Petrography and origin of dedolomites of the Ordovician Majiagou formation in the southeastern Ordos Basin, China: implications for reservoir quality

Dedolomites, the replacement of dolomite by calcite, are widely distributed in the Ordovician Majiagou Formation of the southeastern Ordos Basin, China, which critically affects reservoir quality throughout the region. Two types of dedolomites were recognized in the upper 100 m of the Majiagou Formation, namely brecciated dedolomite and crystalline dedolomite. The petrographic and geochemical data reveal that the investigated dedolomites are often associated with clay minerals and dissolution-collapse breccia, indicating their close relationship with erosional unconformities. The relative negative δ18O and δ13C values and relative high Fe, Mn contents of dedolomite with respect to corresponding dolomite are interpreted as being result from meteoric phreatic water involvement. The dedolomitization process related to subaerial exposure is conventionally interpreted to be formed by dolomite dissolution and calcite precipitation. The rhombic shape crystals in the brecciated dedolomite was formed by an Mg2+-loss process under evaporite solution conditions, which retain the rhombic shape of the dolomite. The crystalline dedolomites, however, were formed by dissolution/precipitation and recrystallization process to form medium to coarse calcite mosaic with very low intercrystalline porosity. The resulting fabrics are mainly controlled by the paleo-topography. The precursor dolomite of the crystalline dedolomite is primarily recrystallized mudstone, which is more soluble and favorable for calcite precipitation. The crystalline dedolomite mostly occurs in the low paleotopographic locations, where the karst-saturated water with respect to CaCO3 is more concentrated, occluding the remaining porosity when excess calcium is supplied. It’s, therefore, recommended to implement drilling in tectonic highland and avoid low paleotopographic locations.

Abstract P401: The Anti-arrhythmic Effects Of VDAC Isoforms Are Mediated By Glutamate 73 Through Regulation Of Mitochondrial Calcium Transport

Mitochondria critically regulate cellular processes such as bioenergetics, metabolism, calcium homeostasis and apoptosis. VDAC proteins are abundant proteins that control the passage of ions and metabolites across the outer mitochondrial membrane. We have previously shown that activation of VDAC2, is able to buffer excess calcium and thereby suppress calcium overload induced arrhythmogenic events in vitro and in vivo. However, the mechanism by which VDAC2 regulates calcium transport and cardiac contractions remained unclear. It is also unclear whether all three VDAC isoforms (VDAC1,2 and 3) possess similar cardioprotective activity. The zebrafish tremblor/ncx1 mutant lacks functional NCX1 in cardiomyocytes leading to calcium overload, and the manifestation of fibrillation-like phenotypes. Using the tremblor/ncx1 mutant as a model, we observed isoform-specific differences between the VDAC family members. VDAC1 and VDAC2 enhanced mitochondrial calcium trafficking and restore rhythmic contraction in tremblor mutants, whereas, VDAC3 did not. We found that the differing rescue capabilities of VDAC proteins were dependent upon residues in their N-terminal halves. Phylogenetic analysis further revealed the presence of an evolutionarily conserved glutamate at position 73 (E73) within VDAC1 and VDAC2, but a glutamine (Q73) in VDAC3. Excitingly, we showed that replacing VDAC2 E73 with Q73 ablated its calcium transporting activity. Conversely, substituting the Q73 with E73 allows VDAC3 to gain calcium trafficking and cardioprotective abilities. Overall, our study demonstrates an essential role for the evolutionarily conserved glutamate-73 in determining the anti-arrhythmic effect of VDAC isoforms through their regulation of mitochondrial calcium uptake.

“It’s Time To Get Leave,” Says Fetuin-A to Calcium Phosphate

Calcium and phosphate are important components of your teeth and bones. Proper incorporation of calcium and phosphate into teeth and bones is called mineralization. If there is too much calcium or phosphate in your blood stream, your body keeps mineralization under control with a protein called fetuin-A. Fetuin-A accompanies calcium and phosphate as they travel through the blood stream, preventing dangerous mineralization from happening in other bodily tissues and helping the excess calcium and phosphate to leave the body through the kidneys.

MON-334 Severe Hypercalcemia Following Hip Joint Implantation of Stimulan® Calcium Sulfate Antibiotic Beads

