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Background: Postpartum Depression (PPD) is a serious depression that develops in the first year, with unknown explained reasons. Many studies evaluated the impact of Vitamin D (VD) levels on depression during pregnancy and postnatal. This narrative review aims to review any association between serum VD levels during pregnancy and the development of PPD. Materials and Methods: PPD data from published trials and research articles (period from 2012 to 2022) were assessed through PubMed, Scopus, Science Direct, and Google Scholar using the following terms: Depression, pregnancy, 25-hydroxyvitamin D (25OH VD), vitamin D deficiency (VDD) and postpartum (PP). Articles were selected manually and with careful tracking to avoid duplication. Articles that investigated any association between VD levels during pregnancy and PPD in the time frame were included in the study, while articles investigating VD levels of PP without depression were excluded. Results: In this narrative review, five out of seven studies showed an association between PPD and VDD during pregnancy. Danish National Birth Cohort (DNBC), Edinburgh Postnatal Depression Scale (EPDS) and Center for Epidemiologic Studies Depression Scale (CES-D) enrolled among different studies from 3 days to 1 year PP to assess PPD. Conclusions: Pregnant women with VDD are significantly associated with PPD. Longitudinal follow-up studies are needed to evaluate the association between VDD with PPD. Screening VD levels among pre-postnatal mothers may be essential for awareness programs that can be implemented to promote remission of postnatal depression.

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Objectives: The association between vitamin D receptor (VDR) polymorphisms and metabolic syndrome (MS) remains debatable. The current study aimed to determine the correlation of VDR gene polymorphisms with MS among Jordanian women. Methods: This case-control study enrolled 100 women with MS and 100 age-matched women as control at Al-Hikma Modern Hospital in Jordan between January 2019 and January 2020. The levels of glycated hemoglobin, fasting glucose, triglyceride, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and 25-hydroxy vitamin D (25(OH)D) were determined from serum samples of all participants. DNA was extracted from whole blood samples, and VDR gene polymorphisms Apa1, Taq1, Bsm1, and Fok1 were analyzed by polymerase chain reaction and restriction fragment length polymorphism. Results: There was a significant difference between MS patients and control in terms of body mass index (34.3±3.1 vs. 28.1±2.5), glycated hemoglobin (5.9±1.1 vs. 4.6±1.2), fasting blood glucose (6.4±1.6 vs. 5.2±1.4), and total cholesterol (6.5±1.2 vs. 5.3±1.8). The results also demonstrated a statistical difference in the number of MS patients and control with 25(OH)D deficiency (69.0 vs. 33.0), 25(OH)D insufficiency (25.0 vs. 42.0), and 25(OH)D sufficiency (6.0 vs. 25.0) (p < 0.001). MS was significantly associated with VDR polymorphisms among Apa1 and Fok1 genes. The genotype distribution for CC (47.0% vs. 53.0%; p = 0.002) and CA (37.0% vs. 45.0%; p = 0.001) genotypes among Apa1 VDR polymorphism, as well as among TT genotype (38.0% vs. 20.0%; p = 0.025) among Fok1 VDR gene polymorphism significantly differed between MS patients and healthy individuals. However, no associations were detected among Taq1 and Bsm1 VDR genotypes. Conclusions: VDR gene polymorphism of Apa1 and Fok1 variants may increase the risk of metabolic syndrome among Jordanian women.

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Background and aims: Diabetic foot is one of the most severe complications in patients with diabetes mellitus and has been linked to 25-OH-vitamin D status. This study aims to determine the prevalence of 25-OH-vitamin D deficiency and its association with diabetic foot. Methods: Patients with type 2 diabetes mellitus were enrolled in this study. The patients were divided into the diabetic foot group (n = 95) and the non-diabetic foot group (n = 388). Weight, height, and waist circumference were measured. The 25-OH-vitamin D and the other biochemical tests were extracted from the electronic medical records. The difference in clinical parameters between the diabetic foot group and the non-diabetic foot group was analyzed, and the risk factors of the diabetic foot group were analyzed using logistic regression. Results: The prevalence of 25-OH-vitamin D deficiency was 44.6%, accounting for 57.9% of all the diabetic foot group patients and only 41.0% of the non-diabetic foot group patients. The mean serum 25-OH-vitamin D level was significantly different between the diabetic foot group and the non-diabetic foot group (19.8 ± 9.5 vs 24.1 ± 11.8; P = .011). Serum 25-OH-vitamin D and B12 were found to have a significant positive correlation (r = 0.410, P = <.01). The 25-OH-vitamin D level and body mass index were independently associated with diabetic foot (P = .043, OR = 1.21; P = .009, OR = 1.47), respectively. Conclusions: The 25-OH-vitamin D deficiency was higher in the diabetic foot group. More research is needed to understand the role of 25-OH-vitamin D in the development of diabetic foot.

