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Weekend Admission Increases Risk of Readmissions Following Elective Cervical Spinal Fusion
Renee Ren,Calista Dominy,Brian Bueno,Sara Pasik,Jonathan Markowitz,Brandon Yeshoua,Brian Cho,Varun Arvind,Aly A. Valliani,Jun Kim,Samuel Cho 대한척추신경외과학회 2023 Neurospine Vol.20 No.1
Objective: The “weekend effect” occurs when patients cared for during weekends versus weekdays experience worse outcomes. But reasons for this effect are unclear, especially amongst patients undergoing elective cervical spinal fusion (ECSF). Our aim was to analyze whether index weekend admission affects 30- and 90-day readmission rates post-ECSF. Methods: All ECSF patients > 18 years were retrospectively identified from the 2016–2018 Healthcare Cost and Utilization Project Nationwide Readmissions Database (NRD), using unique patient linkage codes and International Classification of Diseases, Tenth Revision codes. Patient demographics, comorbidities, and outcomes were analyzed. Univariate logistic regression analyzed primary outcomes of 30- and 90-day readmission rates in weekday or weekend groups. Multivariate regression determined the impact of complications on readmission rates. Results: Compared to the weekday group (n = 125,590), the weekend group (n = 1,026) held a higher percentage of Medicare/Medicaid insurance, incurred higher costs, had longer length of stay, and fewer routine home discharge (all p < 0.001). There was no difference in comorbidity burden between weekend versus weekday admissions, as measured by the Elixhauser Comorbidity Index (p = 0.527). Weekend admissions had higher 30-day (4.30% vs. 7.60%, p < 0.001) and 90-day (7.80% vs. 16.10%, p < 0.001) readmission rates, even after adjusting for sex, age, insurance status, and comorbidities. All-cause complication rates were higher for weekend admissions (8.62% vs. 12.7%, p < 0.001), specifically deep vein thrombosis, infection, neurological conditions, and pulmonary embolism. Conclusion: Index weekend admission increases 30- and 90-day readmission rates after ECSF. In patients undergoing ECSF on weekends, postoperative care for patients at risk for specific complications will allow for improved outcomes and health care utilization.
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Cho, Young-Keol,Kim, Jung-Eun,Lee, Sun-Hee,Foley, Brian T.,Choi, Byeong-Sun The Korean Society of Ginseng 2019 Journal of Ginseng Research Vol.43 No.2
Background: To date, no study has described disease progression in Asian patients infected with HIV-1 subtype D. Methods: To determine whether the disease progression differs in patients infected with subtypes D and B prior to starting combination antiretroviral therapy, the annual decline (AD) in $CD^{4+}$ T cell counts over $96{\pm}59months$ was retrospectively analyzed in 163 patients and compared in subtypes D and B based on the nef gene. Results: $CD^{4+}$ T cell AD was significantly higher in the six subtype D-infected patients than in the 157 subtype B-infected patients irrespective of Korean Red Ginseng (KRG) treatment (p < 0.001). Of these, two subtype D-infected patients and 116 subtype B-infected patients had taken KRG. AD was significantly lower in patient in the KRG-treated group than in those in the $KRG-na{\ddot{i}}ve$ group irrespective of subtype (p < 0.05). To control for the effect of KRG, patients not treated with KRG were analyzed, with AD found to be significantly greater in subtype D-infected patients than in subtype B-infected patients (p < 0.01). KRG treatment had a greater effect on AD in subtype D-infected patients than in subtype B-infected patients (4.5-fold vs. 1.6-fold). Mortality rates were significantly higher in both the 45 $KRG-na{\ddot{i}}ve$ (p < 0.001) and all 163 (p < 0.01) patients infected with subtype D than subtype B. Conclusion: Subtype D infection is associated with a >2-fold higher risk of death and a 2.9-fold greater rate of progression than subtype B, regardless of KRG treatment.
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Cho, Hye-Jin,Jung, Eun-Young,Oh, Sung-Hoon,Yoon, Brian,Suh, Hyung-Joo,Lee, Hyun-Sun The Korean Society of Food Science and Nutrition 2010 Preventive Nutrition and Food Science Vol.15 No.2
Thirty-four strains of Lactobacillus species were isolated from soil and eight of these isolates (M1-4 and P1-4) were capable of growing on red ginseng agar. The M1 and P2 strains were determined to be L. plantarum and other strains (M2, M3, M4, P1, P3 and P4) were determined to be L. brevis. Fermentation of red ginseng extract (RGE) with strains M1, M2, P2 and P4 resulted in a low level of total carbohydrate content (174.3, 170.0, 158.8 and 164.8 mg/mL, respectively). RGE fermented by M3 showed a higher level of uronic acid than the control. The polyphenol levels in RGE fermented by M1, P1 and P2 (964.9, 941.7 and $965.3\;{\mu}g/mL$, respectively) were higher than the control ($936.8\;{\mu}g/mL$). Total saponin contents in fermented RGE (except M1) were higher than the control. RGE fermented by M2 and M3 had the highest levels of total ginsenosides (31.7 and 32.7 mg/mL, respectively). The levels of the ginsenoside Rg3 increased from 2.6 mg/mL (control) to 3.0 mg/mL (M2) or 3.1 mg/mL (M3). RGE fermented by M2 and M3 also had the highest levels of Rg5+Rk1 (7.7 and 8.3 mg/mL, respectively). Metabolite contents of ginsenoside (sum of CK, Rh1, Rg5, Rk1, Rg3 and Rg2) of M2 (13.0 mg/mL) and M3 (13.9 mg/mL) were also at a high level among the fermented RGE. Protopanaxadiol and protopanaxatriol content of ginsenoside of M2 (10.9 and 5.4 mg/mL, respectively) and M3 (11.0 and 5.7 mg/mL, respectively) were at higher levels than other fermented RGE.
