Characterization of various types of cell death (e.g., apoptosis, necrosis, autophagy) currently requires the use of indirect markers1,2 and a combination of different assays (e.g., morphological, immunohistochemical, biochemical, and molecular methods); however, it is not possible to directly investigate the intracellular events leading to cell death.
Even though purely qualitative histopathological appraisals have shown their worth as phenotypic anchoring of toxicological research that employ various biochemical and molecular methods, retrieving statistically compliant figures from histopathological data is indisputably recognized as a more robust approach.
Nineteen Lactobacillus spp. were isolated and subsequently identified based on biochemical and molecular methods.
These powerful biochemical and molecular methods have revolutionized biological research.
All isolates were previously identified as GBS using both biochemical and molecular methods [ 14].
Among 125 patients in this study, 25 samples were diagnosed as nontuberculosis mycobacteria by biochemical and molecular methods.
All initial isolates and those that appeared phenotypically different from previously received isolates from individual patients were evaluated for genomovar and species identity by a polyphasic scheme involving both biochemical analyses and molecular methods (recA PCR and 16s rRNA RFLP) (Table 2).
We have used a combination of virological, biochemical, and molecular modeling methods to derive the mechanism by which this mutation confers resistance to TFV.
Similarly, different types of foci have been identified in the FSU (including the foci in Russia, Kazakhstan, Georgia, Armenia, Azerbaijan, Turkmenistan, Uzbekistan, Tadjikistan and Kirghizia ) and Mongolia, and Russian scientists have classified isolates from these foci into different subspecies by various biochemical and molecular biological methods [3].
By using a series of biochemical and molecular biology methods with specific inhibitors for MAP kinases, AP1, NF-κB, dominant-negative constructs for IκBα, and islets from Fos-/ mice, we demonstrated that MCP-1 induced amylin expression in murine pancreatic β cells through JNK/ERK1/2-AP1 and NF-κB pathways.
We propose a discovery-based strategy to find global flux differences in this population versus a control, in order to find targets for more detailed follow-up using classical biochemical and molecular biology methods.
