Gotowa bibliografia na temat „823/.914”

Los cambios sociales, económicos y culturales en los últimos años han ocasionado nuevas demandas y reajustes en la vida y las conductas de las personas, trayendo como consecuencias reacciones negativas como el estrés prolongado y la rumiación que facilita el engancharse en temas y errores cometidos. Por todo esto, contar con instrumentos que operacionalicen dichas variables dará paso a tener medidas actuales, confiables y certeras. Se trabajó con un muestreo por conveniencia conformado por 388 personas, de edades entre los 17 a 62 años. Como resultado el análisis factorial confirmatorio arrojó para la escala de Estrés un Alpha total de .823 con dos factores (Control y Descontrol). Para la escala de Rumiación se encontró un Alpha total de .914 con dos factores también (Malestar y Reflexión obsesiva). En lo que respecta a las correlaciones se hallaron asociaciones entre los factores de Estrés con Rumiación. De igual manera, se logró desarrollar dos escalas validez y confiables para evaluar las escalas expuestas.

Background: Fatigue is a pervasive symptom among patients with chronic kidney disease (CKD) that is associated with several adverse outcomes, but the incidence of hospitalization for fatigue is unknown. Objective: To explore the association between estimated glomerular filtration rate (eGFR) and incidence of hospitalization for fatigue. Design: Population-based retrospective cohort study using a provincial administrative dataset. Setting: Alberta, Canada. Patients: People above age 18 who had at least 1 outpatient serum creatinine measurement taken in Alberta between January 1, 2009, and December 31, 2016. Measurements: The first outpatient serum creatinine was used to estimate GFR. Hospitalization for fatigue was identified using International Classification of Diseases, Tenth Revision (ICD-10) code R53.x. Methods: Patients were stratified by CKD category based on their index eGFR. We used negative binomial regression to determine if there was an increased incidence of hospitalization for fatigue by declining kidney function (reference eGFR ≥ 60 mL/min/1.73m2). Estimates were stratified by age, and adjusted for age, sex, socioeconomic status, and comorbidity. Results: The study cohort consisted of 2 823 270 adults, with a mean age of 46.1 years and median follow-up duration of 6.0 years; 5 422 hospitalizations for fatigue occurred over 14 703 914 person-years of follow-up. Adjusted rates of hospitalization for fatigue increased with decreasing kidney function, across all age strata. The highest rates were seen in adults on dialysis (adjusted incident rate ratios 24.47, 6.66, and 3.13 for those aged 18 to 64, 65 to 74, and 75+, respectively, compared with eGFR ≥ 60 mL/min/1.73m2). Limitations: Fatigue hospitalization codes have not been validated; reference group limited to adults with at least 1 outpatient serum creatinine measurement; remaining potential for residual confounding. Conclusions: Declining kidney function was associated with increased incidence of hospitalization for fatigue. Further research into ways to address fatigue in the CKD population is warranted. Trial Registration: Not applicable (not a clinical trial).

