No abstract

Pyrite is widely distributed in the Longmaxi marine shale in the Upper Yangtze area of China. Pyrite, one of the important components of shale, has an important influence on the enrichment of shale gas. However, there are currently only a few studies on this topic. Based on shale samples from drilling cores using field emission scanning electron microscopy, the pore characteristics of pyrite from the Longmaxi Formation in the Upper Yangtze area of China are studied. The results showed that the intergranular pores of pyrite and abundant organic pores in the organic matter pyrite assemblages are developed in the Longmaxi Formation shale in the study area. Most pyrite framboid pores have triangular or irregular quadrilateral shapes, with pore diameters ranging from 0 to 240 nm. Pores with diameters of 80–240 nm are the major reservoir spaces for shale gas within the pyrite framboids. The average contribution rate of pyrite framboids to shale pores reaches 3.21%, and the highest contribution is 5.66%, indicating that the pyrite pores may have a favorable contribution to the shale reservoir pore system, but the contribution degree is low.

Rationale: Autosomal dominant hypocalcaemia type 1 (ADH1) is a genetic disease characterized by benign hypocalcemia, inappropriately low parathyroid hormone levels and mostly hypercalciuria. It is caused by the activating mutations of the calcium-sensing receptor gene ( CASR ), which produces a left-shift in the set point for extracellular calcium. Patient concerns: A 50-year-old man presenting with muscle spasms was admitted into the hospital. He has a positive familial history for hypocalcemia. Auxiliary examinations demonstrated hypocalcemia, hyperphosphatemia, normal parathyroid hormone level and nephrolithiasis. A missense heterozygous variant in CASR , c 613C > T (p. Arg205Cys) which has been reported in a familial hypocalciuric hypercalcemia type 1 patient was found in the patient's genotype. It is the first time that this variant is found associating with ADH1. The variant is predicted vicious by softwares and cosegregates with ADH1 in this pedigree. CASR Arg205Cys was deduced to be the genetic cause of ADH1 in the family. Diagnosis: The patient was diagnosed with ADH1 clinically and genetically. Interventions: Oral calcitriol, calcium and hydrochlorothiazide were prescribed to the patient. Outcomes: After the treatments for 1 week, the patient's symptom was improved and the re-examination revealed serum calcium in the normal range. A 3-month follow-up showed his symptom was mostly relieved. Lessons: The variant of CASR Arg205Cys, responsible for ADH1 in this family, broadened the genetic spectrum of ADH1. Further and more studies are required to evaluate the correlation between genotype and phenotype in ADH1 patients.