Search

Radiative decays of the radially excited charmonium resonance, (Formula presented) into (Formula presented) (Formula presented) and (Formula presented) final states have been measured in a sample of (Formula presented) (Formula presented) events collected by the BES Collaboration. The branching ratios (Formula presented) and (Formula presented) are obtained. When compared to the corresponding radiative (Formula presented) decays, the observed (Formula presented) radiative decay rates into (Formula presented) and (Formula presented) are consistent with the prediction of the “12%” rule. © 2003 The American Physical Society.

Radiative decays of the radially excited charmonium resonance, (Formula presented) into (Formula presented) (Formula presented) and (Formula presented) final states have been measured in a sample of (Formula presented) (Formula presented) events collected by the BES Collaboration. The branching ratios (Formula presented) and (Formula presented) are obtained. When compared to the corresponding radiative (Formula presented) decays, the observed (Formula presented) radiative decay rates into (Formula presented) and (Formula presented) are consistent with the prediction of the “12%” rule. © 2003 The American Physical Society.

The Beijing Spectrometer (BES) detector is a general purpose solenoid detector at the Beijing Electron Positron Collider in Beijing, China. The recent upgrade of the initial BES detector to the improved BES II detector is described. A new drift chamber, time-of-flight counter, luminosity monitor compatible with a low-β lattice was built as well as the vertex chamber.

The Beijing Spectrometer (BES) detector is a general purpose solenoid detector at the Beijing Electron Positron Collider in Beijing, China. The recent upgrade of the initial BES detector to the improved BES II detector is described. A new drift chamber, time-of-flight counter, luminosity monitor compatible with a low-β lattice was built as well as the vertex chamber.

The first measurement of (Formula presented) and an upper limit for (Formula presented) are determined from 22.3 (Formula presented) of (Formula presented) annihilation data at a c.m. energy of 4.03 GeV. The data were recorded by the Beijing Spectrometer (BES) at BEPC. A recoil charge method is applied to charm threshold data to determine the charge of the D meson in the recoil from (Formula presented) reconstructed (Formula presented) (Formula presented) mesons. The branching fractions (Formula presented) and (Formula presented) are determined from 10 events with a reconstructed D and a recoiling (Formula presented) In addition, a 90% C.L. upper limit of (Formula presented) is determined from a search for semileptonic decays of the (Formula presented) © 2000 The American Physical Society.

Using a sample of 3.8 M (Formula presented) events accumulated with the BES detector, the process (Formula presented) is studied. The angular distributions are compared with the general decay amplitude analysis of Cahn. We find that the dipion system requires some D wave amplitude, as well as S wave. On the other hand, the (Formula presented) relative angular momentum is consistent with being pure S wave. The decay distributions have been fit to heavy quarkonium models, including the Novikov-Shifman model. This model, which is written in terms of the parameter (Formula presented) predicts that D wave pions should be present. We determine (Formula presented) based on the joint (Formula presented) distribution. The fraction of D wave amplitude as a function of (Formula presented) is found to decrease with increasing (Formula presented) in agreement with the model. We have also fit the Mannel-Yan model, which is another model that allows D wave pions. © 2000 The American Physical Society.

The cross section for charmed meson production at √s=4.03 and 4.14 GeV has been measured with the Beijing Spectrometer. The measurement was made using 22.3 pb-1 of e+e- data collected at 4.03 GeV and 1.5 pb-1 of e+e- data collected at 4.14 GeV. Inclusive observed cross sections for the production of charged and neutral D mesons and momentum spectra are presented. Observed cross sections were radiatively corrected to obtain tree level cross sections. Measurements of the total hadronic cross section are obtained from the charmed meson cross section and an extrapolation of results from below the charm threshold. ©2000 The American Physical Society.

Using a sample of 3.8 M (Formula presented) events accumulated with the BES detector, the process (Formula presented) is studied. The angular distributions are compared with the general decay amplitude analysis of Cahn. We find that the dipion system requires some D wave amplitude, as well as S wave. On the other hand, the (Formula presented) relative angular momentum is consistent with being pure S wave. The decay distributions have been fit to heavy quarkonium models, including the Novikov-Shifman model. This model, which is written in terms of the parameter (Formula presented) predicts that D wave pions should be present. We determine (Formula presented) based on the joint (Formula presented) distribution. The fraction of D wave amplitude as a function of (Formula presented) is found to decrease with increasing (Formula presented) in agreement with the model. We have also fit the Mannel-Yan model, which is another model that allows D wave pions. © 2000 The American Physical Society.

The first measurement of (Formula presented) and an upper limit for (Formula presented) are determined from 22.3 (Formula presented) of (Formula presented) annihilation data at a c.m. energy of 4.03 GeV. The data were recorded by the Beijing Spectrometer (BES) at BEPC. A recoil charge method is applied to charm threshold data to determine the charge of the D meson in the recoil from (Formula presented) reconstructed (Formula presented) (Formula presented) mesons. The branching fractions (Formula presented) and (Formula presented) are determined from 10 events with a reconstructed D and a recoiling (Formula presented) In addition, a 90% C.L. upper limit of (Formula presented) is determined from a search for semileptonic decays of the (Formula presented) © 2000 The American Physical Society.

Hadronic decays of the P-wave spin-triplet charmonium states (Formula presented) are studied using a sample of (Formula presented) decays collected by the BES detector operating at the BEPC storage ring. Branching fractions for the decays (Formula presented) (Formula presented) (Formula presented) (Formula presented) (Formula presented) and (Formula presented) are measured for the first time, and those for (Formula presented) (Formula presented) (Formula presented) and (Formula presented) are measured with improved precision. In addition, we determine the masses of the (Formula presented) and (Formula presented) to be (Formula presented) and (Formula presented) © 1999 The American Physical Society.

A sample of 3.79 × 106ψ(2S) events is used to study the decays of charmonium to axial-vector plus pseudoscalar mesons. The branching fraction for the decay ψ(2S) → b±1(1235)π∓ agrees with expectations based on scaling the corresponding J/ψ branching fraction. Flavor-SU(3)-violating K1(1270)- K1(1400) asymmetries with opposite character for ψ(2S) and J/ψ decays are observed. This contrasting behavior cannot be accommodated by adjustments of the singlet-triplet mixing angle. © 1999 The American Physical Society.