Maddox Dairy, located in Riverdale, CA, USA, is a Holstein herd that milks 3500 cows with a 305-day mature-equivalent milk production of 12 800 kg, and they have been producing high genetic animals by embryo transfer (ET) since the early 1980s. Invivo-derived embryos from Holstein donors were transferred fresh (grade 1 or 2) or frozen (grade 1), at morula (4), early blastocyst (5), or blastocyst (6) stage, to virgin heifers (VH, natural oestrus, 13-15 months old) or lactating cows (LC, Presynch-Ovsynch, 86 days in milk, first or second lactation) 6 to 9 days after oestrus. Pregnancy diagnosis was done by transrectal ultrasonography at 32-46 days in VH and by the IDEXX PAG test at 30 days in LC. June, July, August, September, and October were called critical months (first service AI conception rate drops below 44%) and compared with the other months. The data from 32 503 ETs between January 2008 and December 2018 are summarised on Table 1. Pregnancy rates (PR) are lower for LC recipients than for VH. Embryo transfers performed 7 or 8 days after oestrus had higher PR in both types of recipients and embryos, but Day 6 and 9 oestrus are also used with fair results. The season does not seem to affect PR. There is not enough difference in the combination of stage and days from oestrus for invivo-derived embryos. These numbers do not belong to a planned experiment. Several management changes during the years were made, which make it very difficult to apply statistical methods to analyse the data correctly. They are used as a tool to make decisions in an attempt to improve future results. Table 1.Pregnancy rate (PR) of virgin heifers (top) and lactating cows (bottom)-fresh (SH) and frozen (OZ) invivo-derived embryo transfer1 Heat-months SH-ST4 SH-ST5 SH-ST6 SH-All OZ-ST4 OZ-ST5 OZ-ST6 OZ-All PR% n PR% n PR% n PR% n PR% n PR% n PR% n PR% n Heifers 6 d-CM 62 934 66 243 68 69 63 1246 56 473 58 219 62 42 57 734 6 d-OM 62 1623 67 489 69 211 64 2323 56 600 55 296 48 137 55 1033 6 d-T 62 2557 67 732 69 280 63 3569 56 1073 57 515 51 179 56 1767 7 d-CM 64 1506 68 495 67 221 65 2222 60 822 62 340 63 156 61 1318 7 d-OM 66 2723 68 1021 69 510 67 4254 57 1120 59 581 57 231 58 1932 7 d-T 66 4229 68 1516 69 731 67 6476 58 1942 60 921 60 387 59 3250 8 d-CM 65 1348 64 518 67 322 65 2188 59 595 64 258 63 108 61 961 8 d-OM 66 2166 68 886 70 510 67 3562 61 770 60 364 51 130 60 1264 8 d-T 66 3514 67 1404 69 832 66 5750 60 1365 62 622 56 238 60 2225 9 d-CM 60 109 56 43 70 20 60 172 60 5 33 6 50 4 47 15 9 d-OM 58 129 63 57 60 40 60 226 63 16 50 18 75 4 58 38 9 d-T 59 238 60 100 63 60 60 398 62 21 46 24 63 8 55 53 All-CM 64 3897 66 1299 67 632 65 5828 58 1895 61 823 63 310 60 3028 All-OM 65 6641 67 2453 69 1271 66 10 365 58 2506 58 1259 53 502 58 4267 All-T 65 10 538 67 3752 69 1903 66 16 193 58 4401 60 2082 57 812 59 7295 Lactating cows 6 d-CM 54 265 48 86 50 12 53 363 38 141 31 77 50 10 36 228 6 d-OM 49 463 52 203 45 56 50 723 46 101 48 54 59 27 48 182 6 d-T 51 728 51 289 46 68 51 1086 41 242 38 131 57 37 42 410 7 d-CM 54 755 59 274 56 103 55 1137 43 928 48 450 43 192 45 1570 7 d-OM 55 914 66 367 54 109 58 1393 46 1052 45 564 47 353 46 1969 7 d-T 55 1669 63 641 55 212 57 2530 45 1980 46 1014 46 545 45 3539 8 d-CM 63 252 68 82 76 33 65 368 48 219 56 80 42 33 50 332 8 d-OM 61 257 64 161 53 47 61 466 50 191 53 77 56 16 51 284 8 d-T 62 509 65 243 63 80 63 834 49 410 55 157 47 49 50 616 All-CM 56 1272 58 442 60 148 57 1868 44 1288 47 607 43 235 45 2130 All-OM 55 1634 62 731 51 212 56 2582 47 1344 46 695 48 396 47 2435 All-T 55 2906 60 1173 55 360 57 4450 45 2632 47 1302 46 631 46 4565 1ST=stage; CM=critical months (June, July, August, September, and October); OM=other months.