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The calcium-activated chloride channel anoctamin 1 acts as a heat sensor in nociceptive neurons
Cho, Hawon,Yang, Young Duk,Lee, Jesun,Lee, Byeongjoon,Kim, Tahnbee,Jang, Yongwoo,Back, Seung Keun,Na, Heung Sik,Harfe, Brian D,Wang, Fan,Raouf, Ramin,Wood, John N,Oh, Uhtaek Nature Publishing Group, a division of Macmillan P 2012 NATURE NEUROSCIENCE Vol.15 No.7
Nociceptors are a subset of small primary afferent neurons that respond to noxious chemical, thermal and mechanical stimuli. Ion channels in nociceptors respond differently to noxious stimuli and generate electrical signals in different ways. Anoctamin 1 (ANO1 also known as TMEM16A) is a Ca<SUP>2+</SUP>-activated chloride channel that is essential for numerous physiological functions. We found that ANO1 was activated by temperatures over 44 째C with steep heat sensitivity. ANO1 was expressed in small sensory neurons and was highly colocalized with nociceptor markers, which suggests that it may be involved in nociception. Application of heat ramps to dorsal root ganglion (DRG) neurons elicited robust ANO1-dependent depolarization. Furthermore, knockdown or deletion of ANO1 in DRG neurons substantially reduced nociceptive behavior in thermal pain models. These results indicate that ANO1 is a heat sensor that detects nociceptive thermal stimuli in sensory neurons and possibly mediates nociception.
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Cho, Kyoung-Ah,Kim, Hyuk,Lee, Brian Seonghwa,Kwon, Woon-Yong,Kim, Mi-Seon,Seo, Kwang-Suk,Kim, Hyun-Jeong The Korean Dental Society of Anesthsiology 2014 Journal of Dental Anesthesia and Pain Medicine Vol.14 No.1
Background: Various medical emergency situations can occur during dental practices. Cardiac arrest is known to comprise approximately 1% of emergency situation. Thus, it is necessary for dentists to be able to perform cardiopulmonary resuscitation (CPR) to increase the chance of saving patient's life in emergency situation. In this paper, we conducted a survey study to evaluate to what extent dentists actually understood CPR practice and if they had experience in handling emergency situations in practice. Method: The survey was done for members of the Korean Dental Society of Anesthesiology (KDSA), who had great interest in CPR and for whom survey-by-mail was convenient. We had selected 472 members of the KDSA with a dental license and whose office address and contact information were appropriate, and sent them a survey questionnaire by mail asking about the degree of their CPR understanding and if they had experience of handling emergency questions before. Statistical analyses -frequency analysis, chi-square test, ANOVA, and so on- were performed by use of IBM SPSS Statistics 19 for each question. Result: Among 472 people, 181 responded (38.4% response rate). Among the respondents were 134 male and 47 female dentists. Their average age was $40.4{\pm}8.4$. In terms of practice type, there were 123 private practitioners (68.0%), 20 professors (11.0%), 16 dentists-in-service (8.8%), 13 residents (specialist training) (7.2%) and 9 military doctors (5%). There were 125 dentists (69.1%) who were specialists or receiving training to be specialist, most of whom were oral surgeon (57, 31.5%) and pediatric dentists (56, 30.9%). There were 153 people (85.0%) who received CPR training before, and 65 of them (35.9%) were receiving regular training. When asked about the ratio of chest pressure vs mouth-to-mouth respiration when conducting CPR, 107 people (59.1%) answered 30:2. However, only 27.1% of them answered correctly for a question regarding CPR stages, C(Circulation)- A(Airway)- B(Breathing)- D(Defibrillation), which was defined in revised 2010 CPR practice guideline. Dentists who had experience of handling emergency situations in their practice were 119 (65.6%). The kinds of emergency situations they experienced were syncope (68, 37.6%), allergic reactions to local anesthetic (44, 24.3%), hyperventilation (43, 23.8%), seizure (25, 13.8%), hypoglycemia (15, 8.3%), breathing difficulty (14, 7.8%), cardiac arrest (11, 6.1%), airway obstruction (6, 3.3%), intake of foreign material and angina pectoris (4, 2.2%), in order of frequency. Most respondents answered that they handled the situation appropriately under the given emergency situation. In terms of emergency equipment they had blood pressure device (70.2%), pulse oximetry (69.6%), Bag-Valve-Mask (56.9%), emergency medicine (41.4%), intubation kit (29.8%), automated external defibrillator (23.2%), suction kit (19.3%) and 12 people (6.6%) did not have any equipment. In terms of confidence in handling emergency situation, with 1-10 point scale, their response was $4.86{\pm}2.41$ points. The average point of those who received regular training was $5.92{\pm}2.20$, while those who did not was $4.29{\pm}2.29$ points (P<0.001) Conclusion: The result showed they had good knowledge of CPR but the information they had was not up-to-date. Also, they were frequently exposed to the risk of emergency situation during their dental practice but the level of confidence in handling the emergency situation was intermediate. Therefore, regular training of CPR to prepare them for handling emergency situation is deemed necessary.
