A comparative study of three different methods of shoot meristem excision for induction of embryogenic calli in coconut

A protocol was standardized to maximize yields of embryogenic calli from shoot meristem culture of coconut. Three different shoot meristem excision methods were tested viz., excision of shoot meristem aseptically from in vitro germinated embryo after 10-12 days, excision of shoot meristem from in vitro germinated embryo subjected to GA3 treatment for five days and excision of shoot meristem from fresh embryo. The primary calli induction after 30 days of culture incubation for the three treatments were 21%, 27%  and 79% respectively.  Further, the primary calli formed from the shoot meristem excised from fresh embryo gave rise to 56% of embryogenic calli. The calli obtained from the shoot meristem which were excised from in vitro germinated embryo formed less percentage of embryogenic calli because of the presence of cotyledonary tissues which inhibited the multiplication of meristematic tissues. In the case of shoot meristem extracted from GA3-treated embryos, the percentage of non-embryogenic calli was more compared to the shoot meristem excised from fresh embryo. It was observed that the addition of GA3 in the initial stages of culture inhibited the formation of embryogenic calli and favored direct shoot development. Currently, the shoot meristem excised from fresh embryo is being employed for scaling up the planting material production from released varieties of coconut

"A Free thenar flap – A case report"

We present a case report of a free thenar flap surgery done for a volar right hand middle finger, distal and middle phalanx degloving injury. A free thenar flap is a fasciocutaneous sensate flap supplied by a constant branch of the superficial radial artery and its variable nerve supply. It has a distinct advantage of low donor site morbidity, better cosmesis and texture of the flap. No immobilization is required postop. The donor site can be closed primiarily

U(n) Spectral Covers from Decomposition

We construct decomposed spectral covers for bundles on elliptically fibered Calabi-Yau threefolds whose structure groups are S(U(1) x U(4)), S(U(2) x U(3)) and S(U(1) x U(1) x U(3)) in heterotic string compactifications. The decomposition requires not only the tuning of the SU(5) spectral covers but also the tuning of the complex structure moduli of the Calabi-Yau threefolds. This configuration is translated to geometric data on F-theory side. We find that the monodromy locus for two-cycles in K3 fibered Calabi-Yau fourfolds in a stable degeneration limit is globally factorized with squared factors under the decomposition conditions. This signals that the monodromy group is reduced and there is a U(1) symmetry in a low energy effective field theory. To support that, we explicitly check the reduction of a monodromy group in an appreciable region of the moduli space for an $E_6$ gauge theory with (1+2) decomposition. This may provide a systematic way for constructing F-theory models with U(1) symmetries.Comment: 41 pages, 14 figures; v2: minor improvements and a reference adde

Elastin Peptides Signaling Relies on Neuraminidase-1-Dependent Lactosylceramide Generation

The sialidase activity of neuraminidase-1 (Neu-1) is responsible for ERK 1/2 pathway activation following binding of elastin peptide on the elastin receptor complex. In this work, we demonstrate that the receptor and lipid rafts colocalize at the plasma membrane. We also show that the disruption of these microdomains as well as their depletion in glycolipids blocks the receptor signaling. Following elastin peptide treatment, the cellular GM3 level decreases while lactosylceramide (LacCer) content increases consistently with a GM3/LacCer conversion. The use of lactose or Neu-1 siRNA blocks this process suggesting that the elastin receptor complex is responsible for this lipid conversion. Flow cytometry analysis confirms this elastin peptide-driven LacCer generation. Further, the use of a monoclonal anti-GM3 blocking antibody shows that GM3 is required for signaling. In conclusion, our data strongly suggest that Neu-1-dependent GM3/LacCer conversion is the key event leading to signaling by the elastin receptor complex. As a consequence, we propose that LacCer is an early messenger for this receptor

Cyclen-Based Cationic Lipids for Highly Efficient Gene Delivery towards Tumor Cells

Gene therapy has tremendous potential for both inherited and acquired diseases. However, delivery problems limited their clinical application, and new gene delivery vehicles with low cytotoxicity and high transfection efficiency are greatly required.In this report, we designed and synthesized three amphiphilic molecules (L1-L3) with the structures involving 1, 4, 7, 10-tetraazacyclododecane (cyclen), imidazolium and a hydrophobic dodecyl chain. Their interactions with plasmid DNA were studied via electrophoretic gel retardation assays, fluorescent quenching experiments, dynamic light scattering and transmission electron microscopy. The in vitro gene transfection assay and cytotoxicity assay were conducted in four cell lines.Results indicated that L1 and L3-formed liposomes could effectively bind to DNA to form well-shaped nanoparticles. Combining with neutral lipid DOPE, L3 was found with high efficiency in gene transfer in three tumor cell lines including A549, HepG2 and H460. The optimized gene transfection efficacy of L3 was nearly 5.5 times more efficient than that of the popular commercially available gene delivery agent Lipofectamine 2000™ in human lung carcinoma cells A549. In addition, since L1 and L3 had nearly no gene transfection performance in normal cells HEK293, these cationic lipids showed tumor cell-targeting property to a certain extent. No significant cytotoxicity was found for the lipoplexes formed by L1-L3, and their cytotoxicities were similar to or slightly lower than the lipoplexes prepared from Lipofectamine 2000™.Novel cyclen-based cationic lipids for effective in vitro gene transfection were founded, and these studies here may extend the application areas of macrocyclic polyamines, especially for cyclen

