Effect of soluble corn fibre and calcium supplementation on bone mineral content and bone mineral density in preadolescent Malaysian children-a double-blind randomised controlled trial (PREBONE-Kids Study).

Soluble corn fibre (SCF) with calcium did not improve bone indices after 1 year in preadolescent children. INTRODUCTION: SCF has been reported to improve calcium absorption. We investigated the long-term effect of SCF and calcium on bone indices of healthy preadolescent children aged 9-11 years old. METHODS: In a double-blind, randomised, parallel arm study, 243 participants were randomised into four groups: placebo, 12-g SCF, 600-mg calcium lactate gluconate (Ca) and 12-g SCF + 600-mg calcium lactate gluconate (SCF + Ca). Total body bone mineral content (TBBMC) and total body bone mineral density (TBBMD) were measured using dual-energy X-ray absorptiometry at baseline, 6 and 12 months. RESULTS: At 6 months, SCF + Ca had a significant increase in TBBMC from baseline (27.14 ± 6.10 g, p = 0.001). At 12 months, there was a significant increase in TBBMC from baseline in the SCF + Ca (40.28 ± 9.03 g, p = 0.001) and SCF groups (27.34 ± 7.93 g, p = 0.037). At 6 months, the change in TBBMD in the SCF + Ca (0.019 ± 0.003 g/cm2) and Ca (0.014 ± 0.003 g/cm2) groups was significantly different (p < 0.05) from SCF (0.004 ± 0.002 g/cm2) and placebo (0.002 ± 0.003 g/cm2). However, the changes in TBBMD and TBBMC were not significantly different among groups at 12 months. CONCLUSION: SCF did not increase TBBMC and TBBMD in Malaysian children after 1 year although calcium supplementation increased TBBMD at 6 months. Further work is needed to fully understand the mechanism and health benefits of prebiotics in this study population. CLINICAL TRIAL REGISTRATION: https://clinicaltrials.gov/ct2/show/NCT03864172.

The Effect of Pre- and Postharvest Calcium Gluconate Treatments on Physicochemical Characteristics and Bioactive Compounds of Sweet Cherry during Cold Storage.

The effects of pre- and postharvest calcium gluconate (Ca-Glu) treatments on some physicochemical characteristics and bioactive compounds of sweet cherry cv. Sweetheart during cold storage were investigated. For preharvest treatments, the Ca-Glu (1%) solution was applied to the cherry trees two times at 21 and 35 days after full bloom stage. Control trees were sprayed with distilled water at the same days. Sweet cherries, sprayed with and without Ca-Glu, were dipped into cold water (4 °C) containing calcium gluconate (1%) for 30 s and only in cold water (4 °C) as control, after harvest Following each treatment, cherries were placed in plastic boxes and stored at 1 ± 0.5 °C and 90 ± 5% relative humidity for 3 weeks. The weight losses of cherries increased over time but calcium (Ca) treatments, especially pre-and postharvest combination, limited these increases compared to control groups. The best result for suppressing the respiration rate of cherries was also obtained from combined treatment. Moreover, combined treatment delayed the losses of titratable acidity, fruit firmness, decay rate and sensory quality in sweet cherries during storage comparison with the pre or postharvest application of Ca-Glu alone. The effect of Ca-Clu treatments on stem chlorophyll content and antioxidant activity was not significant. Preharvest and combined treatments retarded the loss of ascorbic acid content of cherries compared to postharvest and control treatments. The total phenolic and anthocyanin content increased regularly throughout storage, regardless of treatment; however, Ca treatments delayed the accumulation of these compounds. As a result, the combined Ca-Glu treatment could be a promising method for maintaining some physicochemical characteristics and bioactive compounds in sweet cherries during cold storage.

Effect of feeding calcium gluconate embedded in a hydrogenated fat matrix on feed intake, gastrointestinal fermentation and morphology, intestinal brush border enzyme activity and blood metabolites in growing lambs.

