Fluvoxamine Ameliorates the Damage to the Neuro-Behavioral Status of Rats Caused by the Administration of Valproic Acid by Preventing Cognitive Memory Deficits and Decreased Hippocampal Cellular Proliferation.

Fluvoxamine is a major antidepressant of the selective serotonin-reuptake inhibitor class, previously studied as a drug that improves cognitive memory by enhancing hippocampal cell division and proliferation. Valproic acid (VPA) is a commonly used antiepileptic drug and mood stabilizer that has negative effects on cognitive memory as it inhibits cellular division and proliferation in the hippocampus. This study assessed the protective effects of fluvoxamine treatment versus the memory impairment, decreased hippocampal cellular proliferation, and weight loss produced by VPA treatment. The cognitive memory of 40 male Sprague-Dawley rats was assessed by the novel object location (NOL) test. Immunostaining by Ki67 and glutathione peroxidase 1 (GPX-1) was performed to quantify the number of dividing cells in the subgranular zone (SGZ) of the dentate gyrus and to assess the antioxidant activity of different treatments, respectively. Results showed that the VPA group had fewer Ki67-positive cells than the control group (p < 0.001), indicating reduced hippocampal proliferation. In contrast, the VPA and fluvoxamine combination group showed increased proliferation (p < 0.001) compared to VPA alone. Notably, fluvoxamine treatment significantly differed in cell counts compared to other groups (p < 0.001). Fluvoxamine also attenuated the weight loss caused by VPA (p < 0.0001). Our data suggested that fluvoxamine therapy attenuated the VPA-induced decrease in SGZ cellular proliferation, memory, and weight in rats.

Association of Parental Consanguinity With Papillary Thyroid Carcinoma: A Case-Control Study.

CONTEXT: Papillary thyroid carcinoma (PTC) is the most common type of nonmedullary thyroid carcinoma. Uncommonly, PTC is associated with multiple genetic alterations and chromosomal abnormalities and displays familial patterns of inheritance. Parental consanguinity increases susceptibility to many genetic disorders. OBJECTIVE: This work aimed to investigate the association of parental consanguinity with PTC. METHODS: This case-control study of PTC patients compared with healthy controls took place in a tertiary referral hospital. We recruited 200 PTC patients who were managed at the endocrinology outpatient clinics of the Jordan University Hospital, and we recruited 515 healthy controls from a nonclinical setting. We interviewed all participants and collected sociodemographic data. We reviewed the family pedigrees of each participant four generations back and excluded any participant who was related. We established whether the parents of each participant were first cousins, first cousins once removed, second cousins, or unrelated. We then used binary logistic regression to assess the association of parental consanguinity with PTC adjusted for age, sex, smoking status, body mass index, and parental education. RESULTS: We recruited 715 participants. The numbers of PTC patients and healthy controls were 200 (28.0%) and 515 (72.0%), respectively. The rate of parental consanguinity was 25.5% in PTC patients and 12.2% in healthy controls. Parental consanguinity was significantly associated with PTC (adjusted odds ratio, 2.60; 95% CI, 1.63-4.17; P < .001). CONCLUSION: Parental consanguinity is a risk factor for PTC. Our findings should be considered during familial risk assessment and genetic counseling, especially in populations with high rates of consanguinity.