When MLS is utilized in stop-and-go mode, similar point cloud data to that collected by TLS are obtained. In such scenarios, multi-sensor positioning and orientation sensors can be used to directly register several scans into a single point cloud, even without the use of separate calibration targets. In the continuous mode, MLS collects similar data to that of ALS. The area covered in the same time span is greater than with the stop-and-go mode, but the produced data set is sparser.The data collected by MLS systems is less precise in comparison with TLS because positioning errors propagate in the MLS point cloud. Another challenge of applying MLS is that the mobility of the platform in forest environments may be limited. Forest ground is characterized by rugged terrain and obstacles, such as rocks, dead wood and undergrowth.

The ground condition may be not easy or even suitable for vehicle movement. In a pilot study, the applied platform was an all-terrain vehicle (ATV) [27].Personal laser scanning (PLS) is an emerging concept [28]. The idea first appeared as a backpack-type MLS system, where th
DNA-modifying enzymes have been used for many years as drug targets in chemotherapeutic anticancer therapy, which exploits the high transcription and replication rates of cancer cells. As a consequence there has been a growing interest in using genetic and bio-enzymatic information related to these enzymes to predict drug response. An example of DNA-modifying enzymes that are targeted by chemoterapeutic agents is the human enzyme, topoisomerase I (hTopI).

hTopI is an essential nuclear enzyme which releases the topological stress resulting during processes such as transcription and replication, where the two DNA strands in the DNA double helix are locally unwound. Enzymatically, hTopI acts through the transient cleavage and subsequent religation of one strand of the DNA helix [1]. The enzyme is overexpressed in a wide range of cancers [2] and it is the sole cellular target of anticancer drugs from the camptothecin (CPT) family mainly used in systemic treatment of colon-, ovarian- and small cell lung cancer [3�C5]. Recently drugs of the CPT family have also been used for treatment of upper gastrointestinal-, cervical-, and pancreatic cancer [6�C9]. CPT exhibits its toxicity AV-951 by intercalating between the bases of the DNA in the hTopI-induced nicks and is stabilized through interactions to both the DNA and hTopI [10]. CPT poisons the cells mainly through the generation of double-stranded DNA breaks caused by S-phase specific collision of replication forks with the hTopI-DNA complexes [11]. However, CPT also damages non-dividing cells through collision of the complexes with DNA repair processes and transcription forks [12].