Gluconate salts have been identified as a butyrate precursor when fed to non-ruminant species and may increase the butyrate concentration in the large intestine supporting gastrointestinal health and development. The objective of this study was to evaluate the dose response of hydrogenated fat-embedded calcium gluconate (HFCG) on performance and gastrointestinal tract (GIT) development in growing lambs. Thirty-two wether lambs were used in a randomized complete block design and assigned to 1 of 4 treatments differing in the inclusion of HFCG: 0.0% (CON), 0.075% (LOW), 0.30% (MED), and 0.60% of the diet (HIGH). Lambs were allocated into individual pens and fed ad libitum with feed delivered twice daily. Feed intake was recorded daily, and body weight (BW) was assessed at the beginning and the end of the 29-d period. Blood was sampled on day 21, prior to feeding and 6 h post-feeding to evaluate changes in ß-hydroxybutyrate, glucose, and insulin concentrations. Total fecal collection was conducted during days 25 to 28 to assess apparent total tract digestibility. On day 29, lambs were slaughtered, and the entire GIT was separated by region to enable sampling of tissue and digesta. Data were analyzed to assess linear, quadratic, and cubic effects of HFCG dose. Final BW, average daily gain, and dry matter intake decreased linearly (P ≤ 0.02) with increasing HFCG. Increasing inclusion of HFCG linearly decreased (P = 0.01) the thickness of the stratum corneum in ruminal papillae but did not affect other strata (P ≥ 0.34). Omasal digesta weight linearly decreased (P = 0.01) as the concentration of HFCG increased and abomasal digesta weight was cubically affected (P = 0.03) the increasing dose of HFCG. Short-chain fatty acid concentration in the cecum was cubically affected (P < 0.01) with increasing dose of HFCG where low dose had the greatest concentration. Moreover, increasing the dietary supply of HFCG linearly increased the proportion of acetate (P = 0.04) in the cecum and linearly decreased the proportion of propionate in the digesta of both the cecum (P < 0.01) and colon (P = 0.01). Colon crypt depth was quadratically (P = 0.03) affected with the increasing dose of HFCG, where lambs fed MED had greatest crypt depth. We conclude that feeding HFCG to growing lambs did not increase butyrate concentration in the large intestine and consequently does not increase the absorptive surface area of the whole tract, the size of the GIT, or the functionality of the intestine.

Gluconate salts have been reported to be metabolized by microbes in the gastrointestinal tract to yield butyrate. Butyrate has shown potential to enhance functionality of the gastrointestinal tract by increasing the absorptive surface area, enzyme activity, and the barrier function. This study evaluated the inclusion of four levels of hydrogenated fat-embedded Ca-gluconate (HFCG; 0.0%, 0.075%, 0.30%, and 0.60% of the diet) designed to increase the production of butyrate in the large intestine. Thirty-two wether lambs were fed for 28 d, slaughtered, and eviscerated to allow complete evaluation of the gastrointestinal tract and its contents. Growth and dry matter intake decreased linearly with increasing dose of HFCG. Dose of HFCG cubically affected short-chain fatty acid concentration in the cecum with increased concentrations at the 0.075% dose. Moreover, increasing dose of HFCG linearly increased the proportion of acetate and linearly decreased the proportion of propionate in the cecum without altering the proportion of butyrate. Thus, the supplementation of HFCG did not increase butyrate concentration in the large intestine and did not enhance gastrointestinal tract function.

Enhanced mechanical properties and biocompatibility on BC/HAp composite through calcium gluconate fortified bacterial.

Bacterial cellulose/hydroxyapatite (BC/HAp) composite is an outstanding candidate for bone tissue engineering. The conventional biomimetic mineralization method takes a long time with unsatisfactory mechanical properties and biocompatibility. Herein, we modified the BC by changing the carbon source to calcium gluconate during the biosynthesis process of BC by bacteria, providing nucleation sites for further mineralization in simulated body fluid. Results show spherical porous HAp in the size of 100-200 nm was fully filled in the three-dimensional network structure of BC nanofibers uniformly within five days of mineralization. Molecular dynamics simulation shows that the aggregation of cellulose units in aqueous solution can enhance the adsorption of calcium ions. By this means, we significantly improved the mechanical properties and biocompatibility of the BC/HAp composite, as well as simplified the preparation process, compared to conventional method, which, therefore, suggests, it could be further studied for biomedical applications such as bone tissue engineering.

