Efficacy of pretreatment with remimazolam on prevention of propofol-induced injection pain in patients undergoing gastroscopy.

To evaluate the efficacy of remimazolam pretreatment in preventing propofol-induced injection pain (PIP) in patients undergoing gastroscopy. One hundred and forty patients (ASA I-II, aged 18-65 years, BMI 18-28 kg/m2) who were to undergo gastroscopy were randomized into either a saline group (group S) or a remimazolam group (group R) (n = 70 for each) on a computer-generated random number basis. The patients in group S received normal saline (0.1 ml/kg) and those in group R were administered remimazolam (0.1 mg/kg) via intravenous infusion for 60 s. 30 s after the injection of normal saline or remimazolam, patients received intravenously propofol (0.5 ml/s) until loss of consciousness. A different anesthesiologist who was unaware of the pretreatment was responsible for maintaining the outcome. The primary endpoint of our study was the incidence of PIP, which was measured using a 4-point scale. Secondary endpoints include the intensity of PIP, vital signs, characteristics of surgery and recovery, and adverse events. The incidence of PIP was significantly lower in group R than in group S (13 vs 51%, p < 0.001), and a lower percentage of patients presented with moderate PIP (3 vs 20%, p < 0.001). Moreover, lower consumption of propofol, shorter recovery time, and greater patient satisfaction were observed in group R than in group S. Pretreatment with remimazolam can effectively reduce the incidence and intensity of PIP in gastroscopy and shorten the recovery time without severe adverse effects.Clinical Trials Registration: Trial Registration: Chinese Clinical Trial Registry (identifier: ChiCTR2200063793). Registry time: 16/09/2022. Registry name: Efficacy of Pre-Treatment with Remimazolam on Prevention of Propofol-Induced Injection Pain in Patients Undergoing Gastroscopy. The date of patient enrollment began from 2022-9-17 to 2022-10-10. The link to the registration: https://www.chictr.org.cn/showproj.html?proj=176004 .

Primary adrenal diffuse large B cell Lymphoma with Tumor thrombus in central adrenal vein: a case report and literature review.

BACKGROUND: Primary adrenal lymphoma (PAL) is a rare disease confined wholly or chiefly to extramural involvement. Tumor thrombus in the central adrenal vein, renal vein, and inferior vena cava has been reported in adrenal pheochromocytoma, adrenocortical carcinoma, adrenal metastasis carcinoma, and adrenal leiomyosarcoma. Primary adrenal diffuse large B cell lymphoma with tumor thrombus in the central adrenal vein has rarely been reported in the current study. ( We searched in PubMed, Web of Science databases, Embase, and Medline in the English language from 1970 to December 2022. The keywords used were "Primary adrenal lymphoma " and " tumor thrombus".) CASE PRESENTATION: In this report, we discuss the case of a 57-year-old woman who complained of abdominal discomfort following cold stimulation, low back pain, anorexia, fatigue, and weight loss for 1 year. Contrast-enhanced spiral computed tomography (CT) showed mild-to-moderate enhancement of the bilateral masses and central adrenal vein tumor thrombus. After an exhaustive study, the patient was diagnosed with primary adrenal diffuse large B-cell lymphoma. In the diagnosis of PAL, the possibility of a tumor embolism in the central adrenal vein, renal vein, or inferior vena cava should be considered, although this is rare.

Giant seminal vesicle cyst with hemorrhage in Zinner syndrome: A case report.

RATIONALE: Zinner syndrome (ZS) is a rare congenital malformation of the urogenital tract that is associated with seminal vesicle cysts, ejaculatory duct obstruction, and ipsilateral renal agenesis. This unique condition was first reported by Zinner (1914). ZS is caused by malformation of the distal mesonephric duct during embryogenesis. To our knowledge, no giant seminal vesicle cysts with hemorrhage in ZS have been reported in the current study. PATIENT CONCERNS: A 63-year-old man presented with chronic hypogastralgia with no history of lower urinary tract symptoms, hematuria, or trauma. Physical examination revealed no localized uplift or percussive pain in either kidney. No tenderness in the ureter stroke region, no localized eminence in the suprapubic region of the bladder, and no tenderness in the bladder region was observed. Digital rectal examination revealed a cystic mass with a smooth surface in the anterior wall of the rectum with no tenderness or unclear boundaries. No blood staining was observed in the finger sheaths. DIAGNOSES: Computed tomography scan revealed that the right kidney was absent, with a mass similar to a cord above the right seminal vesicle cyst. Contrast-enhanced pelvic magnetic resonance imaging (MRI) confirmed a short T1 and T2 signal shadow similar to a cord above the right seminal vesicle cyst. The boundary was clear, with the upper part leading to the "renal region" and the lower part connecting to the right seminal vesicle cyst. Contrast-enhanced MRI showed local parenchymal cysts with cyst wall enhancement but no intrathecal enhancement. This suggested a hemorrhagic cyst. A diagnosis of Zinner syndrome was established. INTERVENTIONS: The patient was diagnosed with a giant seminal vesicle cyst with hemorrhage in ZS. The patient had no obvious symptoms; therefore, regular follow-ups were performed. OUTCOMES: MRI of the patient 1 month later showed that the hematoma in the seminal vesicle cyst was not absorbed. LESSONS: Giant seminal vesicle cysts with hemorrhage in ZS are rare. To patients without symptom, regular follow-up can be adopted.

