Although many studies have explored the mechanisms of skeletal muscle growth and adaptation with hypoxia exercise interventions, less attention has been given to the potential for vascular adaptation and regenerative capacity. This study shows for the first time an acute upregulation of the angiotensin-converting enzyme 2 and increase in CD34+ vasculogenic cells following an acute bout of blood flow restriction with low-intensity exercise. These rapid changes collectively promote skeletal muscle angiogenesis. Therefore, this study supports the potential of hypoxic exercise interventions with low intensity for vascular and muscle health.

Aging increases risk for ischemic vascular diseases. Bone marrow-derived hematopoietic stem/ progenitor cells (HSPCs) are known to stimulate vascular regeneration. Activation of either the Mas receptor (MasR) by angiotensin-(1-7) (Ang-(1-7)) or angiotensinconverting enzyme-2 (ACE2) stimulates vasoreparative functions in HSPCs. This study tested if aging is associated with decreased ACE2 expression in HSPCs and if Ang-(1-7) restores vasoreparative functions. Flow cytometric enumeration of Lin − CD45 low CD34 + cells was carried out in peripheral blood of male or female individuals (22-83 years of age). Activity of ACE2 or the classical angiotensin-converting enzyme (ACE) was determined in lysates of HSPCs. Lin − Sca-1 + cKit + (LSK) cells were isolated from young (3-5 months) or old (20-22 months) mice, and migration and proliferation were evaluated. Old mice were treated with Ang-(1-7), and mobilization of HSPCs was determined following ischemia induced by femoral ligation. A laser Doppler blood flow meter was used to determine blood flow. Aging was associated with decreased number (Spearman r = − 0.598, P < 0.0001, n = 56), decreased ACE2 (r = − 0.677, P < 0.0004), and increased ACE activity (r = 0.872, P < 0.0001) (n = 23) in HSPCs. Migration or proliferation of LSK cells in basal or in response to stromal-derived factor-1α in old cells is attenuated compared to young, and these dysfunctions were reversed by Ang-(1-7). Ischemia increased the number of circulating LSK cells in young mice, and blood flow to ischemic areas was recovered. These responses were impaired in old mice but were restored by treatment with Ang-(1-7). These results suggest that activation of ACE2 or MasR would be a promising approach for enhancing ischemic vascular repair in aging.

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Introduction: One to three per 1,000 live births suffers from significant hearing impairment. However, 2 to 4 per 100 infants who survived neonatal intensive care have some degree of sensorineural hearing loss. If hearing impairment in newborns is detected earlier, early management can prevent undesirable and often irreversible damage due to late detection.  Early detection and the treatment of hearing impairment in children are essential for the development of communication skills, social skills, emotional well-being, and positive self-esteem. Unfortunately, this disability remains undetected for many newborns until it is too late to prevent undesirable and often irreversible damage. Unfortunately, not many studies were done on this topic in Bangladesh. The magnitude of the burden of hearing impairment in the study place might be identified by this study.  The objective of the study: Hearing screening was done to see the status of hearing impairment in newborns admitted to NICU. Methodology: A prospective observational study was conducted in the department of neonatology, BSMMU. Newborn admitted to the NICU during the study period was the study population. The newborn who met the inclusion criteria was screened with TEOAE close to discharge from the NICU or before one month of age. A second screen was done with TEOAE again after one month of 1st screen but prior to 3 months of postnatal age if referred in 1st screen. Diagnostic ABR was done prior to 3 months of the postnatal age if referred in both the 1st and 2nd screen. Results: 426 valid recordings from 493 newborns admitted to the NICU enrolled consecutively constitute the basis of this study. Fourteen newborns were found to have hearing impairment among 426 newborns (3.3%). 2 newborns had unilateral hearing loss, and their hearing losses were moderate in nature. The other 12 newborns in their 24 ears had different grades of hearing loss. It was mild hearing loss in 3 ears, moderate in 9 ears, severe in 8 ears, and profound in 4 ears. Conclusion: Hearing screening showed that 3.3% of newborns in the NICU have a hearing impairment. It is still an underestimation considering the number of newborns who were lost to follow-up. TAJ 2022; 35: No-1: 77-82

Adult hematopoietic stem/progenitor cells (HSPCs) participate in the cardiovascular repair by stimulating regeneration and angiogenic functions of endothelium. Long‐term diabetes is associated with impaired vasoprotective functions of HSPCs. Transforming growth factor β (TGFβ1) is pleiotropic regulator of HSPC functions. Previous studies have shown that transient silencing of TGFβ1 expression improves in vivo migratory functions of diabetic HSPCs partly by restoring nitric oxide (NO) generation. This study tested the hypothesis that restoration of NO by TGFβ1‐silencing is mediated by thrombospondin‐1 (TSP1)/CD47 pathway. TSP1 is known to attenuate NO generation via inhibition of endothelial nitric oxide synthase (eNOS). HSPCs were isolated from peripheral blood samples obtained from either male or female healthy (n=25) or diabetic (both type 1 and type 2) (n=27) individuals (50–80 years of age) by immunomagnetic enrichment. TGFβ1 expression was transiently blocked by using TGFβ1‐antisense delivered in the form of phosphorodiamidate morpholino oligomer (PMO‐TGFβ1). TGFβ1 and TSP1 gene expressions were determined in HSPCs treated with either PMO‐control or PMO‐TGFβ1. NO generation induced by stromal‐derived factor‐1α (SDF) was determined by DAF‐FM flow cytometry. Diabetic cells have higher expression of TGFβ1 or TSP1 compared to that observed in cells derived from healthy individuals (n=10). Treatment with TGFβ1‐PMO decreased the expression of TGFβ1, which was associated with decreased TSP1 expression. CD47 expression is similar in healthy or diabetic individuals. NO generation by SDF is attenuated in diabetic compared to healthy cells (P<0.01, n=5). PMO‐TGFβ1‐treated diabetic cells showed increased generation of NO in response to SDF compared to PMO‐control‐treatment (P<0.01, n=5). Future studies will determine the effect of TSP1 on SDF/NO generation in cells with or without CD47‐siRNA, to further support the hypothesis. Collectively, these studies indicate the involvement of TGFβ1/TSP1/CD47/eNOS pathway in diabetic impairment of NO generation however involvement of other pathways cannot be ruled out. Support or Funding Information This study is partly supported by funding from NIH National Institute of Aging (AG056681).