Myocardial Viability Imaging using Manganese-Enhanced MRI in the First Hours after Myocardial Infarction.

Early measurements of tissue viability after myocardial infarction (MI) are essential for accurate diagnosis and treatment planning but are challenging to obtain. Here, manganese, a calcium analogue and clinically approved magnetic resonance imaging (MRI) contrast agent, is used as an imaging biomarker of myocardial viability in the first hours after experimental MI. Safe Mn2+ dosing is confirmed by measuring in vitro beating rates, calcium transients, and action potentials in cardiomyocytes, and in vivo heart rates and cardiac contractility in mice. Quantitative T1 mapping-manganese-enhanced MRI (MEMRI) reveals elevated and increasing Mn2+ uptake in viable myocardium remote from the infarct, suggesting MEMRI offers a quantitative biomarker of cardiac inotropy. MEMRI evaluation of infarct size at 1 h, 1 and 14 days after MI quantifies myocardial viability earlier than the current gold-standard technique, late-gadolinium-enhanced MRI. These data, coupled with the re-emergence of clinical Mn2+ -based contrast agents open the possibility of using MEMRI for direct evaluation of myocardial viability early after ischemic onset in patients.

Destruction of Staphylococcus aureus biofilms by combining an antibiotic with subtilisin A or calcium gluconate.

In S. aureus biofilms, bacteria are embedded in a matrix of extracellular polymeric substances (EPS) and are highly tolerant to antimicrobial drugs. We thus sought to identify non-antibiotic substances with broad-spectrum activity able to destroy the EPS matrix and enhance the effect of antibiotics on embedded biofilm bacteria. Among eight substances tested, subtilisin A (0.01 U/mL) and calcium gluconate (CaG, Ca2+ 1.25 mmol/L) significantly reduced the biomass of biofilms formed by at least 21/24 S. aureus isolates. Confocal laser scanning microscopy confirmed that they both eliminated nearly all the proteins and PNAG from the matrix. By contrast, antibiotics alone had nearly no effect on biofilm biomass and the selected one (oxytetracycline-OTC) could only slightly reduce biofilm bacteria. The combination of OTC with CaG or subtilisin A led to an additive reduction (average of 2 log10 CFU/mL) of embedded biofilm bacteria on the isolates susceptible to OTC (MBC < 10 µg/mL, 11/24). Moreover, these two combinations led to a reduction of the embedded biofilm bacteria higher than 3 log10 CFU/mL for 20-25% of the isolates. Further studies are now required to better understand the factors that cause the biofilm produced by specific isolates (20-25%) to be susceptible to the combinations.

Trauma-induced primary hypoparathyroidism following severe bite wound injury to the neck in a dog.

OBJECTIVE: To describe the clinical presentation and outcome of a dog with primary hypoparathyroidism secondary to cervical bite wounds. CASE SUMMARY: A 3-year-old male intact Chihuahua presented after being attacked by a large breed dog. The dog sustained severe cervical lacerations, exposing the trachea and jugular veins. A portion of the right thyroid gland was missing. The dog was stabilized before wound debridement and closure. Ionized calcium concentrations were within reference range at the time of presentation. Forty-eight hours after the initial trauma, the dog was presented in lateral recumbency with signs of hypovolemic shock, muscle tremors, and hyperthermia. Bloodwork showed severe ionized hypocalcemia with low normal parathyroid hormone concentration consistent with acute primary hypoparathyroidism. The dog was managed initially with IV calcium gluconate and calcitriol, then long-term oral calcium carbonate and vitamin D3. After 6 months, the dog was successfully weaned off calcium supplementation. NEW OR UNIQUE INFORMATION PROVIDED: This is the first described case of traumatic primary hypoparathyroidism after a bite injury to the neck in a dog.

Analysis of Epineurial Lidocaine Injection for Nerve Transfers in a Rat Sciatic Nerve Model.

