Evaluation of the ileal digestibility and excreta retention of phosphorus for feed phosphates in broiler chickens and in Pekin ducks.

The study aimed to determine the ileal phosphorus (P) digestibility (iPD) and the excreta P retention (ePR) of 5 monodicalcium phosphate (MCP) samples and 3 dicalcium phosphate (DCP) samples in broiler chickens and in Pekin ducks using the substitution method. A total of 720, 21-d-old Arbor Acres broiler chickens in experiment 1 and 720, 15-d-old Pekin ducks in experiment 2 were randomly allocated to 9 dietary treatments with 8 replicate cages (10 birds/cage) based on the similar mean body weight, respectively. The collection of excreta (for 72 h after a 3-d acclimation) and ileal digesta (after 6 d of feeding experimental diets) was done. The results showed the average iPD/ePR of MCP and DCP for broilers were 83.11%/74.52% and 75.34%/69.46% and for ducks were 79.37%/80.02% and 75.74%/76.44%, respectively. The iPD/ePR of MCP in broilers and the ePR of MCP in ducks were markedly higher (P < 0.05) than those of DCP. Our data suggest that using the substitution method to evaluate the bioavailability of feed phosphates has its own advantages; MCP has higher biological availability than DCP for broilers and ducks.

[A clinical analysis of 22 patients with drug-induced liver injury caused by traditional Chinese medicine Periploca forrestii Schltr].

Objective: To investigate the clinical features, diagnosis, treatment, and prognosis of patients with liver injury caused by Periploca forrestii Schltr. Methods: A retrospective analysis was performed for the general data, clinical manifestations, and laboratory examinations of 22 patients who were diagnosed with liver injury caused by Periploca forrestii Schltr. from November 2014 to December 2015, and their clinical type was determined according to the classification criteria of drug-induced liver injury recommended by the Council for International Organizations of Medical Sciences. Results: There were 12 female and 10 male patients. The mean medication time ranged from 1 week to 2 months, and as for biochemical markers, there were mainly abnormalities in alanine aminotransferase(ALT), aspartate aminotransferase(AST), total bilirubin(TBil), alkaline phosphatase(ALP), and gamma-glutamyl transpeptidase(GGT). ALT and AST increased in all the patients, with mean levels of 676.68±481.11 U/L and 527.36±361.14 U/L, respectively; TBil increased to a mean level of 170.26±147.30 µmol/L in 19 patients; ALP increased to a mean level of 135.61±59.26 U/L in 13 patients; GGT increased to a mean level of 195.65±138.48 U/L in 20 patients. As for clinical typing, 18 patients had liver cell injury, none had cholestasis, 3 had a mixed type, and 1 had an unclassified type. One patient died and all the other patients fully recovered. Conclusion: Periploca forrestii Schltr. had complex constituents, and liver injury caused by this drug is mainly liver cell injury. The pathogenesis of liver injury caused by Periploca forrestii Schltr. is presumed to be related to patients' idiosyncratic reaction to its constituents.

Clinical application of total parenteral nutrition in patients with peritoneal carcinomatosis.

Cancer patients with terminal stage peritoneal carcinomatosis are often unable to eat, rendering total parenteral nutrition (TPN) as the only option to avoid starvation. In this retrospective study, we reviewed the medical records of 46 patients with peritoneal carcinomatosis and compared them to the records of 51 patients who had gastrointestinal malignancy without evidence of peritoneal carcinomatosis. The factors evaluated include demographic data, cause of primary malignancy, ascites formation, anthropometric measurements, laboratory tests, and outcome measurements as well as factors associated with greater than 90-day survival. In-hospital mortality was observed in 31 of the 46 patients with peritoneal carcinomatosis, with a median survival time of 40 days (4-148 days) for all 46 patients. The median duration of TPN administration in the peritoneal carcinomatosis group was 24.1 ± 27.4 days (3-68 days). Severe infection related to TPN application was seen in 5/46 (10.7%) patients with peritoneal carcinomatosis and 6/51 (9.8%) patients without peritoneal carcinomatosis. The length of survival varied widely among terminal patients with peritoneal carcinomatosis. The average survival time in peritoneal carcinomatosis patients receiving TPN was short, indicating that the nutrition support of TPN was relatively suboptimal. Ascites was not a prognostic factor for peritoneal carcinomatosis, while body mass index was a predictor for 90-day survival.