Hadronic decays of the P-wave spin-triplet charmonium states (Formula presented) are studied using a sample of (Formula presented) decays collected by the BES detector operating at the BEPC storage ring. Branching fractions for the decays (Formula presented) (Formula presented) (Formula presented) (Formula presented) (Formula presented) and (Formula presented) are measured for the first time, and those for (Formula presented) (Formula presented) (Formula presented) and (Formula presented) are measured with improved precision. In addition, we determine the masses of the (Formula presented) and (Formula presented) to be (Formula presented) and (Formula presented) © 1999 The American Physical Society.

The decays of the ψ(2S) into vector plus tensor meson final states have been studied for the first time using the BES detector. We determine upper limits on branching fractions for ψ(2S) decays into ωf2, ρa2, K*0K*02 + c.c., and φf'2(1525) that are, in each case, significantly smaller than the corresponding branching fractions for the J/ψ meson, scaled according to the expectations of perturbative QCD. © 1998 The American Physical Society.

The processes ψ(2S) → I π+ π−, γK+ K−, and γpp¯ have been studied using a sample of 3.79 × 106 ψ(2S) decays. We determine the total width of the χc0 to be γtotχc0 = 14.3 ± 2.0 ± 3.0 MeV. We present the first measurement of the branching fraction B(χc0 → pp¯) = (15.9 ± 4.3 ± 5.3) × 10−5, where the first error is statistical and the second one is systematic. Branching fractions of χc0, 2 → π+ π− and K+ K− are also reported. © 1998 American Physical Society.

Purely leptonic decays of the charged D meson have been studied using the reaction e+e- → D*+D- at a center of mass energy of 4.03 GeV. A search was performed for D → μνμ recoiling against a D0 or D+ which had been reconstructed from its hadronic decay products. A single event candidate was found in the reaction e+e- → D*+D-, where D*+ → π+D0 with the D0 → K-π+, and the recoiling D- decaying via D- → μ-ν̄μ. This yields a branching fraction value B(D → μνμ) = 0.08+0.16+0.05-0.05-0.02%, and a corresponding value of the pseudoscalar decay constant fD = 300+180+80-150-40 MeV. © 1998 Elsevier Science B.V. All rights reserved.

Purely leptonic decays of the charged D meson have been studied using the reaction e+e- → D*+D- at a center of mass energy of 4.03 GeV. A search was performed for D → μνμ recoiling against a D0 or D+ which had been reconstructed from its hadronic decay products. A single event candidate was found in the reaction e+e- → D*+D-, where D*+ → π+D0 with the D0 → K-π+, and the recoiling D- decaying via D- → μ-ν̄μ. This yields a branching fraction value B(D → μνμ) = 0.08+0.16+0.05-0.05-0.02%, and a corresponding value of the pseudoscalar decay constant fD = 300+180+80-150-40 MeV. © 1998 Elsevier Science B.V. All rights reserved.

A search is performed for the production of the (Formula presented) in (Formula presented) annihilation at a center-of-mass energy of 4.03 GeV using the BES detector operated at the Beijing Electron Positron Collider (BEPC). The kinematic features of the reconstructed (Formula presented) signal are consistent with its being produced only in association with an energetic photon resulting from initial state radiation (ISR). Limits are placed on (Formula presented) production from the decay of unknown charmonia or metastable hybrids that might be produced in (Formula presented) annihilations at 4.03 GeV. Under the assumption that the observed cross section for (Formula presented) production is due entirely to ISR, the partial width (Formula presented) of the (Formula presented) is measured to be (Formula presented). © 1998 The American Physical Society.

The absolute inclusive branching fraction of (Formula presented) has been measured from data collected by the BES detector at a center-of-mass energy of 4.03 GeV, corresponding to an integrated luminosity of 22.3 pb(Formula presented). At this energy, direct pair production (Formula presented) has been observed. We have selected (Formula presented) candidate events by reconstructing five hadronic decay modes (Formula presented), (Formula presented), (Formula presented), (Formula presented) and (Formula presented) and have searched for inclusive (Formula presented)’s in the recoiling (Formula presented). We observed three recoiling (Formula presented)’s in the 166.4 (Formula presented) 31.8 (Formula presented) candidate events, which leads to the absolute branching fraction (Formula presented) and (Formula presented). © 1998 The American Physical Society.

The absolute inclusive branching fraction of (Formula presented) has been measured from data collected by the BES detector at a center-of-mass energy of 4.03 GeV, corresponding to an integrated luminosity of 22.3 pb(Formula presented). At this energy, direct pair production (Formula presented) has been observed. We have selected (Formula presented) candidate events by reconstructing five hadronic decay modes (Formula presented), (Formula presented), (Formula presented), (Formula presented) and (Formula presented) and have searched for inclusive (Formula presented)’s in the recoiling (Formula presented). We observed three recoiling (Formula presented)’s in the 166.4 (Formula presented) 31.8 (Formula presented) candidate events, which leads to the absolute branching fraction (Formula presented) and (Formula presented). © 1998 The American Physical Society.

A search is performed for the production of the (Formula presented) in (Formula presented) annihilation at a center-of-mass energy of 4.03 GeV using the BES detector operated at the Beijing Electron Positron Collider (BEPC). The kinematic features of the reconstructed (Formula presented) signal are consistent with its being produced only in association with an energetic photon resulting from initial state radiation (ISR). Limits are placed on (Formula presented) production from the decay of unknown charmonia or metastable hybrids that might be produced in (Formula presented) annihilations at 4.03 GeV. Under the assumption that the observed cross section for (Formula presented) production is due entirely to ISR, the partial width (Formula presented) of the (Formula presented) is measured to be (Formula presented). © 1998 The American Physical Society.