PURPOSE: Nerve transfers for peripheral nerve injuries can result in variable outcomes. We investigated the neuroprotective effect of epineurial lidocaine injection in the donor nerve prior to transection, with the hypothesis that proximal axon loss would be decreased with consequent increased neuroregeneration and functional recovery. METHODS: A rat sciatic nerve model was used with 4 intervention groups: (1) lidocaine; (2) lidocaine/calcium gluconate (CG); (3) CG; or (4) saline (control). Behavioral testing and qualitative and quantitative histological evaluation was performed at 8 and 12 weeks. Histological assays included transmission electron microscopy, retrograde fluorogold labeling, and whole mount immunostaining. RESULTS: Functional assessments through the sciatic functional index and Basso, Beattie, and Bresnahan scale showed a statistically significant increase in recovery at 8 and 12 weeks with lidocaine treatment. Significantly higher axonal counts were obtained in the lidocaine-treated groups. Fragmentation and increased myelin damage was present in the CG and saline groups. Retrograde fluorogold labeling showed a statistically significant increase in the number of L4-6 dorsal root ganglion neurons in the lidocaine-treated groups. Whole mount immunostaining identified extension of the axonal growth cone past the nerve coaptation site in lidocaine-treated groups, but not in CG and saline groups. CONCLUSIONS: Our results suggest that epineurial lidocaine injection prior to donor nerve transection for nerve transfer has a neuroprotective effect, resulting in increased proximal axon counts and improved functional recovery. CLINICAL RELEVANCE: These findings may have direct clinical application because epineurial lidocaine can be used in surgery as a simple and inexpensive intervention for promoting improved clinical outcomes after nerve transfer.

Effects of calcium gluconate on lipopolysaccharide-induced acute lung injury in mice.

Lipopolysaccharide (LPS), which can cause acute airway inflammatory reactions, constitutes one of the most common substances to establish acute lung injury (ALI) models in mice. Studies suggest that calcium gluconate offers the possibility of suppressing the immune response, and this study was intended to explore the effects of calcium gluconate on LPS-induced ALI in mice. Mice inhaled with LPS were intraperitoneally injected with calcium gluconate (12.5, 25, 50 mg/kg). IL-1ß, IL-6 and TNF-α levels in bronchoalveolar lavage fluid (BALF) were determined by ELISA. The expression of signaling proteins, phosphorylation extracellular regulated protein kinases (p-ERK), was detected using Western Blot in lung tissues. In our study, the release of inflammatory cytokines IL-1ß, IL-6 and TNF-α in BALF increased after inhalation of LPS. Post-treatment with calcium gluconate inhibited LPS-induced airway inflammatory injury and the release of inflammatory cytokines. In addition, LPS promoted the expression of signaling protein p-ERK while calcium gluconate was capable of reversing this change. Overall, calcium gluconate inhibits LPS-induced ALI in mice, which may take effects through the inhibition of ERK phosphorylation.

Citrate shows protective effects on cardiovascular and renal function in ischemia-induced acute kidney injury.

BACKGROUND: Ischemia and reperfusion (I/R) is one of the major causes of acute kidney injury (AKI). Citrate reduces hypoxia-induced mitochondrial energetic deficits in isolated proximal tubules. Moreover, citrate anticoagulation is now frequently used in renal replacement therapy. In the present study a rat model of I/R-induced AKI was utilized to examine renal protection by citrate in vivo. METHODS: AKI was induced by bilateral renal clamping (40 min) followed by reperfusion (3 h). Citrate was infused at three different concentrations (0.3 mmol/kg/h; 0.6 mmol/kg/h and 1.0 mmol/kg/h) continuously for 60 min before and 45 min after ischemia. Plasma calcium concentrations were kept stable by infusion of calcium gluconate. The effect of citrate was evaluated by biomonitoring, blood and plasma parameters, histopathology and tissue ATP content. RESULTS: In comparison to the normoxic control group bilateral renal ischemia led to an increase of creatinine and lactate dehydrogenase activity and a decrease in tissue ATP content and was accompanied by a drop in mean arterial blood pressure. Infusion of 1.0 mmol/kg/h citrate led to lower creatinine and reduced LDH activity compared to the I/R control group and a tendency for higher tissue ATP content. Pre-ischemic infusion of 1.0 mmol/kg/h citrate stabilized blood pressure during ischemia. CONCLUSIONS: Citrate has a protective effect during I/R-induced AKI, possibly by limiting the mitochondrial deficit as well as by beneficial cardiovascular effects. This strengthens the rationale of using citrate in continuous renal replacement therapy and encourages consideration of citrate infusion as a therapeutic treatment for AKI in humans.

