Blood Phosphate Levels Research Articles

Improvement of Bone Metabolism in Prepubertal Girls with Turner Syndrome Following Long-term Pegylated Growth Hormone Treatment.

The study aims to assess the improvement in bone metabolism in prepubertal girls with Turner Syndrome (TS) after long-term polyethylene glycol recombinant human Growth Hormone (PEG-rhGH) treatment. A 12-month longitudinal prospective study was conducted with 28 prepubertal girls diagnosed with TS. Participants were divided into two groups: 18 received PEG-rhGH therapy (0.1-0.25 mg/kg/week) and 10 did not. Anthropometric measurements, bone turnover markers (BTMs), and serum levels of IGF-1, calcium, and phosphate were collected at baseline and after 12 months. BTMs included bone alkaline phosphatase (BAP), Type I collagen propeptide (CICP), Type I collagen telopeptide (CTX), and fibroblast growth factor 23 (FGF23). After 12 months of PEG-rhGH therapy, the treatment group showed significant increases in growth velocity (GV) and height standard deviation scores (HtSDS). Serum IGF-1 levels increased rapidly within one month and remained elevated. BTMs indicated enhanced bone formation, significantly increasing BAP and CICP, while CTX levels remained low. FGF23 levels initially rose slightly but declined below baseline by 12 months. Elevated blood phosphate levels were observed. PEG-rhGH therapy in children with TS significantly improves linear growth and enhances bone formation markers, benefiting bone metabolism.

The effect of local injections of a vitamin d receptor activator into the parathyroid glands on the level of parathyroid hormone and mineral metabolism in patients with secondary hyperparathyroidism in chronic kidney disease

Aim: to assess the dynamics of laboratory parameters (total calcium, inorganic phosphorus, albumin, and alkaline phosphatase levels) and parathyroid hormone (PTH) concentrations after administrating local injections of vitamin D receptor activators into the parathyroid glands of patients with secondary hyperparathyroidism in chronic kidney disease. The intial PTH concentration ranged from 300 to 600 pg/ml. This range was chosen to explore a more active strategy for managing the disease at its early stages and preventing the induction and progression of cardiovascular complications associated with secondary hyperparathyroidism.Methods: the study included 48 patients diagnosed with end-stage of chronic kidney disease, who were treated in the nephrology and dialysis department. The main group consisted of 34 patients who received two consecutive injections of a vitamin D receptor activator (Paricalcitol) into the most enlarged and technically accessible parathyroid gland under ultrasound guidance. The control group included 14 patients who continued with conservative treatment due to technical infeasibility of performing the injections. Effectiveness was assessed by comparing laboratory parameters before the intervention and six months after the injections in the main group, and among patients continuing standard medical therapy for secondary hyperparathyroidism.Results: the results showed a statistically significant reduction in parathyroid hormone levels after 3 and 6 months of treatment. In the control group, which continued to receive standard drug therapy, PTH and blood phosphate levels continued to rise. No undesirable effects or complications, such as hypocalcemia, bleeding, allergic reactions, and recurrent laryngeal nerve paralysis, were not observed throughout the observation period.Conclusion: this research confirms the efficacy of local injections of vitamin D receptor activators (Paricalcitol) in reducing PTH levels without significant complications or changes in calcium levels. This method could be employed to correct and prevent secondary hyperparathyroidism complications in early stages among patients with end-stage chronic kidney disease, offering a safer and more effective treatment option.

Prospective multicenter study to describe the prevalence, outcomes, and management of phosphate disorders in intensive care patients: Study protocol for part B of the international GUTPHOS study

