An integrative review of maternal distress during neonatal intensive care hospitalization

Archives of Women's Mental Health - To synthesize literature addressing maternal distress and associated variables in response to infant hospitalization in the NICU. CINAHL, Medline, PubMed,...     

SARS-CoV-2-induced immunodysregulation and the need for higher clinical suspicion for co-infection and secondary infection in COVID-19 patients

Cases of co-infection and secondary infection emerging during the current Coronavirus Disease-19 (COVID-19) pandemic are a major public health concern. Such cases may result from immunodysregulation induced by the SARS-CoV-2 virus. Pandemic preparedness must include identification of disease natural history and common secondary infections to implement clinical solutions.     

Sexual Orientation Demographic Data in a Clinical Cohort of Transgender Patients

Background  There are specific issues regarding sexual orientation (SO) collection and analysis among transgender and nonbinary patients. A limitation to meaningful SO and gender identity (GI) data collection is their consideration as a fixed trait or demographic data point. Methods  A de-identified patient database from a single electronic health record (EHR) that allows for searching any discrete data point in the EHR was used to query demographic data (sex assigned at birth and current GI) for transgender individuals from January 2011 to March 2020 at a large urban tertiary care academic health center. Results  A cohort of transgender individuals were identified by using EHR data from a two-step demographic question. Almost half of male identified (46.70%, n  = 85) and female identified (47.51%, n  = 86) individuals had “heterosexual/straight” input for SO. Overall, male and female identified (i.e., binary) GI aggregate categories had similar SO responses. Assigned male at birth (AMAB) nonbinary individuals ( n  = 6) had “homosexual/gay” SO data input. Assigned female at birth (AFAB) nonbinary individuals ( n  = 56) had almost half “something else” SO data input (41.67%, n  = 15). Individuals with “choose not to disclose” for GI ( n  = 249) almost all had “choose not to disclose” SO data (96.27%, n  = 232). Conclusion  Current SO categories do not fully capture transgender individuals'' identities and experiences, and limit the clinical and epidemiological utility of collecting this data in the current form. Anatomical assumptions based on SO should be seen as a potential shortcoming in over-reliance on SO as an indicator of screening needs and risk factors.     

Patients at elevated risk of major adverse events following endarterectomy for asymptomatic carotid stenosis

Background

Carotid endarterectomy (CEA) as treatment in patients with asymptomatic carotid stenosis is the subject of much debate.

Methods

The National Surgical Quality Improvement Program database from 2005 to 2012 was queried. Patients undergoing CEA for asymptomatic carotid stenosis were identified. Preoperative risk factors and patient demographics were compared using chi-square analysis and logistic regression to determine their relation with stroke and death.

Results

During an 8-year period, 24,211 CEAs performed for asymptomatic carotid stenosis were identified. Patients with dependent functional status (12.5%), recent myocardial infarction (6.3%), chronic heart failure (5.0%), hypoalbuminemia (4.8%), angina (4.1%), dialysis dependence (3.4%), steroid dependence (3.4%), chronic obstructive pulmonary disease (3.3%), and American Society of Anesthesiologists > 3 (3.2%) had a clinically significant increase in risk of stroke and death. Patients with none of the above risk factors had a stroke and death rate of 1.08%, which was significantly less than the overall stroke and death rate (P < .001).

Conclusions

A high-risk subset of patients undergoing CEA for asymptomatic carotid stenosis can be identified. If patient selection is optimized and perioperative morbidity and mortality are minimized, CEA will continue to play an important role in stroke prevention for those with significant asymptomatic carotid stenosis.     

Molecular Basis of Intervertebral Disc Degeneration and Herniations: What Are the Important Translational Questions?

Background

Intervertebral disc degeneration is a common condition with few inexpensive and effective modes of treatment, but current investigations seek to clarify the underlying process and offer new treatment options. It will be important for physicians to understand the molecular basis for the pathology and how it translates to developing clinical treatments for disc degeneration. In this review, we sought to summarize for clinicians what is known about the molecular processes that causes disc degeneration.

Results

A healthy disc requires maintenance of a homeostatic environment, and when disrupted, a catabolic cascade of events occurs on a molecular level resulting in upregulation of proinflammatory cytokines, increased degradative enzymes, and a loss of matrix proteins. This promotes degenerative changes and occasional neurovascular ingrowth potentially contributing to the development of pain. Research demonstrates the molecular changes underlying the harmful effects of aging, smoking, and obesity seen clinically while demonstrating the variable influence of exercise. Finally, oral medications, supplements, biologic treatments, gene therapy, and stem cells hold great promise but require cautious application until their safety profiles are better outlined.

Conclusions

Intervertebral disc degeneration occurs where there is a loss of homeostatic balance with a predominantly catabolic metabolic profile. A basic understanding of the molecular changes occurring in the degenerating disc is important for practicing clinicians because it may help them to inform patients to alter lifestyle choices, identify beneficial or harmful supplements, or offer new biologic, genetic, or stem cell therapies.     

MDX‐1097 induces antibody‐dependent cellular cytotoxicity against kappa multiple myeloma cells and its activity is augmented by lenalidomide

MDX‐1097 is an antibody specific for a unique B cell antigen called kappa myeloma antigen (KMA) that consists of cell membrane‐associated free kappa light chain (κFLC). KMA was detected on kappa human multiple myeloma cell lines (κHMCLs), on plasma cells (PCs) from kappa multiple myeloma (κMM) patients and on κPC dyscrasia tissue cryosections. In primary κMM samples, KMA was present on CD38+ cells that were CD138 and CD45 positive and/or negative. MDX‐1097 exhibited a higher affinity for KMA compared to κFLC and the latter did not abrogate binding to KMA. MDX‐1097‐mediated antibody‐dependent cellular cytotoxicity (ADCC) and in vitro exposure of target cells to the immunomodulatory drug lenalidomide resulted in increased KMA expression and ADCC. Also, in vitro exposure of peripheral blood mononuclear cells (PBMCs) to lenalidomide enhanced MDX‐1097‐mediated ADCC. PBMCs obtained from myeloma patients after lenalidomide therapy elicited significantly higher levels of MDX‐1097‐mediated ADCC than cells obtained prior to lenalidomide treatment. These data establish KMA as a relevant cell surface antigen on MM cells that can be targeted by MDX‐1097. The ADCC‐inducing capacity of MDX‐1097 and its potentiation by lenalidomide provide a powerful rationale for clinical evaluation of MDX‐1097 alone and in combination with lenalidomide.