB, xestospongin C (3-10 µM) inhibited ATP-induced Ca[sup 2+] release and capacitative Ca[sup 2+] entry. Further, xestospongin C inhibited capacitative Ca[sup 2+] entry induced by thapsigargin (1 µM) and ionomycin (0.5 µM). 5 The data are consistent with a mechanism of capacitative Ca[sup 2+] entry in vascular endothelial cells which requires (a) IP[sub 3] receptor binding and/or an event distal to the activation of the ER receptor and (b) a spatial relationship, dictated by the cytoskeleton, between Ca[sup 2+] release and entry pathways. [ABSTRACT FROM AUTHOR]

1. Agonists increase endothelial cell intracellular Ca(2+), in part, by capacitative entry, which is triggered by the filling state of intracellular Ca(2+) stores. It has been suggested that depletion of endoplasmic reticulum (ER) Ca(2+) stores either leads to a physical coupling between the ER and a plasma membrane channel, or results in production of an intracellular messenger which affects the gating of membrane channels. As an axis involving the IP(3) receptor has been implicated in a physical coupling mechanism the aim of this study was to examine the effects of the putative IP(3) receptor antagonists/modulators, 2 aminoethoxydiphenyl borate (2APB) and xestospongin C, on endothelial cell Ca(2+) entry. 2. Studies were conducted in fura 2 loaded cultured bovine aortic endothelial cells and endothelial cells isolated from rat heart. 3. 2APB (30 - 300 microM) inhibited Ca(2+) entry induced by both agonists (ATP 1 microM, bradykinin 0.1 microM) and receptor-independent mechanisms (thapsigargin 1 microM, ionomycin 0.5 and 5 microM). 2APB did not diminish endothelial cell ATP-induced production of IP(3) nor effect in vitro binding of [(3)H]-IP(3) to an adrenal cortex binding protein. Capacitative Ca(2+) entry was also blocked by disruption of the actin cytoskeleton with cytochalasin (100 nM) while the initial Ca(2+) release phase was unaffected. 4. Similarly to 2APB, xestospongin C (3 - 10 microM) inhibited ATP-induced Ca(2+) release and capacitative Ca(2+) entry. Further, xestospongin C inhibited capacitative Ca(2+) entry induced by thapsigargin (1 microM) and ionomycin (0.5 microM). 5. The data are consistent with a mechanism of capacitative Ca(2+) entry in vascular endothelial cells which requires (a) IP(3) receptor binding and/or an event distal to the activation of the ER receptor and (b) a spatial relationship, dictated by the cytoskeleton, between Ca(2+) release and entry pathways. [ABSTRACT FROM AUTHOR]

In this research, Imprecise Data Envelopment Analysis (IDEA) model wasutilized to improve fuzzy multiple responses in robust design. The combinationof process factor levels at each experiment was considered as a DecisionMaking Unit (DMU) with responses treated as inputs and outputs for allDMUs. The Fuzzy C-Means Clustering (FCMC) technique is used to fit theresponse fuzziness by clustering the average values, relative to each response,into a suitable number of clusters with triangular / trapezoidal membershipfunctions. IDEA models were used to estimate the fuzzy triangular / trapezoidalefficiency values for each DMU. Finally, the preference degree-based rankingapproach was used to discriminate between the fuzzy efficiency valuesand identifying the best combination of factors levels that would improvefuzzy multiple responses. Two case studies are utilized to illustrate the proposedapproach, including optimizing wire electrical discharge machining andsputtering process parameters. The results showed that the proposed approachprovides better anticipated improvements than the fuzzy multipleregression based approach. This approach would provide great assistant toprocess engineers in improving process performance with fuzzy multipleresponses over a wide range of business applications. [ABSTRACT FROM AUTHOR]