Right supernumerary kidney with urothelial carcinoma: A case report.

RATIONALE: A supernumerary kidney is an extremely rare renal anomaly. Currently, <100 cases are reported in the literature. There are only 2 right unilateral supernumerary kidneys reported in the literature thus far, but no confirmed cases of urothelial carcinoma in supernumerary kidneys. We report a case of a right supernumerary with urothelial carcinoma, which is, to the best of our knowledge, reported for the first time. PATIENT CONCERNS: A 73-year-old female patient presented with intermittent, painless, whole course and gross hematuria for about 3 months. Her physical and laboratory examinations did not reveal any significant findings except positive occult blood in routine urine examination. Contrast-enhanced spiral computed tomography revealed a dysplastic supernumerary kidney under the normal right kidney. DIAGNOSES: The ureteroscopy showed that the ureter was Y-shaped in the middle part. The medial ureter led to a normal kidney. The lateral ureter was just 2 cm and led to a small cavity in which there was a mass whose biopsy showed urothelial carcinoma. The patient was subsequently diagnosed with a right supernumerary kidney with urothelial carcinoma. INTERVENTION: Nephroureterectomy, including the right normal and supernumerary kidneys, and partial cystectomy by laparoscopy were performed after the ureteroscopy. The patient then received 6 cycles of gemcitabine and cisplatin regimen chemotherapy and regular intravesical epirubicin chemotherapy. OUTCOMES: No recurrence or metastasis was found on follow-up computed tomography performed 13 months postoperatively. LESSONS: A supernumerary kidney is an extremely rare renal anomaly. Malignancy can occur in supernumerary kidneys.

The biological effect and mechanism of the Wnt/ß-catenin signaling pathway on malignant melanoma A375 cells.

The present study aimed to determine the influence of the Wnt/ß-catenin signaling pathway on the proliferation, invasion, migration and apoptosis of malignant melanoma (MM) A375 cells. ß-catenin interfering lentivirus liquid (ß-catenin-RNAi-LV) and empty vector lentivirus liquid (ß-catenin-negative-LV) were used to infect A375 cells. Infected cells were obtained and marked as A375-RNA interference (A375-RNAi) or A375-negative, respectively. Western blotting was used to measure the expression of ß-catenin in infected cells and uninfected cells were utilized as a control. An MTT assay was adopted to measure cell proliferation and the clone formation of cells was assessed. In addition, the Transwell method was used to detect cell invasion and migration in vitro and flow cytometry was utilized to determine cell apoptosis. Western blot analysis demonstrated that ß-catenin was highly expressed in uninfected A375 cells but exhibited reduced expression in A375-RNAi cells. These results indicate that ß-catenin expression is effectively silenced by ß-catenin-RNAi-LV. The proliferative and clone forming abilities of A375-RNAi cells were impaired compared with A375-negative and A375 cells. Additionally, the apoptosis rate was increased and the invasion and migration of A375-RNAi cells was decreased. However, no significant differences were identified in the proliferation, clone formation, apoptosis rate, invasion and migration of A375-negative cells compared with A375 cells. Therefore, the current study demonstrated that the inhibition of ß-catenin expression or activity inhibits cell proliferation and invasion and migration, further downregulating the expression of anti-apoptotic genes and accelerating cellular apoptosis.

MiR-122 targets VEGFC in bladder cancer to inhibit tumor growth and angiogenesis.

Previous studies indicate that microRNA-122 (miR-122) is down-regulated in several cancer cells and regulates cell apoptosis, proliferation, metastasis, and tumor angiogenesis. However, the mount of miR-122 in bladder cancer and the pivotal molecular mechanisms of miR-122 used to regulate bladder carcinogenesis and angiogenesis remain to be clarified. Here, we reveal that miR-122 expression is down-regulated in human bladder cancer tissues and cell lines. MiR-122 represses vascular endothelial growth factor C (VEGFC) post-transcriptional expression by directly binding to its 3'-UTR. The protein kinase B (AKT) and mammalian target of rapamycin (mTOR), which are the most important downstream molecules of VEGFC, are also decreased in bladder cancer cell after miR-122 overexpression. Furthermore, miR-122 over-expression decreases bladder cancer cell migration, invasion, colony formation in vitro and slow bladder cancer growth and angiogenesis in vivo. Finally, miR-122 sensitizes bladder cancer cells to cisplatin-induced apoptosis. Taken together, these studies suggest that miR-122 serves as a tumor suppressor and down-regulating VEGFC expression, leading to the inhibition of bladder cancer growth and angiogenesis.