A review of the role of assistive technology for people with dementia in the hours of darkness.

Assistive Technology (AT) has been utilized to support people with dementia (PwD) and their carers in the home. Such support can extend the time that PwD can remain safely at home and reduce the burden on the tertiary healthcare sector. Technology can assist people in the hours of darkness as well as during the day. The objective of this literature review is to evaluate reported healthcare technologies appropriate to night time care. This paper summarises and categorises the current evidence base. In all, 131 abstracts were returned from a database search, yielding fifty four relevant papers which were considered in detail. While night-time specific studies identified very few papers (4 papers, 7%), most of the more general AT findings could be adopted to benefit night-time assistance. Studies have used technology for prompting and reminding as loss of time and forgetfulness are major problems; for monitoring daily activities in a sensor enriched environment and utilised location aware technologies to provide information to enhance safety. Technology also supports a range of therapies to alleviate symptoms. Therapies include the delivery of music and familial pictures for reminiscing, the use of light therapy to enhance wellbeing and the provision of mental tasks to stimulate the brain and maintain activity levels.

Tissue culture-induced locus-specific alteration in DNA methylation and its correlation with genetic variation in Codonopsis lanceolata Benth. et Hook. f.

We have reported recently that tissue culture induced a high level of genetic variation at the primary nucleotide sequence in regenerants of medicinal plant Codonopsis lanceolata. It is not known, however, whether epigenetic variation in the form of alteration in DNA methylation also occurred in these plants. Here, we investigated possible alterations in level and pattern of cytosine methylation at the CCGG sites in the same set of regenerants relative to the donor plant, by the MSAP method employing a pair of isoschizomers, HpaII and MspI, which recognize the same restriction site but are differentially sensitive to cytosine methylation at the CCGG sites. A total of 1,674 MSAP profiles were resolved using 39 primer combinations. Of these, 177 (10.5%) profiles were polymorphic among the regenerants and/or between the regenerant(s) and the donor plant, in EcoRI + HpaII or EcoRI + MspI digest but not in both, indicating alteration in cytosine methylation patterns of specific loci, though their estimated total level of methylation remained more or less the same as the donor plant. Gel blot analysis validated most of the variant MSAP profiles as bona fide alteration in methylation patterns. Correlation analysis between the MSAP data and the previously reported ISSR and RAPD data revealed significant correlations, suggesting their possible intrinsic interrelatedness. Thirty-seven typical variant MSAP profiles were isolated and sequenced, of which 5 showed significant homology to known-function genes, 2 to chloroplast sequences, whilst the rest 30 did not find a match in the database.

Stimulated D(1) dopamine receptors couple to multiple Galpha proteins in different brain regions.

Previous studies have revealed that activation of rat striatal D(1) dopamine receptors stimulates both adenylyl cyclase and phospholipase C via G(s) and G(q), respectively. The differential distribution of these systems in brain supports the existence of distinct receptor systems. The present communication extends the study by examining other brain regions: hippocampus, amygdala, and frontal cortex. In membrane preparations of these brain regions, selective stimulation of D(1) dopamine receptors increases the hydrolysis of phosphatidylinositol/phosphatidylinositol 4,5-biphosphate. In these brain regions, D(1) dopamine receptors couple differentially to multiple Galpha protein subunits. Antisera against Galpha(q) blocks dopamine-stimulated PIP(2) hydrolysis in hippocampal and in striatal membranes. The binding of [(35)S]GTPgammaS or [alpha-(32)P]GTP to Galpha(i) was enhanced in all brain regions. Dopamine also increased the binding of [(35)S]GTPgammaS or [alpha-(32)P]GTP to Galpha(q) in these brain regions: hippocampus = amygdala > frontal cortex. However, dopamine-stimulated binding of [(35)S]GTPgammaS to Galphas only in the frontal cortex and striatum. This differential coupling profile in the brain regions was not related to a differential regional distribution of the Galpha proteins. Dopamine induced increases in GTPgammaS binding to Galpha(s) and Galpha(q) was blocked by the D(1) antagonist SCH23390 but not by D(2) receptor antagonist l-sulpiride, suggesting that D(1) dopamine receptors couple to both Galpha(s) and Galpha(q) proteins. Co-immunoprecipitation of Galpha proteins with receptor-binding sites indicate that in the frontal cortex, D(1) dopamine-binding sites are associated with both Galpha(s) and Galpha(q) and, in hippocampus or amygdala, D(1) dopamine receptors couple solely to Galpha(q). The results indicate that in addition to the D(1)/G(s)/adenylyl cyclase system, brain D(1)-like dopamine receptor sites activate phospholipase C through Galpha(q) protein.

