U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 4151 - 4160 of 4377 results

Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.
Nickel(II) chloride (NiCl2), a water soluble salt of Nickel, is a toxic and carcinogenic environmental and occupational pollutant, which has been shown to be carcinogenic to the lungs and nasal passages, in cases of long-term inhalation exposure. It was approved that NiCl2 was a potential genotoxicity caused indirect DNA damage by the production of ROS. In addition was conducted studies to evaluate the precise mechanism of Ni toxicology. And it was shown, thet NiCl2 induced and caused cell cycle G2/M phase arrest via p53-dependent pathway and generated inflammatory response by NF-κB pathway activation.

Showing 4151 - 4160 of 4377 results