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Restoring everyday civil life from the devastating pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can be only by the development of an efficient vaccine. As of April 12, 2022, 497,960,492 confirmed cases of COVID-19 were reported, including 6,181,850 lives having been lost worldwide and completely paralyzing the d global economy. Detection of a novel coronavirus SARS-CoV-2 in Wuhan, in December 2019, and the genetic sequence of SARS-CoV-2 that was published on January 11, 2020, leads to a global race, to prepare for a preventive vaccine. No single institution can develop a vaccine individually because there are many stages for developing and producing a successful vaccine. Since this virus threatens the health, the economy, and society the demand for a fast-track vaccine is understandable. This article tries to give an overview of vaccine 'candidates' development and clinical trials, and it mentions some challenges of using these vaccines for managing SARS-CoV-2.

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BACKGROUND: Polycystic ovary syndrome (PCOS) is a common heterogeneous disorder characterized by chronic anovulation, infertility, polycystic ovaries, and hyperandrogenic signs. OBJECTIVE: The aim of this study was to determine the association of luteinizing hormone/chorionic gonadotropin hormone receptor LHCGR polymorphism (rs2293275) with oligomenorrhea, amenorrhea, hirsutism, acne, infertility, LH, LH/FSH ratio, and body mass index (BMI) among PCOS females. METHODS: This genetic case-control study recruited 55 PCOS and 55 control females, diagnosed based on the Rotterdam criteria. LH and FSH were measured by the Roche cobas c 502 automated analyzer. Genotypic analysis was carried out using the polymerase chain reaction-restriction fragment length polymorphism and restriction endonuclease digestion. RESULTS: BMI was higher for PCOS patients (28.5 ± 6.59) compared to controls (25.1 ± 5.77), and ovulatory dysfunction was seen among 90% of PCOS females. Oligomenorrhea was common in PCOS (73%), and hirsutism and acne were detected in PCOS (80% and 40%; respectively). LH ≥10 were recoded among 51%, while LH/FSH ≥1.5 was recorded among 33% PCOS females. There is a statistical difference between rs2293275 polymorphism in the AG genotype between PCOS patients and controls. PCOS patients have a significantly higher mean LH level compared to controls (8.36 ± 4.86 and 5.67 ± 2.51, respectively) and showed higher LH/FSH value (1.46 ± 0.81) compared to (0.87 ± 0.30) controls. GG and AG genotypes of LHCGR showed statistically significant higher LH (8.22 ± 4.11; 9.02 ± 3.87) and LH/FSH values (1.57 ± 0.56; 1.64 ± 0.89) compared to controls. CONCLUSION: LHCGR (rs2293275) GA and GG genetic variants could modulate the hormonal levels of PCOS LH levels and the LH/FSH ratio and associated with hirsutism, oligomenorrhea, BMI, and LH/FSH ratio as risk factors.

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Context: The whole universe is facing a coronavirus catastrophe, and prompt treatment for the health crisis is primarily significant. The primary way to improve health conditions in this battle is to boost our immunity and alter our diet patterns. A common bulb veggie used to flavor cuisine is garlic. Compounds in the plant that are physiologically active are present, contributing to its pharmacological characteristics. Among several food items with nutritional value and immunity improvement, garlic stood predominant and more resourceful natural antibiotic with a broad spectrum of antiviral potency against diverse viruses. However, earlier reports have depicted its efficacy in the treatment of a variety of viral illnesses. Nonetheless, there is no information on its antiviral activities and underlying molecular mechanisms. Objectives: The bioactive compounds in garlic include organosulfur (allicin and alliin) and flavonoid (quercetin) compounds. These compounds have shown immunomodulatory effects and inhibited attachment of coronavirus to the angiotensin-converting enzyme 2 (ACE2) receptor and the Mpro of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Further, we have discussed the contradictory impacts of garlic used as a preventive measure against the novel coronavirus. Method: The GC/MS analysis revealed 18 active chemicals, including 17 organosulfur compounds in garlic. Using the molecular docking technique, we report for the first time the inhibitory effect of the under-consideration compounds on the host receptor ACE2 protein in the human body, providing a crucial foundation for understanding individual compound coronavirus resistance on the main protease protein of SARS-CoV-2. Allyl disulfide and allyl trisulfide, which make up the majority of the compounds in garlic, exhibit the most potent activity. Results: Conventional medicine has proven its efficiency from ancient times. Currently, our article's prime spotlight was on the activity of Allium sativum on the relegation of viral load and further highlighted artificial intelligence technology to study the attachment of the allicin compound to the SARS-CoV-2 receptor to reveal its efficacy. Conclusions: The COVID-19 pandemic has triggered interest among researchers to conduct future research on molecular docking with clinical trials before releasing salutary remedies against the deadly malady.