Background: The obesity epidemic is a significant health concern, affecting nearly a third of all United States citizens according to the 2013-2014 National Health and Nutrition Examination Survey. Obesity contributes to multiple metabolic and cardiovascular risk factors including diabetes mellitus, hypertension, and dyslipidemia. The atherosclerotic cardiovascular disease (ASCVD) risk calculator is a frequently used tool that aggregates various risk factors to assist physicians in detecting patients that may benefit from statin therapy and risk factor modification. However, this calculator does not directly factor in obesity, which has been found to be associated with multiple cardiovascular comorbidities. Our goal was to assess the correlation between body mass index (BMI) and ASCVD risk scores in order to identify potential targets for intervention to further decrease ASCVD risk. Methods: We obtained data from the medical record data warehouse of a primary care outpatient clinic predominantly run by internal medicine residents within a large safety-net hospital from January to December 2015. Patients with a diagnosis of dyslipidemia or hyperlipidemia were identified and electronic medical records were reviewed. ASCVD risk scores were calculated using the American College of Cardiology ASCVD risk estimator. Linear and logistical regression analyses were performed using SPSS software to assess the correlation between BMI and ASCVD risk. Results: The patient population was predominantly African American (92%, 1771 of 1919). Obesity (BMI ≥30) was present in 63% (1207 of 1919) of patients. ASCVD scores could be calculated for 914 patients and 90% (823 of 914) of these patients had ASCVD risk scores ≥7.5. However, only 84% (691 of 823) of these patients with elevated ASCVD scores were on a statin. Analyses did not reveal a correlation between BMI and ASCVD risk. However, elevated BMI (>25) conferred an increased odds ratio (O.R.) of having elevated ASCVD risk (>22.5% O.R. 1.58; p value 0.02) in comparison to normal or underweight BMI. Conclusion: Obesity rates appear to be higher in our patient population in comparison to national estimates but our mathematical model cannot be used to explain any correlation between BMI and ASCVD risk scores. Obesity did not confer an increased ASCVD risk in comparison to being overweight (BMI 25-29.9). However, both overweight and obese patients had a higher likelihood of having a significantly elevated ASCVD risk score. Future aims include initiating a targeted educational intervention for residents in the continuity clinic to ultimately demonstrate that resident driven intervention is an effective way to address obesity and modify ASCVD risk.

Despite the enormous benefits of breastfeeding, its prevalence is suboptimal, with exclusive breastfeeding ranging between 7.3 % and 51% in the Saudi community. The aim of this study was to assess the Saudi community's knowledge regarding breastfeeding, exposure to breastfeeding promotional messages and formula milk advertisement, and acceptability of breastfeeding in public places. It was a cross-sectional study that included Saudis aged 20 to 55 years old between December 2019 and June 2020. It utilized a self-administered questionnaire, which asked about background information, knowledge of breastfeeding, exposure to breastfeeding promoting messages and exposure to formula milk advertisement, and acceptability of breastfeeding versus bottle feeding in public. Data were analyzed using the Statistical Package for the Social Sciences (SPSS v. 22). For the analysis, p-value < 0.05 was considered significant. The sample included for analysis was 914. Mean age of participants was 33.8±9 years. The majority of participants were female 823 (90%); males were 87 (10%). The vast majority (94%) agreed that breast milk is more beneficial than formula milk. Nearly two-thirds (61%) were continuously exposed to messages advertising formula feeding, compared to only 35% who were exposed to messages promoting breastfeeding. The study found that 67.2% accept breastfeeding in public places. Among male participants, only 49% accepted breastfeeding in public places compared to 79% of female participants who accepted it; p-value < 0.001. Acceptability of breastfeeding in public places was significantly higher among participants who had family members who breastfed (68%), compared to those who didn't (50%), (p-value 0.01).