BackgroundAberrations in blood phosphate (Pi) levels, whether presenting as hypo- or hyperphosphatemia, appear to be associated with clinical complications and adverse outcomes in patients admitted to an intensive care unit (ICU). However, the prevalence of Pi disorders and the association with subsequent factors and organ failures leading to death in ICU patients are poorly described. Despite endeavors to understand the etiology and treatment of low Pi levels from systematic reviews and meta-analyses, the literature lacks comprehensive guidance for managing hypophosphatemia. Hyperphosphatemia, on the other hand, appears to be associated with higher mortality among critically ill patients, yet its prevalence among ICU patients, particularly following phosphate repletion, remains unknown. The present study aims to investigate the prevalence of Pi abnormalities upon ICU admission and their incidence during the first week of ICU stay, the factors associated with Pi alterations, and the effect of phosphate repletion on the normalization of Pi levels, and its associations with clinical outcomes. MethodsThis multicentre, prospective, non-interventional cohort study will include at least 1000 consecutive adult ICU patients (≥18 years) as part B of the GUTPHOS study. Sites are eligible if an anticipated minimal inclusion of 50 eligible patients during eight weeks from January 2024 until June 2024 and daily phosphate measurements during the first seven days of ICU stay are expected. All consecutive adult patients admitted to a participating ICU during the recruitment period, lasting up to eight weeks, or up to 120 patients if enrollment reaches that limit earlier, will be included. Study parameters include study site characteristics, patient demographics, daily assessment of Pi levels, Pi-related treatment, feeding details, renal replacement therapy details, the incidence of refeeding-associated hypophosphatemia and administered medication (during the first seven calendar days of ICU stay). There will be a follow-up period of a maximum of 90 days to document 28- and 90-day all-cause mortality as the primary outcome. Multiple logistic regression will be used to assess independent associations with mortality in addition to Receiver Operating Characteristics curves to identify cut-off Pi values associated with mortality and overcorrection. Linear mixed models will be conducted to assess Pi treatment effects. Subgroup analyses will be performed based on Pi abnormalities observed during ICU admission, categorized as normo-, hypo-, hyper-, or mixed, along with its severity (mild, moderate, or severe). DiscussionThe GUTPHOS study will be the first multicentre, prospective observational cohort study to investigate the prevalence, management practices, and consequent outcomes associated with Pi abnormalities during the first week of ICU admission. Its results may bridge the current evidence gap in repletion protocols while establishing the groundwork for a subsequent randomized controlled trial. Clinical trial registryNCT05909722.

Retrospective study on the diagnosis, treatment, and follow-up of 85 cases of hypophosphatemic rickets in children

To study the diagnosis, treatment, and complications of hypophosphatemic rickets (HR) in children, explore effectiveness evaluation indicators for the disease, and understand the pattern in height growth among these patients. A retrospective analysis of the initial clinical data and five-year follow-up data of 85 children with HR treated at Children's Hospital of Nanjing Medical University from January 2008 to December 2022. Among the 85 children with HR, there were 46 males (54%) and 39 females (46%). The age at initial diagnosis ranged from 6 months to 13 years and 9 months, with a median age of 2.75 years. The average height standard deviation score was -2.0±1.1. At initial diagnosis, children exhibited reduced blood phosphate levels and elevated alkaline phosphatase (ALP), with 99% (84/85) presenting with lower limb deformities. The positive rate for PHEX gene mutations was 93% (55/59). One year post-treatment, there was a significant reduction in ALP levels and the gap between the lower limbs (P<0.05). The fastest height growth occurred in the first year after treatment, at 8.23 cm/year, with a peak height velocity (PHV) phase lasting about two years during puberty. The height increased by 9-20 cm in male children during the PHV stage and 10-15 cm in female children. Major complications included nephrocalcinosis and hyperparathyroidism. The incidence rate of nephrocalcinosis in the first year after treatment was 55% (22/40), which increased with the duration of the disease (P<0.001); an increased urinary phosphate/creatinine ratio was positively associated with a higher risk of nephrocalcinosis (OR=1.740, P<0.001). The incidence of hyperparathyroidism in the first year after treatment was 64% (27/42). For children presenting with lower limb deformities, short stature, and slow growth, early testing for blood levels of phosphate, calcium, and ALP, along with imaging examinations of the lower limbs, can aid in the early diagnosis of HR. Genetic testing may be utilized for definitive confirmation when necessary. ALP combined with improvements in skeletal deformities and annual height growth can serve as indicators of therapeutic effectiveness for HR. Compared to normal children, children with HR demonstrate a lower height increase during the PHV phase, necessitating close follow-up and timely adjustment of treatment plans Citation:Chinese Journal of Contemporary Pediatrics, 2024, 26(7): 677-682.

Exploring the Relationship Between Serum Phosphate Levels and Carotid Intima-Media Thickness in Chronic Kidney Disease Patients: A Correlational Analysis.

