BCAA-nitrogen flux in brown fat controls metabolic health independent of thermogenesis.

Brown adipose tissue (BAT) is best known for thermogenesis. Rodent studies demonstrated that enhanced BAT thermogenesis is tightly associated with increased energy expenditure, reduced body weight, and improved glucose homeostasis. However, human BAT is protective against type 2 diabetes, independent of body weight. The mechanism underlying this dissociation remains unclear. Here, we report that impaired mitochondrial catabolism of branched-chain amino acids (BCAAs) in BAT, by deleting mitochondrial BCAA carriers (MBCs), caused systemic insulin resistance without affecting energy expenditure and body weight. Brown adipocytes catabolized BCAA in the mitochondria as nitrogen donors for the biosynthesis of non-essential amino acids and glutathione. Impaired mitochondrial BCAA-nitrogen flux in BAT resulted in increased oxidative stress, decreased hepatic insulin signaling, and decreased circulating BCAA-derived metabolites. A high-fat diet attenuated BCAA-nitrogen flux and metabolite synthesis in BAT, whereas cold-activated BAT enhanced the synthesis. This work uncovers a metabolite-mediated pathway through which BAT controls metabolic health beyond thermogenesis.

A case of mild partial androgen insensitivity syndrome in a juvenile boy.

Androgen insensitivity syndrome (AIS) is a rare disorder with X-linked recessive inheritance in 46 XY patients. The clinical manifestations vary between patients, especially regarding external genitalia development. Herein, the case of AIS in a 13-year-old male, who was born with hypospadias and presented to the hospital with gynaecomastia that had developed from 8 years of age, is reported. No micropenis, cryptorchidism or bifid scrotum were found. Testis volume was 12 ml on both sides. His testosterone and luteinizing hormone levels were normal compared with sex- and age-adjusted reference range. His bone age was approximately 13 years according to Greulich-Pyle assessment. Sequence analysis of the androgen receptor (AR) gene revealed a mutation (c.2041A>G) in exon 4, a novel mutation site in the AR gene. Prediction analysis suggested this to be a disease-causing variant. A milder clinical presentation and normal hormone levels in cases of partial AIS might differ from the usually reported signs and symptoms. A diagnosis of AIS should not be ignored in teenage patients who present with gynaecomastia and hypospadias, but normal hormone levels.

CircRNA_102046 Affects the Occurrence and Development of Ischemic Stroke by Regulating the miR-493-5p/ROCK1 Signaling.

In our previous studies, the results have revealed that circRNA_102046 is significantly upregulated in plasma of patients with ischemic stroke, which closely related to NIHSS score. Human neural stem cells (hNSCs) were used for characterization and subcellular localization of circRNA_102046, and hNSCs OGD/R model was generated. The proliferation of cells was examined by CCK-8 assay. The expression levels of associated molecules were evaluated using RT-qPCR, immunofluorescence staining or western blotting. The binding and co-localization of associated molecules were also evaluated by RIP and FISH assay. Furthermore, MCAO mouse model was established to examine the effects of circRNA_102046 on the progression of ischemic stroke. Expression of circRNA_102046 was detected in the cytoplasma of hNSCs. Then OGD/R cell model was established, where the levels of circRNA_102046 was significantly up-regulated. Furthermore, knockdown of circRNA_102046 was able to enhance the proliferation and differentiation of OGD/R hNSCs. In further downstream molecular studies, the results indicated that circRNA_102046 could participate in the occurrence and development of ischemic stroke through targeting miR-493-5p. In addition, ROCK1 was identified as the putative target of miR-493-5p, and circRNA_102046 regulates the proliferation and differentiation of hNSCs via the miR-493-5p/ROCK1 signaling. More importantly, the infarct volumes of MCAO mice were remarkably reduced after the treatment with sh-circRNA_102046, which also up- and down-regulate the expression of miR-493-5p and ROCK1, respectively. Elucidating this novel pathway provides a theoretical basis for the development of new diagnostic approach and targeted treatment for ischemic stroke.

Clinical effect of laparoscopic radical resection of colorectal cancer based on propensity score matching.

