The potential mechanism and clinical application value of remote ischemic conditioning in stroke

Some studies have confirmed the neuroprotective effect of remote ischemic conditioning against stroke. Although numerous animal researches have shown that the neuroprotective effect of remote ischemic conditioning may be related to neuroinflammation, cellular immunity, apoptosis, and autophagy, the exact underlying molecular mechanisms are unclear. This review summarizes the current status of different types of remote ischemic conditioning methods in animal and clinical studies and analyzes their commonalities and differences in neuroprotective mechanisms and signaling pathways. Remote ischemic conditioning has emerged as a potential therapeutic approach for improving stroke-induced brain injury owing to its simplicity, non-invasiveness, safety, and patient tolerability. Different forms of remote ischemic conditioning exhibit distinct intervention patterns, timing, and application range. Mechanistically, remote ischemic conditioning can exert neuroprotective effects by activating the Notch1/phosphatidylinositol 3-kinase/Akt signaling pathway, improving cerebral perfusion, suppressing neuroinflammation, inhibiting cell apoptosis, activating autophagy, and promoting neural regeneration. While remote ischemic conditioning has shown potential in improving stroke outcomes, its full clinical translation has not yet been achieved.

Cardioprotection by remote ischemic conditioning: Mechanisms and clinical evidences

In remote ischemic conditioning(RIC), several cycles of ischemia and reperfusion render distant organ and tissues more resistant to the ischemia-reperfusion injury. The intermittent ischemia can be applied before the ischemic insult in the target site(remote ischemic preconditioning), during the ischemic insult(remote ischemic perconditioning) or at the onset of reperfusion(remote ischemic postconditioning). The mechanisms of RIC have not been completely defined yet; however, these mechanisms must be represented by the release of humoral mediators and/or the activation of a neural reflex. RIC has been discovered in the heart, and has been arising great enthusiasm in the cardiovascular field. Its efficacy has been evaluated in many clinical trials, which provided controversial results. Our incomplete comprehension of the mechanisms underlying the RIC could be impairing the design of clinical trials and the interpretation of their results. In the present review we summarize current knowledge about RIC pathophysiology and the data about its cardioprotective efficacy.

Concepts of hypoxic NO signaling in remote ischemic preconditioning

Acute coronary syndromes remain a leading single cause of death worldwide. Therapeutic strategies to treat cardiomyocyte threatening ischemia/reperfusion injury are urgently needed. Remote ischemic preconditioning(r IPC) applied by brief ischemic episodes to heartdistant organs has been tested in several clinical studies, and the major body of evidence points to beneficial effects of r IPC for patients. The underlying signaling, however, remains incompletely understood. This relates particularly to the mechanism by which the protective signal is transferred from the remote site to the target organ. Many pathways have been forwarded but none can explain the protective effects completely. In light of recent experimental studies, we here outline the current knowledge relating to the generation of the protective signal in the remote organ, the signal transfer to the target organ and the transduction of the transferred signal into cardioprotection. The majority of studies favors a humoral factor that activates cardiomyocyte downstream signaling- receptor-dependent and independently. Cellular targets include deleterious calcium(Ca2+) signaling, reactive oxygen species, mitochondrial function and structure, and cellular apoptosis and necrosis. Following an outline of the existing evidence, we will furthermore characterize the existing knowledge and discuss future perspectives with particular emphasis on the interaction between the recently discovered hypoxic nitrite-nitric oxide signaling in r IPC. This refers to the protective role of nitrite, which can be activated endogenously using r IPC and which then contributes to cardioprotection by rIPC.

Protective effects of remote ischemic preconditioning in rat hindlimb on ischemia- reperfusion injury

Three cycles of remote ischemic pre-conditioning induced by temporarily occluding the bilateral femoral arteries （10 minutes） prior to 10 minutes of reperfusion were given once a day for 3 days before the animal received middle artery occlusion and reperfusion surgery. The results showed that brain infarct volume was significantly reduced after remote ischemic pre-conditioning. Scores in the forelimb placing test and the postural reflex test were significantly lower in rats having undergone remote ischemic pre-conditioning compared with those who did not receive remote ischemic pre-conditioning. Thus, neurological function was better in rats having undergone remote ischemic pre-conditioning compared with those who did not receive remote ischemic pre-conditioning. These results indicate that remote ischemic pre-conditioning in rat hindlimb exerts protective effects in ischemia-reperfusion injury.