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Many cancers might be influenced by obesity, including breast cancer, the leading cause of cancer death among women. Obesity is a complex state associated with multiple physiological and molecular changes capable of modulating the behavior of breast tumor cells and the surrounding microenvironment. This review discussed the inverse association between obesity and breast cancer among premenopausal breast cancer females and the positive association among postmenopausal. Four mechanisms may link obesity and breast cancer including leptin and leptin receptor expression, adipose chronic inflammation, sex hormone alternation, and insulin and insulinlike growth factor 1 (IGF-1) signaling. Leptin has been involved in breast cancer initiation, development, and progression through signaling transduction network. Leptin functions are strengthened through cross talk with multiple oncogenes, cytokines, and growth factors. Adipose chronic inflammation promotes cancer growth and angiogenesis and modifies the immune responses. A pro-inflammatory microenvironment at tumor site promotes cytokines and pro-inflammatory mediators adjacent to the tumor. Leptin stimulates pro-inflammatory cytokines and promotes T-helper 1 responses. Obesity is common of chronic inflammation. In obese patients, white adipose tissue (WAT) will promote pro-inflammatory mediators that will encourage tumor growth and WAT inflammation. Sex hormone alternation of estrogens is associated with increased risk for hormone-sensitive breast cancers. Estrogens cause tumorigenesis by its effect on signaling pathways that lead to DNA damage, stimulation angiogenesis, mutagenesis, and cell proliferation. In postmenopausal females, and due to termination of ovarian function, estrogens were produced extra gonadally, mainly in peripheral adipose tissues where adrenal-produced androgen precursors are converted to estrogens. Active estradiol leads to breast cancer development by binding to ERα, which is modified by receptor's interaction of various signal transduction pathways. Hyperinsulinemia and IGF-1 activate the MAPK and PI3K pathways, leading to cancer-promoting effects. Cross talk between insulin/IGF and estrogen signaling pathways promotes hormone-sensitive breast cancer development. Hyperinsulinemia is a risk factor for breast cancer that explains the obesity-breast cancer association. Controlling IGF-1 level and targeting IGF-1 receptors among different breast cancer subtypes may be useful for breast cancer treatment. This review discussed several leptin signaling pathways, highlighting the potential advantage of targeting leptin as a potential target of the novel therapeutic strategies for breast cancer treatment.

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BACKGROUND: Breast cancer is the most common type of cancer among females. Genetic polymorphisms might have a role in carcinogenesis. The aim of this study was to determine whether C to T base substitution within TaqI Vitamin D receptor (VDR) gene (rs731236) in exon 9 was a risk factor among patients with breast cancer. METHODS: Peripheral blood was drawn from 122 Jordanian breast cancer patients and 100 healthy Jordanian volunteers in Al-Basheer Hospital during the summer months (from June to November of 2013, 2014, and 2015). DNA was amplified using polymerase chain reaction (PCR), followed by TaqI restriction enzyme digestion. Quantification of serum 25-hydroxy Vitamin D (25[OH]D) level was determined by competitive immunoassay Elecsys. RESULTS: Genotypic frequencies for TaqI TT, Tt, and tt genotypes were 41%, 46%, and 13% for breast cancer compared to 42%, 50%, and 8% for control, respectively. Vitamin D serum level was significantly lower in the breast cancer patients (8.1 ± 0.3 ng/ml) compared to the control group (21.2 ± 0.6 ng/ml; P= 0.001). This study showed an inverse association between 25(OH)D serum level and breast cancer risk (odds ratio [OR], 22.72, 95% confidence interval [CI], 10.06-51.29). CONCLUSIONS: An inverse association was found between 25(OH)D serum level and breast cancer risk. Statistical difference was also found between different VDR TaqI genotypes and circulating levels of 25(OH)D among Jordanian females with breast cancer.

