Comparison of clinical efficacy between direct anterior approach and posterolateral approach in primary total hip arthroplasty.

OBJECTIVE: The aim of this study was to retrospectively analyze the clinical efficacy of the direct anterior approach (DAA) vs. posterolateral approach (PLA) in primary total hip arthroplasty (THA). PATIENTS AND METHODS: A total of 382 patients who underwent primary THA in our hospital from March 2016 to March 2021 were identified as research subjects, with 183 patients in the DAA group and 199 in the PLA group. Outcome measures included operation time, intraoperative blood loss, postoperative creatine kinase (CK), Harris score, visual analogue scale (VAS), postoperative hospital stay, and postoperative complications. RESULTS: DAA resulted in significantly longer operative time but lower intraoperative bleeding volume vs. PLA. Three months postoperatively, patients receiving DAA showed significantly lower visual analogue scale (VAS) scores and higher Harris scores than those given PLA. No hip dislocation was observed in the DAA group. CONCLUSIONS: DAA results in less intraoperative hemorrhage and muscle damage, better postoperative recovery, and a lower incidence of hip dislocation.

Central nervous disease in pediatric patients during acute lymphoblastic leukemia (ALL): a review.

Acute lymphoblastic leukemia (ALL) is one of the frequently reported malignancies of childhood age. Earlier it was thought to be a fatal pathological state with no cure, but with advancements in medicine and science, new therapeutic approaches have resulted in better management and cure. However, one of the major hurdles in achieving a complete cure is the relapse of ALL at extra-medullary sites like the central nervous system (CNS). The present review article is focused on recent diagnostic avenues available for the detection of CNS disease during acute lymphoblastic leukemia (ALL) in young patients.

Lymphocyte subsets in children with hemophagocytic lymphohistiocytosis (HLH) and its clinical significance.

OBJECTIVE: To study the peripheral blood lymphocyte subsets in children with hemophagocytic lymphohistiocytosis (HLH) in acute period as well as remission period, and compare them with healthy children to investigate the significance of lymphocyte subsets in the diagnosis, treatment, and prognosis in children with HLH. PATIENTS AND METHODS: From January 2009 to March 2014, 30 HLH patients were enrolled in this study. Among them, 20 were placed in the remission group, while 10 cases were placed in the death group. 6 cases died within 8 weeks due to the illness, and 4 cases died within 9 to 34 weeks. 30 children who were confirmed healthy after physical check-ups in the same period were enrolled in the control group. Peripheral blood was collected from both groups and lymphocyte subsets were studied using flow cytometry. RESULTS: The ratios of CD3+ T and CD8+ T cells increased in the HLH remission group and the death group, while CD4+, CD4+/CD8+ and CD3-CD16+CD56+NK ratios decreased. Difference detected in the proportion of CD19+ B cells was not statistically significant. By comparing lymphocyte subsets in the HLH acute period and the remission period in HLH patients we discovered that the differences in CD3+, CD8+, CD4+ and CD4+/CD8+, CD19+ B cells ratios were not statistically significant (p > 0.05). CD3-CD16+CD56+NK cells ratios in the remission period increased significantly. CONCLUSIONS: The lymphocyte subsets in children with HLH underwent obvious changes and there was an imbalance in cellular immunity. We believe that dynamic detection of changes may help us to evaluate the prognosis and the effect of the treatment.

Macrophage activation syndrome as a complication of juvenile rheumatoid arthritis.