A feasible strategy for focal cerebral ischemiareperfusion injury: remote ischemic postconditioning

It is difficult to control the degree of ischemic postconditioning in the brain and other isch- emia-sensitive organs. Remote ischemic postconditioning could protect some ischemia-sensitive organs through measures on terminal organs. In this study, a focal cerebral ischemia-reperftlsion injury model was established using three cycles of remote ischernic postconditioning, each cycle consisted of 10-minute occlusion of the femoral artery and 10-minute opening. The results showed that, remote ischemic postconditioning significantly decreased the percentage of the in- farct area and attenuated brain edema. In addition, inflammatory nuclear factor-KB expression was significantly lower, while anti-apoptotic Bcl-2 expression was significantly elevated in the ce- rebral cortex on the ischemic side. Our findings indicate that remote ischemic postconditioning attenuates focal cerebral ischemia/reperfusion injury, and that the neuroprotective mechanism is mediated by an anti-apoptotic effect and reduction of the inflammatory response.

Remote ischemic conditioning approach for the treatment of ischemic stroke

Stroke is the leading cause of disability and death in North America.There has been growing interest in identifying neuroprotective strategies to reduce ischemic burden in patients with acute ischemic stroke.However,despite extensive clinical trials,no neuroprotective agent has been found for prevention of ischemic damage.Remote ischemic preconditioning(RIC)is a promising non-invasive strategy that has been proven to provide renal and cardioprotection and has recently found to have a potential broad application in the treatment of neurovascular disease,which has bee linked to its possible effects on the release and activation of endogenous neuroprotective substances against the ischemia/reperfusion injuries in experimental studies.This endogenous neuroprotection might vaccinate neural tissues against effects of acute IR following primary infarction insult.Regardless of the method of RIC administration,through manual or automated blood pressure cuff,RIC procedure is inexpensive and easy to use.Based on the experimental and clinical data,application of RIC avoids possible adverse effects and interactions associated with chemical pharmacological agents.In previous clinical studies RIC was safe and associated with only minor transient adverse effects in few cases,including petechia and minor limb pain,which were mostly resolved shortly after completing the treatment.

Remote ischemic postconditioning protects against gastric mucosal lesions in rats

AIM: To investigate the protective effects of remote ischemic postconditioning (RIP) against limb ischemia-reperfusion (IR)-induced gastric mucosal injury.

Remote ischemic preconditioning protects liver ischemia-reperfusion injury by regulating eNOS-NO pathway and liver microRNA expressions in fatty liver rats

BACKGROUND: Ischemic preconditioning (IPC) is a strategy to reduce ischemia-reperfusion (I/R) injury. The protective effect of remote ischemic preconditioning (RIPC) on liver I/R injury is not clear. This study aimed to investigate the roles of RIPC in liver I/R in fatty liver rats and the involvement of endothelial nitric oxide synthase-nitric oxide (eNOS-NO) pathway and microRNA expressions in this process. METHODS: A total of 32 fatty rats were randomly divided into the sham group, I/R group, RIPC group and RIPC+I/R group. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and nitric oxide (NO) were measured. Hematoxylin-eosin staining was used to observe histological changes of liver tissues, TUNEL to detect hepatocyte apoptosis, and immunohistochemistry assay to detect heat shock protein 70 (HSP70) expression. Western blotting was used to detect liver inducible NOS (iNOS) and eNOS protein levels and realtime quantitative polymerase chain reaction to detect miR-34a, miR-122 and miR-27b expressions. RESULTS: Compared with the sham and RIPC groups, serum ALT, AST and iNOS in liver tissue were significantly higher in other two groups, while serum NO and eNOS in liver tissue were lower, and varying degrees of edema, degeneration and inflammatory cell infiltration were found. Cell apoptosis number was slightly lower in the RIPC+I/R group than that in I/R group. Compared with the sham group, HSP70 expressions were significantly increased in other three groups (all P<0.05). Compared with the sham and RIPC groups, elevated miR-34a expressions were found in I/R and RIPC+I/R groups (P<0.05). MiR-122 and miR-27b were found significantly decreased in I/R and RIPC+I/R groups compared with the sham and RIPC groups (all P<0.05). CONCLUSION: RIPC can reduce fatty liver I/R injury by affecting the eNOS-NO pathway and liver microRNA expressions.