BACKGROUND: The incidence of colorectal cancer (CRC) is increasing annually. Laparoscopic radical resection of CRC is a minimally invasive procedure preferred in clinical practice. AIM: To investigate the clinical effect of laparoscopic radical resection of CRC on the basis of propensity score matching (PSM). METHODS: The clinical data of 100 patients who received inpatient treatment for CRC at Changde Hospital, Xiangya School of Medicine, Central South University (The First People's Hospital of Changde City) were analyzed retrospectively. The control group included patients who underwent open surgery (n = 43), and those who underwent laparoscopic surgery formed the observation group (n = 57). The baseline information of both groups was equipoised using 1 × 1 PSM. Differences in the perioperative parameters, inflammatory response, immune function, degree of pain, and physical status between the groups were analyzed. RESULTS: Thirty patients from both groups were successfully matched. After PSM, baseline data showed no statistically significant differences between the groups: (1) Perioperative parameters: The observation group had a longer surgery time, less intraoperative blood loss, earlier first ambulation and first anal exhaust times, and shorter gastric tube indwelling time than the control group; (2) Inflammatory response: 24 h after surgery, the levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) between groups were higher than preoperatively. IL-6, CRP, and TNF-α levels in the observation group were lower than in the control group; (3) Immune function: At 24 h after surgery, counts of CD4-positive T-lymphocytes (CD4+) and CD4+/CD8-positive T-lymphocytes (CD8+) in both groups were lower than those before surgery, whereas CD8+ was higher than that before surgery. At 24 h after surgery, both CD4+ counts and CD4+/CD8+ in the observation group were higher than those in the control group, whereas CD8+ counts were lower; (4) Degree of pain: The visual analog scale scores in the observation group were lower than those in the control group at 24 and 72 h after surgery; and (5) Physical status: One month after surgery, the Karnofsky performance score in the observation group was higher than that in the control group. CONCLUSION: Laparoscopic radical resection of CRC has significant benefits, such as reducing postoperative pain and postoperative inflammatory response, avoiding excessive immune inhibition, and contributing to postoperative recovery.

High Doses of Exogenous Glucagon Stimulate Insulin Secretion and Reduce Insulin Clearance in Healthy Humans.

Glucagon is generally defined as a counterregulatory hormone with a primary role to raise blood glucose concentrations by increasing endogenous glucose production (EGP) in response to hypoglycemia. However, glucagon has long been known to stimulate insulin release, and recent preclinical findings have supported a paracrine action of glucagon directly on islet ß-cells that augments their secretion. In mice, the insulinotropic effect of glucagon is glucose dependent and not present during basal euglycemia. To test the hypothesis that the relative effects of glucagon on hepatic and islet function also vary with blood glucose, a group of healthy subjects received glucagon (100 ng/kg) during fasting glycemia or experimental hyperglycemia (∼150 mg/dL) on 2 separate days. During fasting euglycemia, administration of glucagon caused blood glucose to rise due to increased EGP, with a delayed increase of insulin secretion. When given during experimental hyperglycemia, glucagon caused a rapid, threefold increase in insulin secretion, as well as a more gradual increase in EGP. Under both conditions, insulin clearance was decreased in response to glucagon infusion. The insulinotropic action of glucagon, which is proportional to the degree of blood glucose elevation, suggests distinct physiologic roles in the fasting and prandial states.

YTHDF2-mediated regulations bifurcate BHPF-induced programmed cell deaths.

N6-methyladenosine (m6A) is a critical regulator in the fate of RNA, but whether and how m6A executes its functions in different tissues remains largely obscure. Here we report downregulation of a crucial m6A reader, YTHDF2, leading to tissue-specific programmed cell deaths (PCDs) upon fluorene-9-bisphenol (BHPF) exposure. Currently, Bisphenol A (BPA) substitutes are widely used in plastic manufacturing. Interrogating eight common BPA substitutes, we detected BHPF in 14% serum samples of pregnant participants. In a zebrafish model, BHPF caused tissue-specific PCDs triggering cardiac and vascular defects. Mechanistically, BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m6A-gch1 for cardiomyocyte ferroptosis, and decreased YTHDF2-mediated m6A-sting1 decay for caudal vein plexus (CVP) apoptosis. The two distinct YTHDF2-mediated m6A regulations and context-dependent co-expression patterns of gch1/ythdf2 and tnfrsf1a/ythdf2 contributed to YTHDF2-mediated tissue-specific PCDs, uncovering a new layer of PCD regulation. Since BHPF/YTHDF2-medaited PCD defects were also observed in mammals, BHPF exposure represents a potential health threat.

LILRB2/PirB mediates macrophage recruitment in fibrogenesis of nonalcoholic steatohepatitis.