Genetic causes of hypercalciuric nephrolithiasis

Renal stone disease (nephrolithiasis) affects 3–5% of the population and is often associated with hypercalciuria. Hypercalciuric nephrolithiasis is a familial disorder in over 35% of patients and may occur as a monogenic disorder that is more likely to manifest itself in childhood. Studies of these monogenic forms of hypercalciuric nephrolithiasis in humans, e.g. Bartter syndrome, Dent’s disease, autosomal dominant hypocalcemic hypercalciuria (ADHH), hypercalciuric nephrolithiasis with hypophosphatemia, and familial hypomagnesemia with hypercalciuria have helped to identify a number of transporters, channels and receptors that are involved in regulating the renal tubular reabsorption of calcium. Thus, Bartter syndrome, an autosomal disease, is caused by mutations of the bumetanide-sensitive Na–K–Cl (NKCC2) co-transporter, the renal outer-medullary potassium (ROMK) channel, the voltage-gated chloride channel, CLC-Kb, the CLC-Kb beta subunit, barttin, or the calcium-sensing receptor (CaSR). Dent’s disease, an X-linked disorder characterized by low molecular weight proteinuria, hypercalciuria and nephrolithiasis, is due to mutations of the chloride/proton antiporter 5, CLC-5; ADHH is associated with activating mutations of the CaSR, which is a G-protein-coupled receptor; hypophosphatemic hypercalciuric nephrolithiasis associated with rickets is due to mutations in the type 2c sodium–phosphate co-transporter (NPT2c); and familial hypomagnesemia with hypercalciuria is due to mutations of paracellin-1, which is a member of the claudin family of membrane proteins that form the intercellular tight junction barrier in a variety of epithelia. These studies have provided valuable insights into the renal tubular pathways that regulate calcium reabsorption and predispose to hypercalciuria and nephrolithiasis

N-Acetylcysteine and Allopurinol Synergistically Enhance Cardiac Adiponectin Content and Reduce Myocardial Reperfusion Injury in Diabetic Rats

Background: Hyperglycemia-induced oxidative stress plays a central role in the development of diabetic myocardial complications. Adiponectin (APN), an adipokine with anti-diabetic and anti-ischemic effects, is decreased in diabetes. It is unknown whether or not antioxidant treatment with N-acetylcysteine (NAC) and/or allopurinol (ALP) can attenuate APN deficiency and myocardial ischemia reperfusion (MI/R) injury in the early stage of diabetes. Methodology/Principal Findings: Control or streptozotocin (STZ)-induced diabetic rats were either untreated (C, D) or treated with NAC (1.5 g/kg/day) or ALP (100 mg/kg/day) or their combination for four weeks starting one week after STZ injection. Plasma and cardiac biochemical parameters were measured after the completion of treatment, and the rats were subjected to MI/R by occluding the left anterior descending artery for 30 min followed by 2 h reperfusion. Plasma and cardiac APN levels were decreased in diabetic rats accompanied by decreased cardiac APN receptor 2 (AdipoR2), reduced phosphorylation of Akt, signal transducer and activator of transcription 3 (STAT3) and endothelial nitric oxide synthase (eNOS) but increased IL-6 and TNF-α (all P<0.05 vs. C). NAC but not ALP increased cardiac APN concentrations and AdipoR2 expression in diabetic rats. ALP enhanced the effects of NAC in restoring cardiac AdipoR2 and phosphorylation of Akt, STAT3 and eNOS in diabetic rats. Further, NAC and ALP, respectively, decreased postischemic myocardial infarct size and creatinine kinase-MB (CK-MB) release in diabetic rats, while their combination conferred synergistic protective effects. In addition, exposure of cultured rat cardiomyocytes to high glucose resulted in significant reduction of cardiomyocyte APN concentration and AdipoR2 protein expression. APN supplementation restored high glucose induced AdipoR2 reduction in cardiomyocytes. Conclusions/Significance: NAC and ALP synergistically restore myocardial APN and AdipoR2 mediated eNOS activation. This may represent the mechanism through which NAC and ALP combination greatly reduces MI/R injury in early diabetic rats. © 2011 Wang et al.published_or_final_versio

Prolotherapy for early osteoarthritis knee

Introduction: Osteoarthritis is most prevalent arthritis in older patients. Present study is to evaluate efficacy of dextrose prolotherapy for treatment of early knee osteoarthritis. Material &amp; Method: This study was done at Bundelkhand Medical College, Sagar. In our study we studied 38 patients of more than 55 years of age. For treatment of Knee OA, 3 sitting of prolotherapy were given one month apart and patient followed up for 1 year. Results: 76% patients showed improvement on second follow-up. On third follow up 89% showed improvement. On further follow up at 6 months 81% of patients were symptomatically improved. These patients remained symptomatically better even at the conclusion of study. Discussion: Definitive mechanism of action of prolotherapy is unknown but probable mechanism is, hypertonic dextrose induced growth factor release and connective tissue healing thereafter. Conclusion: Dextrose prolotherapy injection is safe, reliable and long lasting treatment modality for early osteoarthriti