Introductory Phrases

How to introduce your protocols

Here is a poor introduction from a Materials and Methods section:

‘3-hydroxydecanoic acid (3HD) synthesized by various recombinant E. coli strains harboring tesB.  In order
to evaluate the functionality of thioesterase II in E. coli, pLZZH01 was digested with Cla I and Hinc II.  The
918-bp tesB gene fragment….’

This is misleading, because the digestion does not tell us anything about the function of thioesterase II.  In
reality, it is a procedure that is used to prepare the DNA.  We should rewrite the opening sentences:

‘3-hydroxydecanoic acid (3HD) synthesized by various recombinant E. coli strains harboring tesB.  In order
to evaluate the function of thioesterase II in E. coli, we determined the levels of 3HB produced by various
recombinant E. coli strains harboring tesB.  pLZZH01 was digested with Cla I and Hinc II.  The 918-bp tesB
gene fragment …’


Introduce your results

Sometimes, give a little background information, particularly early in the results section:

We have typically observed that when CGC cultures were treated with 100 mM kainate in NFL at room
temperature for 30 min, 50–70% of the cells were killed (40).  However, in some cases little to no cell death
was observed.  We therefore varied the treatment conditions to identify those associated with more
reproducible levels of cell death.

Or, use logic:

Neurons do not depolarize as efficiently when sodium ions are eliminated from the medium and replaced with
NMDG, because the latter cannot pass through cation channels. We therefore hypothesized that calcium entry
through voltage-gated calcium channels protected CGC from kainate neurotoxicity. To test this possibility, we
determined cell viability following kainate treatment in the presence of cadmium, a general voltage-gated
calcium channel blocker.

Or, use logical connectors.  If the experiments that generated a data set depend on the previous set of results,
you may just continue the thought process:

We then considered possible mechanisms by which calcium could protect neurons from kainate neurotoxicity.
Currents through AMPA- and kainate-type glutamate receptors are potentiated by phosphorylation of Ser/Thr
residues of receptor subunits. Elevated intracellular calcium levels could activate a kinase or phosphatase such
that the phosphorylation of the receptor and subsequent activation of current was mitigated.  However,
kainate neurotoxicity in NL was not observed when cells were treated with the type 1 and 2A protein
phosphatase inhibitor okadaic acid (1 mM).
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Many journals require
subheadings for the
results section.  This
facilitates transitions
between different
groups of results.
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