[Therapeutic effect of Astragalus and Angelica on renal injury induced by ischemia/reperfusion in rats].

OBJECTIVE: To observe the effect of Astragalus and Angelica on acute renal injury. METHODS: Using the ischemia/reperfusion model established by blocking blood flow through clamping of bilateral renal artery for 45 min, the changes of glomerular filtration rate (GFR), renal plasma flow (RPF), fractional excretion of sodium (FENa), urinary volume (UV) and mean arterial pressure (MAP) as well as the morphological change of kidney before and after ischemia/reperfusion were observed. RESULTS: Astragalus and Angelica could promote recovery of RPF and GFR after ischemia/reperfusion, prevent the oliguria or shorten the oliguria period, reduce the increment of FENa and improve the histomorphological injury of kidney. CONCLUSION: Astragalus and Angelica have certain effect in protecting kidney from acute renal injury.

[Effects of total flavones of metasequosia on left ventricular hypertrophy due to pressure overload in rats].

OBJECTIVE: To determine the preventive and regressive effects of total flavones of metasequosia (TFM) on left ventricular hypertrophy in rats. METHOD: Left ventricular hypertrophy was inducedin by partial ligation of abdominal aorta. The rats were given ig TFM(4, 40, 400 mg.kg-1.d-1) for six weeks. RESULT: TFM markedly reduced the HW/BW, LVW/BW, myofibril diameter and Ca2+ content in left ventricles but the systolic blood pressure (SBP) in rats wasn't obviously influenced. CONCLUSION: TFM can prevent and reverse the left ventricular hypertrophy due to pressure overload in rats. The mechanism may be related to its calcium antagonistic properties.

Dynamic complexes of beta2-adrenergic receptors with protein kinases and phosphatases and the role of gravin.

Signals mediated by G-protein-linked receptors display agonist-induced attenuation and recovery involving both protein kinases and phosphatases. The role of protein kinases and phosphatases in agonist-induced attenuation and recovery of beta-adrenergic receptors was explored by two complementary approaches, antisense RNA suppression and co-immunoprecipitation of target elements. Protein phosphatases 2A and 2B are associated with the unstimulated receptor, the latter displaying a transient decrease followed by a 2-fold increase in the levels of association at 30 min following challenge with agonist. Protein kinase A displays a robust, agonist-induced association with beta-adrenergic receptors over the same period. Suppression of phosphatases 2A and 2B with antisense RNA or inhibition of their activity with calyculin A and FK506, respectively, blocks resensitization following agonist removal. Recycling of receptors to the plasma membrane following agonist-promoted sequestration is severely impaired by loss of either phosphatase 2B or protein kinase C. In addition, loss of protein kinase C diminishes association of phosphatase 2B with beta-adrenergic receptors. Overlay assays performed with the RII subunit of protein kinase A and co-immunoprecipitations reveal proteins of the A kinase-anchoring proteins (AKAP) family, including AKAP250 also known as gravin, associated with the beta-adrenergic receptor. Suppression of gravin expression disrupts recovery from agonist-induced desensitization, confirming the role of gravin in organization of G-protein-linked signaling complexes. The Ht31 peptide, which blocks AKAP protein-protein interactions, blocks association of beta-adrenergic receptors with protein kinase A. These data are the first to reveal dynamic complexes of beta-adrenergic receptors with protein kinases and phosphatases acting via an anchoring protein, gravin.

Inhibitory effect of Tripterygium wilfordii multiglycoside on increased glomerular albumin permeability in vitro.