The TRP superfamily of channels (nomenclature as agreed by NC-IUPHAR [176, 1075]), whose founder member is the Drosophila Trp channel, exists in mammals as six families; TRPC, TRPM, TRPV, TRPA, TRPP and TRPML based on amino acid homologies. TRP subunits contain six putative TM domains and assemble as homo- or hetero-tetramers to form cation selective channels with diverse modes of activation and varied permeation properties (reviewed by [730]). Established, or potential, physiological functions of the individual members of the TRP families are discussed in detail in the recommended reviews and in a number of books [401, 686, 1158, 256]. The established, or potential, involvement of TRP channels in disease [1129] is reviewed in [448, 685], [688] and [464], together with a special edition of Biochemica et Biophysica Acta on the subject [685]. Additional disease related reviews, for pain [633], stroke [1138], sensation and inflammation [990], itch [130], and airway disease [310, 1054], are available. The pharmacology of most TRP channels has been advanced in recent years. Broad spectrum agents are listed in the tables along with more selective, or recently recognised, ligands that are flagged by the inclusion of a primary reference. See Rubaiy (2019) for a review of pharmacological tools for TRPC1/C4/C5 channels [806]. Most TRP channels are regulated by phosphoinostides such as PtIns(4,5)P2 although the effects reported are often complex, occasionally contradictory, and likely to be dependent upon experimental conditions, such as intracellular ATP levels (reviewed by [1011, 689, 802]). Such regulation is generally not included in the tables.When thermosensitivity is mentioned, it refers specifically to a high Q10 of gating, often in the range of 10-30, but does not necessarily imply that the channel's function is to act as a 'hot' or 'cold' sensor. In general, the search for TRP activators has led to many claims for temperature sensing, mechanosensation, and lipid sensing. All proteins are of course sensitive to energies of binding, mechanical force, and temperature, but the issue is whether the proposed input is within a physiologically relevant range resulting in a response. TRPA (ankyrin) familyTRPA1 is the sole mammalian member of this group (reviewed by [293]). TRPA1 activation of sensory neurons contribute to nociception [414, 891, 602]. Pungent chemicals such as mustard oil (AITC), allicin, and cinnamaldehyde activate TRPA1 by modification of free thiol groups of cysteine side chains, especially those located in its amino terminus [575, 60, 365, 577]. Alkenals with α, β-unsaturated bonds, such as propenal (acrolein), butenal (crotylaldehyde), and 2-pentenal can react with free thiols via Michael addition and can activate TRPA1. However, potency appears to weaken as carbon chain length increases [26, 60]. Covalent modification leads to sustained activation of TRPA1. Chemicals including carvacrol, menthol, and local anesthetics reversibly activate TRPA1 by non-covalent binding [424, 511, 1084, 1083]. TRPA1 is not mechanosensitive under physiological conditions, but can be activated by cold temperatures [425, 212]. The electron cryo-EM structure of TRPA1 [741] indicates that it is a 6-TM homotetramer. Each subunit of the channel contains two short ‘pore helices’ pointing into the ion selectivity filter, which is big enough to allow permeation of partially hydrated Ca2+ ions. TRPC (canonical) familyMembers of the TRPC subfamily (reviewed by [284, 779, 18, 4, 94, 446, 740, 70]) fall into the subgroups outlined below. TRPC2 is a pseudogene in humans. It is generally accepted that all TRPC channels are activated downstream of Gq/11-coupled receptors, or receptor tyrosine kinases (reviewed by [766, 955, 1075]). A comprehensive listing of G-protein coupled receptors that activate TRPC channels is given in [4]. Hetero-oligomeric complexes of TRPC channels and their association with proteins to form signalling complexes are detailed in [18] and [447]. TRPC channels have frequently been proposed to act as store-operated channels (SOCs) (or compenents of mulimeric complexes that form SOCs), activated by depletion of intracellular calcium stores (reviewed by [742, 18, 771, 821, 1124, 157, 726, 64, 