Bladder smooth muscle cells on electrospun poly(ε-caprolactone)/poly(l-lactic acid) scaffold promote bladder regeneration in a canine model.

Engineering of urinary bladder has been the focus of numerous studies in recent decade. Novel biomaterials, innovative fabrication methods and various modification processes of scaffolds are the critical issues to find supportive matrices. Supportive characteristics of electrospun PCL/PLLA nano-scaffold for bladder augmentation in canine model and the role of bladder cells in regeneration process were appraised. Electrospun PCL/PLLA was fabricated by co-electrospinning of PCL and PLLA. Bladder cells were isolated and transduced with lentiviral particles encoding eGFP and JRed proteins. Electrospun PCL/PLLA was seeded with different bladder cells individually or in co-culture condition. Cell-free and cell-seeded electrospun PCL/PLLA scaffolds (10cm2) were surgically implanted in bladders of eight female dogs for three months. To evaluate bladder regeneration, the dogs were sacrificed and their bladders were examined macroscopically and microscopically for presence of tracking proteins, expression of cell-specific markers and histological attributes of regenerated tissues. All animals survived the experiment with no complication. In smooth muscle transplanted group complete regeneration and covering of scaffold were observed. Other groups revealed partial regeneration. A well-developed layer of urothelium was formed in all groups in regenerated parts. Smooth muscle transplanted group showed the most developed muscle layer. Regenerated tissue demonstrated typical expression of cell-specific markers. No expression of eGFP and JRed was observed. Electrospun PCL/PLLA scaffold with proper handling, suture retention, nano-sized surface features, maintenance of normal phenotype of cells and minimal adverse effects in body can be a supportive substrate for bladder wall regeneration when seeded with bladder smooth muscle cells.

Retinal manifestations of patients with human immunodeficiency virus, a multiethnics study in Malaysia.

AIM: To investigate the fundus findings of patients infected with human immunodeficiency virus (HIV) in correlation to Highly Active Antiretroviral Therapy (HAART) and CD4 count. METHODS: Two hundred and two patients of the three major races (Chinese, Malay and Indian) in Malaysia were recruited in this population-based cross-sectional study. This consisted of confirmed HIV sero-positive patients with HAART treatment (n=95) or without HAART therapy (n=107) from December 2007 to March 2008. They were further classified into the HIV infected group, AIDS related complex (ARC) group and AIDS group. Each group was then subdivided according to their CD4 count. Clinical fundus findings were recorded. RESULTS: Sixty six patients (32.7%) showed presence of fundus manifestation, majority of which was HIV microangiopathy (89%) and the rest being Cytomegalovirus (CMV) retinitis (11%). The most common fundus lesion was cotton wool spot (34%). There was a higher incidence of fundus manifestation in the non HAART group than the HAART group (P=0.04) and in patients with CD4 count less than 200 cells/ml in both groups (P=0.01). The HAART therapy had remarkably reduced the percentage of fundus manifestation by 20% but CD4 count remains the marker for fundus manifestations. There were no significant differences noted in the retinal manifestation among the different races. (ANOVA, P=0.25). CONCLUSION: The fundus manifestations were higher in patients with CD4<200 cells/ml and in the non HAART group. Hence the HAART therapy is capable of reducing the incidence of fundus manifestations, however the CD4 count determines the occurrence of fundus manifestations.

A regression model for correcting intraocular lens power after refractive surgery independent of preoperative data.

PURPOSE: To find a method of calculating intraocular lens (IOL) power that may be independent of preoperative data in eyes that have previously undergone myopic laser in situ keratomileusis (LASIK). METHODS: In 148 eyes of 75 patients, before and 6 months after LASIK, IOL power was calculated with SRK/T formula utilizing the spherical equivalent as the desired target refraction. Assuming that LASIK does not alter the crystalline lens refractive properties, IOL calculation error (CER) was estimated with this formula: CER = [pre-LASIK IOL power]/[post-LASIK IOL power]. Then the authors used postoperative biometry and Orbscan II corneal topography data in multiple regression models to find the best variables to predict the CER. Predicted amount of error which is calculated independent of preoperative data could be used to correct the post-LASIK calculated IOL: [corrected post-LASIK IOL power] = CER x [post-LASIK IOL power]. RESULTS: A regression model with these predictors was found: axial length in millimeters (L), radius of the anterior corneal surface best fitted sphere in millimeters divided by radius of the posterior corneal surface best fitted sphere in millimeters (AntBFS/PostBFS), corneal central 5 millimeters mean power in diopters divided by corneal central 3 millimeters mean power in diopters (mean 5 mm/mean 3 mm), the post-LASIK IOL power, and the post-LASIK simulated K reading. The model R square was 0.88. CONCLUSIONS: There is correlation between post-LASIK biometry values and IOL power correction factor. This study presents a new model for further investigation.

Myelomatosis with type III hyperlipoproteinemia: clinical and metabolic studies.

We investigated the metabolism of intermediate-density lipoproteins (IDL [1.006 to 1.019 g per milliliter]) and low-density lipoproteins (LDL [1.019 to 1.063 g per milliliter]) in two men with Type III hyperlipoproteinemia associated with myelomatosis. In vivo kinetic studies using radiolabeled autologous lipoproteins demonstrated a greatly reduced fractional catabolic rate of IDL, relative to control values (patients vs. normal, 0.006 and 0.025 per hour vs. 0.20 +/- 0.08 per hour [mean +/- S.E.M]) and a greatly prolonged IDL-to-LDL conversion time (45 and 17 hours vs. 5.4 +/- 1.6 hours). In studies in vitro, LDL from both patients failed to bind to the LDL receptor of normal blood lymphocytes, whereas LDL from subjects with familial Type III hyperlipoproteinemia bound normally to the receptor. In one patient immunoglobulin was shown to be associated with IDL and LDL. Thus, hyperlipoproteinemia reflected an impaired metabolism of IDL, probably secondary to the binding of immunoglobulin to the lipoproteins. A similar impairment of receptor-mediated LDL catabolism did not elevate the plasma LDL concentration because of the low IDL-to-LDL conversion rate.