The absolute inclusive semileptonic branching fraction of the [Formula presented] meson has been measured based on [Formula presented] of [Formula presented] collision data collected with the Beijing Spectrometer at [Formula presented] At this energy, the [Formula presented] are produced in pairs: [Formula presented] We reconstructed [Formula presented] [Formula presented] events in five hadronic decay modes. In the recoil system of these events, several [Formula presented] inclusive semileptonic decays were observed and the branching fraction is estimated to be [Formula presented] © 1997 The American Physical Society.

The absolute inclusive semileptonic branching fraction of the [Formula presented] meson has been measured based on [Formula presented] of [Formula presented] collision data collected with the Beijing Spectrometer at [Formula presented] At this energy, the [Formula presented] are produced in pairs: [Formula presented] We reconstructed [Formula presented] [Formula presented] events in five hadronic decay modes. In the recoil system of these events, several [Formula presented] inclusive semileptonic decays were observed and the branching fraction is estimated to be [Formula presented] © 1997 The American Physical Society.

The cross section for e+e-→ρπ has been measured by the BES detector at BEPC at center-of-mass energies covering a 40 MeV interval spanning the J/ψresonance. The data are used to search for the vector gluonium state hypothesized by Brodsky, Lepage, and Tuan as an explanation of the ρπ puzzle in charmonium physics. The shape of the ρπ cross section is compatible with that of the total hadronic cross section. No distortions indicating the presence of a vector glueball are seen. © 1996 The American Physical Society.

A data-driven energy scan in the immediate vicinity of the τ pair production threshold has been performed using the Beijing Spectrometer at the Beijing Electron-Positron Collider. Approximately 5pb-1 of data, distributed over 12 scan points, have been collected. A previous mass value for the τ lepton, obtained using only the eµ final state, has been published. In this paper, the final BES result on the mass measurement is presented. The analysis is based on the combined data from the ee, eµ, eh, µµ, µh, and hh final states, where h denotes a charged Π or K. A maximum likelihood fit to the τ pair production cross section data yields the value mT=1776.96-0.21 -0.17+0.18+0.25. © 1995 The American Physical Society.

A data-driven energy scan in the immediate vicinity of the τ pair production threshold has been performed using the Beijing Spectrometer at the Beijing Electron-Positron Collider. Approximately 5pb-1 of data, distributed over 12 scan points, have been collected. A previous mass value for the τ lepton, obtained using only the eµ final state, has been published. In this paper, the final BES result on the mass measurement is presented. The analysis is based on the combined data from the ee, eµ, eh, µµ, µh, and hh final states, where h denotes a charged Π or K. A maximum likelihood fit to the τ pair production cross section data yields the value mT=1776.96-0.21 -0.17+0.18+0.25. © 1995 The American Physical Society.

The Beijing Spectrometer (BES) experiment has observed purely leptonic decays of the Ds meson in the reaction e+e-→Ds+Ds- at a c.m. energy of 4.03 GeV. Three events are observed in which one Ds decays hadronically to φπ, K̄*0K, or K̄0K, and the other decays leptonically to μνμ or τντ. With the assumption of μ-τ universality, values of the branching fraction, B(Ds→μνμ)=(1.5-0.6-0.2+1.3+0.3)%, and the Ds pseudoscalar decay constant, fDs=(4.3-1.3-0.4+1.5+0.4)×102 MeV, are obtained. © 1995 The American Physical Society.

Background: Oncocytic thyroid carcinoma (OTC) is a rare subtype of thyroid cancer known for its distinctive morphology and high likelihood of recurrence, setting it apart from follicular thyroid carcinoma (FTC). Despite this, there is limited research comparing the clinicopathological characteristics and outcomes of OTC and FTC., Methods: We retrospectively searched through the Surveillance, Epidemiology, and End-Results (SEER) database (2004-2015) for histologically diagnosed OTC and FTC patients. Kaplan-Meier analysis, propensity score matching (PSM), univariate Cox proportional risk regression model, and subgroup analysis were employed to investigate the prognostic effect of clinicopathological features and treatment regimens on survival outcomes of OTC and FTC patients., Results: 2329 OTC patients and 5679 FTC patients were included in the study. OTC patients were prone to older age, white race, lymph node metastasis, distal metastasis, extension and multiple primary tumors compared with FTC patients. After using a 1:1 PSM matching ratio, there were no significant differences in demographic and clinicopathological characteristics between the matched groups. Further Cox regression analysis showed that OTC patients had lower overall survival (OS) and cancer-specific survival (CSS) in contrast with FTC patients. Subgroup survival analysis suggested that the OTC patients were related to lower OS in subgroups including those over 55 years old, male sex, white ethnicity, extrathyroidal extension, single primary tumor, surgery and without chemotherapy compared with the FTC patients in these subgroups. In addition, the OTC patients were connected with lower CSS in subgroups including male sex, white ethnicity, married status, tumor size is less than 20 mm or more than 40 mm, N0 stage, localized stage, single primary tumor, surgery, radiotherapy, and without chemotherapy compared with the FTC patients in these subgroups. Meanwhile, the OTC patients had lower CSS compared to FTC patients regardless of age and extrathyroidal extension., Conclusions: The results suggested that OTC patients have unique clinical features and poorer prognoses compared to FTC patients. Surgical resection and radioactive iodine therapy are recommended for OTC patients and FTC patients. It is worth noting that the prognosis of OTC relies largely on the selection of treatment strategies. Therefore, our results highlighted the clinical significance of the early distinguishment and the correct choice of treatment in OTC patients., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Although anesthesia provides favorable conditions for surgical procedures, recent studies have revealed that the brain remains active in processing noxious signals even during anesthesia. However, whether and how these responses affect the anesthesia effect remains unclear. The ventrolateral periaqueductal gray (vlPAG), a crucial hub for pain regulation, also plays an essential role in controlling general anesthesia. Hence, it was hypothesized that the vlPAG may be involved in the regulation of general anesthesia by noxious stimuli. Here, we found that acute noxious stimuli, including capsaicin-induced inflammatory pain, acetic acid-induced visceral pain, and incision-induced surgical pain, significantly delayed recovery from sevoflurane anesthesia in male mice, whereas this effect was absent in the spared nerve injury-induced chronic pain. Pretreatment with peripheral analgesics could prevent the delayed recovery induced by acute nociception. Furthermore, we found that acute noxious stimuli, induced by the injection of capsaicin under sevoflurane anesthesia, increased c-Fos expression and activity in the GABAergic neurons of the ventrolateral periaqueductal gray. Specific reactivation of capsaicin-activated vlPAG GABA neurons mimicked the effect of capsaicin and its chemogenetic inhibition prevented the delayed recovery from anesthesia induced by capsaicin. Finally, we revealed that the vlPAG GABA neurons regulated the recovery from anesthesia through the inhibition of ventral tegmental area dopaminergic neuronal activity, thus decreasing dopamine (DA) release and activation of DA D 1 -like receptors in the brain. These findings reveal a novel, cell- and circuit-based mechanism for regulating anesthesia recovery by nociception, and it is important to provide new insights for guiding the management of the anesthesia recovery period., Competing Interests: The authors declare no competing financial interests., (Copyright © 2024 the authors.)