[Experimental research on the effects of different activators on the formation of platelet-rich gel and the release of bioactive substances in human platelet-rich plasma].

Objective: To explore the effects of calcium gluconate and thrombin on the formation of platelet-rich gel (PRG) and the release of bioactive substances in human platelet-rich plasma (PRP) and the clinical significance. Methods: Six healthy blood donors who met the inclusion criteria were recruited in our unit from May to August in 2016. Platelet samples of each donor were collected for preparation of PRP. (1) PRP in the volume of 10 mL was collected from each donor and divided into thrombin activation group (TA, added with 0.5 mL thrombin solution in dose of 100 U/mL) and calcium gluconate activation group (CGA, added with 0.5 mL calcium gluconate solution in dose of 100 g/L) according to the random number table, with 5 mL PRP in each group. Then the PRP of the two groups was activated in water bath at 37 ℃ for 1 h. The formation time of PRG was recorded, and the formation situation of PRG was observed within 1 hour of activation. After being activated for 1 h, one part of PRG was collected to observe the distribution of fibrous protein with HE staining, and another part of PRG was collected to observe platelet ultrastructure under transmission electron microscope (TEM). After being activated for 1 h, the supernatant was collected to determine the content of transforming growth factor ß(1, )platelet-derived growth factor BB (PDGF-BB), vascular endothelial growth factor, basic fibroblast growth factor (bFGF), epidermal growth factor, and insulin-like growth factorⅠby enzyme-linked immunosorbent assay. (2) Another 10 mL PRP from each donor was collected and grouped as above, and the platelet suspension was obtained after two times of centrifugation and resuspension with phosphate buffered saline, respectively. And then they were treated with corresponding activator for 1 h as that in experiment (1). Nanoparticle tracking analyzer was used to detect the concentrations of microvesicles with different diameters and total microvesicles derived from platelet. Data were processed with t test. Results: (1) The formation time of PRG in group TA was (228±40) s, and the PRG volume reached the maximum at this moment. The PRG volume shrunk to the minimum after 30 minutes of activation. The formation time of PRG in group CGA was (690±71) s, and the PRG volume reached the maximum at this moment. After 55 minutes of activation, the PRG volume shrunk to the minimum. The formation time of PRG in group TA was obviously shorter than that in group CGA (t=15.17, P<0.01). (2) HE staining showed that after 1 hour of activation, the red-stained area of fibrous protein in PRG of group TA was large and densely distributed, while that of group CGA was small and loosely distributed. TEM revealed that after 1 hour of activation, the platelets in PRG of group TA were fragmented, while lysing platelet structure, lysing α granule structure, intact α granule structure, and intact dense body structure were observed in PRG of group CGA. (3) The content of PDGF-BB released by PRP in group TA was (7.4±0.8) ng/mL, which was obviously higher than that in group CGA [(4.9±0.5) ng/mL, t=5.41, P<0.01]. The content of bFGF released by PRP in group CGA was (960±151) pg/mL, which was significantly higher than that in group TA [(384±56) pg/mL, t=8.75, P<0.01]. The content of the other 4 growth factors released by PRP in the two groups was close (with t values from 0.11 to 1.97, P values above 0.05). (4) The concentrations of total microvesicles, microvesicles with diameter more than 100 nm, and exosomes with diameter less than or equal to 100 nm derived from platelet in group CGA were (165.8±15.1)×10(8)/mL, (142.4±12.3)×10(8)/mL, and (23.4±2.9)×10(8)/mL respectively, which were significantly higher than those in group TA [(24.7±4.6)×10(8)/mL, (22.6±4.0)×10(8)/mL, and (2.1±0.7)×10(8)/mL, with t values from 17.36 to 22.66, P values below 0.01]. Conclusions: Calcium gluconate can slowly activate PRP, resulting in slowly shrunk PRG with high content of bFGF and high concentration of microvesicles, which is suitable for repairing articular cavity and sinus tract wound. Thrombin can rapidly activate PRP, resulting in quickly shrunk PRG with high content of PDGF-BB and a certain concentration of microvesicles, which is suitable for repairing acute trauma.

