Abstract The successful transfer of R-cytoplasm (Ogura)-induced cytoplasmic male sterility has aroused great interest in the development of hybrids in cabbage. An experiment was conducted from 2018 to 2020 to study the per se performance and estimate heterosis in cabbage (Brassica oleracea L. var. capitata L.), This crop is highly cross-pollinated; thus, exploitation of heterosis is an additional advantage. The experimental material consisted of an F1 population of 18 crosses, resulting from three lines (CMS) crossed with six testers in a Line × Tester design, plus a standard check (Pusa Cabbage Hybrid-1). The per se performance and estimates of heterosis of the cross combinations L1 × T2, L2 × T2, L2 × T5, L3 × T2 and L3 × T5 were high for various horticultural parameters. Hence, after multilocation testing, these parents and crosses can be released to substitute existing cabbage varieties/hybrids.

Abstract Background: Excitotoxicity-induced in vivo injury models are vital to reflect the pathophysiological features of acute spinal cord injury (SCI) in humans. The duration and concentration of chemical treatment controls the extent of neuronal cell damage. The extent of injury is explained in relation to locomotor and behavioural activity. Several SCI in vivo methods have been reported and studied extensively, particularly contusion, compression, and transection models. These models depict similar pathophysiology to that in humans but are extremely expensive (contusion) and require expertise (compression). Chemical excitotoxicity-induced SCI models are simple and easy while producing similar clinical manifestations. The kainic acid (KA) excitotoxicity model is a convenient, low-cost, and highly reproducible animal model of SCI in the laboratory. The basic impactor approximately cost between 10,000 and 20,000 USD, while the kainic acid only cost between 300 and 500 USD, which is quite cheap as compared to traditional SCI method. Methods: In this study, 0.05 mM KA was administered at dose of 10 μL/100 g body weight, at a rate of 10 μL/min, to induce spinal injury by intra-spinal injection between the T12 and T13 thoracic vertebrae. In this protocol, detailed description of a dorsal laminectomy was explained to expose the spinal cord, following intra-spinal kainic acid administration at desired location. The dose, rate and technique to administer kainic acid were explained extensively to reflect a successful paraplegia and spinal cord injury in rats. The postoperative care and complication post injury of paraplegic laboratory animals were also explained, and necessary requirements to overcome these complications were also described to help researcher. Results: This injury model produced impaired hind limb locomotor function with mild seizure. Hence this protocol will help researchers to induce spinal cord injury in laboratories at extremely low cost and also will help to determine the necessary supplies, methods for producing SCI in rats and treatments designed to mitigate post-injury impairment. Conclusions: Kainic acid intra-spinal injection at the concentration of 0.05 mM, and rate 10 μL/min, is an effective method create spinal injury in rats, however more potent concentrations of kainic acid need to be studied in order to create severe spinal injuries.