Both peripheral and central corticotropin-releasing factor (CRF) systems have been implicated in regulating pain sensation. However, compared with the peripheral, the mechanisms underlying central CRF system in pain modulation have not yet been elucidated, especially at the neural circuit level. The corticoaccumbal circuit, a structure rich in CRF receptors and CRF-positive neurons, plays an important role in behavioral responses to stressors including nociceptive stimuli. The present study was designed to investigate whether and how CRF signaling in this circuit regulated pain sensation under physiological and pathological pain conditions. Our studies employed the viral tracing and circuit-, and cell-specific electrophysiological methods to label the CRF-containing circuit from the medial prefrontal cortex to the nucleus accumbens shell (mPFC CRF -NAcS) and record its neuronal propriety. Combining optogenetic and chemogenetic manipulation, neuropharmacological methods, and behavioral tests, we were able to precisely manipulate this circuit and depict its role in regulation of pain sensation. The current study found that the CRF signaling in the NAc shell (NAcS), but not NAc core, was necessary and sufficient for the regulation of pain sensation under physiological and pathological pain conditions. This process was involved in the CRF-mediated enhancement of excitatory synaptic transmission in the NAcS. Furthermore, we demonstrated that the mPFC CRF neurons monosynaptically connected with the NAcS neurons. Chronic pain increased the protein level of CRF in NAcS, and then maintained the persistent NAcS neuronal hyperactivity through enhancement of this monosynaptic excitatory connection, and thus sustained chronic pain behavior. These findings reveal a novel cell- and circuit-based mechanistic link between chronic pain and the mPFC CRF  → NAcS circuit and provide a potential new therapeutic target for chronic pain., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

The dorsal raphe nucleus (DRN) is an important nucleus in pain regulation. However, the underlying neural pathway and the function of specific cell types remain unclear. Here, we report a previously unrecognized ascending facilitation pathway, the DRN to the mesoaccumbal dopamine (DA) circuit, for regulating pain. Chronic pain increased the activity of DRN glutamatergic, but not serotonergic, neurons projecting to the ventral tegmental area (VTA) (DRN Glu -VTA) in male mice. The optogenetic activation of DRN Glu -VTA circuit induced a pain-like response in naive male mice, and its inhibition produced an analgesic effect in male mice with neuropathic pain. Furthermore, we discovered that DRN ascending pathway regulated pain through strengthened excitatory transmission onto the VTA DA neurons projecting to the ventral part of nucleus accumbens medial shell (vNAcMed), thereby activated the mesoaccumbal DA neurons. Correspondingly, optogenetic manipulation of this three-node pathway bilaterally regulated pain behaviors. These findings identified a DRN ascending excitatory pathway that is crucial for pain sensory processing, which can potentially be exploited toward targeting pain disorders., (Copyright © 2024 the authors.)

This study examined whether plasma FXII levels reflect disease activity in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Plasma FXII levels were detected by ELISA in 127 patients with AAV, and their associations with disease activity and plasma myeloperoxidase (MPO)-ANCA titre were examined. Immunofluorescent co-staining of FXII and neutrophils was performed on the renal tissues of patients with AAV. MPO expression in renal biopsy tissues was determined by immunohistochemical staining. The association between plasma FXII levels and histological activity was assessed in 82 patients who underwent kidney biopsy. Plasma FXII levels were considerably increased in patients with clinically active AAV compared to those in clinical remission and healthy individuals. Plasma FXII levels correlated positively with creatinine (r = 0.377), CRP (r = 0.222), urine red blood cell (r = 0.203), serum MPO-ANCA titer (r = 0.353), white blood cell (r = 0.194), percentage of glomeruli with crescents (P = 0.001), capillary breaks (P = 0.001), interstitial inflammation (P < 0.001) and fibrinoid necrosis (p < 0.001) on kidney biopsy. The plasma FXII optimal cut-off value for evaluating AAV activity was 24.5 μg/mL (sensitivity = 0.81, specificity = 0.82, P = 0.0001), which was superior to that achieved using conventional serologic biomarkers. Co-expression of FXII and neutrophils was higher, with increased MPO expression, in renal tissue with pathologically active AAV than that observed in pathologically inactive tissues. In conclusion, elevated plasma FXII levels reflect AAV clinical and histologic activity, and can serve as markers of active AAV., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

A comorbidity of chronic pain is sleep disturbance. Here, we identify a dual-functional ensemble that regulates both pain-like behaviour induced by chronic constrictive injury or complete Freund's adjuvant, and sleep wakefulness, in the nucleus accumbens (NAc) in mice. Specifically, a select population of NAc neurons exhibits increased activity either upon nociceptive stimulation or during wakefulness. Experimental activation of the ensemble neurons exacerbates pain-like (nociceptive) responses and reduces NREM sleep, while inactivation of these neurons produces the opposite effects. Furthermore, NAc ensemble primarily consists of D1 neurons and projects divergently to the ventral tegmental area (VTA) and preoptic area (POA). Silencing an ensemble innervating VTA neurons selectively increases nociceptive responses without affecting sleep, whereas inhibiting ensemble-innervating POA neurons decreases NREM sleep without affecting nociception. These results suggest a common NAc ensemble that encodes chronic pain and controls sleep, and achieves the modality specificity through its divergent downstream circuit targets., (© 2023. Springer Nature Limited.)