Inhibition of immunocyte infiltration and activation has been suggested to effectively ameliorate nonalcoholic steatohepatitis (NASH). Paired immunoglobulin-like receptor B (PirB) and its human ortholog receptor, leukocyte immunoglobulin-like receptor B (LILRB2), are immune-inhibitory receptors. However, their role in NASH pathogenesis is still unclear. Here, we demonstrate that PirB/LILRB2 regulates the migration of macrophages during NASH by binding with its ligand angiopoietin-like protein 8 (ANGPTL8). Hepatocyte-specific ANGPTL8 knockout reduces MDM infiltration and resolves lipid accumulation and fibrosis progression in the livers of NASH mice. In addition, PirB-/- bone marrow (BM) chimeras abrogate ANGPTL8-induced MDM migration to the liver. And yet, PirB ectodomain protein could ameliorate NASH by sequestering ANGPTL8. Furthermore, LILRB2-ANGPTL8 binding-promoted MDM migration and inflammatory activation are also observed in human peripheral blood monocytes. Taken together, our findings reveal the role of PirB/LILRB2 in NASH pathogenesis and identify PirB/LILRB2-ANGPTL8 signaling as a potential target for the management or treatment of NASH.

Case report: Autosomal recessive type 3 Stickler syndrome caused by compound heterozygous mutations in COL11A2.

Background: Stickler syndrome (SS) is a group of hereditary collagenopathies caused by a variety of collagen and non-collagen genes. Affected patients have characteristic manifestations involving ophthalmic, articular, craniofacial and auditory disorders. SS is classified into several subtypes according to clinical and molecular features. Type 3 SS is an ultra-rare disease, known as non-ocular SS or otospondylomegaepiphyseal dysplasia (OSMED) with only a few pathogenic COL11A2 variants reported to date. Case presentation: A 29-year-old Chinese male was referred to our hospital for hearing loss and multiple joint pain. He presented a phenotype highly suggestive of OSMED, including progressive sensorineural deafness, spondyloepiphyseal dysplasia with large epiphyses, platyspondyly, degenerative osteoarthritis, and sunken nasal bridge. We detected compound heterozygous mutations in COL11A2, both of which were predicted to be splicing mutations. One is synonymous mutation c.3774C>T (p.Gly1258Gly) supposed to be a splice site mutation, the other is a novel intron mutation c.4750 + 5 G>A, which is a highly conservative site across several species. We also present a review of the current known pathogenic mutation spectrum of COL11A2 in patients with type 3 SS. Conclusion: Both synonymous extonic and intronic variants are easily overlooked by whole-exome sequencing. For patients with clinical manifestations suspected of SS syndrome, next-generation whole-genome sequencing is necessary for precision diagnosis and genetic counseling.

Sphenoid sinus is a rare site for tumor-induced osteomalacia: A case report and literature review.

Background: In this paper, we present a rare case of tumor-induced osteomalacia (TIO) and a literature review of this rare disease. Methods: A case of TIO of the isolated sphenoid sinus was reported. Furthermore, the clinical features of TIO in the sphenoid sinus and other sinonasal sinuses were also reviewed and summarized. Results: A 35-year-old man with muscle weakness and lower back pain came to the Department of Neurology. No obvious neurological disease was found; however, magnetic resonance imaging of the extremities accidentally showed a tumor in the axilla. Bone scintigraphy showed suspicious bone metastasis. Hypophosphatemia was neglected. Interestingly, 2-deoxy-2-[fluorine-18]fluoro-d-glucose positron emission tomography/computed tomography (18F-FDG PET/CT) detected a tumor in the axilla and another in the sphenoid sinus, but only the tumor in the sphenoid sinus had somatostatin receptor (SSTR) expression in 68-gallium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid octreotate (Ga-68 DOTATATE) PET/CT. The sphenoid sinus tumor was proven to be a phosphaturic mesenchymal tumor (PMT), and the phosphate levels returned to normal after surgery. The literature review showed only 17 cases of TIOs that occurred in the sphenoid sinus, with an average age of 43.3 ± 13.7 years. Only three cases of TIOs in the sphenoid sinus did not invade the nasal cavity or other paranasal sinuses, which could be identified as isolated sphenoid sinus diseases. We compared the clinical features of sphenoid TIOs with those of non-sphenoid sinonasal TIOs, and it was found that the concentration of 1,25-dihydroxy vitamin D in the group with sphenoid TIOs was much higher than that in the group with non-sphenoid sinonasal TIOs. A total of 153 cases of TIOs in the sinonasal sinus were reviewed. The ethmoid sinus was found to be the major site (64.7%), followed by the nasal cavity (50.3%), maxillary sinus (19.0%), frontal sinus (16.4%), and sphenoid sinus (11.8%). There were 66 patients (43.1%) who showed tumors invading more than one sinus. Most of the tumors (69.3%) were diagnosed as PMTs by pathology, followed by hemangiopericytoma (14.3%). Immunostaining was beneficial in the differential diagnosis of these tumors; however, larger sample sizes are needed for better accuracy. Conclusion: TIO in the sinonasal sinus, especially in the sphenoid sinus, is rare. Moreover, isolated sphenoid sinus disease can be easily misdiagnosed. When the clinical manifestation of osteomalacia is atypical, associating it with sphenoid sinus disease is even more difficult. Thus, TIO in the sphenoid sinus needs further exploration.