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Breast cancer is a global health concern among women worldwide. Estrogen receptor alpha (ERα) mediates diverse polymorphic effects in breast tissues that may relate to breast cancer susceptibility. The aim of this study was to evaluate the effect of -397 PvuII (T/C) and -351 XbaI (A/G) restriction fragment length polymorphism within intron 1 of ERα, and its effect on breast cancer susceptibility. A total of 156 women who were histopathologically diagnosed with breast cancer and 142 healthy Jordanian women were enrolled in this case-control study. Genomic DNA was extracted from whole peripheral blood, and the desired fragment was amplified using polymerase chain reaction followed by restriction digestion with PvuII and XbaI restriction enzymes. The results showed no significant association between PvuII polymorphism and breast cancer risk. However, a significant association was found between XbaI polymorphism and reduction in breast cancer risk within the "x" allele of heterozygotes (odds ratio [OR] 0.199, 95% confidence interval [CI] 0.09-0.044) and heterozygotes (OR 0.208, 95% CI 0.09-0.047). The combined analysis of PvuII and XbaI polymorphisms revealed a synergistic effect of Pp/Xx and pp/xx genotypes and a significant reduction in breast cancer risk with these genotypes. The results also showed no statistical differences among PvuII or XbaI polymorphisms based on stage, ER, progesterone receptor and expression of hormone receptor such as human epidermal growth factor receptor 2. This case-control study showed that XbaI polymorphism of alpha estrogen gene modified and reduced breast cancer susceptibility among Jordanians.

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INTRODUCTION: Interleukin-10 (IL-10) is a multifactorial cytokine with a complex biological role in breast cancer. The aims of this study were to investigate any association between IL-10 gene promoter polymorphisms, 1082A>/G, -819T>C, and -592A>C, or haplotypes and breast cancer risk among Jordanian women and to evaluate any association between the most common haplotype with clinicopathological features of breast cancer. PATIENTS AND METHODS: A total of 202 breast cancer patients and 210 age-matched healthy control subjects were genotyped for -1082A/G, -819T/C, and -592A/C single nucleotide polymorphisms in the promoter region of the IL-10 gene by polymerase chain reaction-restriction fragment length polymorphism. Study patients and control subjects were recruited from Prince Hamzah Hospital, Amman, Jordan (2012-2013). Ethical approval and signed consent forms were signed by all participants. DNA was extracted, and polymerase chain reaction fragments were amplified and restriction digested by MnII, MaeIII, and RsaI. RESULTS: This study showed no statistically significant difference between -1082A/G, -819T/C, and -592A/C IL-10 genotypes or alleles among breast cancer patients or controls. Four different haplotypes ATA, ACC, GTA, and ACA within the IL-10 promoter gene were determined among both breast cancer and control groups. The most frequent haplotype was ACC among breast cancer patients and controls (41.6% and 40.7%, respectively). No statistical differences in these haplotypes among breast cancer patients or controls were determined. Analysis of the most common ACC haplotype showed statistical difference in positive estrogen receptor (P=0.022), positive progesterone receptor (P=0.004), cancer grade (P=0.0001), and cancer stage (P=0.009) among the ACC haplotype compared to non-ACC haplotype. CONCLUSION: To our knowledge, this is the first report studying the association of IL-10 haplotype with breast cancer risk events among Jordanian females. The most frequent IL-10 haplotype among Jordanian breast cancer females is ACC haplotype. Patients carrying the ACC haplotype are associated with higher positive estrogen and progesterone receptors and advanced breast cancer grade and stage. These patients also had lower survival rate in the Kaplan-Meier survival plot compared to those with non-ACC haplotype.

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BACKGROUND: Prostate cancer (PCa) is one of the most commonly diagnosed neoplasms and the second leading cause of cancer death in men in the Western world. Vitamin D (1,25dihydroxy vitamin D) is linked to many biological processes that influence oncogenesis but data on relations between its genetic variants and cancer risk have been inconsistent. The aim of this study was to determine associations between a vitamin D genetic polymorphism and 25-hydroxyvitamin D [25(OH)D] levels and prostate cancer. MATERIALS AND METHODS: Genomic DNA was extracted from 124 Jordanian prostate cancer patients and 100 healthy volunteers. Ethical approval was granted from the ethical committee at Hashemite University and written consent was given by all patients. PCR was used to amplify the vitamin D receptor Fok1 polymorphism fragment. 25(OH)D serum levels were measured by competitive immunoassay. RESULTS: All genotypes were in Hardy-Weinberg equilibrium. Genotype frequency for Fok1 genotypes FF, Ff and ff was 30.7%, 61.3% and 8.06%, for prostate cancer patients, while frequencies for the control group was 28.0%, 66.0% and 6.0%, respectively, with no significant differences. Vitamin D serum level was significantly lower in prostate cancer patients (mean 7.7 ng/ml) compared to the control group (21.8 ng/ml). No significant association was noted between 25(OH)D and VDR Fok1 gene polymorphism among Jordanians overall, but significant associations were evident among prostate cancer patients (FF, Ff and ff : 25(OH)D levels of 6.2, 8.2 and 9.9) and controls (19.0, 22.5 and 26.3, respectively). An inverse association was noted between 25(OH)D serum level less than 10 ng/ml and prostate cancer risk (OR 35.5 and 95% CI 14.3- 88.0). CONCLUSIONS: There is strong inverse association between 25(OH)D serum level less than 10 ng/ml level and prostate cancer risk.