Although it has become a consensus in the field of colorectal surgery to perform radical tumor treatment and functional protection under the minimally invasive concept, there exist many controversies during clinical practice, including the concept of embryonic development of abdominal organs and membrane anatomy, the principle of membrane anatomy related to right hemicolectomy, D3 resection, and identification of the inner boundary. In this paper, we analyzed recently reported literature with high-level evidence and clinical data from the author's hospital to recognize and review the membrane anatomy-based laparoscopic assisted right hemicolectomy for right colon cancer, emphasizing the importance of priority of surgical dissection planes, vascular orientation, and full understanding of the fascial space, and proposing that the surgical planes should be dissected in the parietal-prerenal fascial space, and the incision should be 1 cm from the descending and horizontal part of the duodenum. The surgery should be performed according to a standard procedure with strict quality control. To identify the resection range of D3 dissection, it is necessary to establish a clinical, imaging, and pathological evaluation model for multiple factors or to apply indocyanine green and nano-carbon lymphatic tracer intraoperatively to guide precise lymph node dissection. We expect more high-level evidence of evidence-based medicine to prove the inner boundary of laparoscopic assisted radical right colectomy and a more rigorous consensus to be established.

Our recent study demonstrated the critical role of the mesolimbic dopamine (DA) circuit and its brain-derived neurotropic factor (BDNF) signaling in mediating neuropathic pain. The present study aims to investigate the functional role of GABAergic inputs from the lateral hypothalamus (LH) to the ventral tegmental area (VTA; LH GABA →VTA) in regulating the mesolimbic DA circuit and its BDNF signaling underlying physiological and pathologic pain. We demonstrated that optogenetic manipulation of the LH GABA →VTA projection bidirectionally regulated pain sensation in naive male mice. Optogenetic inhibition of this projection generated an analgesic effect in mice with pathologic pain induced by chronic constrictive injury (CCI) of the sciatic nerve and persistent inflammatory pain by complete Freund's adjuvant (CFA). Trans-synaptic viral tracing revealed a monosynaptic connection between LH GABAergic neurons and VTA GABAergic neurons. Functionally, in vivo calcium/neurotransmitter imaging showed an increased DA neuronal activity, decreased GABAergic neuronal activity in the VTA, and increased dopamine release in the NAc, in response to optogenetic activation of the LH GABA →VTA projection. Furthermore, repeated activation of the LH GABA →VTA projection was sufficient to increase the expression of mesolimbic BDNF protein, an effect seen in mice with neuropathic pain. Inhibition of this circuit induced a decrease in mesolimbic BDNF expression in CCI mice. Interestingly, the pain behaviors induced by activation of the LH GABA →VTA projection could be prevented by pretreatment with intra-NAc administration of ANA-12, a TrkB receptor antagonist. These results demonstrated that LH GABA →VTA projection regulated pain sensation by targeting local GABAergic interneurons to disinhibit the mesolimbic DA circuit and regulating accumbal BDNF release. SIGNIFICANCE STATEMENT The mesolimbic dopamine (DA) system and its brain-derived neurotropic factor (BDNF) signaling have been implicated in pain regulation, however, underlying mechanisms remain poorly understood. The lateral hypothalamus (LH) sends different afferent fibers into and strongly influences the function of mesolimbic DA system. Here, utilizing cell type- and projection-specific viral tracing, optogenetics, in vivo calcium and neurotransmitter imaging, our current study identified the LH GABA →VTA projection as a novel neural circuit for pain regulation, possibly by targeting the VTA GABA-ergic neurons to disinhibit mesolimbic pathway-specific DA release and BDNF signaling. This study provides a better understanding of the role of the LH and mesolimbic DA system in physiological and pathological pain., (Copyright © 2023 the authors.)

The paucity of medications with novel mechanisms for pain treatment combined with the severe adverse effects of opioid analgesics has led to an imperative pursuit of non-opioid analgesia and a better understanding of pain mechanisms. Here, we identify the putative glutamatergic inputs from the paraventricular thalamic nucleus to the nucleus accumbens (PVT Glut →NAc) as a novel neural circuit for pain sensation and non-opioid analgesia. Our in vivo fiber photometry and in vitro electrophysiology experiments found that PVT Glut →NAc neuronal activity increased in response to acute thermal/mechanical stimuli and persistent inflammatory pain. Direct optogenetic activation of these neurons in the PVT or their terminals in the NAc induced pain-like behaviors. Conversely, inhibition of PVT Glut →NAc neurons or their NAc terminals exhibited a potent analgesic effect in both naïve and pathological pain mice, which could not be prevented by pretreatment of naloxone, an opioid receptor antagonist. Anterograde trans-synaptic optogenetic experiments consistently demonstrated that the PVT Glut →NAc circuit bi-directionally modulates pain behaviors. Furthermore, circuit-specific molecular profiling and pharmacological studies revealed dopamine receptor 3 as a candidate target for pain modulation and non-opioid analgesic development. Taken together, these findings provide a previously unknown neural circuit for pain sensation and non-opioid analgesia and a valuable molecular target for developing future safer medication., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Corticotropin-releasing factor (CRF) neurones in the paraventricular nucleus (PVN) of the hypothalamus (PVN CRF neurones) can promote wakefulness and are activated under anaesthesia. However, whether these neurones contribute to anaesthetic effects is unknown., Methods: With a combination of chemogenetic and molecular approaches, we examined the roles of PVN CRF neurones in isoflurane anaesthesia in mice and further explored the underlying cellular and molecular mechanisms., Results: PVN neurones exhibited increased Fos expression during isoflurane anaesthesia (mean [standard deviation], 218 [69.3] vs 21.3 [7.3]; P<0.001), and ∼75% were PVN CRF neurones. Chemogenetic inhibition of PVN CRF neurones facilitated emergence from isoflurane anaesthesia (11.7 [1.1] vs 13.9 [1.2] min; P=0.001), whereas chemogenetic activation of these neurones delayed emergence from isoflurane anaesthesia (16.9 [1.2] vs 13.9 [1.3] min; P=0.002). Isoflurane exposure increased CRF protein expression in PVN (4.0 [0.1] vs 2.2 [0.3], respectively; P<0.001). Knockdown of CRF in PVN CRF neurones mimicked the effects of chemogenetic inhibition of PVN CRF neurones in facilitating emergence (9.6 [1.1] vs 13.0 [1.4] min; P=0.003) and also abolished the effects of chemogenetic activation of PVN CRF neurones on delaying emergence from isoflurane anaesthesia (10.3 [1.3] vs 16.0 [2.6] min; P<0.001). Acute, but not chronic, stress delayed emergence from isoflurane anaesthesia (15.5 [1.5] vs 13.0 [1.4] min; P=0.004). This effect was reversed by chemogenetic inhibition of PVN CRF neurones (11.7 [1.6] vs 14.7 [1.4] min; P=0.001) or knockdown of CRF in PVN CRF neurones (12.3 [1.5] vs 15.3 [1.6] min; P=0.002)., Conclusions: CRF neurones in the PVN of the hypothalamus neurones modulate isoflurane anaesthesia and acute stress effects on anaesthesia through CRF signalling., (Copyright © 2023 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.)