BACKGROUND: Tripterygium wilfordii Hook F is a medicinal plant used for the treatment of glomerulonephritis in China. We studied the effect of Tripterygium wilfordii multiglycoside (TWG) on glomerular albumin permeability (Palbumin) in vitro. METHODS: Isolated rat glomeruli were incubated with protamine (600 micrograms/ml) for 30 min, or with human recombinant tumour necrosis factor (TNF-alpha 0.4 ng/ml), superoxide (10 units/ml), or serum from a focal segmental glomerular sclerosis (FSGS) patient for 10 min at 37 degrees C. TWG, 1 mg/ml, was added in parallel tubes to study the effect on Palbumin. Control glomeruli were incubated under identical conditions. The albumin reflection coefficient (sigma albumin) was calculated from the change in glomerular volume in response to an applied oncotic gradient. Convectional permeability (Palbumin) was calculated as (1 - sigma albumin). RESULTS: Compared with controls, protamine increased the Palbumin of glomeruli (0.83 +/- 0.05, n = 25, vs 0.18 +/- 0.03, n = 20); pretreatment with TWG blocked this effect (0.13 +/- 0.04, n = 25). TNF-alpha also increased the Palbumin (0.79 +/- 0.04, n = 24 vs 0.04 +/- 0.07, n = 19); preincubation with TWG blocked this effect (0.03 +/- 0.09, n = 24). Palbumin of glomeruli incubated with xanthine and xanthine oxidase, resulting in the production of superoxide, also increased as compared to controls (0.85 +/- 0.04, n = 15 vs 0.08 +/- 0.05, n = 14); TWG blocked this effect as well (0.21 +/- 0.08, n = 14). FSGS serum also increased Palbumin of glomeruli significantly (0.88 +/- 0.02, n = 49 vs 0.00 +/- 0.02, n = 49); preincubation with TWG blocked this effect (0.05 +/- 0.07, n = 30). TWG by itself had no effect on Palbumin (0.19 +/- 0.10, n = 15). CONCLUSIONS: Our results show that TWG blocks protamine, TNF-alpha, superoxide, and FSGS serum-mediated increase in glomerular albumin permeability in vitro. We conclude that reduction of proteinuria by Tripterygium wilfordii multiglycoside in various kinds of glomerular diseases in vivo might be due to protection of the glomerular filtration barrier.

Cocaine administration in pregnant rabbits alters cortical structure and function in their progeny in the absence of maternal seizures.

Previous studies have reported that cocaine exposure in utero results in structural and functional alterations in the development of the anterior cingulate cortex (ACC). In the present study, the effects of maternal cocaine dosage and of cocaine-elicited maternal seizures on the progeny were studied. The incidence of maternal generalized tonic clonic seizures (GTCSs) elicited by cocaine was recorded. No GTCSs were elicited in pregnant rabbits by doses of 2 or 3 mg/kg of cocaine, but GTCSs were sometimes elicited by the highest dose (4 mg/kg per injection). We analyzed the offspring of cocaine-exposed and control animals using three assays of ACC development: (i) the structure of apical dendrites of pyramidal neurons, (ii) the distribution of a calcium binding protein (parvalbumin) in the dendrites of GABAergic neurons, and (iii) coupling of D1-like receptors and their G proteins. In all progeny of rabbits exposed to 3 or 4 mg/kg of cocaine during pregnancy, there was a significant change in the structure of apical dendrites, a significant increase in the number of dendrites of GABAergic neurons which were parvalbumin immunoreactive, and a significant reduction in D1/G protein coupling. In assays of apical dendrites, the effects on offspring of rabbits given 2 mg/kg cocaine were as pronounced as in offspring of rabbits given 3 or 4 mg/kg, but the effects on parvalbumin immunoreactivity and D1/G protein coupling were reduced at this low dose. Thus, previous findings of ACC developmental abnormalities in offspring of rabbits given a dose of 4 mg/kg were replicated, the effects were shown to be dose-related and to be independent of maternal seizures. A mechanism by which dysfunction of the D1 receptor system could mediate cocaine-associated changes in all three parameters of ACC structure and function is discussed.

Receptor-mediated activation of G proteins is increased in postmortem brains of bipolar affective disorder subjects.

