Three cases of neonatal pericardial effusion related to umbilical venous catheterization / 中华实用儿科临床杂志

A retrospective case review was conducted of 3 cases with umbilical venous catheterization(UVC) related pericardial effusions in the Neonatal Intensive Care Unit of Zhongnan Hospital of Wuhan University from December 2020 to April 2022.All 3 cases were preterm infants with gestational ages of 33 + 4, 31 and 27 + 6 weeks, respectively.UVC was inserted routinely in 24 hours after birth.Three neonates developed tachycardia or bradycardia, dyspnea, decreased oxygen saturation and muffled heart sound at the 1 st to 4 th day after catheterization.Echocardiography indicated pericardial effusion, so the 3 neonates underwent pericardiocentesis and drainage.Among the 3 neonates, 2 cases improved and have good prognosis, 1 case died.UVC can cause pericardial effusion, which occurs mostly in the early stage after catheterization.Pericardial effusion and tamponade should be considered when patients show unexplained sudden clinical deterioration after catheterization, such as dyspnea, cyanosis, tachycardia or bradycardia, etc.Once diagnosed, umbilical vein catheter should be removed in time and pericardiocentesis and drainage should be performed for decompression.Early diagnosis and intervention can effectively improve the prognosis.

Biological characteristics of Chinese hamster infected with Babesia / 中国比较医学杂志

Objective To establish a Chinese hamster model of babesia infection, to find the changing pattern of organs and biochemical parameters in Chinese hamster infected with Babesia, and to promote the detection and treatment of babesiosis.Methods Healthy 5-week old Chinese hamsters were infected by intraperitoneal injection of blood containing Babesia.Blood samples were collected at 0, 2, 4, 6, 8, 10, 12, 14, 16, 23, 30, and 37 days after infection from 5 hamsters at each time point.Blood smears were prepared to detect the parasites using Giemsa staining.ELISA assay was employed to test the IL-2 concentration.The blood biochemical indexes were detected using an automatic biochemical analyzer.DNA was extracted from the whole blood and REAL-TIME RCR was performed to determine the reproduction of Babesia.Aftert the animals were sacrificed, the heart, lung, spleen, liver, and kidney were taken to analyze the changes of organ coefficients.Results The highest level of Babesia in the hamsters occurred on day 4 after the Babesia injection, and then showing a decreasing tendency.However, there was a transient increase on the 12th day after infection.The liver and spleen displayed most extensive response to the infection showing hepatomegaly and splenomegaly, but the variation of heart and kidneys coefficients was within the norm.There were prominent changes of blood cells, especially leucocytes, with two peaks at day 10 and 23 after the Babesia infection.The peak changes of blood biochemical indexes occurred at day 12 after infection.The concentration of serum IL-2 reached a peak on the 10th day after infection.Conclusions The Chinese hamsters display typical characteristics of tick-borne diseases such as hepatomegaly and splenomegaly.The immunological system is activated along with the infection and reaches a highest stage in the second week.Afterwards the Babesia can live in the hamster body for a long period of time.The results of this study provide useful information supporting further studies on the detection, treatment and prevention of Babesiosis.

Role of protein kinase C in the activation of store-operated Ca(2+) entry in airway smooth muscle cells / 华中科技大学学报（医学）（英德文版）

Store-operated Ca(2+) channels (SOCs) are plasma membrane Ca(2+) permeable channels activated by depletion of intracellular Ca(2+) store. Ca(2+) entry through SOCs is known as store-operated Ca(2+) entry (SOCE), which plays an important role in the functional regulation of airway smooth muscle cells (ASMCs). Protein kinase C (PKC) has been shown to have an activating or inhibiting effect on SOCE, depending on cell types and PKC isoforms that are involved. In ASMCs, the effect of PKC on SOCE has not been elucidated so far. In this study, the role of PKC in the activation of SOCE in rat ASMCs was examined by using Ca(2+) fluorescence imaging technique. The results showed that acute application of PKC activators PMA and PDBu did not affect SOCE induced by the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin. The non-selective PKC inhibitor chelerythrine significantly inhibited thapsigargin- and bradykinin-induced SOCE. RT-PCR assay identified PKCα, δ and ɛ isoforms in rat ASMCs. PKCα-selective inhibitor Gö6976 and PKCɛ-inhibiting peptide Epsilon-V1-2 had no effect on SOCE; by contrast, PKCδ-selective inhibitor rottlerin attenuated SOCE dramatically, suggesting that PKCδ was the major PKC isoform involved in the activation of SOCE in ASMCs. Moreover, PKC down-regulation by extended exposure to high doses of PMA or PDBu also reduced SOCE, confirming the essential role of PKC in the activation of SOCE in ASMCs. In addition, PKC down-regulation did not influence the expression of stromal interaction molecule 1 (STIM1) and Orai1, two elementary molecules in the regulation and activation of SOCs. These results identified PKCδ as an essential PKC isoform involved in the activation of SOCE, and confirmed that PKC regulates the function of ASMCs in a SOCE-dependent manner.