The neurotrophin brain-derived neurotrophic factor (BDNF), which acts as a transducer, is responsible for improving cerebral stroke, neuropathic pain, and depression. Exercise can alter extracellular nucleotide levels and purinergic receptors in central nervous system (CNS) structures. This inevitably activates or inhibits the expression of BDNF via purinergic receptors, particularly the P2X receptor (P2XR), to alleviate pathological progression. In addition, the significant involvement of sensitive P2X4R in mediating increased BDNF and p38-MAPK for intracerebral hemorrhage and pain hypersensitivity has been reported. Moreover, archetypal P2X7R blockade induces mouse antidepressant-like behavior and analgesia by BDNF release. This review summarizes BDNF-mediated neural effects via purinergic receptors, speculates that P2X4R and P2X7R could be priming molecules in exercise-mediated changes in BDNF, and provides strategies for the protective mechanism of exercise in neurogenic disease., (© 2022. The Author(s).)

Introduction: The COVID-19 pandemic has led to major changes in the provision of surgical services and also affected patients' health-seeking behaviour. This contributes to delayed presentation of many surgical conditions resulting in poorer outcomes. Colorectal cancer (CRC) patients who present with acute surgical emergencies such as complete bowel obstruction, perforation, bleeding or sepsis often require immediate intervention. This study aimed to assess the impact of COVID-19 pandemic on the proportion of emergency surgery in CRC patients., Materials and Methods: This is a retrospective cohort study. All CRC patients who underwent elective and emergency surgery from January until December 2019 (pre-COVID era) and September 2020 until August 2021 (COVID era) were included. Patient demographics, presentation, tumour stage, surgery performed and waiting time for surgery were collected. Data were then compared., Results: Seventy-seven and 76 new cases of CRC underwent surgery before and during COVID-19, respectively. The proportions of emergency surgery before and during COVID-19 are 29% vs 33% (p=0.562). Of those who required emergency surgery, the proportions of patients who required stoma formation are 59% vs 72% (p= 0.351). There was no difference in median waiting time for patients requiring elective surgery (p= 0.668)., Conclusion: The proportion of emergency surgery for CRC patients is not statistically higher during the pandemic.

It is a promising method to identify structural damage using bridge dynamic response under moving vehicle excitation, but the lack of accurate information about road roughness and vehicle parameters will lead to the failure of this method. The paper proposed a step-by-step EKF damage identification method, which transforms the inversion problem of unknown structural parameters under unknown loads (vehicle and road roughness) into two separate inversion problems: moving contact force identification and damage parameters identification. Firstly, the VBI model is converted into bridge vibration model under a moving contact force, and the moving contact force covering the information of road roughness and vehicle parameters can be calculated by EKF iteration. Secondly, the moving contact force identified in the first step is loaded on the bridge as a known condition, and the bridge damage problem is also solved by the EKF method. Numerical analyses of a simply-supported bridge under the moving vehicle are conducted to investigate the accuracy and efficiency of the proposed method. Effects of the vehicle speed, the damage cases, the measurement noise, and the roughness levels on the accuracy of the identification results are investigated. The results demonstrate the proposed algorithm is efficient and robust, and the algorithm can be developed into an effective tool for structural health monitoring of bridges., (© 2022. The Author(s).)

Objective: To investigate the role of clock gene BMAL1 in exercise-induced skeletal muscle injury recovery. Methods: Two hundred and eight 8-week-old SD rats were randomly divided into the control group (Group C, n =104) and the exercise group (Group E, n =104). Group E performed a 90-minute downhill run on the treadmill. After exercise, the gastrocnemius muscle of 8 rats in Group C and Group E were collected at 0 h, 6 h, 12 h, 18 h, 24 h, 30 h, 36 h, 42 h, 48 h, 54 h, 60 h, 66 h and 72 h. The expression of skeletal muscle core clock gene, BMAL1 was measured by real-time fluorescence quantitative PCR. The parameters of fitting cosine curve were obtained by cosine analysis software circacompare (R package), and the change trend of rhythmic oscillation was analyzed. The ultrastructure of skeletal muscle fibers was observed by transmission electron microscope. The expressions of skeletal muscle BMAL1 and DESMIN were detected by Western blot; Immunofluorescence was used to observe the localization and contents of BMAL1 and DESMIN. Results: In Group C, three complete circadian rhythm cycles of mRNA BMAL1 were observed within 72 hours; in Group E, the circadian rhythm of BMAL1 mRNA disappeared at 0 h～24 h. Compared with Group C, the expression level of BMAL1 mRNA was significantly increased at 0 h, 6 h, 12 h, and 18 h after exercise in Group E ( P ＜0.05), and the expression of BMAL1 protein was significantly increased at 0 h and 12 h after exercise( P ＜0.05), and recovered to the level of that in Group C from 24 h to 72 h( P ＞0.05). The expression of DESMIN protein was decreased at 0 h and 12 h after exercise( P ＜0.05), gradually increased at 24 h, increased significantly at 48 h( P ＜0.01), and recovered to the control level at 72 h ( P ＞0.05). In Group E, BMAL1 and DESMIN were co-localized at 0 h, 12 h, and 24 h after exercise; the colocalization at 0 h～24 h showed a trend of first decreasing and then increasing, and the fluorescence intensity at 24 h reached the highest value. Conclusion: The post-exercise clock gene BMAL1 may be involved in the enhanced synergy of regulating the cytoskeletal protein DESMIN, it is thus related to the promotion of muscle fiber structure recovery.

