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NSTableView editing doesn’t work on second NSTableView

I have a NSTableView with rows that I create programatically. Each NSTableView has a context menu that allows to delete the row. If I open this context menu in the first NSTableView, it works fine. If I open it in the second NSTableView, it just doesn’t work.
Any clue how to solve this problem?
This is my action code, I think it’s not enough, right?
– (void)tableViewSelectionDidChange:(NSNotification *)notification
NSInteger oldSelectedRow = [self.tableView selectedRow];

[self.parentController.childsTableView beginUpdates];

[self.tableView setSelectionIndex:oldSelectedRow];

[self.parentController.childsTableView endUpdates];


Here’s an image that shows what I’m talking about:


You don’t need the begin/end updates, just update the display property to reflect what is in the row.
You also don’t need a notification for selection changes. You can update the row’s display property directly by setting it to nil. The controller will then update the table view as part of the regular refresh.
In your selectionDidChange: method, simply set the row’s display property to the new index:
– (void)tableViewSelectionDidChange:(NSNotification *)notification
NSInteger oldSelectedRow = [self.tableView selectedRow];
[self.tableView setSelectionIndex:oldSelectedRow];

NSIndexSet *indexSet = [NSIndexSet indexSetWithIndex:oldSe


is there a setting i can mess with in to make this stop? thank you so much


Does this actually happen after the first time the program has been started, or every time you start your computer? I would definitely give it a try without closing, and see if it continues.

N-acetyltransferase-2 (NAT2) polymorphism analysis in a Senegalese population.
Genetic polymorphisms of the human N-acetyltransferase 2 gene have been linked to the risk of human cancers. We determined the frequency of NAT2 polymorphisms and the acetylation status of benzidine and aromatic amine by testing urine samples from 400 healthy volunteers in Senegal. Two NAT2 genotypes (slow and rapid acetylator phenotypes) were observed in our study population, with a frequency of 37% and 63%, respectively. A strong association between a NAT2 polymorphism at the base 6110G>A (Arg213His) and acetylation phenotype was found in this Senegalese population. The NAT2 genotype distribution was: GG 46%, GA 36%, AA 18%. Among acetylators, the frequency of 13.6% of the AA genotype suggests an epidemiological role for this variant in the development of bladder cancer. The NAT2 genotype distribution was also studied in two unselected patients with bladder cancer and in 400 healthy subjects. NAT2 genotyping showed a lower frequency of the fast acetylator genotype (GA+AA), previously associated with bladder cancer, in the two patient populations. These data suggest a protective role of the slow acetylator genotype (GG) in the bladder carcinogenesis.$ and $e_y$ in $N$ units per time-step, and the acceleration of the $j$th particle in the $k$th arena $a_k^{(j)}$ in $N$ units per time-step. Each particle’s $x$ and $y$-displacements are therefore sampled from a Gaussian distribution with mean $0$ and variance $2s_x$ and $2s_y$, respectively. Finally, the vertical and horizontal linear accelerations are sampled from a Gaussian distribution with mean $0$ and variance $2a_k$ respectively.

Increasing and Decreasing Numbers of Arena Walls

Figure \[fig:rates\] illustrates the behavior of the system as the number



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