158]). However, the weight of the evidence is that they are not directly gated by conventional store-operated mechanisms, as established for Stim-gated Orai channels. TRPC channels are not mechanically gated in physiologically relevant ranges of force. All members of the TRPC family are blocked by 2-APB and SKF96365 [347, 346]. Activation of TRPC channels by lipids is discussed by [70]. Important progress has been recently made in TRPC pharmacology [806, 619, 436, 102, 852, 191, 291]. TRPC channels regulate a variety of physiological functions and are implicated in many human diseases [295, 71, 886, 1034, 1028, 154, 103, 561, 914, 409]. TRPC1/C4/C5 subgroup TRPC1 alone may not form a functional ion channel [229]. TRPC4/C5 may be distinguished from other TRP channels by their potentiation by micromolar concentrations of La3+. TRPC2 is a pseudogene in humans, but in other mammals appears to be an ion channel localized to microvilli of the vomeronasal organ. It is required for normal sexual behavior in response to pheromones in mice. It may also function in the main olfactory epithelia in mice [1117, 723, 724, 1118, 539, 1171, 1112].TRPC3/C6/C7 subgroup All members are activated by diacylglycerol independent of protein kinase C stimulation [347].TRPM (melastatin) familyMembers of the TRPM subfamily (reviewed by [275, 346, 742, 1154]) fall into the five subgroups outlined below. TRPM1/M3 subgroupIn darkness, glutamate released by the photoreceptors and ON-bipolar cells binds to the metabotropic glutamate receptor 6 , leading to activation of Go . This results in the closure of TRPM1. When the photoreceptors are stimulated by light, glutamate release is reduced, and TRPM1 channels are more active, resulting in cell membrane depolarization. Human TRPM1 mutations are associated with congenital stationary night blindness (CSNB), whose patients lack rod function. TRPM1 is also found melanocytes. Isoforms of TRPM1 may present in melanocytes, melanoma, brain, and retina. In melanoma cells, TRPM1 is prevalent in highly dynamic intracellular vesicular structures [398, 708]. TRPM3 (reviewed by [714]) exists as multiple splice variants which differ significantly in their biophysical properties. TRPM3 is expressed in somatosensory neurons and may be important in development of heat hyperalgesia during inflammation (see review [943]). TRPM3 is frequently coexpressed with TRPA1 and TRPV1 in these neurons. TRPM3 is expressed in pancreatic beta cells as well as brain, pituitary gland, eye, kidney, and adipose tissue [713, 942]. TRPM3 may contribute to the detection of noxious heat [1020]. TRPM2TRPM2 is activated under conditions of oxidative stress (respiratory burst of phagocytic cells). The direct activators are calcium, adenosine diphosphate ribose (ADPR) [972] and cyclic ADPR (cADPR) [1121]. As for many ion channels, PI(4,5)P2 must also be present [1112]. Numerous splice variants of TRPM2 exist which differ in their activation mechanisms [239]. Recent studies have reported structures of human (hs) TRPM2, which demonstrate two ADPR binding sites in hsTRPM2, one in the N-terminal MHR1/2 domain and the other in the C-terminal NUDT9-H domain. In addition, one Ca2+ binding site in the intracellular S2-S3 loop is revealed and proposed to mediate Ca2+ binding that induces conformational changes leading the ADPR-bound closed channel to open [387, 1030]. Meanwhile, a quadruple-residue motif (979FGQI982) was identified as the ion selectivity filter and a gate to control ion permeation in hsTRPM2 [1123]. TRPM2 is involved in warmth sensation [849], and contributes to several diseases [76]. TRPM2 interacts with extra synaptic NMDA receptors (NMDAR) and enhances NMDAR activity in ischemic stroke [1167]. Activation of TRPM2 in macrophages promotes atherosclerosis [1168, 1150]. Moreover, silica nanoparticles induce lung inflammation in mice via ROS/PARP/TRPM2 signaling-mediated lysosome impairment and autophagy dysfunction [1031]. Recent studies have designed various compounds for their potential to selectively inhibit the TRPM2 channel, including ACA derivatives A23, and 2,3-dihydroquinazolin-4(1H)-one derivatives [1140, 1142]. TRPM4/5 subgroupTRPM4 and TRPM5 have the distinction within all TRP channels of being impermeable to Ca2+ [1075]. A