Ischemia promotes acyl-CoAs dephosphorylation and propionyl-CoA accumulation.

INTRODUCTION: Our untargeted metabolic data unveiled that Acyl-CoAs undergo dephosphorylation, however little is known about these novel metabolites and their physiology/pathology relevance. OBJECTIVES: To understand the relationship between acyl-CoAs dephosphorylation and energy status as implied in our previous work, we seek to investigate how ischemia (energy depletion) triggers metabolic changes, specifically acyl-CoAs dephosphorylation in this work. METHODS: Rat hearts were isolated and perfused in Langendorff mode for 15 min followed by 0, 5, 15, and 30 minutes of global ischemia. The heart tissues were harvested for metabolic analysis. RESULTS: As expected, ATP and phosphocreatine were significantly decreased during ischemia. Most short- and medium-chain acyl-CoAs progressively increased with ischemic time from 0 to 15 min, whereas a 30-minute ischemia did not lead to further change. Unlike other acyl-CoAs, propionyl-CoA accumulated progressively in the hearts that underwent ischemia from 0 to 30 min. Progressive dephosphorylation occurred to all assayed acyl-CoAs and free CoA regardless their level changes during the ischemia. CONCLUSION: The present work further confirms that dephosphorylation of acyl-CoAs is an energy-dependent process and how this dephosphorylation is mediated warrants further investigations. It is plausible that dephosphorylation of acyl-CoAs and limited anaplerosis are involved in ischemic injuries to heart. Further investigations are warranted to examine the mechanisms of acyl-CoA dephosphorylation and how the dephosphorylation is possibly involved in ischemic injuries.

Terminal group effects of DOPO-conjugated flame retardant on polyamide 6: Thermal stability, flame retardancy and mechanical performances.

Two DOPO-conjugated flame retardants with or without amino terminal groups (DOPO-NH2 and DIDOPO, respectively) were synthesized and incorporated into polyamide 6 (PA6). Results demonstrated the DOPO-NH2 endowed superior thermal, flame retardant and mechanical performances to PA6 composites. With the same loading of 15 wt%, DOPO-NH2 can catalyze the PA6 matrix more effectively and result in more residues at high temperature. The PA6 composites containing DOPO-NH2 exhibited higher LOI (28.0%) compared to 25.0% for the sample containing DIDOPO, and the lower heat release capacity and peak heat release rate. Furthermore, the overall mechanical properties of PA6 composites containing DOPO-NH2 outperformed the samples containing DIDOPO, even superior to that for PA6. Such a significant difference can be mainly attributed to the existence of amino-terminal group, which can interact with carboxyl group in PA6 as confirmed by dynamic mechanical analysis, improving the compatibility between the flame retardant and PA6 matrix.

m6A modification confers thermal vulnerability to HPV E7 oncotranscripts via reverse regulation of its reader protein IGF2BP1 upon heat stress.

