Effects of Maitland mobilization technique on upper extremity function in stroke survivors with spasticity: An experimental study.

BACKGROUND: The recovery of upper limb function is of great significance for stroke patients to regain their self-care ability, yet it is still a difficult point in clinical practice of neurological rehabilitation. This study aimed to investigate the effect of Maitland joint mobilization technique on the recovery of upper extremity function in patients with spasticity after stroke. METHODS: From August to December 2023, 71 patients with upper extremity flexor spasm after stroke were recruited and randomly divided into experimental group (n = 35) and control group (n = 36). The control group was given conventional rehabilitation treatment, while the experimental group was treated with Maitland mobilization technique treatment of upper extremity joints on the basis of the control group. The experiment lasted for 8 weeks. Participants of the 2 groups were observed for Fugl-Meyer motor assessment-upper extremity (FMA-UE), box and block test (BBT) and Brunnstrom stage, modified Ashworth scale (MAS), and functional independence measure (FIM) at pre- and post-8 weeks study. RESULTS: There was no significant difference in gender distribution, hemiplegic side, diagnosis, past history, age, duration, body mass index, and mini-mental state examination between the 2 groups (P > .05). After 8 weeks of intervention, both groups showed significant improvement in FMA-UE, Brunnstrom stage, BBT, FIM, and MAS of the shoulder (P < .05); however, there was no significant change in MAS of the elbow, wrist, and finger joints (P > .05). The posttreatment values showed a significant improvement in FMA-UE, BBT, and FIM in the experimental group compared to the control group. Comparing the changes in pretreatment and posttreatment, FMA-UE, BBT, and FIM in the experimental group were significantly improved compared with those in the control group (P < .05). CONCLUSION: Maitland joint mobilization can improve the motor function of upper extremity and the spasticity of shoulder joint complex in patients with stroke.

UA promotes epithelial­mesenchymal transition in peritoneal mesothelial cells.

Long­term peritoneal dialysis is often limited or interrupted due to the development and progression of peritoneal fibrosis. Accumulating evidence suggests that epithelial­mesenchymal transition (EMT) is a major component of peritoneal injury associated with peritoneal fibrosis in the end stage of renal disease; however, at present, the underlying mechanisms remain unclear. Thus, in the present study, uric acid (UA)­induced EMT of peritoneal mesothelial cells was investigated by western­blot and immunofluorescence staining. The results revealed that peritoneal mesothelial cells stimulated with UA underwent EMT, as demonstrated by the decreased expression of epithelial markers (E­cadherin) and an increased expression of mesenchymal markers (α­smooth muscle actin and vimentin). Additionally, it was reported that UA could facilitate the progression of EMT of peritoneal mesothelial cells via EMT transcription pathways, including transforming growth factor­ß1/mothers against decapentaplegic homolog 3 and P38/mitogen­activated protein kinase by western­blot and reverse transcription semi­quantitative polymerase chain reaction. The results of the present study suggest that UA could promote EMT and may contribute to peritoneal chronic disease. Furthermore, the data obtained suggest that the levels of blood UA may account for the development of EMT; thus, lowering the levels of blood UA may be beneficial to inhibit the occurrence and development of peritoneal fibrosis.

Inhibition of kidney cancer cell growth by Mulberroside-A is mediated via mitochondrial mediated apoptosis, inhibition of cell migration and invasion and targeting EGFR signalling pathway.

PURPOSE: Kidney cancer is a lethal type of malignancy with high mortality. The chemotherapeutic agents used for the treatment of kidney cancer have several adverse effects, therefore, there is need to explore new molecules for the treatment of this disease. In the current study, the anticancer activity of plant-derived stilbenoid Mulberroside-A (MA) was evaluated against the A498 kidney cancer cell line and the underlying mechanism was explored. METHODS: The A498 cell viability was determined by WST-1 assay. DAPI and AO/EB staining were employed for the detection of apoptosis. Matrigel and wound heal assay were used for cell invasion and migration study, respectively. Protein expression was checked by immunoblotting. RESULTS: The results showed that MA could inhibit the growth of the A498 cells dose-dependently. The IC50 of 20 µM was observed for MA against the kidney cancer A498 cells. The anticancer effects of MA against these cells were due to apoptotic cell death. Apoptosis was associated with alteration of the Bax/bcl-2 ratio. In addition, MA could also suppress the migration and invasion of the kidney cancer A498 cells by targeting EGFR signalling pathway. CONCLUSION: In conclusion, MA may prove beneficial in the treatment of kidney cancer.

Comparison of the Inhibitory Mechanisms of Diethyl Citrate, Sodium Citrate, and Phosphonoformic Acid on Calcification Induced by High Inorganic Phosphate Contents in Mouse Aortic Smooth Muscle Cells.

