Eclampsia as the First Manifestation of Primary Hyperparathyroidism: a Case Report.

BACKGROUND: This study aimed to explore the diagnosis and treatment strategies of eclampsia during pregnancy and postpartum acute pancreatitis caused by primary hyperparathyroidism. METHODS: This study reported a 26-year-old patient who had maternal eclampsia as her first symptom and was admitted to the hospital. The pregnancy was terminated by cesarean section immediately. Postpartum life-threatening complications, such as severe hypercalcemia and acute pancreatitis, occurred afterward. Following completion of the relevant examination, primary hyperparathyroidism was initially considered to be the cause. Symptomatic treatment is ongoing and will be improved, and the patient will be admitted again for parathyroidectomy. RESULTS: The patient gave birth to a premature neonate via cesarean section. The postpartum diagnosis was primary hyperparathyroidism, for which post-surgical pathology showed a parathyroid adenoma. CONCLUSIONS: The clinical manifestations of pregnancy with primary hyperparathyroidism are atypical but may cause serious maternal and fetal complications. Early diagnosis and appropriate treatment can prevent serious prenatal and postnatal complications and foster better pregnancy outcomes.

The Expression and Clinical Value of miR-221 and miR-320 in the Plasma of Women with Gestational Diabetes Mellitus.

BACKGROUND: The goal was to investigate the expression of plasma miR-221 and miR-320 in gestational diabetes mellitus (GDM) and to further explore the relationship between miRNA and risk factors for GDM. METHODS: This study included 85 GDM and 85 age-matched normal pregnant women who visited our hospital from January 2019 to January 2020. Real-time polymerase chain reaction (RT-qPCR) was used to determine the expression of miR-221 and miR-320 in the plasma of pregnant women. The correlation analysis was used to detect the relationship between miR-221, miR-320, and risk factors of GDM, including homeostatic model assessment for insulin resistance (HOMA-IR), percentage of glycosylated hemoglobin (HbA1c), and the prepregnancy BMI. The receiver operating characteristic curve (ROC) was used to determine the diagnostic value of miR-320 and miR-221 in GDM. RESULTS: Compared with normal pregnant women, the expression of miR-221 and miR-320 in GDM was significantly higher (p < 0.05). The results also demonstrate that the expression of miR-221 and miR-320 increases grad-ually with the development of pregnancy in GDM at 24 weeks, 28 weeks, and 32 weeks (p < 0.05). Spearman's correlation analysis confirmed that the expression level of miR-221 and miR-320 in the plasma of GDM is positively correlated with the HOMA-IR and HbA1c, but has no significant correlation with pre-pregnancy BMI. The area under the curve (AUC) values of miR-221 and miR-320 were 0.862 and 0.853, respectively. Meanwhile, the area under the combined detection curve is 0.904. CONCLUSIONS: Plasma miR-221 and miR-320 are significantly elevated in GDM, and are positively correlated with HbA1c and HOMA-IR. The high expression of miR-221 and miR-320 in the peripheral plasma of pregnant women may directly or indirectly participate in the occurrence and development of GDM or may become a new target for the diagnosis, treatment, and prognosis of GDM.

CircAMOTL1 Promotes Tumorigenesis Through miR-526b/SIK2 Axis in Cervical Cancer.

