Characteristics and comorbidity of confirmed COVID-19 death cases at the Arifin Achmad Hospital in Riau province from March 2020 to September 2021.

Objectives: To investigate the characteristics and comorbidity among those who died due to coronavirus disease-2019.

Methods: The cohort retrospective study was conducted at Arifin Achmad Public Hospital, Riau, Indonesia, from January 5 to February 28, 2022, and comprised data of all coronavirus disease-2019 patients who had been treated at the hospital from March 2020 to October 2021. Data was analysed using SPSS version 20.

Decrease of left ventricular function measured by speckle-tracking echocardiography based on systemic lupus erythematosus severity in children.

Introduction: Systemic lupus erythematosus in children generally manifests more severely with a more aggressive disease course. Cardiac involvement in systemic lupus erythematosus often does not show specific signs and symptoms, but speckle-tracking echocardiography can detect cardiac dysfunction. This study aimed to determine the differences in left ventricular function as measured by speckle-tracking echocardiography in children with various severity of systemic lupus erythematosus activity.

Prevalence of hepatitis B and C viruses in healthy Indonesian blood donors.

Blood samples were collected from 7572 healthy volunteer blood donors from 21 of the 27 Indonesian provinces, and tested for antibodies to hepatitis C virus (anti-HCV) using the new second-generation enzyme immunosorbent assay, and also tested for hepatitis B surface antigen (HBsAg). We detected anti-HCV in 2.1% of the blood donors.

Molecular basis for plasma alpha(1,3)-fucosyltransferase gene deficiency (FUT6).

While most humans express an alpha(1,3)-fucosyltransferase in plasma, 9% of individuals on the isle of Java (Indonesia) do not express this enzyme. Ninety-five percent of these plasma alpha(1,3)-fucosyltransferase-deficient individuals have Lewis negative phenotype on red cells, suggesting strong linkage disequilibrium between these two traits. To define the molecular basis for this plasma deficiency and to determine which of two candidate human alpha(1,3)-fucosyltransferase genes encode this enzyme (FUT5 and FUT6), we cloned and analyzed alleles at these two loci from an Indonesian individual deficient in plasma alpha(1,3)-fucosyltransferase activity.