OBJECTIVE: Juvenile rheumatoid arthritis (JRA), also known as juvenile idiopathic arthritis (JIA), is a rare autoimmune joint disorder of children. The concrete causes for the prevalence of the above pathological state are still unknown. In other words, it is an arthritis affecting mainly children and adolescents. Clinically, it has 3 different clinical subtypes. JRA patients are often noticed with some confirmed symptoms including coagulopathy, disseminated intravascular coagulation (DIC) with hepatosplenomegaly, fall in erythrocyte sedimentation rate and higher levels of liver enzymes leading to a life-threatening outcome. The above complications of JRA are recognized as a macrophage activation syndrome (MAS), which is similar to hemophagocytic lymphohistiocytosis (HLH). Pathogenesis of JRA manly involves deregulation of immunological processes with excessive and persistent activation of antigen presenting cells and T-lymphocytes. Further, abnormalities in the functioning of NK cells are often observed in JIA cases. Also, 40% of patients with these abnormalities are habitually associated with perforin gene mutations. Today, MAS remains a clinical and diagnostic challenge. RESULTS: The diagnosis of MAS is mainly based on clinical grounds. However, laboratory evidence of macrophages in the bone marrow performing phagocytosis of variable hematopoietic cells also help in diagnosis. For confirmation of MAS, there must be present either of two clinical or laboratory criteria. Further, laboratory criteria often appear late and are unable to diagnose the complication right at the beginning stage. Important laboratory findings in macrophage activation syndrome associated with JIA include hypertriglyceridemia, anemia, low erythrocyte sedimentation rate, elevated alanine aminotransferase level, higher than normal bilirubin levels, presence of fibrin degradation products, high lactate dehydrogenase level, low sodium, low albumin, and hyperferritinemia. CONCLUSIONS: MAS is a confirmed life threatening complication of patients with JIA. Further, an early diagnosis and treatment of MAS could be a life-saving mode for this syndrome.

A review of risk factors for childhood leukemia.

OBJECTIVE: Leukemia is the most common cancer of childhood, with AML, CML, ALL and CLL being the most common. Environmental and genetic factors have been studied extensively in children with childhood leukemia. Other factors, such as the prenatal parental use of controlled substances, have not been investigated to the same degree. We review what is currently known about environmental and parental factors and the occurrence of leukemia in children. MATERIALS AND METHODS: Electronic databases were searched for studies correlated pediatric leukemia with (1) ionizing radiation; (2) benzene; (3) parental drug use (4) parental alcohol use; (5) genetic factors. RESULTS: The two known significant environment risk factors for the occurrence leukemia are ionizing radiation and benzene. However, at least 4 studies have been published over the last century have looked at other environmental factors such as pesticides and drug and alcohol use as well as genetic factors such as gene fusions and translocations. CONCLUSIONS: We determined the risk of environmental and genetic factors that could be the cause of childhood leukemia in an effort to reduce the incidence of this disease.

Pentamethylquercetin generates beneficial effects in monosodium glutamate-induced obese mice and C2C12 myotubes by activating AMP-activated protein kinase.

AIMS/HYPOTHESIS: Pentamethylquercetin (PMQ) has recently been shown to have glucose-lowering properties. Here, we aimed to characterise the effectiveness and underlying mechanisms of PMQ for ameliorating metabolic disorders in vivo and vitro. METHODS: We generated a mouse model of obesity by neonatal administration of monosodium glutamate (MSG) and used it to assess the properties of PMQ as a treatment for metabolic disorders. We also investigated the possible underlying mechanisms of PMQ in the prevention of metabolic disorders. RESULTS: Compared with normal mice, MSG mice had metabolic disorders, including central obesity, hyperinsulinaemia, insulin resistance, hyperglycaemia, hyperlipidaemia, decreased phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), and downregulated levels of GLUT4 in gastrocnemius muscles. In MSG mice, PMQ treatment (5, 10, 20 mg/kg daily) reduced body weight gain, waist circumference, adipose tissue mass, serum glucose, triacylglycerol and total cholesterol, while improving insulin resistance, activating AMPK and increasing ACC phosphorylation and GLUT4 abundance. In C2C12 myotubes, PMQ (10 µmol/l) increased glucose consumption by ∼65%. PMQ treatment (1-10 µmol/l) also activated AMPK, increased ACC phosphorylation and GLUT4 abundance, and upregulated the expression of some key genes involved in fatty acid oxidation. CONCLUSIONS/INTERPRETATION: These findings suggest that PMQ can ameliorate metabolic disorders at least in part via stimulation of AMPK activity.

