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Microsoft SQL Server Optimizing Queries

We have 2 databases, one called groups and the other called message. A user has a table called messages for the messages to be stored in (this is the default). However the user also has a table called groups for the groups the user is part of (this is a users only table, and it will never have any rows added to it).
In each of the tables are a groupID field and a messageID field.
The user selects a group by clicking a checkbox and this also fires off an insert into the groups table.
Now, the table message already has a unique index on ID fields (name, email), however the default index on the table is on ID field which is not unique and still a index. So when a user posts his post, the database runs the query and it says “please insert with a unique ID, and a unique index exists on ID, so it will automatically ignore the primary. If you leave it blank, then the users post is sent to the MySQL instead.”
My question is, do I need to set a primary key on the table, or will this automatically create one for me?
I’m not really sure what to expect if I tell the database it’s primary key is set on the ID field. It’s also not showing any tables when I look for key_column_usage.
Thanks

A:

You need to create unique index on columns that are unique.
CREATE UNIQUE INDEX id_table_name ON table_name (columns)

You can get more information about it from this link
If this does not work, please share the error message.

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If a function can be defined in several ways as a limit, is it continuous?

If a function $f : \mathbb{R}^m \to \mathbb{R}^n$ is defined by
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for $A_t$ a symm

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The present inventors have also carried out a comparative study of the intracellular and the secreted IGF1R in melanoma cells, for determining whether the expression and/or the phosphorylation status of the two receptors might be different.
It has been observed that melanoma cells constitutively secrete IGF1, while it is unclear whether in this pathological condition the secretion of IGF2 is also present or not. In any case, the secretion of IGF2 is reduced by IGF1-neutralizing antibodies.
In order to block the autocrine activity of IGF1 on IGF1R, in vitro experiments have been carried out wherein human melanoma cells have been treated with IGF1-neutralizing antibodies. The results obtained show that, upon treatment of the cells with the anti-IGF1 antibodies, the phosphorylation of the IGF1R is inhibited.
In order to block the autocrine activity of IGF1 on WM-115 cells, tyrphostins have been employed. The inhibition of the IGF1R with a small molecule inhibitor affects also the phosphorylation of the IGF1R.
Finally, in order to inhibit the autocrine activity of IGF1 on WM-115 cells, mAb have been employed. The results obtained show that, upon treatment of the cells with the anti-IGF1 antibodies, the phosphorylation of the IGF1R is inhibited.
IGF1R is also expressed in normal cells such as, for example, in fibroblast growth factor (FGF) responsive cells. In fact
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