Growing Cellulose Spheres for Consumption & Encapsulation

Make a product from kombucha mat that normally goes unused. Create cellulose spheres that will appeal to consumers

Predicting Elective Orthopaedic Sports Medicine Surgical Cancellations Based on Patient Demographics.

Purpose:To evaluate whether patient demographics are associated with cancellation of elective orthopaedic sports medicine surgical procedures. Methods:We retrospectively reviewed the electronic medical records of 761 patients who were scheduled to undergo an elective sports medicine orthopaedic operation from January 1, 2015, to December 31, 2017. The patients were divided into 2 groups: those who underwent the scheduled procedure (group A) and those in whom the operation was canceled for any reason prior to the surgical date and not rescheduled (group B). Univariate analysis assessed patient factors consisting of age, sex, race, language, marital status, occupation status, type of insurance (Medicaid or Medicare vs private), smoking history, employment status, and history of surgery to determine which demographic factors led to an increased risk of elective case cancellation. Results:Patients who canceled were significantly older (46.5 years vs 41.5 years, t = 2.432, P = .015) than those who do not. In addition, current smokers (22.5% vs 10.9%, χ2 = 10.85, P = .001), patients with Medicare or Medicaid versus private insurance (16.7% vs 10.0%, χ2 = 5.35, P = .021), non-English-speaking patients (29.5% vs 11.6%, χ2 = 11.43, P = .001), and patients without a history of surgery requiring anesthesia (18.8% vs 9.6%, χ2 = 9.96, P = .002) were all more likely to cancel. When all studied variables were examined in a logistic regression analysis, of the above demographic variables, only insurance status was no longer significant, given its correlation with age and language. Conclusions:Increased age (≥46.5 years), non-English speaking, smoking, lack of a history of surgery requiring anesthesia, and Medicaid or Medicare insurance were found to contribute to an increased risk of elective orthopaedic surgery cancellation. Level of Evidence:Level III, case-control study

Secondary dentin formation mechanism: The effect of attrition

Human dentin consists of a primary layer produced during tooth formation in early child-hood and a second layer which first forms upon tooth eruption and continues throughout life, termed secondary dentin (SD). The effect of attrition on SD formation was considered to be confined to the area subjacent to attrition facets. However, due to a lack of three‐dimensional methodologies to demonstrate the structure of the SD, this association could not be determined. Therefore, in the current study, we aimed to explore the thickening pattern of the SD in relation to the amount of occlusal and interproximal attrition. A total of 30 premolars (50–60 years of age) with varying attrition rates were evaluated using micro‐computerized tomography. The results revealed thickening of the SD below the cementoenamel junction (CEJ), mostly in the mesial and distal aspects of the root (p < 0.05). The pattern of thickening under the tooth cervix, rather than in proximity to attrition facets, was consistent regardless of the attrition level. The amount of SD thickening mildly corre-lated with occlusal attrition (r = 0.577, p < 0.05) and not with interproximal attrition. The thickening of the SD below the CEJ coincided with previous finite element models, suggesting that this area is mostly subjected to stress due to occlusal loadings. Therefore, we suggest that the SD formation might serve as a compensatory mechanism aimed to strengthen tooth structure against deflection caused by mechanical loading. Our study suggests that occlusal forces may play a significant role in SD formation

Spontaneous Expression of the c-sis Gene and Release of a Platelet-derived Growth Factorlike Molecule by Human Alveolar Macrophages

Alveolar macrophages from normal individuals and patients with interstitial lung diseases spontaneously expressed a 4.2-kilobase mRNA complementary to the c-sis gene, a proto-oncogene coding for one of the chains of platelet-derived growth factor (PDGF). Concomitantly, these cells released a mediator with the properties of PDGF, including: (a) chemotactic factor for smooth muscle cells whose activity was resistant to heat and acid, but sensitive to reduction; (b) mitogenic (competence) activity for fibroblasts; (c) ability to compete with PDGF for its receptor, and (d) precipitated by an anti-PDGF antibody. While blood monocytes did not contain c-sis mRNA transcripts, monocytes matured in vitro expressed c-sis, consistent with the concept that expression of c-sis occurs during the differentiation of monocytes into alveolar macrophages. Together with the known actions of PDGF, these observations suggest that the c-sis proto-oncogene and its PDGF product are part of the armamentarium available to the alveolar macrophages for normal lung defense and participation in lung inflammation