OBJECTIVE: This study aimed to investigate the differences and inhibitory effects of diethyl citrate (Et2Cit), sodium citrate (Na3Cit), and phosphonoformic acid (PFA) on calcification induced by high inorganic phosphate (Pi) contents in mouse aortic smooth muscle cells (MOVAS) and to develop drugs that can induce anticoagulation and inhibit vascular calcification (VC). METHODS: Alive and fixed MOVAS were assessed for 14 days in the presence of high Pi with increasing Et2Cit, Na3Cit, and PFA concentrations. Calcification on MOVAS was measured through Alizarin red staining and the deposited calcium amount; apoptosis was detected by annexin V staining; and cell transdifferentiation was examined by measuring smooth muscle lineage gene (α-SMA) expression and alkaline phosphatase activity. RESULTS: Coincubation of MOVAS with Et2Cit, Na3Cit, and PFA significantly decreased Pi-induced VC in live MOVAS, and the apoptotic rate was reduced by low inhibitor concentrations. The 3 inhibitors could prevent the alkaline phosphatase activity induced by high Pi contents and increased the expression of α-smooth muscle actin genes. Thus, the transdifferentiation of MOVAS into osteoblast-like cells was blocked. Their inhibitory effects exhibited concentration dependence. The inhibitory effect of each inhibitor at the same concentration showed the following trend: PFA > Na3Cit > Et2Cit. CONCLUSIONS: Et2Cit, Na3Cit, and PFA prevented the calcification of MOVAS and inhibited the osteochondrocytic conversion of vascular smooth muscle cells. Thus, Et2Cit and Na3Cit as anticoagulants may alleviate VC in clinical applications.

Prevalence of abdominal artery calcification in dialysis patients with end-stage renal disease: a systematic review and meta-analysis.

PURPOSE: To systematically determine the prevalence of abdominal artery calcification (AAC) in dialysis patients with end-stage renal disease (ESRD) and identify reasons for heterogeneity. METHODS: We searched PubMed, EMBASE, and Web of Science from database inception to March 2017. Cross-sectional or cohort (only used baseline data) studies reporting estimates of AAC prevalence in dialysis adult patients with ESRD were included. We performed a random-effects meta-analysis to generate pooled prevalence estimates. Subgroup analyses were used to compare differences within categorical variables (geographic region, AAC detection instruments, dialysis methods, study design, and sample size), and meta-regression analyses to assess the impact of continuous variables (participants' age, duration of dialysis, and male proportion). RESULTS: A total of 44 studies with 9883 dialysis patients were included. The pooled prevalence for AAC was 68.5% (95% CI 63-73.9%). Subgroup analyses suggested that AAC prevalence varied significantly by geographical region and AAC detection instruments, not by dialysis methods, study design and sample size. Meta-regression analysis suggested that positive correlations were found between AAC prevalence and the age of participants as well as the male proportion (r = 1.01477, P = 0.002 and r = 2.034413, P = 0.01, respectively), but not with the duration of dialysis (P = 0.576). CONCLUSION: The pooled and nearest estimate of AAC prevalence among dialysis patients was as high as 65%. Geographical region, AAC detection instruments, age of participants, and male proportion potentially lead to the high variance of the reported prevalence. Considering the high AAC prevalence, effective treatment for preventing vascular calcification in these patients is badly needed.

Changes in urinary nanocrystallites in calcium oxalate stone formers before and after potassium citrate intake.

The property changes of urinary nanocrystallites in 13 patients with calcium oxalate (CaOx) stones were studied before and after ingestion of potassium citrate (K3cit), a therapeutic drug for stones. The analytical techniques included nanoparticle size analysis, transmission electron microscopy, X-ray diffraction, and Fourier-transform infrared spectroscopy. The studied properties included the components, morphologies, zeta potentials, particle size distributions, light intensity autocorrelation curves, and polydispersity indices (PDIs) of the nanocrystallites. The main components of the urinary nanocrystallites before K3cit intake included uric acid, ß-calcium phosphate, and calcium oxalate monohydrate. After K3cit intake, the quantities, species, and percentages of aggregated crystals decreased, whereas the percentages of monosodium urate and calcium oxalate dehydrate increased, and some crystallites became blunt. Moreover, the urinary pH increased from 5.96 ± 0.43 to 6.46 ± 0.50, the crystallite size decreased from 524 ± 320 nm to 354 ± 173 nm, and the zeta potential decreased from -4.85 ± 2.87 mV to -8.77 ± 3.03 mV. The autocorrelation curves became smooth, the decay time decreased from 11.4 ± 3.2 ms to 4.3 ± 1.7 ms, and the PDI decreased from 0.67 ± 0.14 to 0.53 ± 0.19. These changes helped inhibit CaOx calculus formation.