ABSTRACT
Key Clinical Message: Managing acute pancreatitis secondary to hypertriglyceridemia in pregnancy is challenging. The use of intravenous insulin along with lipid lowering drugs can be an option in settings where plasmapharesis and gene therapy are unavailable. Abstract: Acute pancreatitis secondary to hypertriglyceridemia is rare but various studies have highlighted it as the third most common cause following gallstones and alcohol consumption. Managing acute pancreatitis is always challenging; even more challenging during pregnancy. We present a case of a 31-year- old female with a history of recurrent pancreatitis secondary to hypertriglyceridemia with a current episode of acute pancreatitis at 21 weeks of gestation.
ABSTRACT
Spontaneous uterine rupture in an unscarred uterus is very rare. It is found to be rarer after in-vitro fertilization. It is associated with significant morbidity and mortality if not diagnosed and treated promptly. Case presentation: Thirty three years female with twin pregnancy following in-vitro fertilization after 11 years of marriage presented to emergency department with lower abdominal pain at 36 weeks 3 days of gestation and was planned for emergency caesarean section for precious twin pregnancy in labour. Clinical findings and investigation: She was vitally stable and on palpation of abdomen, there was generalized tenderness along with guarding. All the investigations were within normal limits. Intervention and outcome: Emergency caesarean section was performed under subarachnoid block which revealed a 6×2 cm fundal uterine rupture with no active bleeding which was repaired in layers. The babies were extracted with a lower uterine segment incision. First twin cried immediately after birth while the second one needed resuscitation and mechanical ventilation due to perinatal asphyxia. Conclusion: Even though rare in a previously unscarred uterus, uterine rupture can present in different forms and thus, requires vigilant evaluation of the patient and prompt intervention to avoid significant maternal or foetal morbidity and mortality.
ABSTRACT
AIMS: Papillary thyroid cancer (PTC) is one of the subtypes of thyroid cancer with increasing incidence worldwide, but the molecular mechanism is still unclear. BACKGROUND: Papillary thyroid cancer (PTC) is one of the subtypes of thyroid cancer with increasing incidence worldwide, but the molecular mechanism is still unclear. Studies have indicated that nectin cell adhesion molecule 4 (NECTIN4) was an oncogene and played an important role in the development and progression of PTC. Meanwhile, specificity protein 1 (SP1) expresses many important oncogenes and tumor suppressor genes. However, the relationship between NECTIN4 and SP1 in regulating PTC growth is unclear. OBJECTIVE: In the present study, reverse transcription PCR was utilized to detect the mRNA expression of NECTIN4 and SP1 in thyroid cancer cell lines and normal thyroid cell lines. Chromatin immunoprecipitation assays and luciferase reporter assays were used to study whether SP1 could bind to the promoter region of NECTIN4 and activate its transcription. The biological functions of SP1 correlated with NECTIN4 were also performed in TPC-1 and KTC1 cell lines. METHOD: The study revealed that the mRNA expression level of SP1 and NECTIN-4 showed a positive correlation and were upregulated in PTC cell lines. Moreover, the results of ChIP and luciferase reporter assays showed that SP1 could bind to the NECTIN4 promoter regions and activate the transcriptional level of NECTIN4. RESULT: The experiments in vitro showed that SP1 could promote cell proliferation, colony formation, migration, and invasion by regulating NECTIN4 in PTC cells. CONCLUSION: In conclusion, our study, for the first time, demonstrated that SP1 could control the transcriptional regulation of NECTIN4 and accelerate the growth of PTC, which may provide a new potential therapeutic target for PTC patients.
ABSTRACT
High levels of S100A6 have been associated with progression in some types of human cancers. Cancers related to S100A6 have been reported to include lung cancer, cervical cancer, pancreatic cancer, gastric cancer, colon cancer, etc., but its role in the molecular pathogenesis of these cancers is largely unknown. This study investigated the expression and functional roles of S100A6 in human thyroid cancer. The expression level of S100A6 in thyroid cancer cells was determined by bioinformatics and transcriptomic analysis. Furthermore, the potential functions of S100A6 in tumorigenesis were analyzed by cell proliferation, migration, invasion, and Western blot assays in human thyroid cancer cells. Public database queries revealed high S100A6 expression in thyroid cancer. In addition, we also found that high expression of S100A6 was positively correlated with malignant clinicopathological characteristics of thyroid cancer in The Cancer Genome Atlas database. qPCR results confirmed the high expression of S100A6 in thyroid cancer cells. S100A6 silencing inhibited cell proliferation, migration, and invasion. Western blot assays and response experiments showed that S100A6 promotes cell proliferation and tumorigenicity partly through the PI3K/AKT/mTOR signaling pathway. These results suggest that S100A6 affects the progression of thyroid cancer and can be used as a target in the future treatment of thyroid cancer.
