Objective To observe the effects of lα-hydroxyvitamin D3 on renal tubular function in the patients with IgA ne phropathy(IgAN) accompanied with proteinuria.Methods Forty-eight eligible patients with IgAN were selected as the IgAN group and divided into the treatment group and control group according to the random number table method,meanwhile 30 healthy adults undergoing healthy physical examination were selected as the normal group.On the routine treatment such as maintaining the double dose of renin-angiotensin system(RAS) blocker,the treatment group took oral l α-hydroxyvitamin D3 capsule (0.5 μg,once a day);the control group continued to adopt the original treatment scheme.The treatment course lasted for 12 weeks.The changes of urinary cystatin C(Cys-C),α1-microglobulin(α1-MG),N-acetyl-β-D-glucosaminidase (NAG),24 h urinary total protein (UTP),blood urea nitrogen (BUN),serum creatinine (Scr),serum calcium (Ca),serum phosphorus (P) and intact parathyroid hormone (iPTH) in two groups were respectively compared between before and after treatment.Results Compared with the normal group,urinary Cys-C,αl-MG and NAG levels in the IgAN group were significantly increased (P＜ 0.01).After 12-week treatment,the levels of Cys-C,α1-MG and NAG were obviously declined compared with that before treatment and in the control group,the differences were statistically significant (P＜ 0.05),meanwhile the UTP level had statistical difference between the two groups after treatment and between before and after treatment in the same group (P＜0.05),but the decrease in the treatment group was more significant than that in the control group(P＜0.05).There was no statistically significant difference in BUN,Scr,Ca,P and iPTH between the two groups before and after treatment(P＞0.05).Conclusion There exists tubulointerstitial injury in IgAN with proteinuria.1α-hydroxyvitamin D3 can significantly decrease urine protein and improves the renal tubular function in the patients with IgAN.

Purpose To observe the mutation of K-ras gene and expression of Fascin-1 protein in CRC tissues and their relationship with clinical pathological features, and then to analyze the correlation between mutation of K-ras and expression of Fascin-1. Methods In 86 cases of CRC tissues, K-ras mutation was detected by DNA sequencing analysis, and Fascin-1 expression was detected by im-munohistochemical method. Results In CRC tissues the mutation rate of K-ras was 34. 88%, the expression rate of Fascin-1 was 60. 47%. The mutation rate of K-ras in lymph node metastasis group was higher than that of without lymph node metastasis group, and that in distant metastasis group was higher than that of without distant metastasis group(P<0. 05). The expression rate of Fascin-1 in serosa invasion group was higher than that of without serosa invasion group, and that in lymph node metastasis group was higher than that of without lymph node metastasis group, and that in distant metastasis group was higher than that of without distant metastasis group (P<0. 01). There was a correlation between the mutation of K-ras gene and the expression of Fascin-1 in CRC tissues (rp =0. 236, P<0. 05). Conclusions The CRC tissues with mutation of K-ras are more likely to metastasize and the CRC tissues with expression of Fascin-1 are more likely to invade serosa and metastasize. The CRC tissues with mutation of K-ras are more likely to express Fascin-1.