TGF-β1 and serum both stimulate contraction but differentially affect apoptosis in 3D collagen gels

Apoptosis of fibroblasts may be key for the removal of cells following repair processes. Contraction of three-dimensional collagen gels is a model of wound healing and remodeling. Here two potent inducers of contraction, TGF-β1 and fetal calf serum (FCS) were evaluated for their effect on fibroblast apoptosis in contracting collagen gels. Human fetal lung fibroblasts were cultured in floating type I collagen gels, exposed to TGF-β1 or FCS, and allowed to contract for 5 days. Apoptosis was evaluated using TUNEL and confirmed by DNA content profiling. Both TGF-β1 and serum significantly augmented collagen gel contraction. TGF-β1 also increased apoptosis assessed by TUNEL positivity and DNA content analysis. In contrast, serum did not affect apoptosis. TGF-β1 induction of apoptosis was associated with augmented expression of Bax, a pro-apoptotic member of the Bax/Bcl-2 family, inhibition of Bcl-2, an anti-apoptotic member of the same family, and inhibition of both cIAP-1 and XIAP, two inhibitors of the caspase cascade. Serum was associated with an increase in cIAP-1 and Bcl-2, anti-apoptotic proteins. Interestingly, serum was also associated with an apparent increase in Bax, a pro-apoptotic protein. Blockade of Smad3 with either siRNA or by using murine fibroblasts deficient in Smad3 resulted in a lack of TGF-β induction of augmented contraction and apoptosis. Contraction induced by different factors, therefore, may be differentially associated with apoptosis, which may be related to the persistence or resolution of the fibroblasts that accumulate following injury

Population pharmacokinetics of colistin and the relation to survival in critically ill patients infected with colistin susceptible and carbapenem-resistant bacteria

Objectives: The aim was to analyse the population pharmacokinetics of colistin and to explore the relationship between colistin exposure and time to death. Methods: Patients included in the AIDA randomized controlled trial were treated with colistin for severe infections caused by carbapenem-resistant Gram-negative bacteria. All subjects received a 9 million units (MU) loading dose, followed by a 4.5 MU twice daily maintenance dose, with dose reduction if creatinine clearance (CrCL) 2 mg/L in 94% (195/208) and 44% (38/87) of patients with CrCL ≤120 mL/min, and >120 mL/min, respectively. Colistin methanesulfonate sodium (CMS) and colistin clearances were strongly dependent on CrCL. High colistin exposure to MIC ratio was associated with increased hazard of death in the multivariate analysis (adjusted hazard ratio (95% CI): 1.07 (1.03–1.12)). Other significant predictors included SOFA score at baseline (HR 1.24 (1.19–1.30) per score increase), age and Acinetobacter or Pseudomonas as index pathogen. Discussion: The population pharmacokinetic model predicted that >90% of the patients had colistin concentrations

Phospholipase A2-activating protein is associated with a novel form of leukoencephalopathy

Leukoencephalopathies are a group of white matter disorders related to abnormal formation, maintenance, and turnover of myelin in the central nervous system. These disorders of the brain are categorized according to neuroradiological and pathophysiological criteria. Herein, we have identified a unique form of leukoencephalopathy in seven patients presenting at ages 2 to 4 months with progressive microcephaly, spastic quadriparesis, and global developmental delay. Clinical, metabolic, and imaging characterization of seven patients followed by homozygosity mapping and linkage analysis were performed. Next generation sequencing, bioinformatics, and segregation analyses followed, to determine a loss of function sequence variation in the phospholipase A2-activating protein encoding gene (PLAA). Expression and functional studies of the encoded protein were performed and included measurement of prostaglandin E2 and cytosolic phospholipase A2 activity in membrane fractions of fibroblasts derived from patients and healthy controls. Plaa-null mice were generated and prostaglandin E2 levels were measured in different tissues. The novel phenotype of our patients segregated with a homozygous loss-of-function sequence variant, causing the substitution of leucine at position 752 to phenylalanine, in PLAA, which causes disruption of the protein's ability to induce prostaglandin E2 and cytosolic phospholipase A2 synthesis in patients' fibroblasts. Plaa-null mice were perinatal lethal with reduced brain levels of prostaglandin E2 The non-functional phospholipase A2-activating protein and the associated neurological phenotype, reported herein for the first time, join other complex phospholipid defects that cause leukoencephalopathies in humans, emphasizing the importance of this axis in white matter development and maintenance