Objective:To investigate the protective effects of incremental hemodialysis (iHD) combined with furosemide on residual kidney function (RKF) in end-stage renal disease patients who initiate dialysis with preserved RKF.Methods:This was a randomized controlled trial. The patients diagnosed with end-stage renal disease who initiated hemodialysis at the Department of Nephrology, the Affiliated Hospital of Qingdao University from May 2021 to May 2023 were enrolled. The clinical data were collected and analyzed. The patients were randomly assigned to either iHD group (two 4-hour sessions per week or three 3-hour sessions per week, with oral furosemide 40-80 mg twice daily) or the standard HD group (three 4-hour sessions per week, with oral furosemide 40-80 mg twice daily). Differences in clinical characteristics and RKF were assessed between the two groups of patients at 3 months and 6 months, and the differences between the clinical characteristic and the baseline level at 6 months were analyzed, along with the incidence of adverse events.Results:A total of 87 patients met the inclusion and exclusion criteria, of whom 75 completed this study. The mean age was (53.45±12.57) years old, with 37 females (49.33%) and 38 males (50.67%). The patients were assigned to iHD group (39 cases) and standard HD group (36 cases). At 3 months of the trial, compared with standard HD group, the level of serum C-reactive protein was significantly decreased, and the level of eGFR was significantly increased in the iHD group. At 6 months of the trial, the levels of systolic blood pressure, serum β 2-microglobulin, average ultrafiltration volume and C-reactive protein were significantly decreased, and the levels of eGFR, 24-hour urine volume were significantly increased in the iHD group ( P<0.05). The difference in eGFR, urine volume and systolic blood pressure between the iHD group and the baseline level was significantly smaller than that between the standard HD group and the baseline level (all P<0.05). In contrast, the differences in C-reactive protein was significantly greater than that in standard HD group and the baseline level ( P<0.05). At the 3rd, 6th month of the trial, the 24-h urine volumes of iHD group and standard HD group were (955±219) ml/24 h vs. (847±143) ml/24 h, (914±151) ml/24 h vs. (827±124) ml/24 h, showing statistically significant differences ( t=2.510, P=0.014; t=2.729, P=0.008). Adverse events mainly included pulmonary infections (22 cases), fluid overload during the dialysis interval (or more than 5% of the ideal dry weight, 12 cases), heart failure (4R or 4NR grade, 7 cases), hyperkalemia (6 cases), and thrombosis or failure of vascular access (3 cases). The incidence of adverse events did not differ statistically between the two groups ( P>0.05). Conclusion:iHD combined with furosemide helps preserve RKF and maintain urine output within 6 months compared with standard HD in patients with end-stage renal disease.

Objective:To investigate the protective effects of incremental hemodialysis (iHD) combined with furosemide on residual kidney function (RKF) in end-stage renal disease patients who initiate dialysis with preserved RKF.Methods:This was a randomized controlled trial. The patients diagnosed with end-stage renal disease who initiated hemodialysis at the Department of Nephrology, the Affiliated Hospital of Qingdao University from May 2021 to May 2023 were enrolled. The clinical data were collected and analyzed. The patients were randomly assigned to either iHD group (two 4-hour sessions per week or three 3-hour sessions per week, with oral furosemide 40-80 mg twice daily) or the standard HD group (three 4-hour sessions per week, with oral furosemide 40-80 mg twice daily). Differences in clinical characteristics and RKF were assessed between the two groups of patients at 3 months and 6 months, and the differences between the clinical characteristic and the baseline level at 6 months were analyzed, along with the incidence of adverse events.Results:A total of 87 patients met the inclusion and exclusion criteria, of whom 75 completed this study. The mean age was (53.45±12.57) years old, with 37 females (49.33%) and 38 males (50.67%). The patients were assigned to iHD group (39 cases) and standard HD group (36 cases). At 3 months of the trial, compared with standard HD group, the level of serum C-reactive protein was significantly decreased, and the level of eGFR was significantly increased in the iHD group. At 6 months of the trial, the levels of systolic blood pressure, serum β 2-microglobulin, average ultrafiltration volume and C-reactive protein were significantly decreased, and the levels of eGFR, 24-hour urine volume were significantly increased in the iHD group ( P<0.05). The difference in eGFR, urine volume and systolic blood pressure between the iHD group and the baseline level was significantly smaller than that between the standard HD group and the baseline level (all P<0.05). In contrast, the differences in C-reactive protein was significantly greater than that in standard HD group and the baseline level ( P<0.05). At the 3rd, 6th month of the trial, the 24-h urine volumes of iHD group and standard HD group were (955±219) ml/24 h vs. (847±143) ml/24 h, (914±151) ml/24 h vs. (827±124) ml/24 h, showing statistically significant differences ( t=2.510, P=0.014; t=2.729, P=0.008). Adverse events mainly included pulmonary infections (22 cases), fluid overload during the dialysis interval (or more than 5% of the ideal dry weight, 12 cases), heart failure (4R or 4NR grade, 7 cases), hyperkalemia (6 cases), and thrombosis or failure of vascular access (3 cases). The incidence of adverse events did not differ statistically between the two groups ( P>0.05). Conclusion:iHD combined with furosemide helps preserve RKF and maintain urine output within 6 months compared with standard HD in patients with end-stage renal disease.