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BACKGROUND: The physiological role of vitamin D extends beyond bone health and calcium-phosphate homeostasis to effects on cancer risk, mainly for colorectal cancer. Vitamin D may have an anticancer effect in colorectal cancer mediated by binding of the active form 1,25(OH)2D to the vitamin D receptor (VDR). The Taq1 VDR gene polymorphism, a C-to-T base substitution (rs731236) in exon 9 may influence its expression and function. The aim of this study was to determine the 25(OH)D vitamin D level and to investigate the association between circulating vitamin D level and Taq1VDR gene polymorphism among Jordanian colorectal cancer patients. MATERIALS AND METHODS: This case control study enrolled ninety-three patients and one hundred and two healthy Jordanian volunteers from AL-Basheer Hospital/Amman (2012-2013). Ethical approval and signed consent forms were obtained from all participants before sample collection. 25(OH)D levels were determined by competitive immunoassay Elecsys (Roche Diagnostic, France). DNA was extracted (Promega, USA) and amplified by PCR followed by VDR Taq1 restriction enzyme digestion. The genotype distribution was evaluated by paired t-test and chi-square. Comparison between vitamin D levels among CRC and control were assessed by odds ratio with 95% confidence interval. RESULTS: The vitamin D serum level was significantly lower among colorectal cancer patients (8.34 ng/ml) compared to the healthy control group (21.02 ng/ml). Patients deficient in vitamin D (less than 10.0 ng/ml) had increased colorectal cancer risk 19.2 fold compared to control. Only 2.2% of CRC patients had optimal vitamin D compared to 23.5% among healthy control. TT, Tt and tt Taq1 genotype frequencies among CRC cases was 35.5%, 50.5% and 14% compared to 43.1%, 41.2% and 15.7% among healthy control; respectively. CRC patients had lower mean vitamin D level among TT (8.91 ± 4.31) and Tt (9.15 ± 5.25) genotypes compared to control ((21.3 ± 8.31) and (19.3 ± 7.68); respectively. CONCLUSIONS: There is significant association between low 25(OH)D serum level and colorectal cancer risk. The VDRTaq1 polymorphism was associated with increased colorectal cancer risk among patient with VDRTaq1 TT and Tt genotypes. Understanding the functional mechanism of VDRTaq1 TT and Tt may provide a strategy for colorectal cancer prevention and treatment.

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BACKGROUND: In the literature, data concerning the relationship between breast cancer and HLA class II gene polymorphisms are limited, so the aim of this study was to determine if HLA-DQB1 and HLA-DRB1 MHC class-II alleles may confer susceptibility or resistance to the disease among Jordanian females. MATERIALS AND METHODS: This case control study enrolled 56 Royal Hospital breast cancer patients and 60 age matched healthy controls, all of whom provided blood samples (2011-2013). A questionnaire was filled after signing a consent form and DNA was extracted, nucleic acids being amplified for assessment of HLA-DQB1 and HLA-DRB1 alleles by muliplex INNO-LiPA and allele typing carried out by reverse hybridization. Comparison of HLA-DQB1 and HLA-DRB1 allele distributions was carried out with paired t-test and chi-square statistics. Risk factors were assessed by odd ratios with 95% confidence intervals. RESULTS: A significant negative correlation was observed between HLADQB1* 02 alleles and breast cancers (p=0.013). No significant associations were observed among HLADQB1* 03, 04, 05 and 06 or among HLA-DRB1* 01, 03, 04, 07, 08, 10, 11, 13, 14 and 15. CONCLUSIONS: HLADQB1* 02 alleles may provide positive protection against breast tumor risk among Jordanians, but not HLADQB1* 03, 04, 05 and 06 or HLA-DRB1* 01, 03, 04, 07, 08, 10, 11, 13, 14 and 15 alleles.

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