Objective: To investigate the effect of long non-coding RNA (lncRNA) lung cancer associated transcript 1 (LUCAT1) on proliferation and migration of clear cell renal cell carcinoma (ccRCC) 786-O cells and the underlying mechanism. Methods: A total of 40 pairs of pathologically confirmed tumor tissues and corresponding adjacent normal tissues from ccRCC patients, who underwent surgical resection in the Department of Urology, the First People's Hospital of Yichang during June 2013 and June 2017, were selected for this study. ccRCC cell lines (786-O, ACHN, UM-RC-2) and normal renal epithelial KiMA cells were also used in this study. qPCR was used to detect the mRNA expressions of LUCAT1, miR-199a-5p and hypoxia inducible fator 1α (HIF-1α) in above mentioned tissues and cell lines; CCK-8 assay was used to evaluate the proliferation of 786-O cells; Transwell assay was used to evaluate the migration of 786-O cells; Dual luciferase reporter gene assay was performed to validate the relationship between LUCAT1 and miR-199a-5p; and Western blotting was conducted to detect the effect of LUCAT1 and miR-199a-5p on the protein expression of HIF-1α. Results: LUCAT1 was significantly up-regulated in ccRCC tissues and cell lines (all P<0.01), and its knockdown significantly inhibited the proliferation and migration of 786-O cells (all P<0.01). miR-199a-5p was low-expressed in ccRCC tissues and cell lines (all P<0.01), StarBase analysis showed that LUCAT1 contained a conserved target site for miR-199a-5p. miR-199a-5p exerted significant suppression on the luciferase activity of LUCAT1-Wt (P<0.01), and LUCAT1 knockdown significantly reduced miR-199a-5p expression (P< 0.01). LUCAT1 was low-expressed in 786-O cells transfected with miR-199a-5p mimics, however, it was attenuated after co-transfection with LUCAT1. The mRNA and protein expressions of HIF-1α in 786-O cells transfected with miR-199a-5p mimics were up-regulated, which was then reversed by LUCAT1 over-expression (P<0.05 or P<0.01). miR-199a-5p over-expression suppressed the proliferation and migration of 786-O cells, which was partially attenuated by LUCAT1 transfection (P<0.05 or P<0.01). Conclusion: LUCAT1 exerts oncogenic function in ccRCC via regulating miR-199a-5p/HIF-1α axis.·

In the aftermath of the pandemic,the government is accelerating the development of top-tier medical resources to broaden the supply and deliver superior healthcare services.However,during this transitional phase,hospitals are experiencing operational challenges due to concurrent construction activities.Notably,a shortage of parking facilities and increased traffic con-gestion continue to impactmedial consultation experience of patients.This paper tries to explore strategies and methods for dynam-ic parking management during hospital campus expansions,offering insights for other medical institutions into grappling with pa-tient parking issues.

BACKGROUND: Although ABO-incompatible (ABOi) kidney transplantation (KT) has been performed successfully, a standard preconditioning regimen has not been established. Based on the initial antidonor ABO antibody titers, an individualized preconditioning regimen is developed, and this study explored the efficacy and safety of the regimen. METHODS: From September 1, 2014, to September 1, 2020, we performed 1668 consecutive living-donor KTs, including 100 ABOi and 1568 ABO-compatible (ABOc) KTs. ABOi KT recipients (KTRs) with a lower antibody titer (≤1:8) were administered oral immunosuppressive drugs (OIs) before KT, while patients with a medium titer (1:16) received OIs plus antibody-removal therapy (plasma exchange/double-filtration plasmapheresis), patients with a higher titer (≥1:32) were in addition received rituximab (Rit). Competing risk analyses were conducted to estimate the cumulative incidence of infection, acute rejection (AR), graft loss, and patient death. RESULTS: After propensity score analyses, 100 ABOi KTRs and 200 matched ABOc KTRs were selected. There were no significant differences in graft and patient survival between the ABOi and ABOc groups (P  = 0.787, P  = 0.386, respectively). After using the individualized preconditioning regimen, ABOi KTRs showed a similar cumulative incidence of AR (10.0% υs . 10.5%, P  = 0.346). Among the ABOi KTRs, the Rit-free group had a similar cumulative incidence of AR ( P  = 0.714) compared to that of the Rit-treated group. Multivariate competing risk analyses revealed that a Rit-free regimen reduced the risk of infection (HR: 0.31; 95% CI: 0.12-0.78, P  = 0.013). Notably, antibody titer rebound was more common in ABOi KTRs receiving a Rit-free preconditioning regimen ( P  = 0.013) than those receiving Rit. ABOi KTRs with antibody titer rebound had a 2.72-fold risk of AR (HR: 2.72, 95% CI: 1.01-7.31, P  = 0.048). ABOi KTRs had similar serum creatinine and estimated glomerular filtration rate compared to those of ABOc KTRs after the first year. CONCLUSIONS An individualized preconditioning regimen can achieve comparable graft and patient survival rates in ABOi KT with ABOc KT. Rit-free preconditioning effectively prevented AR without increasing the risk of infectious events in those with lower initial titers; however, antibody titer rebound should be monitored.
Humans ; Kidney Transplantation/adverse effects* ; Living Donors ; Kidney ; Immunosuppressive Agents/therapeutic use* ; Rituximab/therapeutic use* ; ABO Blood-Group System ; Graft Rejection ; Graft Survival