Background Compelling observational data suggestthat heightened levels of fasting blood phosphate are linked to a higher likelihood of cardiovascular disease, spanning across both the general populace and individuals grappling with chronic kidney disease (CKD). This study aimed to explore the possible correlation between carotid intima-media thickness (CIMT) and blood phosphate levels among those afflicted with chronic renal dysfunction. Objective The primary goal of this study is to determine the potential association between blood phosphate levels and CIMT in patients with CKD. Methodology In the department of nephrology, prospective research was conducted among patients who had a history of CKD. Atotal of 30 patients were included, with 20 males and 10 females. Every case had a thorough physical examination and history. Every patient underwent a laboratory evaluation, which included measurements of the CIMT and renal function testing. At a distance of 1 cm from the carotid bulb, the CIMTwas measured using B-mode ultrasonography. After compilation, the data were examined. Results The majority of the patients, according to this study, were male and over 50 years old. The Stage II patients in the study had a higher mean systolic blood pressure; however, the difference was not statistically significant. Patients with Stage V (D) disease exhibited higher diastolic blood pressure, but not statistically significant. An increase in the mean serum creatinine level that was statistically significant was linked to Stage V (D) renal disease. A higher mean blood urea was linked to Stage V (D) sickness; however, this relationship was not statistically significant. There was no statistical difference in the mean serum calcium levelsbetween the different stages of renal disease. Higher mean blood phosphate levels were linked to Stage III renal disease, but not in a statistically meaningful way. Although it was higher in Stage IV kidney disease, the mean CIMT was not statistically significant between the stages of renal illness. Conclusions Although a positive correlation was shown, a direct relationship between serum phosphate levels was not established by this investigation. The severity of renal disease has been demonstrated to correlate with elevated serum phosphate levels.

Hypophosphatemia and Type-2 Diabetes Mellitus: A Review

Type-2 diabetes is a global public health crisis that threatens the economies of all nations, particularly developing countries. Type-2 diabetes mellitus has been suggested to be the most common endocrine disorder associated with several metabolic disturbances including changes in serum calcium, zinc, magnesium, or phosphate. Moreover, those who have poor glycemic control and longtime diabetes mellitus are more likely to decrease the blood phosphate level. Low serum phosphate level may be associated with morbidity and mortality from cardiovascular disease in these patients. So, the findings of this study may suggest that serum phosphate is an important screening parameter in type-2 diabetic patients especially who have poor glycemic control and longtime diabetes mellitus. Eastern Med Coll J. July 2023; 8 (2): 45-50

Tenapanor-A Novel Approach for Management of Hyperphosphatemia in End Stage Renal Disease: A Clinical Study Aggregate Review

The critical importance of phosphate regulation in chronic kidney disease (CKD) has been well understood for decades. But new findings, frequently applicable to routine medical care, continue to evolve. Poor health outcomes, greater morbidity, lowered quality of life, and a higher death rate from cardiovascular disease are all linked to the development of CKD-bone mineral ailment. Increased blood phosphate levels are linked to an increased risk of mortality in hemodialysis patients due to changes in phosphate breakdown and declining renal function as CKD advances.In this setting, according to CKD-mineral bone disease recommendations, it is critical to regulate serum phosphate levels in patients with CKD-mineral bone problem. If dialysis and dietary intervention fail to control blood phosphate levels, the use of phosphate binders is advised. Although phosphate binders are successful in lowering blood phosphate levels by actively binding to dietary phosphate, certain individuals have adverse effects that may restrict their use.These medications also have a significant pill load, which might result in poor treatment compliance. Tenapanor, a novel medication, works by inhibiting the sodium/hydrogen exporter isoform 3 (NHE3), which lowers intestinal phosphate absorption primarily by decreasing passive paracellular phosphate flow. Tenapanor also reduces the expression of the sodium phosphorus 2b transport protein (NaPi2b), which limits active transcellular phosphate absorption compensation. This is considered to be more effective phosphorous absorption regulator and a better target for tailored medication therapy. This clinical study aggregate report explores the currently published studies that have evaluated Tenapanor for the treatment of hyperphosphatemia in end stage renal disease patients on haemodialysis.&#x0D; Keywords: Tenapanor, phosphate binding agents, hyperphosphatemia, chronic kidney disease, phosphate control, phosphate binders, phosphate absorption, phosphate absorbtion inhibitor.