Summary 1. An exact understanding of signal transduction pathways within intact and functional arteriolar smooth muscle is made difficult by limited access to the intracellular environment due to the cell membrane. The aim of the present studies was to determine the feasibility of using polycationic lipids and reverse permeabilization for the introduction of peptide inhibitors into smooth muscle cells of the intact arteriolar wall. 2. Isolated cannulated arterioles were exposed to polycationic lipid preparations together with varying concentrations of the protein β-galactosidase (30–90 µg/mL). Similar experiments were also performed using cultured smooth muscle cells. Staining for the chromogenic substrate of β-galactosidase (5-bromo-4-chloro-3-indolyl-β-d-galactosidase; X-gal) demonstrated incorporation of the protein into cultured cells but not intact arteriolar smooth muscle. Similarly, polycationic lipid treatment did not enable loading of arteriolar smooth muscle (as assessed by cAMP-mediated vasodilation) with the protein kinase (PK) A inhibitory peptide PKI. 3. In contrast, reverse permeabilization, using high ATP concentrations in the presence of EGTA enabled introduction of PKI and inhibition of forskolin-mediated vasodilatation. Furthermore, arterioles maintained full viability following reverse permeabilization, as demonstrated by an ability to develop spontaneous myogenic tone. 4. Reverse permeabilization provides a method for introducing peptide inhibitors into functional arteriolar smooth muscle and manipulating signal transduction. Protein transfection using polycationic lipids appears to be limited by the barrier provided by the adventitia or inherent differences between cells under cultured conditions compared within the intact arteriole. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Early allograft dysfunction (EAD) is a rare but serious complication encountered among patients undergoing liver transplant surgery. Total plasma exchange (TPE) in EAD has been suggested, but its role is still considered investigational. We retrospectively assessed the efficacy of TPE in EAD and its impact on other parameters of liver function. Materials and methods: Between 1995 and 2001, 25 orthotopic liver transplant recipients developed EAD, which was defined as early postoperative prothrombin time (PT) >17 seconds, aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) >2500 IU/L, and/or the presence of hepatic encephalopathy, and development of renal failure. Daily TPE was performed using the Cobe Spectra TPE (Gambro) for 4 hours until an adequate clinical response, the patient underwent retransplantation, or the patient died. International normalizing ratio (INR), partial thromboplastin time (PTT), fibrinogen, ALT, AST, gamma-glutanyl transpeptidase (GGT), blood urea nitrogen (BUN), ammonia, and total bilirubin were analyzed before and after TPE. Student t and chi-square tests were used for statistical analysis. Results: Twenty-five patients with EAD included 13 females, 12 males of mean age 42.3 years (range, 1–63 years). Coagulopathy and hyperbilirubinemia significantly improved with TPE. Nineteen patients (76%) survived and 2 required retransplantation. Mean number of TPE sessions was 4.3. Conclusion: TPE was effective to correct coagulopathy and improve liver function. These results suggest the benefit of potential temporary liver support until recovery or retransplantation, in the absence of sepsis or multi-system organ failure. [Copyright &y& Elsevier]

Among extracorporeal liver support devices, liver dialysis is cleared by the U.S. Food and Drug Administration to be used for the management of fulminant hepatic failure (FHF). The outcomes of patients following liver dialysis need to be clearly evaluated.Among the 25 patients with FHF admitted to the Liver ICU between May 2000 and November 2002, 12 underwent liver dialysis, including 6 men and 6 women, of mean age 32 years. The causes of FHF were identified as acetaminophen (n = 10), herbal medications (n = 1) and autoimmune disease (n = 1). At presentation, the mean total bilirubin was 9.35 mg/dL (range, 0 to 1.3), mean ALT 3015 U/L (range, 0 to 48), mean AST 3457 (range, 0 to 42), mean ammonia 98 μmol/L (range, 10 to 60) and mean INR 1.88. A control group including 13 patients (2 men and 11 women), of mean age 27.8 years mean total bilirubin 5.66, mean ALT 3494, mean AST 3528, mean ammonia 113 and mean INR 3, were not treated with liver dialysis, due to the lack of machine availability or physician’s choice. The causes of FHF were acute hepatitis B (n = 1), acetaminophen (n = 10) or unknown (n = 2). There was no statistically significant difference in the baseline characteristics of the two groups (P > .05). Among the liver dialysis group, 1 patient died, 2 underwent OLTx, and 9 were discharged home. Among the control group; 4 patients died, 2 underwent OLTx, and 7 were discharged home. Preliminary results seem to support survival benefit among patients who underwent liver dialysis compared to non–liver dialysis; however, further randomized control trials are warranted to verify this observation. [Copyright &y& Elsevier]