Urinary bladder rupture during voiding cystourethrography

Voiding cystourethrography (VCUG) is a commonly performed diagnostic procedure for the evaluation of vesicoureteral reflux with urinary tract infection or congenital renal diseases in children. The procedure is relatively simple and cost-effective, and complications are very rare. The iatrogenic complication of VCUG range from discomfort, urinary tract infection to bacteremia, as well as bladder rupture. Bladder rupture is a rare complication of VCUG, and only a few cases were reported. Bladder rupture among healthy children during VCUG is an especially uncommon event. Bladder rupture associated with VCUG is usually more common in chronically unused bladders like chronic renal failure. Presented is a case of bladder rupture that occurred during a VCUG in a healthy 9-month-old infant, due to instilled action of dye by high pressure. This injury completely healed after 7 days of operation, and it was confirmed with a postoperative cystography. The patient's bladder volume, underlying disease, velocity of the contrast media instilled, catheter size, and styles of instillation are important factors to prevent bladder rupture during VCUG. Management of bladder rupture should be individualized, but the majority of infants are treated with the operation. In conclusion, bladder rupture is a rare complication, however, delicate attention is needed in order to prevent more dire situations

A case of malignant hyperthermia during anesthesia induction with sevoflurane -A case report-

We experienced a case of malignant hyperthermia (MH) in 6-year-old boy during anesthesia induction for strabismus surgery. It has been generally reported that sevoflurane can induce the delayed onset of MH in the absence of succinylcholine. Our case of MH was elicited after about 2-3 min of sevoflurane administration with N2O, O2 and rocuronium. However, we successfully treated the patient by early recognition of his condition and administering symptomatic treatment and dantrolene

Management of Complex Regional Pain Syndrome Type 1 With Total Spinal Block

Complex regional pain syndrome (CRPS) is a painful and disabling disorder that can affect one or more extremities. Unfortunately, the knowledge concerning its natural history and mechanism is very limited and many current rationales in treatment of CRPS are mainly dependent on efficacy originated in other common conditions of neuropathic pain. Therefore, in this study, we present a case using a total spinal block (TSB) for the refractory pain management of a 16-year-old male CRPS patient, who suffered from constant stabbing and squeezing pain, with severe touch allodynia in the left upper extremity following an operation of chondroblastoma. After the TSB, the patient's continuous and spontaneous pain became mild and the allodynia disappeared and maintained decreased for 1 month

A study of the relationship between clinical phenotypes and plasma iduronate-2-sulfatase enzyme activities in Hunter syndrome patients

PurposeMucopolysaccharidosis type II (MPS II or Hunter syndrome) is a rare lysosomal storage disorder caused by iduronate-2-sulfatase (IDS) deficiency. MPS II causes a wide phenotypic spectrum of symptoms ranging from mild to severe. IDS activity, which is measured in leukocyte pellets or fibroblasts, was reported to be related to clinical phenotype by Sukegawa-Hayasaka et al. Measurement of residual plasma IDS activity using a fluorometric assay is simpler than conventional measurements using skin fibroblasts or peripheral blood mononuclear cells. This is the first study to describe the relationship between plasma IDS activity and clinical phenotype of MPS II.MethodsWe hypothesized that residual plasma IDS activity is related to clinical phenotype. We classified 43 Hunter syndrome patients as having attenuated or severe disease types based on clinical characteristics, especially intellectual and cognitive status. There were 27 patients with the severe type and 16 with the attenuated type. Plasma IDS activity was measured by a fluorometric enzyme assay using 4-methylumbelliferyl-α-iduronate 2-sulphate.ResultsPlasma IDS activity in patients with the severe type was significantly lower than that in patients with the attenuated type (P=0.006). The optimal cut-off value of plasma IDS activity for distinguishing the severe type from the attenuated type was 0.63 nmol·4 hr-1·mL-1. This value had 88.2% sensitivity, 65.4% specificity, and an area under receiver-operator characteristics (ROC) curve of 0.768 (ROC curve analysis; P=0.003).ConclusionThese results show that the mild phenotype may be related to residual lysosomal enzyme activity

Inhibition of mTORC1 through ATF4-induced REDD1 and Sestrin2 expression by Metformin

Background Although the major anticancer effect of metformin involves AMPK-dependent or AMPK-independent mTORC1 inhibition, the mechanisms of action are still not fully understood. Methods To investigate the molecular mechanisms underlying the effect of metformin on the mTORC1 inhibition, MTT assay, RT-PCR, and western blot analysis were performed. Results Metformin induced the expression of ATF4, REDD1, and Sestrin2 concomitant with its inhibition of mTORC1 activity. Treatment with REDD1 or Sestrin2 siRNA reversed the mTORC1 inhibition induced by metformin, indicating that REDD1 and Sestrin2 are important for the inhibition of mTORC1 triggered by metformin treatment. Moreover, REDD1- and Sestrin2-mediated mTORC1 inhibition in response to metformin was independent of AMPK activation. Additionally, lapatinib enhances cell sensitivity to metformin, and knockdown of REDD1 and Sestrin2 decreased cell sensitivity to metformin and lapatinib. Conclusions ATF4-induced REDD1 and Sestrin2 expression in response to metformin plays an important role in mTORC1 inhibition independent of AMPK activation, and this signalling pathway could have therapeutic value.This research was supported by grants from the Korea Institute of Radiological and Medical Sciences (KIRAMS), funded by the Ministry of Science and ICT (MSIT), Republic of Korea (Nos. 50336–2021; 50531–2021; and 50544–2021)

Correction to: Failure to maintain full-term pregnancies in pig carrying klotho monoallelic knockout fetuses

An amendment to this paper has been published and can be accessed via the original article

ZNF507 affects TGF-β signaling via TGFBR1 and MAP3K8 activation in the progression of prostate cancer to an aggressive state

Background: The progression of prostate cancer (PC) to the highly aggressive metastatic castration-resistant prostate cancer (mCRPC) or neuroendocrine prostate cancer (NEPC) is a fatal condition and the underlying molecular mechanisms are poorly understood. Here, we identified the novel transcriptional factor ZNF507 as a key mediator in the progression of PC to an aggressive state. Methods: We analyzed ZNF507 expression in the data from various human PC database and high-grade PC patient samples. By establishment of ZNF507 knockdown and overexpression human PC cell lines, we assessed in vitro PC phenotype changes including cell proliferation, survival, migration and invasion. By performing microarray with ZNF507 knockdown PC cells, we profiled the gene clusters affected by ZNF507 knockdown. Moreover, ZNF507 regulated key signal was evaluated by dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. Finally, we performed xenograft and in vivo metastasis assay to confirm the effect of ZNF507 knockdown in PC cells. Results: We found that ZNF507 expression was increased, particularly in the highly graded PC. ZNF507 was also found to be associated with metastatic PC of a high grade. Loss- or gain-of-function–based analysis revealed that ZNF507 promotes the growth, survival, proliferation, and metastatic properties of PC (e.g., epithelial-mesenchymal transition) by upregulating TGF-β signaling. Profiling of gene clusters affected by ZNF507 knockdown revealed that ZNF507 positively regulated the transcription of TGFBR1, MAP3K8, and FURIN, which in turn promoted the progression of PC to highly metastatic and aggressive state. Conclusions: Our findings suggest that ZNF507 is a novel key regulator of TGF-β signaling in the progression of malignant PC and could be a promising target for studying the development of advanced metastatic PCs. © 2021, The Author(s).1