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Cho, Jun-Ho,Kim, Goo-Young,Pan, Chi-Jiunn,Anduaga, Javier,Choi, Eui-Ju,Mansfield, Brian C.,Chou, Janice Y. Public Library of Science 2017 PLoS genetics Vol.13 No.5
<▼1><P>A deficiency in glucose-6-phosphatase-α (G6Pase-α) in glycogen storage disease type Ia (GSD-Ia) leads to impaired glucose homeostasis and metabolic manifestations including hepatomegaly caused by increased glycogen and neutral fat accumulation. A recent report showed that G6Pase-α deficiency causes impairment in autophagy, a recycling process important for cellular metabolism. However, the molecular mechanism underlying defective autophagy is unclear. Here we show that in mice, liver-specific knockout of G6Pase-α (L-<I>G6pc</I>-/-) leads to downregulation of sirtuin 1 (SIRT1) signaling that activates autophagy via deacetylation of autophagy-related (ATG) proteins and forkhead box O (FoxO) family of transcriptional factors which transactivate autophagy genes. Consistently, defective autophagy in G6Pase-α-deficient liver is characterized by attenuated expressions of autophagy components, increased acetylation of ATG5 and ATG7, decreased conjugation of ATG5 and ATG12, and reduced autophagic flux. We further show that hepatic G6Pase-α deficiency results in activation of carbohydrate response element-binding protein, a lipogenic transcription factor, increased expression of peroxisome proliferator-activated receptor-γ (PPAR-γ), a lipid regulator, and suppressed expression of PPAR-α, a master regulator of fatty acid β-oxidation, all contributing to hepatic steatosis and downregulation of SIRT1 expression. An adenovirus vector-mediated increase in hepatic SIRT1 expression corrects autophagy defects but does not rectify metabolic abnormalities associated with G6Pase-α deficiency. Importantly, a recombinant adeno-associated virus (rAAV) vector-mediated restoration of hepatic G6Pase-α expression corrects metabolic abnormalities, restores SIRT1-FoxO signaling, and normalizes defective autophagy. Taken together, these data show that hepatic G6Pase-α deficiency-mediated down-regulation of SIRT1 signaling underlies defective hepatic autophagy in GSD-Ia.</P></▼1><▼2><P><B>Author summary</B></P><P>GSD-Ia is an autosomal recessive metabolic disorder caused by a deficiency in G6Pase-α, a key enzyme in maintaining blood glucose levels between meals. Despite strong compliance to dietary therapies, GSD-Ia patients continue manifesting metabolic aberrations including excessive accumulation of glycogen and lipid in the liver. Recently, G6Pase-α deficiency has been linked to impairment in autophagy, a recycling process essential for cellular homeostasis. However, the underlying mechanism is unclear. In this study, we show that hepatic G6Pase-α deficiency alters the activity and/or expression of several lipid regulators, leading to hepatic steatosis and reduced expression of SIRT1, an enzyme that regulates the activity of many proteins via deacetylation. The impaired SIRT1 signaling increases the acetylation of ATG proteins critical for autophagic vesicle elongation, and reduces the activity of FoxO factors that can induce autophagy genes. Consistently, the G6Pase-α-deficient liver exhibits autophagy impairment characterized by attenuated expression of many autophagy components, defective autophagic vesicle elongation, impaired autophagosome formation, and reduced autophagy flux. Importantly, SIRT1 overexpression in G6Pase-α-deficient liver corrects autophagy deficiency. Finally, restoration of hepatic G6Pase-α expression corrects metabolic abnormalities, restores SIRT1-FoxO signaling, and normalizes defective autophagy. Collectively, hepatic G6Pase-α deficiency-mediated down-regulation of SIRT1 signaling underlies defective hepatic autophagy in GSD-Ia.</P></▼2>
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