U/Pb zircon geochronology and tempo of the end-permian mass extinction

The mass extinction at the end of the Permian was the most profound in the history of life. Fundamental to understanding its cause is determining the tempo and duration of the extinction. Uranium/lead zircon data from Late Permian and Early Triassic rocks from south China place the Permian-Triassic boundary at 251.4 +/- 0.3 million years ago. Biostratigraphic controls from strata intercalated with ash beds below the boundary indicate that the Changhsingian pulse of the end-Permian extinction, corresponding to the disappearance of about 85 percent of marine species, lasted less than 1 million years. At Meishan, a negative excursion in delta13C at the boundary had a duration of 165,000 years or less, suggesting a catastrophic addition of light carbon.

Effect of selective inhibition of soluble guanylyl cyclase on the K(Ca) channel activity in coronary artery smooth muscle.

Activation of a soluble guanylyl cyclase plays an important role in nitric oxide (NO)-induced vasodilation. Recently, we have reported that NO increases the calcium-activated potassium (K(Ca)) channel activity in vascular smooth muscle cells from coronary arteries. The present study examined the role of the soluble guanylyl cyclase in the control of basal activity of the K(Ca) channels and in mediating NO-induced activation of the K(Ca) channels in vascular smooth muscle cells, using a selective inhibitor of this enzyme, 1H-[1,2,4]oxadiazolo[4,2-alpha]quinoxalin-1-one (ODQ). In the cell-attached patch-clamp mode, addition of ODQ into the bath solution (10 micromol/L) decreased the K(Ca) channel activity by 59% and attenuated activation of the channels induced by the NO donor, deta nonoate, by 70%. ODQ had no effect on 8-bromo-cGMP-induced activation of the K(Ca) channels. Deta nonoate produced a concentration-dependent relaxation of precontracted coronary arteries. When ODQ was added to the bath, the deta nonoate-induced relaxations were inhibited. The IC50 for deta nonoate was decreased by about 25-fold and the maximal effect of deta nonoate was reduced by about 60%. A specific K(Ca) channel inhibitor, iberiotoxin, decreased deta nonoate-induced vasodilation but to a lesser extent than ODQ. However, ODQ was without effect on the vasodilation induced by a prostacyclin analog, iloprost, and by adenosine. These results indicate that a soluble guanylyl cyclase and cGMP play an important role in the control of the K(Ca) channel activity in coronary arterial smooth muscle cells. K(Ca) channel activation participates in the NO-induced vasodilation in coronary circulation.

[Characterization of outward current in mouse ventricular myocytes].

Depolarization-activated, calcium-independent outward currents (Iout) in enzymatically dispersed mouse ventricular myocytes were characterized by whole-cell recording technique. During brief depolarizations to potentials positive to -50 mV, outward K+ currents in these cells rise rapidly to a peak followed by a slower decay to an apparent plateau. The relative peak to plateau amplitudes in a single cell varied as a function of the holding potential (HP) from which the currents were evoked. Reversal potentials for the peak and plateau components were -64.3 +/- 3.9 mV and -53.3 +/- 2.9 mV, respectively (uncorrected for junction potentials). The outward current decay is well described by double exponential fits, whereas the time course of peak Iout decay following a 500 ms prepulse is best fitted by single exponential function, indicating the presence of two distinct components, IKf and IKs, of the outward currents in mouse ventricular cells. Application of 4-AP were accompanied by a marked attenuation of peak Iout and plateau Iout, indicating that both IKf and IKs display similar sensitivities to 4-AP. The steady state inactivation of IKf is found incomplete within the test potential range (-80 - +30 mV) owing probably to the fact that the APD of mouse myocardium is too short.

[Study on treatment of infectious shock with recipe of liqi huoxue and kaibi gutuo].

