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Despite extensive industrial use, the biocompatibility of nanocomposites has not been extensively explored. The present study was designed to report the effect of variable doses of a newly synthesized nanocomposite, Neodymium Zirconate Zinc Sulfide, on selective serum and complete blood count parameters and on the oxidative stress markers from the vital organs of albino mice. Albino mice (C57BL/6 strain, 5 weeks old) of both sexes were orally treated for 11 days, either with 10 mg (low dose) or 20 mg/mL saline/kg body weight (high dose) of Neodymium Zirconate Zinc Sulfide nanocomposite. A control group that was not treated with the nanocomposite but with saline solution was also maintained. Data analysis revealed that high-dose nanocomposite-treated male mice had significantly reduced hemoglobin concentration as compared to the control males. Female mice treated with both doses of nanocomposite had higher serum triglyceride levels than controls. High-dose-treated female mice had elevated serum cholesterol concentration compared to their saline-treated controls. Oxidative stress marker analysis from selected organs indicated that concentrations of malonaldehyde (MDA) in the kidney and liver, Superoxide dismutase (SOD) levels in the brain and catalase in the kidney of male mice treated with the nanocomposite were significantly higher than in the control group, whereas SOD in the heart, MDA in the heart and kidney and catalase levels in the kidney were significantly disrupted in female mice compared to their respective controls.

Brachyolmia is a skeletal disorder with an autosomal mode of inheritance (both dominant and recessive) in which the patients have a short height, scoliosis and a reduced trunk size.From the Muzaffargarh District in Pakistan, a consanguineous family with multiple Brachyolmia-affected subjects were enrolled in the present study. Basic epidemiological data and radiographs were collected for the subjects. Whole exome sequencing (WES) which was followed by Sanger sequencing was applied to report the geneticbasic of Brachyolmia.The WES identified a missense mutation (c.1037 GC, p. R346P) in exon 9 of theWe report a missense mutation (c.1037 GC, p. R346P) in the

Objective: Chronic periodontal disease (CP) is a multifactorial infectious and inflammatory disease that occurs due to the challenge between the immune response of the host and specific periodontal bacteria, and that can lead to tooth loss due to damage inflicted to the supporting tissue. The current study investigates the genotypes of the GSTM1 and GSTT1 genes, along with the allelic frequency of the single nucleotide polymorphism [SNP; rs1695] in the GSTP1 gene and correlates them individually or in various combinations with the incidence of CP. Methods: A total of 203 clinically confirmed CP patients and 201 control subjects were enrolled from Multan and Dera Ghazi Khan Districts in Pakistan from April to July 2022. Multiplex Polymerase Chain Reaction (PCR) and tetra-primer amplification refractory mutation system–polymerase chain reaction (T-ARMS–PCR) approaches were applied to determine the genotypes of the studied GSTs. The association of rs1695 in GSTP1 with CP was studied both individually and in various combinations with GSTM1 and T1. Results: The absence of GSTM1, the presence of GSTT1 and the presence of the mutant allele (G) at rs1695 in GSTP1 were found to be significantly associated with CP. Patients aged between 10 and 30 years were more affected by CP. Conclusion: Our results indicate that the genotypes of the analyzed GSTs affect the levels of protection from oxidative stress and may therefore influence the disease progression in CP.

Background: Brachyolmia is a skeletal disorder with an autosomal mode of inheritance (both dominant and recessive) in which the patients have a short height, scoliosis and a reduced trunk size. Methods: From the Muzaffargarh District in Pakistan, a consanguineous family with multiple Brachyolmia-affected subjects were enrolled in the present study. Basic epidemiological data and radiographs were collected for the subjects. Whole exome sequencing (WES) which was followed by Sanger sequencing was applied to report the geneticbasic of Brachyolmia. Results: The WES identified a missense mutation (c.1037 G > C, p. R346P) in exon 9 of the PAPSS2 gene that was confirmed by the Sanger sequencing in the enrolled subjects. The mutation followed a Mendalian pattern with an autosomal recessive inheritance mode. Multiple sequence alignment by Clustal Omega indicated that the PAPSS2 mutation-containing domain is highly conserved. The HEK293T whole-cell extract that was transfected with the Myc-tagged PCMV6-PAPSS2 of both the wild and mutant constructs were resolved by SDS-PAGE as well as by a Western blot, which confirmed that there are different PAPSS2 protein expression patterns when they were compared between the control and Brachyolmia patients. This difference between the normal and mutated protein was not evident when the three-dimensional computational structures were generated using homology modeling. Conclusion: We report a missense mutation (c.1037 G > C, p. R346P) in the PAPSS2 gene that caused Brachyolmia in a consanguineous Pakistani family.