Newborn phosphocalcic metabolism after intravenous iron administration during pregnancy

Objective Iron deficiency anemia is a very common health problem during pregnancy and intravenous (IV) iron substitution has become part of routine management. However, recent studies have raised concerns about the association of IV iron infusion and the development of secondary transitory hypophosphatemia (HP) in adults, including pregnant women. We aimed to evaluate the impact of IV iron administration during pregnancy on the phosphocalcic metabolism of newborns. Methods A prospective, single-center, observational study was performed from December 2022 to May 2023 at the maternity facility of Geneva University Hospitals. We included women treated with either IV or oral iron during pregnancy. At delivery, a maternal blood sample was collected to assess hemoglobin, hematocrit, and levels of ferritin, phosphate and calcium, as well as an umbilical cord blood sample to assess levels of phosphate and calcium. Univariate and multivariate analyses were performed to evaluate the contribution of IV iron substitution on cord blood phosphatemia and calcemia, considering potential confounding factors. Neonatal HP was defined as a phosphate level <1.3 mmol/L. Results Forty-three pregnant women were included in our study. Among these, 22 were treated with ferric carboxymaltose and 21 with oral iron. There were three cases of maternal HP in the IV iron group (13.6%) and one (4.8%) in the control group (p value for the difference= .607). We observed one case (4.5%) of neonatal HP in the IV iron group and no cases in the control group. Median cord blood phosphatemia and calcemia were 1.7 mmol/L vs. 1.71 mmol/L and 2.67 mmol/L vs. 2.64 mmol/L in the IV iron and oral groups, respectively. After adjustment, IV iron administration had no impact on cord blood phosphate (p= .919) and calcium (p= .891) levels. Conclusion No impact of IV iron administration during pregnancy was observed on the newborn phosphocalcic metabolism.

Phosphate-sensing mechanisms and functions of phosphate as a first messenger.

Bone secrets the hormone, fibroblast growth factor 23 (FGF23), as an endocrine organ to regulate blood phosphate level. Phosphate is an essential mineral for the human body, and around 85% of phosphate is present in bone as a constituent of hydroxyapatite, Ca10(PO4)6(OH)2. Because hypophosphatemia induces rickets/osteomalacia, and hyperphosphatemia results in ectopic calcification, blood phosphate (inorganic form) level must be regulated in a narrow range (2.5 mg/dL to 4.5 me/dL in adults). However, as yet it is unknown how bone senses changes in blood phosphate level, and how bone regulates the production of FGF23. Our previous data indicated that high extracellular phosphate phosphorylates FGF receptor 1 (FGFR1) in an unliganded manner, and its downstream intracellular signaling pathway regulates the expression of GALNT3. Furthermore, the post-translational modification of FGF23 protein via a gene product of GALNT3 is the main regulatory mechanism of enhanced FGF23 production due to high dietary phosphate. Therefore, our research group proposes that FGFR1 works as a phosphate-sensing receptor at least in the regulation of FGF23 production and blood phosphate level, and phosphate behaves as a first messenger. Phosphate is involved in various effects, such as stimulation of parathyroid hormone (PTH) synthesis, vascular calcification, and renal dysfunction. Several of these responses to phosphate are considered as phosphate toxicity. However, it is not clear whether FGFR1 is involved in these responses to phosphate. The elucidation of phosphate-sensing mechanisms may lead to the identification of treatment strategies for patients with abnormal phosphate metabolism.

A competing risk predictive model for kidney failure in patients with advanced chronic kidney disease

Background/purposePredictive modeling aids in identifying patients at high risk of adverse events. Using routinely collected data, we report a competing risk prediction model for kidney failure. MethodsA total of 5138 patients with CKD stages 3b–5 were included and randomized into the development and validation cohorts at a ratio of 7:3. The outcome was end-stage kidney disease, defined as the initiation of dialysis or kidney transplantation. All patients were followed-up until December 31, 2020. A Fine and Gray model was applied to estimate the sub-hazard ratio of kidney failure, with death as a competing event. ResultsIn the development cohort, the mean age was 67.6 ± 13.9 years and 60 % were male. The mean index eGFR and median urinary protein-creatinine ratio (UPCR) were 26.5 ± 12.8 mL/min/1.73 m2 and 1051 mg/g, respectively. The median follow-up duration was 1051 days. The proportion of patients with kidney failure and death was 25.4 % and 14.1 %, respectively. Four models were applied, including eGFR, age, sex, UPCR, systolic and diastolic blood pressure, serum albumin, phosphate, uric acid, haemoglobin, and potassium levels had the best goodness of fit. All models had good discrimination with time-to-event c statistics of 0.89–0.95 in the development cohort and 0.86–0.95 in the validation cohort. The prediction models showed excellent and fairly good calibration at 2 and 5-year risk, respectively. ConclusionUsing real-world data, our competing risk model can accurately predict progression to kidney failure over 2 years in patients with advanced CKD.