Human papillomavirus (HPV)-induced carcinogenesis critically depends on the viral early protein 7 (E7), making E7 an attractive therapeutic target. Here, we report that the E7 messenger RNA (mRNA)-containing oncotranscript complex can be selectively targeted by heat treatment. In HPV-infected cells, viral E7 mRNA is modified by N6-methyladenosine (m6A) and stabilized by IGF2BP1, a cellular m6A reader. Heat treatment downregulates E7 mRNA and protein by destabilizing IGF2BP1 without the involvement of canonical heat-shock proteins and reverses HPV-associated carcinogenesis in vitro and in vivo. Mechanistically, heat treatment promotes IGF2BP1 aggregation only in the presence of m6A-modified E7 mRNA to form distinct heat-induced m6A E7 mRNA-IGF2BP1 granules, which are resolved by the ubiquitin-proteasome system. Collectively, our results not only show a mutual regulation between m6A RNA and its reader but also provide a heat-treatment-based therapeutic strategy for HPV-associated malignancies by specifically downregulating E7 mRNA-IGF2BP1 oncogenic complex.

Dose-response association between sedentary time and incident of diabetes in Chinese middle-aged and older adults: The 4C study.

AIMS: To investigate the dose-response relationship of total sedentary time with incident diabetes in Chinese middle-aged and older adults. METHODS: The present study followed 100,525 participants aged ≥ 40 years old from the China Cardiometabolic Disease and Cancer Cohort (4C) Study, which was a prospective study conducted in 25 communities across mainland China. Associations between sedentary time and incident diabetes were assessed with Cox regression and restricted cubic splines. RESULTS: During a median follow-up of 3.8 years, 7,529 participants developed diabetes. After adjustment for multiple variables, high levels of sedentary time (≥ 30 h/week) was associated with increased risk for developing diabetes (hazards ratio, 1.08; 95 % confidence intervals 1.02, 1.14) compared with low levels of sedentary time (<20 h/week). Restricted cubic spline analyses revealed an inverted U-shaped relation between sedentary time with diabetes. Subgroup analyses found that the observed association remained significant in subgroup of individuals with body mass index (BMI) ≥ 25 kg/cm2 or diastolic blood pressure (DBP) ≥ 90 mm Hg. However, the significant association was diminished in participants with sufficient physical activity (PA) (P = 0.22). CONCLUSIONS: The multicenter, population-based, prospective study suggested an inverted U-shaped relation between sedentary time with diabetes. PA alleviated the deleterious effects associated with sedentary time.

Paradoxical activation of transcription factor SREBP1c and de novo lipogenesis by hepatocyte-selective ATP-citrate lyase depletion in obese mice.

Hepatic steatosis associated with high-fat diet, obesity, and type 2 diabetes is thought to be the major driver of severe liver inflammation, fibrosis, and cirrhosis. Cytosolic acetyl CoA (AcCoA), a central metabolite and substrate for de novo lipogenesis (DNL), is produced from citrate by ATP-citrate lyase (ACLY) and from acetate through AcCoA synthase short chain family member 2 (ACSS2). However, the relative contributions of these two enzymes to hepatic AcCoA pools and DNL rates in response to high-fat feeding are unknown. We report here that hepatocyte-selective depletion of either ACSS2 or ACLY caused similar 50% decreases in liver AcCoA levels in obese mice, showing that both pathways contribute to the generation of this DNL substrate. Unexpectedly however, the hepatocyte ACLY depletion in obese mice paradoxically increased total DNL flux measured by D2O incorporation into palmitate, whereas in contrast, ACSS2 depletion had no effect. The increase in liver DNL upon ACLY depletion was associated with increased expression of nuclear sterol regulatory element-binding protein 1c and of its target DNL enzymes. This upregulated DNL enzyme expression explains the increased rate of palmitate synthesis in ACLY-depleted livers. Furthermore, this increased flux through DNL may also contribute to the observed depletion of AcCoA levels because of its increased conversion to malonyl CoA and palmitate. Together, these data indicate that in fat diet-fed obese mice, hepatic DNL is not limited by its immediate substrates AcCoA or malonyl CoA but rather by activities of DNL enzymes.

Tirzepatide induces a thermogenic-like amino acid signature in brown adipose tissue.

