OBJECTIVETo describe the clinical manifestations and lung imaging characteristics of the human transmissible highly pathogenic H5N1 avian influenza.

METHODSThe clinical manifestations and lung imaging characteristics of human transmissible highly pathogenic H5N1 avian influenza in one patient were reviewed and analyzed.

RESULTSThe patient had the clear history of occupational exposure. The fever and symptoms of influenza were prominent at onset and associated with the symptoms of the digestive tract. The laboratory findings comprised the significant decrease of the white blood cell count and the lymphocyte number and the impairment of the liver function and the myocardial enzymes. The disease progressed rapidly and multiple organs including lung, heart, liver and kidneys were involved. It was ineffective to administer anti-fungal, anti-virus and anti-inflammation medicines. It was in vain to use mechanical ventilation and pneumothorax intubation and closed drainage as well as the support therapy. In the X-ray film, the lesions progressed quickly and changed diversely with absorption and development at the same time. The nasal and throat swabs and the gargle specimen were detected with RT-PCR and real time PCR by Chinese Center for Disease Control and Prevention. The results showed that both the specific HA and NA genes of the avian influenza virus H5N1 subtype were positive and in the same time a strain of avian influenza virus A/jiangxi/1/2005H5N1) was separated and obtained from the nasal and throat swabs. The autopsy showed that diffuse injury of alveolus in lungs, DIC and multiple organ injury.

CONCLUSIONThe human transmissible highly pathogenic H5N1 avian influenza is a lethal disease. The disease progresses rapidly with the absorption and development at the same time in the lungs and unfortunately there are no effective therapeutic measures. The prevention of the contagious disease for the occupationally exposed population should be emphasized.

Adult ; Humans ; Influenza A Virus, H5N1 Subtype ; Influenza, Human ; diagnosis ; etiology ; therapy ; Male ; Occupational Exposure ; adverse effects

OBJECTIVETo systemically investigate receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) induced differentiation of osteoclasts.

METHODSMouse protein-protein interaction(PPI) database NIA and published microarray dataset GES16749 were used to construct and analyze PPI network of RANKL and M-CSF induced mouse monocyte RAW264.7.

RESULTSIn the PPI network, transforming growth factor beta receptor 1 (TGFBR1), Rous sarcoma oncogene (SRC), myelocytomatosis oncogene(MYC) and integrin beta 3 (ITGB3) were able to interact with more proteins and they were the key nodes in the signaling transduction.

CONCLUSIONTGFBR1, SRC, MYC and ITGB3 might be the key points of RANKL and M-CSF induced differentiation of osteoclasts.

Animals ; Carrier Proteins ; Cell Differentiation ; Macrophage Colony-Stimulating Factor ; Membrane Glycoproteins ; Mice ; Osteoclasts ; Protein Interaction Maps ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B

OBJECTIVETo study the adaptive alterations of elastic fibers in the bilaminar zone (BZ) of rabbit temporomandibular joint (TMJ) following disc displacement.

METHODSTwenty-eight Japanese white rabbits were used in this study. The right temporomandibular joints of 20 of 28 rabbits were subjected to the surgical procedure of anterior disc displacement (ADD). Four rabbits in the surgical group were sacrificed at 2, 4, 6, 8 and 12 weeks after operation. Their temporomandibular joints were studied histochemically.

RESULTSElastic fibers were reduced in number and ran irregularly in the superior lamina of BZ from ADD rabbits. The jungly elastic fibers (EFs) could still be seen at 2 weeks after operation. At 4 weeks, the number of EFs decreased significantly; EFs lost their jungly arrangement and were shaped like rough dots, of which the arrangement and the lengths were different. Six weeks after operation, many EFs were replaced by distorted, uneven, non-oriented fine EFs, distributed unevenly and some thick or fine EFs that ran irregularly. The number of EFs decreased further and their arrangement was more deranged at 8 weeks. At 10 and 12 weeks, EFs in the superior lamina of BZ were similar to those at 8 weeks.

CONCLUSIONOur results show that EFs lost their function as well as their distribution and arrangement after disc displacement.

Adaptation, Physiological ; Animals ; Behavior, Animal ; Elastic Tissue ; pathology ; Extracellular Matrix ; pathology ; Joint Dislocations ; pathology ; Rabbits ; Temporomandibular Joint Disc ; pathology ; Temporomandibular Joint Disorders ; pathology

OBJECTIVETo introduce the applied anatomy of pedicled buccal fat pad (BFP) graft and a series of histological changes in the healing process of BFP as an uncovered pedicled graft.