This study examined the expression of cell adhesion molecule 1 (CADM1) in pancreatic cancer and the possible mechanism. The expression of CADM1 was detected by immunohistochemistry in tissues of pancreatic cancer, pancreatitis, and normal pancreas. The plasmid pcDNA3.1-Hygro(+)/CADM1 was transfected into PANC-1 cells (a pancreatic cancer cell line). The expression of CADM1 in the transfected cells was determined by RT-PCR and Western blotting. Cell growth was measured by the MTT method and cell apoptosis by flow cytometry. The results showed that CADM1 was weakly expressed in tissues of pancreatic cancer in contrast to its high expression in normal pancreatic and pancreatitis tissues. The expression level of CADM in pancreatic caner was intensely correlated with the differentiation degree, lymph node metastasis and TNM stages. The growth of CADM1-transfected PANC-1 cells was significantly suppressed in vitro by a G1 cell cycle arrest and apoptosis occurrence. It was concluded that re-expression of CADM1 inhibits the growth of pancreatic cancer cells and induces their apoptosis in vitro. As a tumor suppressor gene, CADM1 plays an important role in the occurrence, progression and metastasis of pancreatic cancer.

This study examined the expression of cell adhesion molecule 1 (CADM1) in pancreatic cancer and the possible mechanism.The expression of CADM1 was detected by immunohistochemistry in tissues of pancreatic cancer,pancreatitis,and normal pancreas.The plasmid pcDNA3.1-Hygro(+)/CADM1 was transfected into PANC-1 cells (a pancreatic cancer cell line).The expression of CADM1 in the transfected cells was determined by RT-PCR and Western blotting.Cell growth was measured by the MTT method and cell apoptosis by flow cytometry.The results showed that CADM1was weakly expressed in tissues of pancreatic cancer in contrast to its high expression in normal pancreatic and pancreatitis tissues.The expression level of CADM in pancreatic caner was intensely correlated with the differentiation degree,lymph node metastasis and TNM stages. The growth of CADM1-transfected PANC-1 cells was significantly suppressed in vitro by a G1 cell cycle arrest and apoptosis occurrence.It was concluded that re-expression of CADM1 inhibits the growth of pancreatic cancer cells and induces their apoptosis in vitro.As a tumor suppressor gene,CADM1 plays an important role in the occurrence,progression and metastasis of pancreatic cancer.

To study the possible mechanism of the effect of glucagon-like peptide-1 (GLP-1) on injury to neonatal rat cardiomyocytes induced by hypoxia-reoxygenation. Lactate dehydrogenase activity [(210.0±11.5) vs (101.4±6.5) U/L] ,apoptosis rate [(8. 138±1. 512) vs(0. 575±0. 168)%] ,and caspase-3 activity [(44.52± 5.69)vs(19.98±1.97) ,all P<0.01] were all increased after hypoxia-reoxygenation. GLP-1 appears to directly act on cardiomyocytes and to protect them from hypoxia-reoxygenation injury [lactate dehydrogenase (190.2±9.0) U/ L, apoptosis rate (2.688±0.580) %, caspase-3 activity 30.34±4.18] mainly by inhibiting the apoptosis probably via the PBK/Akt signaling pathways.