BACKGROUND: Cervical cancer is one of the most common malignancies in women, leading to major health problems for its high morbidity and mortality. Numerous studies have demonstrated that circular RNAs (circRNAs) could be participated in the progression of multifarious diseases, especially plentiful carcinomas. CircAMOTL1 (angiomotin-like1, ID: hsa_circ_0004214), which is located on human chromosome 11:9 4532555-94533477, is involved in the occurrence of breast cancer, etc. However, the intrinsic and concrete molecular mechanism of circAMOTL1 in cervical carcinomas remained thoroughly unclear, which was also the bottleneck of circRNAs studies in cancer. METHODS: The relative expression levels of circAMOTL1 and miR-526b in cervical carcinoma patients' specimens and cervical carcinoma cell lines were detected by RT-qPCR. Through experiments including loss-function and overexpression, the biological effects of circAMOTL1 and miR-526b on the proliferation, migration, apoptosis, and tumorigenicity were explored in cervical carcinomas. Dual luciferase reporter gene analysis, western blot, and other methods were adopted to explore the circAMOTL1 potential mechanism in cervical carcinomas. RESULTS: In our experiments, our researches displayed that circAMOTL1 was significantly higher expression in cervical carcinomas specimens and cell lines. Further experiments illustrated that the knockdown of circAMOTL1 could restrain the malignant phenotype, AKT signaling, and epithelial-mesenchymal transition (EMT) of in cervical carcinomas cells. Meanwhile miR-526b was downregulated in cervical carcinomas and even miR-526b could partially reverse circAMOTL1 function in malignant cervical tumor cells. CircAMOTL1 acts as a microRNA (miRNA) sponge that actively regulates the expression of salt-inducible kinase 2 (SIK2) to sponge miR-526b and subsequently increases malignant phenotypes of cervical carcinomas cells. In a word, circAMOTL1 acts a carcinogenic role and miR-526b serves as the opposite function of antioncogene in the cervical carcinoma pathogenesis. CONCLUSION: CircAMOTL1-miR-526b-SIK2 axis referred to the malignant progression and development of cervical carcinomas. CircAMOTL1 expression was inversely correlated with miR-526b and positively correlated with SIK2 mRNA in cervical cancer tissues. Thus, circAMOTL1 exerted an oncogenic role in cervical cancer progression through sponging miR-526b. Taken together, our study revealed that circAMOTL1 acted as an oncogene and probably was a potential therapeutic target for the cervical cancer.

miR­22­3p enhances multi­chemoresistance by targeting NET1 in bladder cancer cells.

With the discovery of new chemotherapeutic drugs, chemotherapy becomes increasingly valuable. However, the resistance of tumor cells to chemotherapeutic agents significantly limits the effectiveness and causes chemotherapy failure. MicroRNAs have been shown to regulate drug resistance in many types of cancer. In the present study, we measured the chemosensitivity of five bladder cancer (BCa) cell lines to seven commonly used chemotherapeutic drugs by Vita­Blue assay. We then identified the most sensitive (5637) and most tolerant cell lines (H­bc) and conducted a multi­group test. This test included expression group analyses of coding and non­coding genes (miR­omic and RNA­seq). Based on our analyses, we selected miR­22­3p as a target. We then determined its own target gene [neuroepithelial cell transforming 1 (NET1)] by bioinformatic analysis and confirmed this finding by TaqMan­quantitative reverse transcription polymerase chain reaction (qRT­PCR), western blot analysis and luciferase reporter assay. The effect of miR­22­3p on BCa multi­chemoresistance was also determined by transfecting cells with the miR­22­3p­mimic or miR­22­3p­antagomiR. We assessed the involvement of NET1 in BCa chemoresistance by siRNA­mediated NET1 inhibition or pINDUCER21­enhanced green fluorescent protein­NET1­mediated overexpression. Plate colony formation and apoptosis assays were conducted to observe the effects of miR­22­3p and NET1 on BCa chemoresistance. In conclusion, our results suggest that miR­22­3p promotes BCa chemoresistance by targeting NET1 and may serve as a new prognostic biomarker for BCa patients.

miR-193a-3p regulation of chemoradiation resistance in oesophageal cancer cells via the PSEN1 gene.

Chemoradiation therapy is an important component of the curative treatment for oesophageal carcinomas. These therapeutic effects are prevented in patients according to radioresistance and multi-drug resistance, and the cause of such resistance remains unclear. In this study, we identified the role of miR-193a-3p in modulating the radioresistance and chemoresistance of oesophageal cancer cells. We found that KYSE150 and KYSE410 cells could be characterized as relatively radiation-sensitive and radiation-resistant cells, respectively. Similarly, KYSE150 and KYSE410 cells were found to be chemosensitive and chemoresistant, respectively. Over-expression of miR-193a-3p increased the radioresistance and chemoresistance of oesophageal squamous cell carcinoma (ESCC) cells. In contrast, the down-regulation of miR-193a-3p decreased the radioresistance and chemoresistance of ESCC cells. In addition, miR-193a-3p inducing DNA damage has also been demonstrated through measuring the level of gamma-H2AX associated with miR-193a-3p. Moreover, a small interfering RNA(siRNA)-induced repression of the PSEN1 gene had an effect similar to that of miR-193a-3p up-regulation. The above processes also inhibited oesophageal cancer cells apoptosis. These findings suggest that miR-193a-3p contributes to the radiation and chemotherapy resistance of oesophageal carcinoma by down-regulating PSEN1. Thus, miR-193a-3p and PSEN1 might be potential biomarkers for chemoradiation resistant cancers.

