Depression before and during-COVID-19 by Gender in the Korean Population.

This study explored the association between Coronavirus disease (COVID-19) and depression by comparing Patient Health Questionnaire-9 (PHQ-9) results pre-pandemic (2019) and after the start of the pandemic (2020). Data of 444,051 participants (200,206 male (45.1%); 243,845 female (54.9%)) were obtained from the Korean Community Health Survey conducted from 2019 to 2020. The independent variable of interest in this study was the year, divided into binary categories, 2019 and 2020. The dependent variable was depression, measured by the PHQ-9 scale. This dependent variable was also binary, dividing those who are considered depressed or not by a cut-off score of 10. A logistic regression model was employed to examine the association. Our results reveal that compared to participants in 2019, patients from the study sample of 2020 were marginally more likely to be depressed, especially female patients (male OR: 1.092, 95% CI [0.998 to 1.195], female OR: 1.066, 95% CI [1.002 to 1.134]). Moreover, using the participants from the year 2019 as a reference group, those who appeared anxious in response to the COVID-19-related questions in the survey showed more tendency to have a PHQ-9 score of 10 or more. Compared to participants from the 2019 group, those from 2020 more likely to be depressed were those with no-one to contact in case of emergency due to COVID-19 (male OR: 1.45, 95% CI [1.26 to 1.66], female OR: 1.46, 95% CI [1.33 to 1.60]), and individuals with concerns regarding economic loss (male OR: 1.18, 95% CI [1.07 to 1.30], female OR: 1.11, 95% CI [1.04 to 1.18]) and infection of a vulnerable family member at home due to COVID-19 (male OR: 1.16, 95% CI [1.05 to 1.28], female OR: 1.09, 95% CI [ 1.02 to 1.16]).

G769A variation of inhibin alpha-gene in korean women with premature ovarian failure.

Premature ovarian failure (POF) is menopause before the age of 40 years. The frequency of POF is about 1% of all women. Recently inhibin alpha gene (INHalpha) has been indicated as candidate in POF pathogenesis. Inhibin, a glycoprotein, is a gonadal hormone, which can inhibit the synthesis and secretion of pituitary follicle-stimulating hormone (FSH), which has an important role in the recruitment and development of ovarian follicles during the folliculogenesis. G769A variation of INHalpha, alanine, is highly conserved across species, and has an important role of its receptor binding. We screened a G769A transition in the INHalpha from the total population of the patients of 84 women with POF and 100 normal fertile women. We found no variation between the normal subjects and the POF patients. G769A variation of INHalpha is rare in Korea women with POF.

Molecular and cytogenetic characterization of two azoospermic patients with X-autosome translocation.

PURPOSE: To report two azoospermic patients with reciprocal X-autosome translocations. METHODS: Cytogenetic analysis utilizing GTG-banding and Yq microdeletions shown by polymerase chain reaction (PCR) with 12 sequence-tagged site (STS) markers for Y chromosome microdeletions. RESULTS: Cytogenetic analysis showed one man with 46,Y,t(X;19)(q22;q13.3) and the other with 46,Y,t(X;8)(p22;q11). Neither had any Yq microdeletions shown. The patient with 46,Y, t(X;8)(p22;q11) showed a slightly lower than normal testosterone level. By NCBI-Blast search, we found four testis-specific genes, t-complex-associated-testis-expressed 1-like (TCTE1L), Ferritin, heavy polypeptide-like 17 (FTHL17), Testis expressed sequence 13A (TEX13A), and Testis expressed sequence 13B (TEX13B) located near breakpoints on X chromosome. FTHL17, TEX13A, and TEX13B are spermatogonially-expressed, germ-cell-specific genes. CONCLUSION: This is the first clinical report of azoospermia with reciprocal X-autosome translocations on Xp22 and q22. These translocations on Xp22 and q22 may be direct genetic risk factors for azoospermia.

Expression of the mitochondrial ATPase6 gene and Tfam in Down syndrome.

We investigated the expression of the mitochondrial ATPase6 gene whose product is active in oxidative phosphorylation (OXPHOS), and compared it to the expression of Tfam, an important regulator of the transcription and replication of mtDNA. Our aim was to examine a possible relation between mitochondrial gene expression and Down syndrome. The expression of ATPase6 and Tfam was analyzed by RT-PCR amplification of the mRNA in cultured amniocytes from Down syndrome and normal fetuses. The band intensities obtained were normalized against those of HPRT. The Down syndrome fetuses were found to have lower ATPase6 and Tfam expression than the normal fetuses. This finding suggests that mitochondrial dysfunction resulting from decreased ATPase6 and Tfam expression during meiotic oocyte maturation of oocytes might affect ATP generation and cause the nondisjunctional error. Hence this study suggests that mitochondrial dysfunction may be associated with the developmental mechanism of Down syndrome.