B-005 Blood pH and Phosphate Tend to Follow an Inversely Correlated Homeostatic Status

Abstract Background Phosphorus containing biomolecules perform an essential biochemical function in maintaining extra and intracellular acid-base status. Maintaining normal concentration (2.5–4.5 mg/dl) of phosphorus is indispensable for optimal cellular function and homeostasis. Serum concentration of phosphorus (mainly inorganic orthophosphates) is an indicator of H2PO4−/HPO42− acid-base buffer condition. Disturbance of pH could be an immediate impact of many respiratory and metabolic morbidities. Extra/intracellular redistribution of phosphates in response to an abnormal pH is an established homeostatic phenomenon. Failure to maintain an appropriate phosphate level to support the extra/intracellular redistribution may result in a pH shock. Therefore, it is important to have a clear understanding on how blood phosphate and pH levels are interconnected which could assist in guiding therapeutic interventions to fix phosphate abnormalities and acid-base disturbances. This study examined the homeostatic correlation between blood pH and phosphate level among hospitalized and ambulatory patients. Methods Serum phosphorus concentration and pH were retrieved from the biochemical profiles and arterial blood gas data of hospitalized and ambulatory patients who presented or admitted our tertiary care level university hospital during the first week of July, 2021. Logarithmic (base ten) values of phosphorus concentration were determined to normalize the distribution of the phosphorus data more uniform. Correlation analyses between phosphorus/log[phosphorus] and pH were performed by GraphPad PRISM version 8. Results A total of 101 corresponding blood gases and phosphate levels were obtained. Both phosphorus and log [phosphorus] values of the patients displayed an inverse correlation with arterial pH (Figure 1a and b). Pearson r values demonstrated a negative correlation between phosphorus/log [phosphorus] and pH (−0.6737 and −0.6450, respectively).Fig. 1. Conclusion Monitoring of phosphate levels provide an early indication of acid base status. Phosphorus level maintains an inverse correlation with pH profile. Therefore, a therapeutic manipulation of phosphorus or pH may have a mutual effect requiring further investigation.

The Synergistic Effect of Zuogui Pill and Eldecalcitol on Improving Bone Mass and Osteogenesis in Type 2 Diabetic Osteoporosis.

Background and Objectives: The incidence of diabetic osteoporosis, an important complication of diabetes mellitus, is increasing gradually. This study investigated the combined effect of the Zuogui pill (ZGP) and eldecalcitol (ED-71), a novel vitamin D analog, on type 2 diabetic osteoporosis (T2DOP) and explored their action mechanism. Materials and Methods: Blood glucose levels were routinely monitored in db/db mice while inducing T2DOP. We used hematoxylin and eosin staining, Masson staining, micro-computed tomography, and serum biochemical analysis to evaluate changes in the bone mass and blood calcium and phosphate levels of mice. Immunohistochemical staining was performed to assess the osteoblast and osteoclast statuses. The MC3T3-E1 cell line was cultured in vitro under a high glucose concentration and induced to undergo osteogenic differentiation. Quantitative real-time polymerase chain reaction, Western blot, immunofluorescence, ALP, and alizarin red staining were carried out to detect osteogenic differentiation and PI3K-AKT signaling pathway activity. Results: ZGP and ED-71 led to a dramatic decrease in blood glucose levels and an increase in bone mass in the db/db mice. The effect was strongest when both were used together. ZGP combined with ED-71 promoted osteoblast activity and inhibited osteoclast activity in the trabecular bone region. The in vitro results revealed that ZGP and ED-71 synergistically promoted osteogenic differentiation and activated the PI3K-AKT signaling pathway. The PI3K inhibitor LY294002 or AKT inhibitor ARQ092 altered the synergistic action of both on osteogenic differentiation. Conclusions: The combined use of ZGP and ED-71 reduced blood glucose levels in diabetic mice and promoted osteogenic differentiation through the PI3K-AKT signaling pathway, resulting in improved bone mass. Our study suggests that the abovementioned combination constitutes an effective treatment for T2DOP.