Long-term limb nerve injury often leads to mirror-image pain (MIP), an abnormal pain sensation in the limb contralateral to the injury. Although it is clear that MIP is mediated in part by central nociception processing, the underlying mechanisms remain poorly understood. The anterior cingulate cortex (ACC) is a key brain region that receives relayed peripheral nociceptive information from the contralateral limb. In this study, we induced MIP in male mice, in which a unilateral chronic constrictive injury of the sciatic nerve (CCI) induced a decreased nociceptive threshold in both hind limbs and an increased number of c-Fos-expressing neurons in the ACC both contralateral and ipsilateral to the injured limb. Using viral-mediated projection mapping, we observed that a portion of ACC neurons formed monosynaptic connections with contralateral ACC neurons. Furthermore, the number of cross-callosal projection ACC neurons that exhibited c-Fos signal was increased in MIP-expressing mice, suggesting enhanced transmission between ACC neurons of the two hemispheres. Moreover, selective inhibition of the cross-callosal projection ACC neurons contralateral to the injured limb normalized the nociceptive sensation of the uninjured limb without affecting the increased nociceptive sensation of the injured limb in CCI mice. In contrast, inhibition of the non-cross-callosal projection ACC neurons contralateral to the injury normalized the nociceptive sensation of the injured limb without affecting the MIP exhibited in the uninjured limb. These results reveal a circuit mechanism, namely, the cross-callosal projection of ACC between two hemispheres, that contributes to MIP and possibly other forms of contralateral migration of pain sensation. SIGNIFICANCE STATEMENT Mirror-image pain (MIP) refers to the increased pain sensitivity of the contralateral body part in patients with chronic pain. This pathology requires central processing, yet the mechanisms are less known. Here, we demonstrate that the cross-callosal projection neurons in the anterior cingulate cortex (ACC) contralateral to the injury contribute to MIP exhibited in the uninjured limb, but do not affect nociceptive sensation of the injured limb. In contrast, the non-cross-callosal projection neurons in the ACC contralateral to the injury contribute to nociceptive sensation of the injured limb, but do not affect MIP exhibited in the uninjured limb. Our study depicts a novel cross-callosal projection of ACC that contributes to MIP, providing a central mechanism for MIP in chronic pain state., (Copyright © 2021 the authors.)

The mortality rate of young female COVID-19 patients is reported to be lower than that of young males but no significant difference in mortality was found between female and male COVID-19 patients aged over 65 years, and the underlying mechanism is unknown. We retrospectively analyzed clinical characteristics and outcomes of severely ill pre- and post-menopausal COVID-19 patients and compared with age-matched males. Of the 459 patients included, 141 aged ≤55, among whom 19 died (16 males vs. 3 females, p<0.005). While for patients >55 years (n=318), 115 died (47 females vs. 68 males, p=0.149). In patients ≤55 years old, the levels of NLR, median LDH, median c-reactive protein and procalcitonin were significantly higher while the median lymphocyte count and LCR were lower in male than in female (all p<0.0001). In patients over 55, these biochemical parameters were far away from related normal/reference values in the vast majority of these patients in both genders which were in contrast to that seen in the young group. It is concluded that the mortality of severely ill pre-menopausal but not post-menopausal COVID-19 female patients is lower than age-matched male. Our findings support the notion that estrogen plays a beneficial role in combating COVID-19.

The same doses of anesthesia may yield varying depths of anesthesia in different patients. Clinical studies have revealed a possible causal relationship between deep anesthesia and negative short- and long-term patient outcomes. However, a reliable index and method of the clinical monitoring of deep anesthesia and detecting latency remain lacking. As burst-suppression is a characteristic phenomenon of deep anesthesia, the present study investigated the relationship between burst-suppression latency (BSL) and the subsequent burst-suppression ratio (BSR) to find an improved detection for the onset of intraoperative deep anesthesia. The mice were divided young, adult and old group treated with 1.0% or 1.5% isoflurane anesthesia alone for 2 h. In addition, the adult mice were pretreated with intraperitoneal injection of ketamine, dexmedetomidine, midazolam or propofol before they were anesthetized by 1.0% isoflurane for 2 h. Continuous frontal, parietal and occipital electroencephalogram (EEG) were acquired during anesthesia. The time from the onset of anesthesia to the first occurrence of burst-suppression was defined as BSL, while BSR was calculated as percentage of burst-suppression time that was spent in suppression periods. Under 1.0% isoflurane anesthesia, we found a negative correlation between BSL and BSR for EEG recordings obtained from the parietal lobes of young mice, from the parietal and occipital lobes of adult mice, and the occipital lobes of old mice. Under 1.5% isoflurane anesthesia, only the BSL calculated from EEG data obtained from the occipital lobe was negatively correlated with BSR in all mice. Furthermore, in adult mice receiving 1.0% isoflurane anesthesia, the co-administration of ketamine and midazolam, but not dexmedetomidine and propofol, significantly decreased BSL and increased BSR. Together, these data suggest that BSL can detect burst-suppression and predict the subsequent BSR under isoflurane anesthesia used alone or in combination with anesthetics or adjuvant drugs. Furthermore, the consistent negative correlation between BSL and BSR calculated from occipital EEG recordings recommends it as the optimal position for monitoring burst-suppression., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Wang, Guo, Liu, Kong, Xu, Zhou, Su, Dai, Ding and Cao.)