Guanine nucleotide binding proteins (G proteins) have been implicated in the pathophysiology of bipolar affective disorder. In the present investigation receptor-mediated G protein activation and changes in G protein trimeric state were examined in frontal cortical membranes obtained from postmortem brains of bipolar affective disorder subjects and from age-, sex-, and postmortem interval-matched controls. Stimulation of cortical membranes with serotonin, isoproterenol, or carbachol increased guanosine 5'-O-(3-[35S]thiophosphate) ([35S]GTP gamma S) binding to specific G alpha proteins in a receptor-selective manner. The abilities of these receptor agonists to stimulate the binding of [35S]GTP gamma S to the G alpha proteins was enhanced in membranes from bipolar brains. Immunoblot analyses showed increases in the levels of membrane 45- and 52-kDa G alpha S proteins but no changes in the amounts of G alpha i, G alpha o, G alpha Z, G alpha q/11, or G beta proteins in membrane or cytosol fractions of bipolar brain homogenates. Pertussis toxin (PTX)-activated ADP-ribosylations of G alpha i and G alpha o were enhanced by approximately 80% in membranes from bipolar compared with control brains, suggesting an increase in the levels of the trimeric state of these G proteins in bipolar disorder. Serotonin-induced, magnesium-dependent reduction in PTX-mediated ADP-ribosylation of G alpha i/G alpha o in cortical membranes from bipolar brains was greater than that observed in controls, providing further evidence for enhanced receptor-G protein coupling in bipolar brain membranes. In addition, the amounts of G beta proteins that coimmunoprecipitated with the G alpha proteins were also elevated in bipolar brains. The data show that in bipolar brain membrane there is enhanced receptor-G protein coupling and an increase in the trimeric state of the G proteins. These changes may contribute to produce exaggerated transmembrane signaling and to the alterations in affect that characterize bipolar affective disorder.

Pulmonary artery perfusion of doxorubicin with blood flow occlusion: pharmacokinetics and treatment in a metastatic sarcoma model.

BACKGROUND: We compared pharmacokinetics, toxicity, and treatment efficacy of pulmonary artery perfusion of low-dose doxorubicin with blood flow occlusion to intravenous doxorubicin injection in a metastatic sarcoma model in the rat. METHODS: Animals received left pulmonary artery perfusion with 0.1, 0.2, or 0.5 mg/kg doxorubicin at a rate of 0.1 mL/min for 1 minute with 20 minutes of blood flow occlusion. Doxorubicin levels of the lung, heart, and serum were assayed. Body weights after treatment were recorded and right pneumonectomy was performed. The results were compared with those in rats that received 5 mg/kg doxorubicin by intravenous injection or the saline group. Pulmonary sarcoma metastases were treated with 0.5 mg/kg doxorubicin through lung perfusion or intravenously, or with saline solution. RESULTS: Doxorubicin levels in the lung, heart, and serum were 112.1 +/- 9.2 micrograms/g, 1.7 +/- 0.2 microgram/g, and 0.3 +/- 0.1 microgram/mL in the group with 0.5 mg/kg doxorubicin perfusion, versus 24.8 +/- 1.9 microgram/g, 10.1 +/- 1.3 microgram/g, and 0.7 +/- 0.2 microgram/mL in the intravenous group (p < 0.05). Animals had normal growth patterns and survived after right pneumonectomy in the perfused group, whereas the intravenous group failed to thrive. No tumors were found or a significant reduction in nodules was noted in the lungs treated with perfusion as compared with untreated right lungs or the intravenous and saline groups. CONCLUSION: This chemotherapy model has important pharmacokinetic advantages and causes an increased treatment response for pulmonary metastatic sarcoma with minimal systemic and local toxicity as compared with systemic doxorubicin administration.

[Studies on the chemical constituents of Arctium lappa L].

Six compounds were isolated from the seeds of Arctium lappa L. One of them is a new lignan named neoarctin B(VI). The structure has been elucidated on the basis of spectral (UV, IR, 1H-NMR, 13C-NMR, DEPT, 2D-NMR and MS) analysis. The other five compounds were identified as daucosterol (I), arctigenin (II), arctiin (III), matairesinol (IV) and lappaol F (V).

[Experimental study on selenium preventing nasopharyngeal carcinoma].