splice variant of TRPM4 (i.e.TRPM4b) and TRPM5 are molecular candidates for endogenous calcium-activated cation (CAN) channels [327]. TRPM4 is active in the late phase of repolarization of the cardiac ventricular action potential. TRPM4 deletion or knockout enhances beta adrenergic-mediated inotropy [593]. Mutations are associated with conduction defects [404, 593, 880]. TRPM4 has been shown to be an important regulator of Ca2+ entry in to mast cells [995] and dendritic cell migration [52]. TRPM5 in taste receptor cells of the tongue appears essential for the transduction of sweet, amino acid and bitter stimuli [537] TRPM5 contributes to the slow afterdepolarization of layer 5 neurons in mouse prefrontal cortex [513]. Both TRPM4 and TRPM5 are required transduction of taste stimuli [246]. TRPM6/7 subgroupTRPM6 and 7 combine channel and enzymatic activities (‘chanzymes’) [172]. These channels have the unusual property of permeation by divalent (Ca2+, Mg2+, Zn2+) and monovalent cations, high single channel conductances, but overall extremely small inward conductance when expressed to the plasma membrane. They are inhibited by internal Mg2+ at ~0.6 mM, around the free level of Mg2+ in cells. Whether they contribute to Mg2+ homeostasis is a contentious issue. PIP2 is required for TRPM6 and TRPM7 activation [811, 1080]. When either gene is deleted in mice, the result is embryonic lethality [413, 1068]. The C-terminal kinase region of TRPM6 and TRPM7 is cleaved under unknown stimuli, and the kinase phosphorylates nuclear histones [479, 480]. TRPM7 is responsible for oxidant- induced Zn2+ release from intracellular vesicles [3] and contributes to intestinal mineral absorption essential for postnatal survival [622]. The putative metal transporter proteins CNNM1-4 interact with TRPM7 and regulate TRPM7 channel activity [40, 467]. TRPM8Is a channel activated by cooling and pharmacological agents evoking a ‘cool’ sensation and participates in the thermosensation of cold temperatures [63, 178, 224] reviewed by [1013, 562, 457, 649]. Direct chemical agonists include menthol and icilin[1089]. Besides, linalool can promote ERK phosphorylation in human dermal microvascular endothelial cells, down-regulate intracellular ATP levels, and activate TRPM8 [68]. Recent studies have found that TRPM8 has typical S4-S5 connectomes with clear selective filters and exowell rings [512], and have identified cryo-electron microscopy structures of mouse TRPM8 in closed, intermediate, and open states along the ligand- and PIP2-dependent gated pathways [1114]. Moreover, the last 36 amino acids at the carboxyl terminal of TRPM8 are key protein sequences for TRPM8's temperature-sensitive function [194]. TRPM8 deficiency reduced the expression of S100A9 and increased the expression of HNF4α in the liver of mice, which reduced inflammation and fibrosis progression in mice with liver fibrosis, and helped to alleviate the symptoms of bile duct disease [556]. Channel deficiency also shortens the time of hypersensitivity reactions in migraine mouse models by promoting the recovery of normal sensitivity [12]. A cyclic peptide DeC‐1.2 was designed to inhibit ligand activation of TRPM8 but not cold activation, which can eliminate the side effects of cold dysalgesia in oxaliplatin-treated mice without changing body temperature [9]. Analysis of clinical data shows that TRPM8-specific blockers WS12 can reduce tumor growth in colorectal cancer xenografted mice by reducing transcription and activation of Wnt signaling regulators and β-catenin and its target oncogenes, such as C-Myc and Cyclin D1 [732]. TRPML (mucolipin) familyThe TRPML family [783, 1135, 776, 1087, 190] consists of three mammalian members (TRPML1-3). TRPML channels are probably restricted to intracellular vesicles and mutations in the gene (MCOLN1) encoding TRPML1 (mucolipin-1) cause the neurodegenerative disorder mucolipidosis type IV (MLIV) in man. TRPML1 is a cation selective ion channel that is important for sorting/transport of endosomes in the late endocytotic pathway and specifically, fission from late endosome-lysosome hybrid vesicles and lysosomal exocytosis [823]. TRPML2 and TRPML3 show increased channel activity in low luminal sodium and/or increased luminal pH, and