Background: The γ-aminobutyric acid-mediated (GABAergic) inhibitory system in the brain is critical for regulation of sleep-wake and general anesthesia. The lateral septum contains mainly GABAergic neurons, being cytoarchitectonically divided into the dorsal, intermediate, and ventral parts. This study hypothesized that GABAergic neurons of the lateral septum participate in the control of wakefulness and promote recovery from anesthesia., Methods: By employing fiber photometry, chemogenetic and optogenetic neuronal manipulations, anterograde tracing, in vivo electrophysiology, and electroencephalogram/electromyography recordings in adult male mice, the authors measured the role of lateral septum GABAergic neurons to the control of sleep-wake transition and anesthesia emergence and the corresponding neuron circuits in arousal and emergence control., Results: The GABAergic neurons of the lateral septum exhibited high activities during the awake state by in vivo fiber photometry recordings (awake vs. non-rapid eye movement sleep: 3.3 ± 1.4% vs. -1.3 ± 1.2%, P < 0.001, n = 7 mice/group; awake vs. anesthesia: 2.6 ± 1.2% vs. -1.3 ± 0.8%, P < 0.001, n = 7 mice/group). Using chemogenetic stimulation of lateral septum GABAergic neurons resulted in a 100.5% increase in wakefulness and a 51.2% reduction in non-rapid eye movement sleep. Optogenetic activation of these GABAergic neurons promoted wakefulness from sleep (median [25th, 75th percentiles]: 153.0 [115.9, 179.7] s to 4.0 [3.4, 4.6] s, P = 0.009, n = 5 mice/group) and accelerated emergence from isoflurane anesthesia (514.4 ± 122.2 s vs. 226.5 ± 53.3 s, P < 0.001, n = 8 mice/group). Furthermore, the authors demonstrated that the lateral septum GABAergic neurons send 70.7% (228 of 323 cells) of monosynaptic projections to the ventral tegmental area GABAergic neurons, preferentially inhibiting their activities and thus regulating wakefulness and isoflurane anesthesia depth., Conclusions: The results uncover a fundamental role of the lateral septum GABAergic neurons and their circuit in maintaining awake state and promoting general anesthesia emergence time., (Copyright © 2021, the American Society of Anesthesiologists. All Rights Reserved.)

Objective: To observe the effects of acupuncture on the endoplasmic reticulum (ER) functional enzymes sarcoplasmic reticulum Ca 2+ -ATPase (SERCA), protein disulfide isomerase (PDI), glucose-regulated protein 78(GRP78) and PERK pathways in rats with exercise-induced skeletal muscle damage, and to explore the mechanisms of acupuncture in preventing and treating exercise-induced skeletal muscle damage. Methods: Eight-week-old male SD rats were randomly divided into control group (group C, n =6), exercise group (group E, n =30), acupuncture group (group A, n =30) and exercise acupuncture group (group EA, n =30). Among them, the E and EA group were established an exercise-induced skeletal muscle damage model by a single eccentric exercise, and acupuncture intervention was applied 0.5 cm above the Achilles tendon of the rat's calf immediately after EA exercise, and in group A, acupuncture intervention was applied during the same period. Each group was divided into 0 h/12 h/24 h/48 h/72 h ( n =6) according to different sampling time points after exercise and acupuncture intervention, and soleus muscle was collected at the corresponding time for index test. The ultrastructure of muscle fibers was observed by transmission electron microscopy; the contents of SERCA and PDI were determined by ELISA; and the expressions of ER stress marker proteins GRP78 and p-PERK and p-eIF2α were detected by Western blot. Results: Compared with group C, there were no significant differences in the indicators of group A at all time points ( P ＞ 0.05), the ultrastructure of muscle fibers in group E showed different damages, SERCA content was significantly decreased from 0 h to 48 h ( P ＜0.05), PDI content was significantly increased from 0 h to 72 h ( P ＜0.05), GRP78 expression was significantly increased from 0 h to 72 h ( P ＜0.05), p-PERK expression was significantly increased from 0 h to 24 h ( P ＜0.05), and p-eIF2α expression was consistent with p-PERK. Compared with the corresponding times in group E, the ultrastructure of muscle fibers in group EA was significantly alleviated, SERCA content was significantly increased from 48 h and 72 h ( P ＜0.05), PDI content was significantly increased from 0 h to 72 h ( P ＜0.05), and GRP78 expression was significantly decreased from 0 h to 72 h ( P ＜0.05). Conclusion: Acupuncture can effectively ameliorate exercise-induced skeletal muscle damage and alleviate ER stress after a large load eccentric exercise. The mechanism of them may be related to the up-regulation of protein disulfide isomerase PDI and the inhibition of ER stress PERK pathway.

Mesocorticolimbic dopaminergic (DA) neurons have been implicated in regulating nociception in chronic pain, yet the mechanisms are barely understood. Here, we found that chronic constructive injury (CCI) in mice increased the firing activity and decreased the KCNQ channel-mediated M-currents in ventral tegmental area (VTA) DA neurons projecting to the nucleus accumbens (NAc). Chemogenetic inhibition of the VTA-to-NAc DA neurons alleviated CCI-induced thermal nociception. Opposite changes in the firing activity and M-currents were recorded in VTA DA neurons projecting to the medial prefrontal cortex (mPFC) but did not affect nociception. In addition, intra-VTA injection of retigabine, a KCNQ opener, while reversing the changes of the VTA-to-NAc DA neurons, alleviated CCI-induced nociception, and this was abolished by injecting exogenous BDNF into the NAc. Taken together, these findings highlight a vital role of KCNQ channel-mediated modulation of mesolimbic DA activity in regulating thermal nociception in the chronic pain state.