METHODSThe healing processes of BFP are demonstrated via uncovered pedicled grafts on rabbits in histological examination. Uncovered buccal fat pads were used to repair soft tissue defects in rabbit oral cavities.

RESULTSThe uncovered buccal fat pads showed complete epithelialization of their oral surfaces at 6 to 8 weeks after surgery and were slowly replaced by fibrous tissue.

CONCLUSIONSAdvantages of the pedicled buccal fat pad graft include an anatomic region that is consistent and easy to excise. The operation can be performed in one incision, affecting neither appearance nor function of the area. Use of the buccal fat pad provides a good reconstruction of soft tissue defects in the mouth.

Adipose Tissue ; transplantation ; Animals ; Cheek ; Female ; Male ; Oral Surgical Procedures ; methods ; Rabbits ; Reconstructive Surgical Procedures ; methods ; Surgical Flaps ; Wound Healing

Objective We aimed to investigate(i)the preventive and therapeutic effects of Huogu Muli Prescription(HGMLP),a Chinese medical compound consisting of epimedii folium,drynariae rhizoma,and ostreae concha,on postmenopausal osteoporosis(PMOP)rats and(ii)whether it exerts its effects by regulating the osteoclast-osteogenesis balance.Methods Forty-eight female Sprague-Dawley rats were randomly divided into the following six groups:(i)the sham-operated group,(ii)the model group,(iii)the Qianggu Capsule group,(iv)the calcium carbonate group,and(v,vi)the HGMLP low-dose and high-dose groups(n = 8 rats per group).After adaptive feeding,rats in all groups except the sham-operated group were treated with bilateral ovarian castration to establish the PMOP model.Each day,rats in the Qianggu Capsule group received 0.054 g/kg Qianggu Capsule suspension intragastrically,rats in the calcium carbonate group received 1.670 g/kg calcium carbonate suspension intragastrically,and rats in the HGMLP low-dose and high-dose groups received 0.188 g/kg and 0.375 g/kg HGMLP intragastrically.Rats in the sham-operated group and the model group received an equal volume of normal saline intragastrically.After 90 consecutive days,serum estradiol(E2),estrogen receptor α(ERα),procollagen typeⅠN propeptide(PINP),and tartrate-resistant acid phosphatase 5b(TRACP-5b)were detected by ELISA.Total antioxidant capacity(T-AOC),superoxide dismutase(SOD),catalase(CAT),and malondialdehyde(MDA)levels were measured by colorimetry.Bone mineral density(BMD),trabecular number(Tb.N),trabecular separation/spacing(Tb.Sp),trabecular thickness(Tb.Th),and structure model index(SMI)were measured by Micro-CT,and the microstructure of cancellous bone was observed.The expressions of osteoprotegerin(OPG),receptor activator of nuclear factor-κB(RANK),RANK ligand(RANKL),phosphorylation of forkhead box O3(FoxO3α),Wnt2,β-catenin,and peroxisome proliferator-activated receptor γ(PPARγ)in rat femur tissue were detected by Western blotting.Results(i)The serum levels of E2 and ERα increased in the Qianggu Capsule group and HGMLP groups,compared with the model group(all P<0.05).(ii)Compared with the model group,the serum levels of PINP,TRACP-5b decreased and PINP/TRACP-5b increased in both the Qianggu Capsule group and HGMLP high-dose group(all P<0.05).(iii)The activities of T-AOC,AOD,and CAT in the Qianggu Capsule group and HGMLP groups were higher than those in the model group,while the content of MDA lower(all P<0.05).(iv)Compared with the model group,the femoral BMD,Tb.Th,and Tb.N increased in the Qianggu Capsule group and HGMLP groups,while the femoral Tb.Sp and SMI decreased(all P<0.05);the femoral BMD increased and the Tb.Sp decreased in the calcium carbonate group(all P<0.05).(v)The protein expressions of RANKL,RANK,FoxO3α,and PPARγ in the Qianggu Capsule group and HGMLP groups were lower than those in the model group,while the protein expressions of OPG,Wnt2,and β-catenin were higher(all P<0.05).Conclusion HGMLP can significantly increase estrogen levels,inhibit osteoclast differentiation,and inhibit bone resorption in the PMOP rats.It also alleviates oxidative stress,promotes osteogenic differentiation,inhibits lipogenic differentiation,improves bone formation,and recovers the balance between osteoclasts and osteoblasts,thus achieving prevention and treatment of PMOP.The potential mechanism of HGMLP may be related to regulation via the OPG/RANKL/RANK or FoxO3α/Wnt2/β-catenin/PPARγ pathways.