Case Report on Hypophosphatemic Rickets

In children with rickets, osteoid fails to mineralize. This condition is sometimes accompanied by a vitamin D deficiency or a drop in blood phosphate levels, which causes hypophosphatemia. This case report describes a 4-year-old youngster with persistent respiratory conditions since he was nine months old. At an outpatient tubulopathies clinic, throughout a 24-month study, information on the patient's metabolic profile, creatinine clearance, nutritional status, weight, and body composition was gathered. Clinical and laboratory evidence of hypophosphatemia rickets was present in the patient. The patient's bone metabolism had changed. He had been bedridden for some time and was mechanically ventilated. Our case improved after receiving phosphate, calcium, and calcitriol multiple as treatment. The patient improved, eventually walking alone and breathing on his own. Additionally, weight and structural development are enhanced with transient gallstones. The clearance of creatinine was constant. The medication improved his test results and nutritional status. Following two years of treatment, he fully recovered. Early detection can help kids receive additional support earlier and prevent them from falling behind. All age groups can benefit from multimodality treatment, which is essential for managing the condition. The current example is presented since it is so uncommon.

Exploring the interplay between kidney health, vitamin D levels, and mineral/bone disorders in chronic kidney disease (CKD)

Introduction: CKD is associated with a number of problems of mineral and bone metabolism, including vitamin D deficiency and secondary hyperparathyroidism. The relationships between a lack of vitamin D, circulating indicators of mineral and bone diseases (MBD), and renal function in CKD are not well understood. This cross-sectional research included 1,060 individuals with CKD stages 2 to 5 from the Institute of Kidney Disease (IKD), Peshawar. In addition to other indicators of bone metabolism, we evaluated the estimated glomerular filtration rate (eGFR), blood levels of Calcifediol, calcium, phosphate, and intact parathyroid hormone (PTH). The results of interest were blood calcium, phosphate, and PTH levels as well as other indicators of bone metabolism. These markers also included circulating markers of MBD. Results: Higher blood Parathyroid Hormones levels, in addition to lower levels of blood calcium and phosphate, were all associated with vitamin D deficiency and decreased eGFR. Additionally, vitamin D deficiency has been independently linked to lower levels of other bone metabolism indicators, including tartrate-resistant acid phosphatase-5b and bone-specific alkaline phosphatase. In patients with CKD, abnormalities in mineral and bone metabolism, including greater PTH levels and lower calcium and phosphate levels, are independently correlated with reduced eGFR and vitamin D insufficiency.

Kidney glycolysis serves as a mammalian phosphate sensor that maintains phosphate homeostasis.

How phosphate levels are detected in mammals is unknown. The bone-derived hormone fibroblast growth factor 23 (FGF23) lowers blood phosphate levels by reducing kidney phosphate reabsorption and 1,25(OH)2D production, but phosphate does not directly stimulate bone FGF23 expression. Using PET scanning and LC-MS, we found that phosphate increases kidney-specific glycolysis and synthesis of glycerol-3-phosphate (G-3-P), which then circulates to bone to trigger FGF23 production. Further, we found that G-3-P dehydrogenase 1 (Gpd1), a cytosolic enzyme that synthesizes G-3-P and oxidizes NADH to NAD+, is required for phosphate-stimulated G-3-P and FGF23 production and prevention of hyperphosphatemia. In proximal tubule cells, we found that phosphate availability is substrate-limiting for glycolysis and G-3-P production and that increased glycolysis and Gpd1 activity are coupled through cytosolic NAD+ recycling. Finally, we show that the type II sodium-dependent phosphate cotransporter Npt2a, which is primarily expressed in the proximal tubule, conferred kidney specificity to phosphate-stimulated G-3-P production. Importantly, exogenous G-3-P stimulated FGF23 production when Npt2a or Gpd1 were absent, confirming that it was the key circulating factor downstream of glycolytic phosphate sensing in the kidney. Together, these findings place glycolysis at the nexus of mineral and energy metabolism and identify a kidney-bone feedback loop that controls phosphate homeostasis.