Role of protein kinase C in the activation of store-operated Ca(2+) entry in airway smooth muscle cells / 华中科技大学学报（医学）（英德文版）

Store-operated Ca(2+) channels (SOCs) are plasma membrane Ca(2+) permeable channels activated by depletion of intracellular Ca(2+) store. Ca(2+) entry through SOCs is known as store-operated Ca(2+) entry (SOCE), which plays an important role in the functional regulation of airway smooth muscle cells (ASMCs). Protein kinase C (PKC) has been shown to have an activating or inhibiting effect on SOCE, depending on cell types and PKC isoforms that are involved. In ASMCs, the effect of PKC on SOCE has not been elucidated so far. In this study, the role of PKC in the activation of SOCE in rat ASMCs was examined by using Ca(2+) fluorescence imaging technique. The results showed that acute application of PKC activators PMA and PDBu did not affect SOCE induced by the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin. The non-selective PKC inhibitor chelerythrine significantly inhibited thapsigargin- and bradykinin-induced SOCE. RT-PCR assay identified PKCα, δ and ɛ isoforms in rat ASMCs. PKCα-selective inhibitor Gö6976 and PKCɛ-inhibiting peptide Epsilon-V1-2 had no effect on SOCE; by contrast, PKCδ-selective inhibitor rottlerin attenuated SOCE dramatically, suggesting that PKCδ was the major PKC isoform involved in the activation of SOCE in ASMCs. Moreover, PKC down-regulation by extended exposure to high doses of PMA or PDBu also reduced SOCE, confirming the essential role of PKC in the activation of SOCE in ASMCs. In addition, PKC down-regulation did not influence the expression of stromal interaction molecule 1 (STIM1) and Orai1, two elementary molecules in the regulation and activation of SOCs. These results identified PKCδ as an essential PKC isoform involved in the activation of SOCE, and confirmed that PKC regulates the function of ASMCs in a SOCE-dependent manner.

Effects of down-regulation of protein kinase C on activation of storeoperated Ca~(2+) channels and the proliferation of airway smooth muscle cells / 中国病理生理杂志

AIM:To investigate the effects of down-regulation of protein kinase C (PKC) on the activity of storeoperated Ca2 + channels (SOC) and the proliferation of airway smooth muscle cells (ASMCs). METHODS:Rat bronchial smooth muscle cells were isolated and cultured. Fluo-3 /AM fluorescence was measured by laser confocal microscope to assessing intracellular Ca2 +. Downregulation of PKC activity was achieved by incubation of ASMCs with PKC activator phorbol-12-myristate-13-acetate (PMA,10 ?mol/L) or phorbol 12,13 -dibutyrate (PDBu,1 ?mol/L) for 24 h. The proliferation of ASMCs was assayed by calculating the reduction rates of Alamar blue. RESULTS:Down-regulation of PKC activity by longterm exposure of PMA or PDBu inhibited the proliferation of ASMCs,the similar results were obtained by using PKC inhibitor chelerythrine. Both downregulation of PKC activity and inhibition of PKC activity by chelerythrine reduced Ca2 + entry through SOC channels. Low concentration of PMA (0. 1 ?mol/L) promoted the proliferation of ASMCs,and this effect was inhibited by SOC blocker SKF-96365. CONCLUSION:Inhibition or down -regu-lation of PKC activity results in the inhibition of SOC channels,suggesting that PKC is involved in the activation of these channels. Ca2 + entry through SOC channels might contribute to PKC-promoted proliferation of ASMCs.