Intracellular calcium increases in vascular smooth muscle cells with progression of chronic kidney disease in a rat model.

Background: Vascular smooth muscle cells (VSMCs) exhibit phenotypic plasticity, promoting vascular calcification and increasing cardiovascular risk. Changes in VSMC intracellular calcium ([Ca 2+ ] i ) are a major determinant of plasticity, but little is known about changes in [Ca 2+ ] i in chronic kidney disease (CKD). We have previously demonstrated such plasticity in aortas from our rat model of CKD and therefore sought to examine changes in [Ca 2+ ] i during CKD progression. Materials and Methods: We examined freshly isolated VSMCs from aortas of normal rats, Cy/+ rats (CKD) with early and advanced CKD, and advanced CKD rats treated without and with 3% calcium gluconate (CKD + Ca 2+ ) to lower parathyroid hormone (PTH) levels. [Ca 2+ ] i was measured with fura-2. Results: Cy/+ rats developed progressive CKD, as assessed by plasma levels of blood urea nitrogen, calcium, phosphorus, parathyroid hormone and fibroblast growth factor 23. VSMCs isolated from rats with CKD demonstrated biphasic alterations in resting [Ca 2+ ] i : VSMCs from rats with early CKD exhibited reduced resting [Ca 2+ ] i , while VSMCs from rats with advanced CKD exhibited elevated resting [Ca 2+ ] i . Caffeine-induced sarcoplasmic reticulum (SR) Ca 2+ store release was modestly increased in early CKD and was more drastically increased in advanced CKD. The advanced CKD elevation in SR Ca 2+ store release was associated with a significant increase in the activity of the sarco-endoplasmic reticulum Ca 2+ ATPase (SERCA); however, SERCA2a protein expression was decreased in advanced CKD. Following SR Ca 2+ store release, recovery of [Ca 2+ ] i in the presence of caffeine and extracellular Ca 2+ was attenuated in VSMCs from rats with advanced CKD. This impairment, together with reductions in expression of the Na + /Ca 2+ exchanger, suggest a reduction in Ca 2+ extrusion capability. Finally, store-operated Ca 2+ entry (SOCE) was assessed following SR Ca 2+ store depletion. Ca 2+ entry during recovery from caffeine-induced SR Ca 2+ store release was elevated in advanced CKD, suggesting a role for exacerbated SOCE with progressing CKD. Conclusions: With progressive CKD in the Cy/+ rat there is increased resting [Ca 2+ ] i in VSMCs due, in part, to increased SOCE and impaired calcium extrusion from the cell. Such changes may predispose VSMCs to phenotypic changes that are a prerequisite to calcification.

The Effects of Topical Application of Polycal (a 2:98 (g/g) Mixture of Polycan and Calcium Gluconate) on Experimental Periodontitis and Alveolar Bone Loss in Rats.

The aim of this study was to observe whether Polycal has inhibitory activity on ligation-induced experimental periodontitis and related alveolar bone loss in rats following topical application to the gingival regions. One day after the ligation placements, Polycal (50, 25, and 12.5 mg/mL solutions at 200 µL/rat) was topically applied to the ligated gingival regions daily for 10 days. Changes in bodyweight, alveolar bone loss index, and total number of buccal gingival aerobic bacterial cells were monitored, and the anti-inflammatory effects were investigated via myeloperoxidase activity and levels of the pro-inflammatory cytokines IL-1ß and TNF-α. The activities of inducible nitric oxide synthase (iNOS) and lipid peroxidation (MDA) were also evaluated. Bacterial proliferation, periodontitis, and alveolar bone loss induced by ligature placements were significantly inhibited after 10 days of continuous topical application of Polycal. These results indicate that topical application of Polycal has a significant inhibitory effect on periodontitis and related alveolar bone loss in rats mediated by antibacterial, anti-inflammatory, and anti-oxidative activities.