OBJECTIVES: Tirzepatide, a dual GIP and GLP-1 receptor agonist, delivered superior glycemic control and weight loss compared to selective GLP-1 receptor (GLP-1R) agonism in patients with type 2 diabetes (T2D). These results have fueled mechanistic studies focused on understanding how tirzepatide achieves its therapeutic efficacy. Recently, we found that treatment with tirzepatide improves insulin sensitivity in humans with T2D and obese mice in concert with a reduction in circulating levels of branched-chain amino (BCAAs) and keto (BCKAs) acids, metabolites associated with development of systemic insulin resistance (IR) and T2D. Importantly, these systemic effects were found to be coupled to increased expression of BCAA catabolic genes in thermogenic brown adipose tissue (BAT) in mice. These findings led us to hypothesize that tirzepatide may lower circulating BCAAs/BCKAs by promoting their catabolism in BAT. METHODS: To address this question, we utilized a murine model of diet-induced obesity and employed stable-isotope tracer studies in combination with metabolomic analyses in BAT and other tissues. RESULTS: Treatment with tirzepatide stimulated catabolism of BCAAs/BCKAs in BAT, as demonstrated by increased labeling of BCKA-derived metabolites, and increases in levels of byproducts of BCAA breakdown, including glutamate, alanine, and 3-hydroxyisobutyric acid (3-HIB). Further, chronic administration of tirzepatide increased levels of multiple amino acids in BAT that have previously been shown to be elevated in response to cold exposure. Finally, chronic treatment with tirzepatide led to a substantial increase in several TCA cycle intermediates (α-ketoglutarate, fumarate, and malate) in BAT. CONCLUSIONS: These findings suggest that tirzepatide induces a thermogenic-like amino acid profile in BAT, an effect that may account for reduced systemic levels of BCAAs in obese IR mice.

Effects of Small Peptide Supplementation on Growth Performance, Intestinal Barrier of Laying Hens During the Brooding and Growing Periods.

The growing period is a critical period for growth and development in laying hens. During this period, chicks grow rapidly, but are accompanied by unstable digestive function, incomplete organ development, and high mortality. Small peptide, a feed additive, which has been proved to promote intestinal development and immunity in poultry. In order to elucidate the effects of small peptides on growth performance, immunity, antioxidant capacity, and intestinal health of growing laying hens, a total of 900 Tianfu green shell laying hens (1-day-old) were randomly divided into 5 treatments with 6 replicates of 30 birds each in this 18-week trial. Dietary treatments included a corn-soybean meal-based diet supplemented with 0 g/kg, 1.5 g/kg, 3.0 g/kg, 4.5 g/kg and 6.0 g/kg small peptide, respectively. The results showed that the supplementation of small peptides significantly increased growth rate (P<0.05) in laying hens, as well as elevated the serum immunoglobulins (P<0.05) and antioxidant indices (P<0.05), however, it decreased inflammation parameters (P<0.05). The supplementation of small peptides enhanced the intestinal function by promoting gut development (P<0.05) and improving gut integrity (P<0.05), barrier function (P<0.05) and the diversity of gut microbiota (P<0.05) in the growing hens. The best performance was recorded among the hens fed 4.5 g/kg level of small peptide. Taken together, these results showed that small peptide supplementation could improve the economic value of growing hens by promoting growth rate, disease resistance, and the optimal amount of addition for Tianfu green shell laying hens was 4.5 g/kg.

Multi-Band Polarization-Insensitive Metamaterial Absorber for Microwave Based on Slotted Structure and Magnetic Rubber.

A design method of five-band polarization-insensitive metamaterial absorber (MMA) based on the slotted structures and the magnetic rubber is proposed for L-, S-, C-, X-, and Ku-band applications. The slotted structures of the top layer, which evolved from two square rings, are used to excite multi-resonance. The range of the electromagnetic (EM) parameters of a magnetic rubber substrate, which is used to adjust the equivalent impedance of the absorber to match the free space impedance in different bands, is estimated using the impedance matching principle. A series of magnetic rubber substrates based on the estimated EM parameters are prepared and measured, whose thickness is only 0.7 mm, meeting the thin design requirements. The absorption of the proposed absorber greater than 90% at 1.7 GHz, 3.87 GHz, 5.96 GHz, 9.4-10.4 GHz, and 14 GHz is achieved when the doping amount of the carbonyl iron powders is 200%. The absorbing performance of the absorber with measured EM parameter agrees well with the theoretical estimates, which validates the accuracy of the proposed design method.

Variation in the sexual behavior and blood count parameters induced by sleep deprivation in male rats.