Assessing the Progression of Early Atherosclerosis Mice Using a Fluorescence Nanosensor for the Simultaneous Detection and Imaging of pH and Phosphorylation

AbstractThe inflammatory microenvironment involves changes in pH and protein phosphorylation state and is closely related to the occurrence and development of atherosclerosis (AS). Herein, we constructed a dual‐detection fluorescence nanosensor PCN‐NP‐HPZ based on post modification of MOFs, which realized the simultaneous detection and imaging of pH and phosphorylation through the pH‐sensitive group piperazine and the ZrIV node of the MOFs. The sensors were used to monitor changes in blood pH and phosphate levels at different time stages during atherosclerotic plaque formation. Two‐photon fluorescence imaging was also performed in the vascular endothelium. Blood tests combined with two‐photon fluorescence images indicated that in the early stage of AS, blood and tissue pH levels were lower than that of the normal mice, while phosphate and tissue phosphorylation levels were higher than that of the normal mice. The present study provides a new analysis method for the assessment of early atherosclerotic disease.

Assessing the Progression of Early Atherosclerosis Mice Using a Fluorescence Nanosensor for the Simultaneous Detection and Imaging of pH and Phosphorylation.

The inflammatory microenvironment involves changes in pH and protein phosphorylation state and is closely related to the occurrence and development of atherosclerosis (AS). Herein, we constructed a dual-detection fluorescence nanosensor PCN-NP-HPZ based on post modification of MOFs, which realized the simultaneous detection and imaging of pH and phosphorylation through the pH-sensitive group piperazine and the ZrIV node of the MOFs. The sensors were used to monitor changes in blood pH and phosphate levels at different time stages during atherosclerotic plaque formation. Two-photon fluorescence imaging was also performed in the vascular endothelium. Blood tests combined with two-photon fluorescence images indicated that in the early stage of AS, blood and tissue pH levels were lower than that of the normal mice, while phosphate and tissue phosphorylation levels were higher than that of the normal mice. The present study provides a new analysis method for the assessment of early atherosclerotic disease.

Dental Manifestations of Vitamin D Resistant Rickets in Orthopantomogram

Vitamin D is crucial for maintaining healthy bones by sustaining appropriate calcium and phosphorus levels in the blood. It is one factor responsible for maintenance of blood calcium and phosphate levels. Hence there exists Calcium, Vitamin D and Phosphorus axis. Rickets refers to any condition of Vitamin D, Calcium and phosphorus axis which causes hypominaralized bone matrix. It is a typical bone condition that causes problems with the calcium and phosphate balance and can cause low height and anomalies in the joints. Radiological findings, biochemical testing, and history and physical examinations can all be used to diagnose rickets, Depending on amounts of phosphate or calcium. It is classified into two broad groups Calcipenic and Phosphopenic .Knowledge of rickets classification is vital for quick diagnosis and adequate therapy. This article gives a brief overview of different types of rickets as well as describe dental manifestations of vitamin D resistant rickets in orthopantomogram in a 13 year old girl

Joint inference of physiological network and survival analysis identifies factors associated with aging rate

We describe methodology for joint reconstruction of physiological-survival networks from observational data capable of identifying key survival-associated variables, inferring a minimal physiological network structure, and bridging this network to the Gompertzian survival layer. Using synthetic network structures, we show that the method is capable of identifying aging variables in cohorts as small as 5,000 participants. Applying the methodology to the observational human cohort, we find that interleukin-6, vascular calcification, and red-blood distribution width are strong predictors of baseline fitness. More important, we find that red blood cell counts, kidney function, and phosphate level are directly linked to the Gompertzian aging rate. Our model therefore enables discovery of processes directly linked to the aging rate of our species. We further show that this epidemiological framework can be applied as a causal inference engine to simulate the effects of interventions on physiology and longevity.

Blood alcohol levels after standardized intake of alcohol are related to measured blood phosphate levels

The role of blood phosphate in alcohol metabolism has not been studied. In this explorative experimental study, the relationship between blood phosphate levels and metabolism of alcohol was investigated. Twenty young male volunteers were given alcohol relative to body weight to make them reach a theoretical blood alcohol concentration (BAC) of 0.12%. Ten measurements of BAC were taken across the time from intake, to peak and total elimination. The results indicated that individuals with high blood phosphate levels achieved a lower BAC maximum than those with low blood phosphate levels. The difference between the highest and lowest maximum BAC was as much as 30–40% and correlated negatively to physiological blood phosphate levels. The results suggest that phosphate plays a role in prehepatic, possibly gastric, alcohol metabolism. The Alcohol Dehydrogenase enzyme 7 (ADH7) is represented in the upper gastrointestinal tract and may be the enzyme responsible for this variation in the blood alcohol concentration reached.