Limb remote ischemic postconditioning protects integrity of the blood-brain barrier after stroke

Integrity of the blood-brain barrier structure is essential for maintaining the internal environment of the brain.Development of cerebral infarction and brain edema is strongly associated with blood-brain barrier leakage.Therefore,studies have suggested that protecting the blood-brain barrier may be an effective method for treating acute stroke.To examine this possibility,stroke model rats were established by middle cerebral artery occlusion and reperfusion.Remote ischemic postconditioning was immediately induced by three cycles of 10-minute ischemia/10-minute reperfusion of bilateral hind limbs at the beginning of middle cerebral artery occlusion reperfusion.Neurological function of rat models was evaluated using Zea Longa’s method.Permeability of the blood-brain barrier was assessed by Evans blue leakage.Infarct volume and brain edema were evaluated using 2,3,5-triphenyltetrazolium chloride staining.Expression of matrix metalloproteinase-9 and claudin-5 m RNA was determined by real-time quantitative reverse transcription-polymerase chain reaction.Expression of matrix metalloproteinase-9 and claudin-5 protein was measured by western blot assay.The number of matrix metalloproteinase-9-and claudin-5-positive cells was analyzed using immunohistochemistry.Our results showed that remote ischemic postconditioning alleviated disruption of the blood-brain barrier,reduced infarct volume and edema,decreased expression of matrix metalloproteinase-9 m RNA and protein and the number of positive cells,increased expression of claudin-5 m RNA and protein and the number of positive cells,and remarkably improved neurological function.These findings confirm that by suppressing expression of matrix metalloproteinase-9 and claudin-5 induced by acute ischemia/reperfusion,remote ischemic postconditioning reduces blood-brain barrier injury,mitigates ischemic injury,and exerts protective effects on the brain.

Remote ischemic perconditioning prevents liver transplantation-induced ischemia/reperfusion injury in rats: Role of ROS/RNS and e NOS

AIM To investigate the underlying mechanisms of the protective role of remote ischemic perconditioning (RIPerC) in rat liver transplantation. METHODS Sprague-Dawley rats were subjected to sham, orthotopic liver transplantation (OLT), ischemic postconditioning (IPostC) or RIPerC. After 3 h reperfusion, blood samples were taken for measurement of alanine aminotransferase, aspartate aminotransferase, creatinine (Cr) and creatinine kinase-myocardial band (CK-MB). The liver lobes were harvested for the following measurements: reactive oxygen species (ROS), H2O2, mitochondrial membrane potential (Delta psi m) and total nitric oxide (NO). These measurements were determined using an ROS/H2O2, JC1 and Total NOx Assay Kit, respectively. Endothelial NO synthase (eNOS) was analyzed by reverse transcription-polymerase chain reaction (RTPCR) and western blotting, and peroxynitrite was semiquantified by western blotting of 3-nitrotyrosine. RESULTS Compared with the OLT group, the grafts subjected to RIPerC showed significantly improved liver and remote organ functions (P < 0.05). ROS (P < 0.001) including H2O2 (P < 0.05) were largely elevated in the OLT group as compared with the sham group, and RIPerC (P < 0.05) reversed this trend. The collapse of Delta psi m induced by OLT ischemia/reperfusion (I/R) injury was significantly attenuated in the RIPerC group (P < 0.001). A marked increase of NO content and phosphoserine eNOS, both in protein and mRNA levels, was observed in liver graft of the RIPerC group as compared with the OLT group (P < 0.05). I/R-induced 3-nitrotyrosine content was significantly reduced in the RIPerC group as compared with the OLT group (P < 0.05). There were no significant differences between the RIPerC and IPostC groups for all the results except Cr. The Cr level was lower in the RIPerC group than in the IPostC group (P < 0.01). CONCLUSION Liver graft protection by RIPerC is similar to or better than that of IPostC, and involves inhibition of oxidative stress and up-regulation of the PI3K/Akt/eNOS/NO pathway.

Mitofusin-2 mediated mitochondrial Ca2+ uptake 1/2 induced liver injury in rat remote ischemic perconditioning liver transplantation and alpha mouse liver-12 hypoxia cell line models