Objective To evaluate the role of cholinergic anti-inflammatory pathway in dexmedeto-midine pretreatment-induced reduction of acute lung injury in a rat model of intestinal ischemia-reperfusion ( I∕R) . Methods Twenty-four healthy male Sprague-Dawley rats, aged 2-3 months, weighing 200-250 g, were divided into 4 groups ( n=6) using a random number table method: sham operation group ( S group) , intestinal I∕R group ( II∕R group ) , dexmetomidine group ( DEX group) and α7 nicotinic acetyl-choline receptor antagonistα-bungarotoxin (α-BGT) group (α-BGT group) . Intestinal I∕R was produced by occlusion of the superior mesenteric artery ( SMA) for 60 min followed by 120 min of reperfusion in anesthe-tized rats. Dexmetomidine 5 μg·kg-1 ·h-1 was injected via the tail vein at 1 h before operation in DEX group andα-BGT group. α-BGT 1μg∕kg was intraperitoneally injected at 15 min before dexmetomidine in-jection in α-BGT group. Rats were sacrificed at 120 min of reperfusion, and lung tissues were obtained for microscopic examination of pathological changes ( with a light microscope) and for determination of wet∕dry weight ratio ( W∕D ratio) , tumor necrosis factor-alpha ( TNF-α) and interleukin-6 ( IL-6) contents ( using enzyme-linked immunosorbent assay) , malondialdehyde ( MDA) content ( using thiobarbital acid method) and superoxide dismutase ( SOD) activity ( by xanthine oxidase method) . Results Compared with group S, the W∕D ratio and contents of MDA, TNF-αand IL-6 were significantly increased, and the SOD activi-ty was decreased in II∕R and α-BGT groups, and TNF-α and IL-6 contents were significantly increased in group DEX ( P<0. 05) . Compared with group II∕R, the W∕D ratio and contents of MDA, TNF-αand IL-6 were significantly decreased, SOD activity was increased (P<0. 05), and the pathological changes were significantly attenuated in group DEX. Compared with group DEX, the W∕D ratio and contents of MDA, TNF-α and IL-6 were significantly increased, SOD activity was decreased ( P<0. 05) , and the pathological changes were accentuated in group α-BGT. Conclusion Activation of cholinergic anti-inflammatory path-way is involved in the mechanism by which dexmedetomidine pretreatment reduces acute lung injury in a rat model of intestinal I∕R.

Objective:To observe the protective effects of Zhiganqing Prescription on the liver of C57BL/6J non-alcoholic fatty liver disease (NAFLD) mice induced by high fat diet and its effects on PI3K/Akt/FoxO1 signaling pathway, insulin resistance (IR) and gluconogenesis.Methods:A total of 48 8-week-old male C57BL/6J mice were divided into control group ( n=8) and modeling group ( n=40) according to random number table method. The control group was fed with ordinary diet, and the model group was fed with high-fat diet. The NAFLD model was established after 8 weeks of feeding. The modeling group was divided into model group, Pioglitazone group, Zhiganqing Prescription low-, medium-, and high-dosage group ( n=8 in each group) according to random number table method, and drug intervention lasted for 8 weeks. The body mass of mice was measured regularly during administration. Fasting blood glucose (FBG) levels were measured at 0 and 8 weeks of administration, and oral glucose tolerance tests (OGTT) were conducted. After the experiment, serum levels of GPT, GOT, TC, TG, LDL-C, HDL-C, FINS and C-P were detected and HOMA-IR was calculated. The pathological morphology of liver was observed by HE and PAS staining. The expression levels of PI3K and p-Akt were detected by IHC staining. The protein expression levels of PI3K, Akt, p-Akt, FoxO1, p-FoxO1, G6PC and PCK1 were detected by Western blot. Results:Compared with model group, the body weight of mice in each administration group decreased at 4, 6 and 8 weeks ( P<0.05 or P<0.01). At the 8th week of administration, the levels of FBG and OGTT AUC in each administration group decreased ( P<0.05 or P<0.01), the levels of GPT, TC, TG and LDL-C decreased ( P<0.01), and the GOT levels in Zhiganqing Prescription medium- and high-dosage groups decreased ( P<0.01). The HDL-C level in Zhiganqing Prescription medium-dosage group decreased ( P<0.05 or P<0.01), and the HOMA-IR level in Zhiganqing Prescription low- and medium-dosage groups decreased ( P<0.05 or P<0.01). The levels of FINS and C-P in each administration group increased ( P<0.05 or P<0.01), and the expressions of PI3K protein and p-Akt/Akt, p-FoxO1 /FoxO1 protein in liver tissues increased ( P<0.05 or P<0.01). The protein expressions of G6PC and PCK1 decreased ( P<0.05 or P<0.01). Conclusion:Zhiganqing Prescription can effectively control the body mass, blood glucose, liver function and blood lipids of NAFLD mice, improve IR and gluconeogenesis, the mechanism of which may be related to the activation of PI3K/Akt/FoxO1 signaling pathway.