are activated by similar small molecules [319, 147, 878]. A naturally occurring gain of function mutation in TRPML3 (i.e. A419P) results in the varitint waddler (Va) mouse phenotype (reviewed by [783, 690]). TRPP (polycystin) familyThe TRPP family (reviewed by [216, 214, 300, 1064, 374]) or PKD2 family is comprised of PKD2 (PC2), PKD2L1 (PC2L1), PKD2L2 (PC2L2), which have been renamed TRPP1, TRPP2 and TRPP3, respectively [1075]. It should also be noted that the nomenclature of PC2 was TRPP2 in old literature. However, PC2 has been uniformed to be called TRPP2 [345]. PKD2 family channels are clearly distinct from the PKD1 family, whose function is unknown. PKD1 and PKD2 form a hetero-oligomeric complex with a 1:3 ratio. [906]. Although still being sorted out, TRPP family members appear to be 6TM spanning nonselective cation channels. TRPV (vanilloid) familyMembers of the TRPV family (reviewed by [997]) can broadly be divided into the non-selective cation channels, TRPV1-4 and the more calcium selective channels TRPV5 and TRPV6. TRPV1-V4 subfamilyTRPV1 is involved in the development of thermal hyperalgesia following inflammation and may contribute to the detection of noxius heat (reviewed by [763, 883, 923]). Numerous splice variants of TRPV1 have been described, some of which modulate the activity of TRPV1, or act in a dominant negative manner when co-expressed with TRPV1 [845]. The pharmacology of TRPV1 channels is discussed in detail in [329] and [1018]. TRPV2 is probably not a thermosensor in man [736], but has recently been implicated in innate immunity [547]. Functional TRPV2 expression is described in placental trophoblast cells of mouse [204]. TRPV3 and TRPV4 are both thermosensitive. There are claims that TRPV4 is also mechanosensitive, but this has not been established to be within a physiological range in a native environment [127, 530]. TRPV5/V6 subfamily TRPV5 and TRPV6 are highly expressed in placenta, bone, and kidney. Under physiological conditions, TRPV5 and TRPV6 are calcium selective channels involved in the absorption and reabsorption of calcium across intestinal and kidney tubule epithelia (reviewed by [1060, 205, 651, 270]).TRPV6 is reported to play a key role in calcium transport in the mouse placenta [1059].

Rib Fractures are a common injury in trauma patients and affect 10% of all injured patients who require admission to the hospital. Currently, there is no consensus on the most efficacious treatment for rib fractures with the debate comparing non-surgical versus surgical management. Medical management of rib fractures often requires admission to the intensive care unit with a focus on pain control to allow good pulmonary hygiene. Pain control involved a multimodal approach with current techniques including epidural anesthesia and paravertebral blocks. Although many patients recover with medical management alone, some patients may benefit from surgical stabilization of rib fractures as a means of augmenting pain control. Flail chest is the most evidence-based indication for surgical stabilization of rib fractures SSRF with many studies showing decreased days on mechanical ventilation, risk of pneumonia, intensive care unit length of stay, and hospital length of stay. Additionally, in patients with non-flail chest and ventilator dependent respiratory failure, surgical stabilization of rib fractures may provide an advantage over medical management for pain control. There are relatively few contraindications and complications associated with surgical stabilization of rib fractures. Therefore, with proper patient selection, surgical stabilization of rib fractures can improve outcomes in patients with rib fractures. Medical management with or without surgical intervention requires a multidisciplinary approach to prevent adverse clinical outcomes. Keywords: Surgical stabilization of rib fractures, rib plating, rib fracture, flail chest, non-flail chest Article Details How to Cite RAFFA, Taylor et al. Surgical Stabilization of Rib Fractures: A Review of the Indications, Technique, and Outcomes. Medical Research Archives, [S.l.], v. 11, n. 11, nov. 2023. ISSN 2375-1924. Available at: <https://esmed.org/MRA/mra/article/view/4694>. 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