AIM To investigate the protective mechanism of mitofusin-2 (Mfn2) in rat remote ischemic perconditioning (RIC) models and revalidate it in alpha mouse liver-12 (AML-12) hypoxia cell lines. METHODS Sprague-Dawley rats were divided into three groups (n = 6 each): sham, orthotopic liver transplantation and RIC. After operation, blood samples were collected to test alanine aminotransferase and aspartate aminotransferase. The liver lobes were harvested for histopathological examination, western blotting (WB) and quantitative real-time (qRT)-PCR. AML-12 cell lines were then subjected to normal culture, anoxic incubator tank culture (hypoxia) and anoxic incubator tank culture with Mfn2 knockdown (hypoxia + Si), and data of qRT-PCR, WB, mitochondrial membrane potential (Delta psi m), apoptosis, endoplasmic reticulum Ca2+ concentrations and mitochondrial Ca2+ concentrations were collected. RESULTS Both sham and normal culture groups showed no injury during the experiment. The RIC group showed amelioration of liver function compared with the orthotopic liver transplantation group (P < 0.05). qRTPCR and WB confirmed that Mfn2-mitochondrial Ca2+ uptake 1/2 (MICUs) axis was changed (P < 0.005). In AML-12 cell lines, compared with the hypoxia group, the hypoxia + Si group attenuated the collapse of..m and apoptosis (P < 0.005). The endoplasmic reticulum Ca2+ decrease and mitochondrial Ca2+ overloading observed in the hypoxia group were also attenuated in the hypoxia + Si group (P < 0.005). Finally, qRT-PCR and WB confirmed the Mfn2-MICUs axis change in all the groups (P < 0.005). CONCLUSION Mfn2 participates in liver injury in rat RIC models and AML-12 hypoxia cell lines by regulating the MICUs pathway.

Remote ischemic preconditioning as treatment for non-ischemic gastrointestinal disorders: Beyond ischemia-reperfusion injury

Common gastrointestinal diseases such as radiation enteritis(RE),acute pancreatitis,inflammatory bowel diseases(IBD)and drug-induced hepatotoxicity share pathophysiological mechanisms at the molecular level,mostly involving the activation of many pathways of the immune response,ultimately leading to tissue injury.Increased oxidative stress,inflammatory cytokine release,inflammatory cell infiltration and activation and the up-regulation of inflammatory transcription factors participate in the pathophysiology of these complex entities.Treatment varies in each specific disease,but at least in the cases of RE and IBD immunosuppressors are effective.However,full therapeutic responses are not always achieved.The pathophysiology of ischemiareperfusion(IR)injury shares many of these mechanisms.Brief and repetitive periods of ischemia in an organ or limb have been shown to protect against subsequent major IR injury in distant organs,a phenomenon called remote ischemic preconditioning(RIP).This procedure has been shown to protect the gut,pancreas and liver by modulating many of the same inflammatory mechanisms.Since RIP is safe and tolerable,and has shown to be effective in some recent clinical trials,I suggest that RIP could be used as a physiologicallyrelevant adjunct treatment for non-ischemic gastrointestinal inflammatory conditions.

Effect of remote ischemic preconditioning among donors and recipients following pediatric liver transplantation:A randomized clinical trial

BACKGROUND Studies suggested that remote ischemic preconditioning(RIPC)may effectively lessen the harmful effects of ischemia reperfusion injury during organ transplantation surgery.AIM To investigate the protective effects of RIPC on living liver donors and recipients following pediatric liver transplantation.METHODS From January 2016 to January 2019 at Renji Hospital Affiliated with Shanghai Jiao Tong University School of Medicine,208 donors were recruited and randomly assigned to four groups:S-RIPC group(no intervention;n=55),D-RIPC group(donors received RIPC;n=51),R-RIPC group(recipients received RIPC,n=51)and DR-RIPC group(both donors and recipients received RIPC;n=51).We primarily evaluated postoperative liver function among donors and recipients and incidences of early allograft dysfunction,primary nonfunction and postoperative complications among recipients.RESULTS RIPC did not significantly improve alanine transaminase and aspartate aminotransferase levels among donors and recipients or decrease the incidences of early allograft dysfunction,primary nonfunction,and postoperative complications among recipients.Limited protective effects were observed,including a lower creatinine level in the D-RIPC group than in the S-RIPC group on postoperative day 0(P<0.05).However,no significant improvements were found in donors who received RIPC.Furthermore,RIPC had no effects on the overall survival of recipients.CONCLUSION The protective effects of RIPC were limited for recipients who received living liver transplantation,and no significant improvement of the prognosis was observed in recipients.