Comparative assessment of calcitonin stimulation test using calcium gluconate and pentagastrin and the usefulness of procalcitonin basic and post-stimulation concentrations in the diagnosis of patients after surgery for medullary.

OBJECTIVES: The aim of the study was to compare the calcitonin (CT) stimulation tests with tests of calcium gluconate (CaG) and pentagastrin (PG), their tolerance and usefulness of PCT in the patients' diagnosis with active Medullary thyroid cancer (MCT) after thyroidectomy. METHODS: CT was marked in serum by the immunosorbent sandwich test. PCT was marked by the immunosorbent sandwich test, with the final reading of fluorenscence. PG was given intravenously at a dose of 0.5 mg/kg body weight for 10 seconds. CaG was also given by intravenous injection at a dose of 2.5 mg of elemental Ca/kg body weight at a rate of 5ml/min, for minimum 3 minutes. Blood was taken at the 0 minute, the 3 and 5 minute after getting the stimulating substances. RESULTS: The post-stimulation CT concentration in the 3 and 5 minute of the CaG test vs PG is significantly higher compared to the baseline. The maximal stimulation of the CT is in the 3 minute, but higher concentrations occurred using the CaG. CONCLUSION: The results of the study suggest a similar diagnostic value of the tests with CaG compared to the PG as stimulants. In the present study we noticed a trend of basic and post-stimulation concentrations of PCT to increase in the tests with PG and CaG which correspond with the elevated concentrations of CT.

Physiological adaptive indicators in fasted neonate broiler chicks in response to calcium gluconate injection.

Four hundred and eighty mixed-sex broiler chicks aged 3 h after hatching were allotted according to a completely random design in a 6 × 2 × 2 factorial schedule into two groups of 12 replications of 20 chicks each. The main experimental factors were fasting for 0, 6, 12, 24, 36 and 48 h after chick placement and calcium gluconate (Ca-glu) injection (0 and 0.6 ml). Live body weight (BW) of chicks decreased linearly (Y = 43.36-0.109BW0 h , r(2)  = 0.876) as neonatal fasting extended. Injection of 0.6 ml Ca-glu at 3 h post-hatching did not affect weight loss of chicks. Yolk residuals (YR) utilized linearly (Y = 5.75-0.062YR, r(2)  = 0.956) by 0.062 g/h in neonate fasted chicks up to 48 h, showing no effect of Ca-glu injection. Neonatal fasting periods longer than 12 h increased liver weight (p < 0.05). The mean absolute and proportional (% of BW0 h ) breast and leg weight were reduced linearly as neonatal fasting extended (p < 0.05). Serum glucose concentration increased up to 6 h and then reduced linearly to 150 mg/dl after 48-h fasting. The Ca-glu treatment influenced serum glucose level for a short period up to 6 h of fasting. Serum Ca concentration sharply increased up to threefolds in the birds received Ca-glu injection resulting in acute hypercalcemia, then decreased to the initial level after 24-h feed withdrawal (p < 0.05). The mean serum level for creatinine, uric acid, cholesterol, HDL, albumins and total proteins significantly increased during the fasting periods of 6 to 48 h and significantly elevated in the birds receiving 0.6-ml Ca-glu injection compared with the non-treated chicks (p < 0.05). It was concluded that subcutaneous administration of 0.6 ml Ca-glu in the chick's neck did not suitably support the increased metabolic demands for glucose and calcium in feed-deprived neonate chicks.

Effects of Dulaglutide on Thyroid C Cells and Serum Calcitonin in Male Monkeys.