Objective To explore the effect of diabetes mellitus (DM) on biological behavior of epidermal keratinocyte in rats. Methods A total of 40 Sprague-Dawley rats were randomized into control group and streptozotocin (STZ) -induced diabetes group. Of each group, 10 rats were implemented with deep partial-thickness scalding. The re-epithelialization rate was observed at the 3rd, 7th, 14th and 21th post-burn day. Histological characteristics and thickness of epidermal tissue in both groups were observed. The adhesion rate, cell cycles, apoptosis rate and migration ability of keratinocyte were measured. The accumulation of advanced glycosylation end products (AGEs) of epidermal tissue was observed. Results The percentages of re-epithelialized area at the 7th, 14th and 21th post-burn day were much lower in DM group than in control group (P<0.05). In DM group, the epidermal thickness was reduced obviously with obscure multilayered epithelium and less amount of prickle cells; The adhesion rates of 12, 24 h after culturing keratinocyte and the percentage of G2/M phase cells were lower in DM group than in control group (P<0.05). However, apoptosis rate of keratinocyte was higher, the amount of migration cell was significantly less in DM group than in control group (both P<0.05). There were lots of AGEs accumulated in epidermal tissue in DM group, while there were hardly AGEs in control group. Conclusions Re-epithelization blocked exists on non-healing wound in DM rats, which is related with the impaired keratinocyte biological behavior. A large of AGEs accumulate in the epidermal tissue of DM rats, which may be a important reason to inhibit keratinocyte function in diabetic environment.

Objective To investigate the effects of angiotensin-converting enzyme inhibitor (ACEI) lisinopril on experimental diabetic peripheral neuropathy (DPN) in the earlier stage and its mechanism. Methods Diabetes was induced by streptozotosin (STZ) in rats. After 8 weeks of treatment, the effects of lisinopril on function and structure of peripheral nerves were observed; superoxide dismutase, malondialdehyde, Na+K+-ATPase activity in sciatic nerve and NO, NO synthase levels in plasma were determined, and capillary density of sciatic nerve were also assessed. Results With lisinopril, nerve structure and function was improved, oxidative stress state was ameliorated, and NO level, Na+K+-ATPase activity and capillary density of endoneurium were increased (all P<0.05). Conclusion ACEIs are effective in DPN. The possible mechanisms may be related to the amelioration of ischemic state and related metabolic disorders of the nerves.

Objective The aim of this study is to undemtand the development of peripheral nerve injury on diabetes mellitus.Methods Diabetes was induced by STZ.We determined nerve conduction velocity,thermal pain threshold,morphoh)gy changes of sciatic nerve and quantitative analysis of sural nerve of diabetic model group and normal control group after 2 weeks,4 weeks,6 weeks,8 weeks,12 weeks respectively,and observed dynamically functional and morphologic changes of peripheral nerve of diabetic rats.Results After 2 weeks,diabetic rats showed that motor and sensory nerve conduction velocities slowed down and thermal pain threshold decreased.After 4 weeks.changes of pathology of sciatic nerve were observed.With the duration extending,the damages of nerve were aggravated gradually.Conclusions Neumpathy appeared in earlier stage on experimental diabetic rats and functional changes were preceded to morphologic changes.

Objective To investigate prevention and therapy effects of ACEI on peripheral nerve in the earlier stage of diabetic rats and the influence on microcirculation of experimental DPN.Methods Diabetes was induced by STZ.After 8 weeks of prevention or therapy treatment.the effects of lisinopril on function and structure of diabetic peripheral nerve were observed,the NO,NOS level in plasma and capillary density of sciatic nerve were determined.Results Lisinopril prevention and therapy treatment improved nerve conduction velocity,ameliorated morphology abnormalities in nerve fiber and capillary at different degrees.The NO level and capillary density of endoneurium were increased. Conclusions ACE inhibitors may exert neuroprotective effect through improving abnormality of microcirculation.