[Objective]In recent years, communication skills have been recognized as an essential competence for acupuncturists. This study proposes to develop a scale for measuring the medical communication skills of acupuncturists.
[Materials and Methods]A questionnaire of 20 items was used to measure medical communication skills. These items were adopted from a concept analysis conducted in a previous study.
Cronbach's alpha was used to examine the scale's reliability. The scale's validity was examined by correlation analysis and multiple regression analysis comparisons with normal communication skills subscale scores (ENDCOREs, Encode, Decode, Control, Regulate) and a Japanese version of characteristic trait anxiety scores (STAI, State-Trait Anxiety Inventory).
[Results]Factor analysis, using a principal extraction method and promax rotation, was conducted on responses from 443students and therapists. As a result, the original 20 items were reduced to 16, and the following three factors were extracted:I. Acceptance of patients and self-control;II. Appropriate explanation to patients;and III. Understanding of patient's feelings. These three factors had high degrees of internal consistency (Cronbach's alpha =.872 -.892).
The scores of the three factors correlated significantly with the scores of the six factors of ENDCORE, and with the anxiety scores. Although the results of multiple regression analysis showed that each factor of ENDCORE explained the three factors, the anxiety scores did not influence medical communication skills. The scores for the three factors correlated significantly with self-evaluation scores of medical interview skill. In addition, these three factors were affected by the degree of clinical experience.
[Conclusion]These results suggest that this scale may be a reliable instrument for assessing medical communication skills among Japanese acupuncturists.

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

BACKGROUND: The immunological mechanisms of asthma remission remain unclear although several reports have suggested that balance between T helper (Th) 2 cytokines and regulatory cytokines is related. OBJECTIVE: To study the balance between interleukin (IL) 10 and IL-5 in asthma clinical remission. METHODS: We measured the numbers of IL-5 and IL-10 producing cells in peripheral blood mononuclear cells stimulated with mite antigen obtained from patients with active asthma (group A, n = 18), patients in clinical remission (group R, n = 15) and nonatopic healthy controls (group H, n = 14). RESULTS: The numbers of IL-5 producing cells in groups A and R were significantly higher than in group H. The number of IL-5 producing cells was lower in group R than in group A, although the difference was not statistically significant. The number of IL-10 producing cells was higher in group R than in group A, although again the difference was not statistically significant. There was a significant difference in the number of IL-10 producing cells between groups A and H but not between groups R and H. The ratio of the number of IL-10 to IL-5 producing cells was highest in group H followed by groups R and A, and the differences were statistically significant for each pair of groups. CONCLUSION: Our study suggests that the IL-10/IL-5 balance is related to clinical asthma. The balance differs between patients in clinical remission and healthy controls, suggesting that allergic inflammation may continue even after clinical asthma remission.
Asthma ; Child ; Cytokines ; Humans ; Inflammation ; Interleukin-10 ; Interleukin-5 ; Interleukins ; Mites ; Prognosis

Objective: Sitosterolemia is a rare autosomal recessive disease caused by the deleterious variants of adenosine 5'-triphosphate (ATP)-binding cassette sub-family G member 5 (ABCG5) or ATP-binding cassette sub-family G member 8 (ABCG8). There are only few data on the pathogenicity of ABCG5 and ABCG8. This study aimed to propose a scheme for determining variant pathogenicity and to catalog the putative pathogenic variants in sitosterolemia. Methods: This study enrolled 377 consecutive Japanese patients with hyper-low-density lipoprotein cholesterolemia (mean age: 46.5±19.8 years, with 192 men) who have targetedsequenced data on ABCG5 or ABCG8 (among 21 Mendelian lipid genes for any dyslipidemias) and serum sitosterol levels at Kanazawa University Hospital from 2016 to 2021. Serum sitosterol levels were divided by 0.79 in patients treated with ezetimibe, accounting for the average reduction with this drug. ABCG5 or ABCG8 variants were defined as putative pathogenic if associated with serum sitosterol levels ≥5 µg/mL or homozygous if associated with serum sitosterol levels ≥10 µg/mL. Results: Twenty-three ABCG5 or ABCG8 variants (16 missense, 2 nonsense, 2 frameshift, 2 deletion, and 1 splice mutation) were identified. Based on our definition, 11 putative pathogenic variants (median sitosterol level: 10.1 [6.5–17.1] µg/mL) were found in 36 individuals and 12 benign variants (median sitosterol: 3.5 [2.5–4.1] µg/mL) in 14 individuals. Conclusion The scheme proposed for assessing the pathogenicity of genetic variations (ABCG5 and ABCG8) is useful. Using this scheme, 11 putative pathogenic, and 12 benign variants in ABCG5 or ABCG were classified.

Objective: Scrub typhus is a relatively common life-threating disease; its symptoms are non-specific and similar to those of other viral infections. Therefore, scrub typhus might be underdiagnosed.Patient: Herein, we report a patient with scrub typhus whose clinical course mimicked that of infectious mononucleosis. A 63-year-old male patient with hypertension presented to our hospital complaining of symptoms including prolonged fever, pharyngeal discomfort, and a mild headache. He showed the appearance of a rash after amoxicillin administration. At the same time, he did not show a crusted rash on his body surface.Results: After a comprehensive examination, Epstein-Barr virus and cytomegalovirus infections were ruled out. We suspected that this patient suffered from scrub typhus on the basis of his usual lifestyle. Finally, polymerase chain reaction analysis showed a positive result for deoxyribonucleic acid of Orientia tsutsugamushi in his blood sample. Fortunately, he recovered naturally with only supportive treatment during his hospitalization.Conclusion: We should observe and monitor patients with infectious mononucleosis-like symptoms and emphasize the importance of a clinical interview.

Superior vena cava syndrome (SVCS), which is characterized by facial edema and congestion of the head, upper extremities, and neck, is a life-threatening oncologic emergency. Although a combination of chemotherapy and radiation therapy has been considered as the standard treatment for SVCS, stent implantation to the superior vena cava (SVC) has been recently developed to alleviate edema or dyspnea caused by SVCS. On the other hand, stent implantation to the SVC requires skilled interventional cardiologists or radiologists. In general, those specialists reside in university hospitals or large hospitals in an urban area. In this case report, an 86-year-old man underwent stent implantation to a stenosed SVC in a rural area. Because the patient refused the transfer to the core, urban hospital, we invited a skilled interventional cardiologist from the core hospital and performed stent implantation to the SVC in a small, rural hospital. It is generally difficult to perform stent implantation for SVCS in a small hospital, because skilled operators in the field of interventional cardiology or radiology do not usually perform operations in smaller facilities. Our case indicates the importance of cooperation between rural generalists and urban specialists.