The dynamics of patient visits to traditional Chinese medicine during the 2019 coronavirus pandemic.

BACKGROUND: Large-scale epidemics have changed people's medical behavior, and patients tend to delay non-urgent medical needs. However, the impact of the pandemic on the use of complementary and alternative medicine remains unknown. METHODS: This retrospective study aimed to analyze the changes in the number of traditional Chinese medicine (TCM) patients and examine the epidemic prevention policy during the coronavirus disease 2019 (COVID-19) pandemic. We analyzed the number of TCM patients in Taipei City Hospital from January 2017 to May 2020. We tallied the numbers of patients in each month and compared them with those in the same months last year. We calculated the percentage difference in the number of patients to reveal the impact of the COVID-19 pandemic on TCM utilization. We used the Mann-Whitney U test to examine whether there was a significant difference in the number of patients during the COVID-19 pandemic. RESULTS: We included a total of 1,935,827 TCM visits of patients from January 2017 to May 2020 in this study. During the COVID-19 pandemic, the number of patients decreased significantly, except in February 2020. The number of patients during the COVID-19 pandemic had fallen by more than 15% compared with those in the same months last year. March and April had the greatest number of patient losses, with falls of 32.8 and 40% respectively. TCM patients declined significantly during the COVID-19 pandemic, and mobile medicine provided to rural areas fell considerably. Among all the TCM specialties, pediatrics and traumatology, as well as infertility treatment, witnessed the most significant decline in the number of patients. However, the number of cancer patients has reportedly increased. CONCLUSIONS: The COVID-19 pandemic decreased the utilization rate of TCM, especially for mobile healthcare in rural areas. We suggest that the government pay attention to the medical disparity between urban and rural areas, which are affected by the pandemic, as well as allocate adequate resources in areas deprived of medical care.

The proliferation and migration effects of huangqi on RSC96 Schwann cells.

This study evaluated the proliferation effects of huangqi on neuron regeneration. We investigated the molecular mechanisms, which include: (1) cyclin D1, A, E-cell cycle factors and MAPK signaling proliferation (2) FGF-2-UPA-MMPs migration signaling. After treatment with various Huanqi concentrations (1.25, 12.5, 125, 250 and 500 microg/ml,), we observed that Huanqi can increase Rsc 96 cell proliferation at 12.5 microg/ml (p < 0.01) concentration determined by the MTT and wound healing tests. Examination by RT-PCR and Western blotting assay showed that Huangqi is able to stimulate the mRNA and protein expressions of cyclin D1, A, E, cell cycle controlling proteins and excite ERK and P38 MAPK signaling pathways to promote cell proliferation. Huangqi stimulates the FGF-2-UPA-MMP 9 migration pathway and enhances RSC 96 Schwann cells migration. Using MAPK chemical inhibitors, U0126, SB203580 and SP600125, the proliferative effects of Huangqi on RSC 96 cells were ERK and P38 signaling-dependent. Based on these results, applying an appropriate dose of Huangqi with biomedical materials would be a potential approach to enhancing neuron regeneration.

The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis.

BACKGROUND: nocturnal sustained hypoxia during sleeping time has been reported in severe obesity, but no information regarding the cardiac molecular mechanism in the coexistence of nocturnal sustained hypoxia and obesity is available. This study evaluates whether the coexistence of nocturnal sustained hypoxia and obesity will increase cardiac Fas death receptor and mitochondrial-dependent apoptotic pathway. METHODS: 32 lean and 32 obese 5- to 6-mo-old rats with or without nocturnal sustained hypoxia were studied and assigned to one of four subgroups: normoxia lean (NL), normoxia obese (NO), hypoxia lean (HL, 12% O(2) for 8 h and 21% O(2) 16 h/day, 1 wk), and hypoxia obese (HO). The heart weight index, tail cuff plethysmography, echocardiography, hematoxylin-eosin staining, TUNEL assays, Western blotting, and RT-PCR were performed. RESULTS: systolic and diastolic blood pressures in HO were higher than those in NL, and fractional shortening in HO was reduced compared with others. The whole heart weight, the left ventricular weight, the abnormal myocardial architecture, and TUNEL-positive apoptotic cells, as well as the activity of cardiac Fas-dependent and mitochondrial-dependent apoptotic pathway, were significantly increased in obese group or nocturnal sustained hypoxia group and were further increased when obesity and nocturnal sustained hypoxia coexisted, the evidence for which is based on decreases in an anti-apoptotic protein Bcl2 level and Bid and increases in Fas, FADD, pro-apoptotic Bad, BNIP3, cytosolic cytochrome c, activated caspase-8, activated caspase-9, and activated caspase-3. CONCLUSIONS: The cardiac Fas receptor- and mitochondrial-dependent apoptotic pathways were more activated in obesity with coexistent nocturnal sustained hypoxia, which may represent one possible apoptotic mechanism for the development of heart failure in obesity with nocturnal sustained hypoxia.

Hypoxia-induced compensatory effect as related to Shh and HIF-1alpha in ischemia embryo rat heart.

Chronic cardiac ischemia/hypoxia induces coronary collateral formation and cardiomyocyte proliferation. Hypoxia can induce cellular adaptive responses, such as synthesis of VEGF for angiogenesis and IGF-2 for proliferation. Both reduce apoptotic effects to minimize injury or damage. To investigate the mechanism of neoangiogenesis and proliferation of fetal heart under umbilical cord compression situation, we used H9c2 cardiomyoblast cell culture, and in vivo embryonic hearts as our study models. Results showed hypoxia induced not only the increase of IGF-2 and VEGF expression but also the activation of their upstream regulatory genes, HIF-1alpha and Shh. The relationship between HIF-1alpha and Shh was further studied by using cyclopamine and 2-ME2, inhibitor of Shh and HIF-1alpha signaling, respectively, in the cardiomyoblast cell culture under hypoxia. We found that the two inhibitors not only blocked their own signal pathway, but also inhibited each other. The observations revealed when fetal heart under hypoxia that HIF-1alpha and Shh pathways maybe involve in cell proliferation and neoangiogenesis to minimize injury or damage, whereas the complex cross-talk between the two pathways remains unknown.

Immunoglobulin E and matrix metalloproteinase-9 in patients with different stages of coronary artery diseases.

The aims of this study were to identify levels of total immunoglobulin E (IgE) and matrix metalloproteinase (MMP)-9 in patients with different stages of coronary artery diseases. IgE, MMP-9, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), total cholesterol, low density lipoprotein cholesterol (LDL), high density lipoprotein cholesterol (HDL) and triglyceride (TG) were measured by fluorescence enzyme immunoassay, gelatin zymography, and autoanalyzer in normal subjects (n = 40), patients with stable angina pectoris (SAP, n = 40), patients with unstable angina pectoris (UAP, n = 40), patients with acute myocardial infarction (AMI, n = 40), or post-CABG-surgery of those acute myocardial infarction (P-CABG, n = 40). Compared with normal subjects, increased IgE but unchanged MMP-9, CPK, LDH were found in SAP group and UAP group, whereas IgE, MMP-9, CPK and LDH levels were all significantly increased in AMI group. IgE, MMP-9, CPK and LDH levels in P-CABG group were significantly reduced, compared with AMI group, and were similar to those in normal subjects. Cholesterol, LDL, HDL and TG were not significantly changed in all groups. We suggest that serum total IgE can be an early marker of coronary artery disease and MMP-9 is a marker of acute myocardial infarction.