[The effects of DEHP on morphology and function of progenitor Leydig cell in rat].

OBJECTIVE: To investigate the effects and mechanisms of diethylhexylphthalate (DEHP) on morphology and function of progenitor Leydig cells (PLC) in rats. METHODS: Twenty pregnant SD rats were randomly divided into 4 groups ( n = 5): normal control group, DEHP low dose group , middle dose group, and high dose group, which were treated from postnatal day (PND) 1 to PND 21 of the pubs with DEHP at the doses of 0, 10, 100, 750 mg/(kg · d) in 0.5 ml of corn oil by gavage respectively. At the end of the treatment, the male pups were killed and blood samples were collected for determination of serum testosterone concentration by chemiluminescence method. The body weight, testis weight and anogenital distance (AGD) were measured. The morphology of PLC was observed by light and transmission electron microscopy. The protein expression of steroidogenic acute regulatory protein(StAR) in PLC was determined by immunohistochemistry. The mRNA expression of insulin-like growth factor-I (IGF-I) in the testis was assayed by real-time PCR. RESULTS: Compared with normal control group, the serum testosterone and AGD of male pubs from the middle and high dose groups were declined significantly (P < 0.01), the testis weight and body weight from high dose group were decreased significantly (P < 0.01), while the testis weight increased in the low dose group (P < 0.05). Under light microscope, PLC showed hyperplasia and cluster aggregation in the low dose group and focal hyperplasia in the middle and high dose group. The spermatogenic cells in seminiferous tubules showed decrease, apoptosis and unfix in the high dose group. Under transmission electron microscope, the PLC showed decreased lipid droplets, smooth endoplasmic reticulum and mitochondriae in the treated group. The mRNA expression of IGF-I increased in the low dose group, and the protein expression of StAR decreased in the middle and high dose group. CONCLUSION: Lactating exposure to DEHP may interfere with the synthesis of testosterone of PLC in male pubs, the decrease of StAR and the damage of PLC may be involved in it.

Steroidogenic acute regulatory protein is a useful marker for Leydig cells and sex-cord stromal tumors.

Steroidogenic acute regulatory (StAR) protein is a rate-limiting protein, which is essential for transporting cholesterol into the mitochondria for steroidogenesis. StAR protein could be a marker for steroidogenic tissues. In this study, we investigated StAR protein levels in sex-cord stromal tumors (SCSTs) including 31 adult granulosa cell tumors, 3 juvenile granulosa cell tumors, 10 fibrothecomas, 2 luteinized thecomas, 4 Sertoli-Leydig cell tumors (SLCTs), 4 sclerosing stromal tumor and 3 Leydig cell tumors (LCTs), and 219 non-SCSTs. SCSTs were used for immunohistochemical staining of StAR protein, α-inhibin, calretinin, and CD99. All the 3 LCTs (100%) strongly stained for StAR protein; 30 of the 31 adult granulosa cell tumors (96%) showed focal staining of StAR protein; all the 10 fibrothecomas and 4 sclerosing stromal tumors (100%) were negative for StAR protein staining; StAR protein stained in Leydig cells but not in Sertoli cells in the 4 SLCTs. All the non-SCSTs were negative for StAR protein except for tumor cells in 4 adrenocortical adenomas and 2 adrenocortical carcinomas. Results of the study indicate that StAR protein is a useful marker for differential diagnosis of SCSTs. It is sensitive and specific for Leydig cells in tumors containing this component (LCT, SLCT), and can express focally in granulosa cell tumors. It is negative for Sertoli cells and nonluteinized theca cells.