In this study, we observed the effect of selenium (Se) on nasopharyngeal carcinoma (NPC) induced by dinitrosopi erazine (DNP) in rats through adding sodium selenite into drinking water. One hundred and sixty Wistar rats were divided into five groups: (1) blank control group (BG), no treatment; (2) Se control group (SG), given 50.7 mumol/L Se in drinking water for the first 3 weeks and then 31.7 mumol/L until the end of the experiment; (3) DNP control group (DG), injected subcutaneously 15mg/kg DNP twice a week from the 4th week to the 35th week; (4) Se prevention group (PG), given Se as done in SG and injected DNP as done in DG; (5) Se therapy group (TG), injected DNP as done in DG and given 50.7 mumol/L Se in drinking water from the 36th week to the end of the experiment. The experimental duration was one year. The result showed that there was no NPC in BG and SG and that the incidence of NPC in PG was reduced by 54.3% as compared with that in DG, which was significantly different (P < 0.01). In addition, the incidences of precancerous lesions of nasopharynx were significantly different between the two groups. But the incidences of NPC were not significantly different between TG and DG. In the process of carcinogenesis, the blood Se concentration of DG decreased. The blood Se concentration of rats could be elevated by supplementing Se in drinking water. Our result suggested that elevating the level of Se in rats can prevent the NPC.

The preventive effect of radix Salciae miltiorrhizae on monocrotaline-induced pulmonary hypertension in rats.

The preventive effect of Radix Salciae Miltiorrhizae (RSM) on pulmonary hypertension (PHT) and right ventricular hypertrophy (RVH) induced by monocrotaline (MCT) in rats was observed with the methods of measuring the right ventricular systolic pressure (PVSP), the ratio of the right ventricle to the left ventricle plus interventricular septum RV/(LV+S) and the pulmonary small artery morphological analysis. The results show that RSM can reduce the PHT, and prevent the RVH and the increase of the medial thickness of pulmonary small arteries. It can also prevent the endothelial cell injury produced by MCT. The pharmacological effects of RSM on pulmonary circulation were also discussed.

[The influence of hypertension and antihypertensive agents on experimental IgA nephropathy (IgAN)].

In an attempt to evaluate the influence of hypertension and antihypertensive agents on IgAN, IgAN and hypertension experimental models were induced in SD rats and divided into 4 groups: (1) IgAN(n = 8); (2) IgAN+by hypertension(n = 8); (3) captopril 4mg/100gBW/d, for 42 days administered to rats as group (2) (n = 8); (4) nifedipine 300ug/100gBW/d, for 42 days administered to rats as group (2) (n = 8). Blood pressure was measured at the 12th, 14th, 16th, 18th and 20th week. Urinary protein, serum angiotensin II (AT II) and renal pathologic changes were examined at the 20th week. Our results suggest that hypertension worsens IgAN by glomerular mesangial proliferation in early stages. Though Captopril has the same therapeutic effect on hypertension as Nifedipine does, the former has been proven to have potentially beneficial effects on diminishing proteinuria as well as mesangial lesions. This is consistent with the suppression of serum ATII which favours glomerular microcirculation.

Long-term follow-up of 344 Shanghai psoriatics.

344 patients with psoriasis vulgaris treated in Huashan Hospital, Shanghai were followed up for 7-30 years. 13% of them developed arthralgia and 2% had joint deformities. One patient developed erythroderma due to dexamethasone medication. Internal malignancy occurred in 2 patients (0.58%). The severity of the course of the disease was neither influenced by family history nor alcoholism, but was markedly influenced by the duration of illness and administration of anti-neoplastic drugs.

Lithium inhibition of protein kinase C activation-induced serotonin release.

The effect of lithium on protein kinase C (PKC) stimulation-induced serotonin and norepinephrine release facilitation was examined in [3H]5-HT and [3H]NE preloaded superfused rat brain slices. The facilitation of K+-evoked [3H]5-HT release elicited by the active phorbol esters PMA and PDBu was inhibited by 4 mM but not by 1 mM in vitro lithium. In experiments performed in cortical, hippocampal and hypothalamic slices obtained from animals treated for 3 weeks with lithium-containing diet, PMA-induced facilitation of K+-elicited [3H]5-HT release was found to be inhibited by the treatment (serum lithium less than 1 mEq/l). Basal [3H]5-HT efflux, which was enhanced by PMA in control animals, was also inhibited by lithium treatment. In parietal cortical slices, PMA elicited increase in K+-evoked [3H]NE release was prevented in slices taken from lithium-treated (3 weeks) animals. Lithium treatment did not affect the activity and distribution of protein kinase C in cortical tissue. However, 3 weeks of treatment reduced the PMA-induced translocation of the enzyme. These results suggest that lithium treatment interferes with serotonin and norepinephrine release facilitation which results from the stimulation of PKC by phorbol esters. These actions of the ion may be mediated by its ability to inhibit PMA induced PKC translocation.