Impact of remote ischemic preconditioning on wound healing in small bowel anastomoses

AIM： To investigate the influence of remote ischemic preconditioning （RIPC） on anastomotic integrity. METHODS： Sixty male Wistar rats were randomized to six groups. The control group （n = 10） had an end- to-end ileal anastomosis without RIPC. The preconditioned groups （n = 34） varied in time of ischemia and time of reperfusion. One group received the amino acid L-arginine before constructing the anastomosis （n = 9）. On postoperative day 4, the rats were re-laparotomized, and bursting pressure, hydroxyproline concentration, intra-abdominal adhesions, and a histological score concerning the mucosat ischemic injury were collected. The data are given as median （range）.RESULTS： On postoperative day 4, median bursting pressure was 124 mmHg （60-146 mmHg） in the control group. The experimental groups did not show a statistically significant difference （P 〉 0.05）. Regarding the hydroxyproline concentration, we did not find any significant variation in the experimental groups. We detected significantly less mucosal injury in the RIPC groups. Furthermore, we assessed more extensive intra-abdominal adhesions in the preconditioned groups than in the control group. CONCLUSION： RIPC directly before performing small bowel anastomosis does not affect anastomotic stability in the early period, as seen in ischemic preconditioning.

Conventional, but not remote ischemic preconditioning, reduces iNOS transcription in liver ischemia/reperfusion

AIM:To study the effects of preconditioning on inducible nitric oxide synthase(iNOS)and interleukin 1(IL-1)receptor transcription in rat liver ischemia/reperfusion injury(IRI).METHODS:Seventy-two male rats were randomized into 3 groups:the one-hour segmental ischemia(IRI,n=24)group,the ischemic preconditioning(IPC,n=24)group or the remote ischemic preconditioning(RIPC,n=24)group.The IPC and R-IPC were performed as 10 min of ischemia and 10 min of reperfusion.The iNOS and the IL-1 receptor mRNA in the liver tissue was analyzed with real time PCR.The total Nitrite and Nitrate(NOx)in continuously sampled microdialysate(MD)from the liver was analyzed.In addition,the NOx levels in the serum were analyzed.RESULTS:After 4 h of reperfusion,the iNOS mRNA was significantly higher in the R-IPC(ΔCt:3.44±0.57)group than in the IPC(ΔCt:5.86±0.82)group(P=0.025).The IL-1 receptor transcription activity was reduced in the IPC group(ΔCt:1.88±0.53 to 4.81±0.21),but not in the R-IPC group,during reperfusion(P=0.027).In the MD,a significant drop in the NOx levels was noted in the R-IPC group(12.3±2.2 to 4.7±1.2μmol/L)at the end of ischemia compared with the levels in early ischemia(P=0.008).A similar trend was observed in the IPC group(11.8±2.1 to 6.4±1.5μmol/L),although this difference was not statistically significant.The levels of NOx rose quickly during reperfusion in both groups.CONCLUSION:IPC,but not R-IPC,reduces iNOS and IL-1 receptor transcription during early reperfusion,indicating a lower inflammatory reaction.NOx is consumed in the ischemic liver lobe.

Randomized controlled trial of remote ischemic preconditioning and atrial fibrillation in patients undergoing cardiac surgery

AIM To study whether remote ischemic preconditioning(RIPC) has an impact on clinical outcomes, such as post-operative atrial fibrillation(POAF).METHODS This was a prospective, single-center, single-blinded,randomized controlled study. One hundred and two patients were randomized to receive RIPC(3 cycles of 5 min ischemia and 5 min reperfusion in the upper arm after induction of anesthesia) or no RIPC(control). Primary outcome was POAF lasting for five minutes or longer during the first seven days after surgery. Secondary outcomes included length of hospital stay, incidence of inpatient mortality, myocardial infarction, and stroke. RESULTS POAF occurred at a rate of 54% in the RIPC group and 41.2% in the control group(P = 0.23). No statistically significant differences were noted in secondary outcomes between the two groups. CONCLUSION This is the first study in the United States to suggest that RIPC does not reduce POAF in patients with elective or urgent cardiac surgery. There were no differences in adverse effects in either group. Further studies are required to assess the relationship between RIPC and POAF.

Remote sensing of air pollution incorporating integrated-path differential-absorption and coherent-Doppler lidar

An innovative complex lidar system deployed on an airborne rotorcraft platform for remote sensing of atmospheric pollution is proposed and demonstrated.The system incorporates integrated-path differential absorption lidar(DIAL) and coherent-doppler lidar(CDL) techniques using a dual tunable TEA CO_(2)laser in the 9—11 μm band and a 1.55 μm fiber laser.By combining the principles of differential absorption detection and pulsed coherent detection,the system enables agile and remote sensing of atmospheric pollution.Extensive static tests validate the system’s real-time detection capabilities,including the measurement of concentration-path-length product(CL),front distance,and path wind speed of air pollution plumes over long distances exceeding 4 km.Flight experiments is conducted with the helicopter.Scanning of the pollutant concentration and the wind field is carried out in an approximately 1 km slant range over scanning angle ranges from 45°to 65°,with a radial resolution of 30 m and10 s.The test results demonstrate the system’s ability to spatially map atmospheric pollution plumes and predict their motion and dispersion patterns,thereby ensuring the protection of public safety.