Based on the pathogenesis of infectious shock which were stagnation of Qi, blood stasis, impairment of body resistance and trends to collapse, a series of new preparations of traditional Chinese Medicine was developed, Injection Kangjue Tongmai, Injection Yiqi Jiuyin and Injection Yiqi Huiyang, which could Liqi Huoxue and Kaibi Gutuo (regulate the flow of Qi, promote blood circulation, strengthen the body resistance and remit collapse), the result of 183 cases of infectious shock treated with them showed that the mortality was 4.37%, significantly lower than that of control group (23.0%). All three injections could rapidly elevate blood pressure and stabilize it for prolonged time, increase renal blood flow and lower blood viscosity. In animal experiment, the injections reduced lipid peroxide of vital organs, stabilized bio-membrane, protected the cell structure and maintained their normal functions.

[Effect of jiutuo II injection on shock model of superior mesenteric artery occlusion in rabbit].

Tang's SMAO method was adopted to produce shock model to observe the efficacy of the Jiutuo II(JTII) intravenously given. It was found that JTII could normalize the BP rapidly, which were superior to that of Dopamine and NS groups (P < 0.05, P < 0.01). At the same time, it could decrease mortality rate, comparing with Dopamine and NS the difference was significant (P < 0.05, P < 0.01); and it could also inhibit the formation of lipid peroxides (LPO). The contents of LPO in heart, liver, kidney of shock rabbit were obviously lower than that of Dopamine and NS groups (P < 0.05, P < 0.01). The electron microscopy indicated that the drug could relieve the injury of mitochondria and lysosome in the tissues of heart, liver and kidney and protect the cellular ultrastructure of cardinal viscera. This study suggests that the JTII had good efficacy in treating the shock rabbit caused by SMAO method.

Cardiac angiotensinogen and its local activation in the isolated perfused beating heart.

Increasing evidence suggests that the renin-angiotensin system modulates cardiovascular homeostasis both via its circulating, plasma-borne components and through locally present, tissue-resident systems with site-specific activity. The existence of such a system in the heart has been proposed, based on biochemical studies as well as on the demonstration of renin and angiotensinogen messenger RNA in cardiac tissue. We conducted the present study to determine whether biologically active angiotensin peptides may be cleaved within the heart from locally present angiotensinogen. Isolated, perfused rat hearts were exposed to infusions of purified hog renin; the coronary sinus effluent was collected and subsequently assayed for angiotensin I (Ang I) and angiotensin II (Ang II) by high-pressure liquid chromatography and specific radioimmunoassay. Both Ang I and II were undetectable under control conditions but appeared promptly after the addition of renin. Dose-dependent peak values for Ang I release ranged from 2.42 +/- 0.65 fmol/min to 1.38 +/- 0.18 pmol/min during renin infusions at concentrations between 10 microunits/ml and 5 milliunits/ml. Ang II levels measured in the perfusate reflected a mean fractional intracardiac conversion of Ang I to Ang II of 7.18 +/- 1.09%. Generation of Ang I and Ang II was inhibited in the presence of specific inhibitors of renin and converting enzyme, respectively. To investigate the source of angiotensinogen, we measured spontaneous angiotensinogen release from isolated perfused hearts. In the absence of renin in the perfusate, angiotensinogen was initially released in high, but rapidly declining, concentrations and subsequently at a low, but stable, rate. Prior perfusion with angiotensinogen-rich plasma resulted in enhanced early angiotensinogen release but did not alter the second, delayed phase, suggesting that, in addition to plasma-derived substrate, locally produced angiotensinogen may also participate in the intracardiac formation of angiotensin. Supporting this interpretation, hearts from animals pretreated with dexamethasone showed increased angiotensinogen messenger RNA concentrations as well as increased rates of angiotensinogen release not only during the early but also during the late phase. Our study newly demonstrates that Ang I and II may be formed within the isolated heart from locally present substrate, which appears to be derived in part from the circulating pool and in part from endogenous synthesis. These findings add support to the concept of a functionally active and locally integrated cardiac renin-angiotensin system and emphasize its potential physiological and pathological relevance.