Methomyl is a carbamate insecticide widely used in pesticides. Most of the poisoning methods are through digestive tract, respiratory tract and skin contact. At present, there is no report of poisoning caused by intramuscular injection. A case of poisoning caused by intramuscular injection of methomyl was analyzed retrospectively. About 4 minutes later, cholinergic crisis and central inhibition occurred. Venovenous-Extracorporeal Membrane Oxygenation (VV-ECMO) and atropine were given quickly. Finally, the patient was successfully rescued and had a good prognosis. After intramuscular injection of methomyl, cholinergic crisis can occur rapidly, and the onset rate is significantly faster than that of digestive tract, respiratory tract and skin contact.
Humans ; Retrospective Studies ; Methomyl ; Insecticides ; Pesticides ; Cholinergic Agents

Interleukin (IL)-36 is a family of cytokines that belongs to the larger IL-1 superfamily. IL-36 agonist/antagonist binds to the interleukin-36 receptor involving in physiological inflammation regulation and pathogenesis of many inflammatory diseases. In inflammatory joint diseases, the expression of IL-36 changes, and some studies have initially explored the role of IL-36 in these diseases. In psoriatic arthritis, IL-36 signal mediates plasma cell and fibroblast-like synoviocyte crosstalk presenting IL-36 agonist/antagonist imbalance. In rheumatoid arthritis, IL-36 agonists induce fibroblast-like synoviocyte to produce pro-inflammatory factors, while IL-36 antagonist deficiency leads to lesion progression. In osteoarthritis, IL-36 agonists induce chondrocytes to produce catabolic enzymes and pro-inflammatory factors. This article reviews the expression and function of IL-36 in different inflammatory joint diseases to provide a reference for revealing their pathogenic mechanisms and discovering therapeutic targets.
Humans ; Interleukins ; Arthritis, Rheumatoid ; Osteoarthritis/pathology* ; Arthritis, Psoriatic/metabolism* ; Cytokines

Immune checkpoint inhibitors (ICIs) have demonstrated unparalleled clinical responses and revolutionized the paradigm of tumor treatment, while substantial patients remain unresponsive or develop resistance to ICIs as a single agent, which is traceable to cellular metabolic dysfunction. Although dysregulated metabolism has long been adjudged as a hallmark of tumor, it is now increasingly accepted that metabolic reprogramming is not exclusive to tumor cells but is also characteristic of immunocytes. Correspondingly, people used to pay more attention to the effect of tumor cell metabolism on immunocytes, but in practice immunocytes interact intimately with their own metabolic function in a way that has never been realized before during their activation and differentiation, which opens up a whole new frontier called immunometabolism. The metabolic intervention for tumor-infiltrating immunocytes could offer fresh opportunities to break the resistance and ameliorate existing ICI immunotherapy, whose crux might be to ascertain synergistic combinations of metabolic intervention with ICIs to reap synergic benefits and facilitate an adjusted anti-tumor immune response. Herein, we elaborate potential mechanisms underlying immunotherapy resistance from a novel dimension of metabolic reprogramming in diverse tumor-infiltrating immunocytes, and related metabolic intervention in the hope of offering a reference for targeting metabolic vulnerabilities to circumvent immunotherapeutic resistance.
Humans ; Neoplasms/pathology* ; Immunotherapy/methods* ; Immune Checkpoint Inhibitors/therapeutic use*