BACKGROUND: Sleep is a fundamental biological requirement, and lack of sleep has increasingly been recognized to cause metabolic consequences and adversely affect immune function. Recent articles have pointed to how sleep and sexual functions may be interlinked, involving inflammation, vascular alterations, tissue damage, and endothelial dysfunction. OBJECTIVES: We examined the effect of paradoxical sleep deprivation on sexual behavior and hemogram parameters in male rats. In addition, we also explored whether 7 days of recovery sleep is sufficient to offset these detriments. MATERIALS AND METHODS: Male rats were given sexual experience through training. At the fifth test, the sexually vigorous males were randomly separated into three experimental groups: paradoxical sleep deprivation (rats submitted to 96 h of paradoxical sleep deprivation, n = 6), recovery sleep (recovery sleep 7 days after paradoxical sleep deprivation, n = 6), and control (n = 10). We evaluated the sexual behaviors of three groups. Blood samples were collected to analyze hemogram parameters. RESULTS: In this study, we recognized that repeated copulatory tests can lead to changes in sexual behavior over time. We found that 96 h of acute sleep deprivation impaired the sexual behavior of male rats. Our results demonstrated that 96 h of paradoxical sleep deprivation also increased levels of white blood cell subpopulations, in particular neutrophils. Recovery sleep after sleep deprivation has a certain reversal effect on white blood cell subgroups and impairment of sexual behavior, with some signs that not all levels were back to baseline even after 7 days of recovery. CONCLUSION: In general, we found that 96 h of paradoxical sleep deprivation impaired the sexual behavior of male rats. Our results demonstrated that paradoxical sleep deprivation can cause systemic inflammation by affecting white blood cell subpopulations, in particular neutrophils. Seven days of recovery sleep after sleep deprivation has a certain reversal effect to these impairments.

Metabolic perturbations mediated by propionyl-CoA accumulation in organs of mouse model of propionic acidemia.

Propionic acidemia (PA) is an autosomal recessive metabolic disorder after gene encoding propionyl-CoA carboxylase, Pcca or Pccb, is mutated. This genetic disorder could develop various complications which are ascribed to dysregulated propionyl-CoA metabolism in organs. However, the effect of attenuated PCC on propionyl-CoA metabolism in different organs remains to be fully understood. We investigated metabolic perturbations in organs of Pcca-/-(A138T) mice (a mouse model of PA) under chow diet and acute administration of [13C3]propionate to gain insight into pathological mechanisms of PA. With chow diet, the metabolic alteration is organ dependent. l-Carnitine reduction induced by propionylcarnitine accumulation only occurs in lung and liver of Pcca-/- (A138T) mice. [13C3]Propionate tracing data demonstrated that PCC activity was dramatically reduced in Pcca-/-(A138T) brain, lung, liver, kidney, and adipose tissues, but not significantly changed in Pcca-/-(A138T) muscles (heart and skeletal muscles) and pancreas, which was largely supported by PCCA expression data. The largest expansion of propionylcarnitine in Pcca-/-(A138T) heart after acute administration of propionate indicated the vulnerability of heart to high circulating propionate. The overwhelming propionate in blood also stimulated ketone production from the increased fatty acid oxidation in Pcca-/-(A138T) liver by lowering malonyl-CoA, which has been observed in cases where metabolic decompensation occurs in PA patients. This work shed light on organ-specific metabolic alternations under varying severities of PA.

Significance of peripheral blood indexes in differential diagnoses of SARS-CoV-2 and New Bunia virus.

We aimed to provide a laboratory basis for differential diagnosis of COVID-19 and severe fever with thrombocytopenia syndrome (SFTS). Clinical data were collected from 32 COVID-19 patients (2019-nCoV group), 31 SFTS patients (SFTS group) and 30 healthy controls (control group). For each group of hospitalized patients, a retrospective analysis was performed on specific indices, including cytokines, T-lymphocyte subsets, routine blood parameters, C-reactive protein (CRP) and procalcitonin (PCT), and receiver operating characteristic (ROC) curves for the indices revealed the differences among groups. Compared with the 2019-nCoV group, the SFTS group had a significantly and greatly decreased counts of WBC, absolute lymphocyte, PLT and absolute CD4+ T lymphocyte (P < 0.05); the IL-6, TNF-α, D-D and PCT levels of the SFTS group were higher than those of the 2019-nCoV group (P < 0.05). Compared with those of the SFTS group, the CRP and FIB levels of the 2019-nCoV group were greatly increased (P < 0.05). The ROC curves showed that area under the curves (AUCs) for FIB, PLT and TNF-α were greater than 0.85, demonstrating high diagnostic value. At the initial stage of SARS-CoV-2 or SFTS virus infection, PLT, FIB and TNF-α have definitive clinical value for the early and differential diagnosis of these two infections.