The Influence of Remote Ischemic Conditioning on Focal Brain Ischemia in Rats

Despite obvious progress in the treatment of acute forms of ischemic stroke, the risk of this condition remains unacceptably high. Brain infarction in the middle cerebral artery basin occurs in patients with atherosclerosis. The onset of the brain infarction is facilitated by the cessation of circulation (embolism) in conditions of insufficient collateral circulation. The extent of the infarct zone is determined by neuronal death and impaired microcirculation. The development of new methods for effective targeted restorative stroke therapy is crucial for restorative treatment and reducing the risk of mortality after stroke. Remote ischemic conditioning (RIC) is an approach to limiting reperfusion injury in the ischemic region of the brain after focal ischemia. One of the most commonly used in vivo models in stroke studies is the filament model of Middle Cerebral Artery Occlusion (MCAO) in rats. In our experiment, it was performed for 30 min (J. Koizumi) with subsequent 48-hour reperfusion. Within the first 24 hours after the start of reperfusion several short episodes of ischemia in low limbs were induced. After 48 hours of reperfusion the brains were harvested and stained with TTC. Then we evaluated the effect of RIC within 24 hours ex vivo in rats’ brains, as well as syndecan-1 plasma concentration. Infarct area was assessed by means of Image-Pro program with statistical analysis. Infarct volumes in the model group (31.97% ± 2.5%) were significantly higher compared to the values in the RIC group 48 hours after ischemia-reperfusion (13.6% ± 1.3%) (*P < 0.05). A significant reduction in the area of infarction after RIC is likely due to the effect on the regulation of collateral blood flow in the ischemia area. On the second day after ischemia-reperfusion, tissue swelling was reduced in the RIC group compared to the model group. Analysis of the average concentration of Syndecan-1 revealed the difference between model and RIC groups. Syndecan-1, endothelial glycocalyx protein, might be the regulator which performs vascular control of the interaction with inflammatory cell and is responsible for mediate effect of remote ischemic conditioning on the restriction of ischemic-reperfusion injury.

Characteristics and Preliminary Causes of Tropical Cyclone Remote Precipitation over China

In this study,the characteristics and preliminary causes of tropical cyclone remote precipitation(TRP)over China during the period from 1979 to 2020 are investigated.Results indicated that approximately 72.42%of tropical cyclones(TCs)in the Western Pacific produce TRP over China.The peak months for TRP are July and August.The four key regions of TRP are the adjacent areas between the Sichuan and Shaanxi Provinces,the northern coast of the Bohai Sea,the coast of the Yellow Sea,and the southern coast area.The typical distance between the station with TRP and the TC center ranges from 1500 to 2500 km.Most of these stations are situated north to 60°west of north of the TC.The south–west water vapor transportation on the west side of the TC is crucial to TRP.TRP has a decreasing trend because of the decrease in the number of TCs that generate TRP.From the perspective of large-scale environmental conditions,a decrease in the integrated horizontal water vapor transport in China' Mainland,the weakening of upward motion at approximately 25°–35°N,which is inconducive to convection,and an increase in low-level vertical wind shear,which is unfavorable for the development of TC in areas with high frequencies of TRP-related TCs,are the factors that result in the decreasing trend of TRP.

Remote Control of Bovine Catalase Activity with Specific Frequencies of Human and Bovine Catalase with and without Bound NADP+

Remote control enzyme technology is widely used today through resonance. In this study, we showed that the use of frequencies of the catalase enzyme itself to increase enzymatic rate is successful not only in test tubes but also remotely. The present study also suggests that, under optimal temperature, the use of bovine catalase frequency (the specific frequency of that enzyme) has a superior rate promoting vibration than the human catalase frequency, and so increases very significantly the chemical rate of bovine catalase (about 120% at 40˚C). It also suggests that bovine catalase subjected to bovine and human frequencies with catalase bound NADP+ experienced more resonance weight towards NADP+ and so were more slowly reduced back to catalase bound NADPH, increasing compound II formation rate, and slowing down the catalase activity rate.