Introduction: The diagnosis and management of hypercalcemia in hospitalized patients can be challenging. Hypercalcemia is often associated with significant morbidity and end-organ damage which may delay a patient’s recovery. Case report: A 63-years-old female presented for evaluation of left hip pain and was found to have an infection of the prosthetic joint. Past medical history was significant for type 2 diabetes and atrial fibrillation. No known history of malignancy or excess calcium, vitamins A or D intake. Past surgical history was significant for multiple left hip fixation surgeries and a left hip arthroplasty 4 months prior. Patient’s serum calcium on admission was 8.4 mg/dL (corrected 9.5 mg/dL, range 9.5-10.5 mg/dL), serum creatinine 1.2 mg/dL (range, 0.5 - 1.2 mg/dL). Three days later, she underwent surgical irrigation and debridement of the left hip with placement of 30 cc STIMULAN® antibiotic beads with vancomycin. On postoperative day (POD) 5, patient was found to be confused. Laboratory workup revealed serum calcium 13 mg/dL, ionized calcium 1.91 mmol/L (range, 1.12-1.32 mmol/L), serum creatinine 1.6 mg/dL, intact PTH 10 (range, 15- 65 pg/mL), PTH-rp 15 pg/mL (range, 14-27 pg/mL), 25-OH-vitamin D 18 ng/mL (range, 30-60 ng/mL), 1,25-OH2-vitamin D <8 ng/mL (range, 18-72 ng/mL). Clinical challenge: The differential diagnosis of non-PTH mediated hypercalcemia includes malignancy, granulomatosis and/or excess calcium intake. The patient’s history and laboratory data were not consistent with these etiologies. The temporal nature of the hypercalcemia in relation to implantation of antibiotic beads suggest causality of exogenous calcium sulfate and development of the patient’s hypercalcemia. Mild renal insufficiency, as well as immobilization in the setting of surgery, were likely also contributory. Treatment and outcome: This patient was first treated with aggressive intravenous saline and calcitonin. Serum calcium rose to 13.7 mg/dL and pamidronate 30 mg was administered. Hypercalcemia resolved on POD 11 with improvement in patient functional status. Discussion: Hypercalcemia due to implanted calcium sulfate antibiotic beads is not well described outside of case reports. Kallala found hypercalcemia in less than 0.01% of patients who underwent bead implantation, with all the affected patients presenting with preoperative renal failure. Conclusion: Hypercalcemia in the setting of calcium sulfate antibiotic beads implantation may contribute to a patient’s confusion and increase length-of-stay. We recommend serum calcium and creatinine to be closely monitored during the perioperative period in patients who receive calcium sulfate antibiotic beads. Risk factors for the development of hypercalcemia require additional study, though patients with pre-existing renal insufficiency may not be good candidates for the mechanism of antibiotic administration.

Correction of bone remodeling in experimental osteoporosis

The experimental work analyzes the evaluation of the pharmacological efficacy of 3 experimental samples of the anti-osteoporosic preparation, created on the basis of salts of succinic acid in comparison with the comparison drug. On the experimental model of osteoporosis, according to the application of atomic absorption spectroscopy and flame photometry of the femur, the high efficiency of the new drug in the correction of induced pathology has been proved. The data obtained indicate that when acid salts of the natural conformer of succinic acid are used, it is possible to achieve sufficient saturation of bone tissue with calcium without overloading the body with excess calcium.

Ultrasensitive Wearable Strain Sensors of 3D Printing Tough and Conductive Hydrogels

In this study, tough and conductive hydrogels were printed by 3D printing method. The combination of thermo-responsive agar and ionic-responsive alginate can highly improve the shape fidelity. With addition of agar, ink viscosity was enhanced, further improving its rheological characteristics for a precise printing. After printing, the printed construct was cured via free radical polymerization, and alginate was crosslinked by calcium ions. Most importantly, with calcium crosslinking of alginate, mechanical properties of 3D printed hydrogels are greatly improved. Furthermore, these 3D printed hydrogels can serve as ionic conductors, because hydrogels contain large amounts of water that dissolve excess calcium ions. A wearable resistive strain sensor that can quickly and precisely detect human motions like finger bending was fabricated by a 3D printed hydrogel film. These results demonstrate that the conductive, transparent, and stretchable hydrogels are promising candidates as soft wearable electronics for healthcare, robotics and entertainment.

Acute milk-alkali syndrome

Summary A 74-year-old woman presented with progressive lethargy, confusion, poor appetite and abdominal pain. She was found to have non-PTH-mediated severe hypercalcemia with renal failure and metabolic alkalosis. Extensive workup for hypercalcemia to rule out alternate etiology was unrevealing. Upon further questioning, she was taking excess calcium carbonate (Tums) for her worsening heartburn. She was diagnosed with milk-alkali syndrome (MAS). Her hypercalcemia and alkalosis recovered completely with aggressive hydration along with improvement in her renal function. High index of suspicion should be maintained and history of drug and supplements, especially calcium ingestion, should be routinely asked in patients presenting with hypercalcemia to timely diagnose MAS and prevent unnecessary tests and treatments. Learning points: Suspect milk-alkali syndrome in patients with hypercalcemia, metabolic alkalosis and renal failure, especially in context of ingestion of excess calcium-containing supplements. Careful history of over-the-counter medications, supplements and diet is crucial to diagnose milk-alkali syndrome. Milk-alkali syndrome may cause severe hypercalcemia in up to 25–30% of cases.