Glucagon-like peptide-1 (GLP-1) receptor agonists, used for the treatment of type 2 diabetes, have caused hyperplasia/neoplasia of thyroid C cells in rodent carcinogenicity studies. Studies in monkeys have not identified an effect of GLP-1 receptor agonists on thyroid C cells; however, group sizes were small. Dulaglutide is a once-weekly, long-acting human GLP-1 receptor agonist recently approved in the United States and the European Union. The objective of this study was to determine whether dulaglutide altered C-cell mass in monkeys. Male cynomolgus monkeys (20 per group) were sc injected with dulaglutide 8.15 mg/kg (∼500-fold maximum human plasma exposure) or a vehicle control twice weekly for 52 weeks. Basal and calcium gluconate-stimulated serum calcitonin concentrations were obtained at 3, 6, 9, and 12 months. Thyroid glands were weighed, fixed, and sectioned at 500-µm intervals. C-cell volumes were measured using an automated image analysis. C-cell proliferation was estimated using Ki67/calcitonin colabeling and cell counting. Administration of dulaglutide 8.15 mg/kg twice weekly for 52 weeks did not increase serum calcitonin in monkeys or affect thyroid weight, histology, C-cell proliferation, or absolute/relative C-cell volume. This study represents a comprehensive evaluation of the monkey thyroid C cells after dosing with a GLP-1 receptor agonist, with a large group size, and measurement of multiple relevant parameters. The lack of effect of dulaglutide on C cells is consistent with other studies in monkeys using GLP-1 receptor agonists and suggests that nonhuman primates are less sensitive than rodents to the induction of proliferative changes in thyroid C cells by GLP-1 receptor agonists.

Identification and preservation of the parathyroid gland during total thyroidectomy in dogs with bilateral thyroid carcinoma: a report of six cases.

Simultaneous removal of bilateral thyroid tumors was performed while preserving the parathyroid gland in six dogs. At least one external parathyroid gland was identified in all dogs. In five cases, the external parathyroid gland and its blood supply were preserved intact. In one dog, the vessels supplying the external parathyroid gland had been invaded by the tumor, and the gland was thus removed and reimplanted into the sternohyoid muscle. That dog required postoperative treatment with oral calcium gluconate and vitamin D3. Local tumor recurrence was not observed in any of the cases. The mean survival time was 920 days. We found that the external parathyroid gland could be identified and preserved in most dogs undergoing total thyroidectomy.

Calcium gluconate supplementation is effective to balance calcium homeostasis in patients with gastrectomy.

UNLABELLED: We demonstrate histological evidence for hyperparathyroidism in patients with gastrectomy. This is, at least in part, explained by impaired calcium absorption, resulting in mineralization defects and secondary hyperparathyroidism. Additionally, we demonstrate improved bone mineralization in patients with gastrectomy after gluconate therapy and showed the effectiveness of calcium gluconate over carbonate to balance impaired calcium hemostasis in mice. INTRODUCTION: Gastrectomy and hypochlorhydria due to long-term proton pump inhibitor therapy are associated with increased fracture risk because of intestinal calcium malabsorption. Hence, our objectives were to histologically investigate bone metabolism in patients with gastrectomy and to analyze the impact of calcium gluconate supplementation on skeletal integrity in the setting of impaired gastric acidification. METHODS: Undecalcified bone biopsies of 26 gastrectomized individuals were histologically analyzed. In the clinical setting, we retrospectively identified 5 gastrectomized patients with sufficient vitamin D level, who were additionally supplemented with calcium gluconate and had a real bone mineral density (aBMD) follow-up assessments. A mouse model of achlorhydria (ATP4b-/-) was used to compare the effect of calcium gluconate and calcium carbonate supplementation on bone metabolism. RESULTS: Biopsies from gastrectomized individuals showed significantly increased osteoid, osteoclast, and osteoblast indices and fibroosteoclasia (p < 0.05) as well as impaired calcium distribution in mineralized bone matrix compared to healthy controls. Five gastrectomized patients with sufficient vitamin D level demonstrated a significant increase in aBMD after a treatment with calcium gluconate alone for at least 6 months (p < 0.05). Calcium gluconate was superior to calcium carbonate in maintaining calcium metabolism in a mouse model of achlorhydria. CONCLUSION: Gastrectomy is associated with severe osteomalacia, marrow fibrosis, and impaired calcium distribution within the mineralized matrix. We show that calcium gluconate supplementation can increase bone mineral density in gastrectomized individuals and performs superior to calcium carbonate in restoring calcium/skeletal homoeostasis in a mouse model of achlorhydria.