Squamous cell carcinoma of the lung and pulmonary metastasis of papillary thyroid carcinoma: a case report.

BACKGROUND: The coexistence of malignancies in a patient may be explained by the tumor-to-tumor metastasis phenomenon or multiple primary malignant tumors, both of which are not common findings. Here, we are going to present a case with coexistent papillary thyroid carcinoma and primary squamous cell carcinoma of the lung. CASE PRESENTATION: A 36-year-old Iranian man presented to our clinic for evaluation of constitutional symptoms. His past medical history was significant for papillary thyroid carcinoma due to which he had undergone total thyroidectomy, cervical lymph node dissection, and radioactive iodine therapy 14 years ago. Six months prior to admission, he received radioactive iodine therapy due to the metastatic involvement of both lungs with papillary thyroid carcinoma in another center with consequent improvement in symptoms. Diffuse nodular lesions in both lungs, a lesion in the lower lobe of his left lung, not present 6 months ago, peritoneal carcinomatosis, and several para-aortic lymphadenopathies were detected by imaging studies. A radioactive iodine uptake scan, positron emission tomography/computed tomography scan, and transbronchial biopsy of the lesion in the lung revealed concurrent squamous cell carcinoma of the lung and pulmonary metastasis of papillary thyroid carcinoma. After consultation with an oncologist, our patient received 6 months of chemotherapy; however, he died 8 months after presentation. CONCLUSIONS: Physicians should be aware of the possibility of the emergence of primary malignancies in patients with a history of papillary thyroid carcinoma, especially lung cancer as it is a common site of papillary thyroid carcinoma metastases. Using appropriate diagnostic evaluations in order to choose the best therapeutic option is of utmost importance.

Evidence for the link between defective autophagy and inflammation in peripheral blood mononuclear cells of type 2 diabetic patients

Autophagy was shown to modulate inflammation in immune cells. This study was designed to evaluate the association between autophagy and inflammation in peripheral blood mononuclear cells (PBMCs) of type 2 diabetic (T2D) and non-diabetic (ND) subjects. The autophagy markers were measured by real-time PCR and western blot. The gene expression of pro- and anti-inflammatory cytokines was assessed by real-time PCR. Reduced transcription of BECN1 and LAMP2 and unchanged expression of MAP1LC3B and ATG5 were observed in PBMCs of T2D patients. Decreased LC3B-II and increased p62/SQSTM1 levels were found in PBMCs of diabetic patients. The p-mTOR level was higher in PBMCs of diabetic patients. An increase in both IL-1Beta and TNF-alfa gene expression, along with a decrease in the expression of IL-10, was observed in PBMCs of T2D patients. TNF-α mRNA expression was inversely correlated with the mRNA expression of BECN1 and LAMP2. TNF-alfa and IL-1Beta expression were negatively correlated with the protein levels of LC3B-II. TNF-alfa and IL-1Beta expression had also a positive correlation with protein level of p62. IL-10 mRNA expression was positively correlated with the mRNA expression of BECN1 and LAMP2 and protein levels of LC3B-II and negatively correlated with protein level of p62. In addition, p-mTOR level was positively correlated with IL-1Beta and TNF-alfa mRNA expression. The results revealed a reduced autophagy in PBMCs of T2D patients that is liked with an enhanced inflammation. The suppression of autophagy in PBMCs of diabetic patients may be associated with the activation of the mTOR signaling

Evidence for the link between defective autophagy and inflammation in peripheral blood mononuclear cells of type 2 diabetic patients.

Autophagy was shown to modulate inflammation in immune cells. This study was designed to evaluate the association between autophagy and inflammation in peripheral blood mononuclear cells (PBMCs) of type 2 diabetic (T2D) and non-diabetic (ND) subjects. The autophagy markers were measured by real-time PCR and western blot. The gene expression of pro- and anti-inflammatory cytokines was assessed by real-time PCR. Reduced transcription of BECN1 and LAMP2 and unchanged expression of MAP1LC3B and ATG5 were observed in PBMCs of T2D patients. Decreased LC3B-II and increased p62/SQSTM1 levels were found in PBMCs of diabetic patients. The p-mTOR level was higher in PBMCs of diabetic patients. An increase in both IL-1ß and TNF-α gene expression, along with a decrease in the expression of IL-10, was observed in PBMCs of T2D patients. TNF-α mRNA expression was inversely correlated with the mRNA expression of BECN1 and LAMP2. TNF-α and IL-1ß expression were negatively correlated with the protein levels of LC3B-II. TNF-α and IL-1ß expression had also a positive correlation with protein level of p62. IL-10 mRNA expression was positively correlated with the mRNA expression of BECN1 and LAMP2 and protein levels of LC3B-II and negatively correlated with protein level of p62. In addition, p-mTOR level was positively correlated with IL-1ß and TNF-α mRNA expression. The results revealed a reduced autophagy in PBMCs of T2D patients that is liked with an enhanced inflammation. The suppression of autophagy in PBMCs of diabetic patients may be associated with the activation of the mTOR signaling.

Safety and Effectiveness of Switching from a Basal-only to Biphasic Insulin Aspart 30 Insulin Regimen.

PURPOSE: This sub-analysis of the A1chieve study evaluated the safety and effectiveness of changing from a basal-only insulin regimen to biphasic insulin aspart 30. METHODS: A1chieve was an international, multicenter, prospective, open-label, non-interventional, 24-week study in people with type 2 diabetes mellitus starting/switching to therapy with biphasic insulin aspart 30, insulin detemir, or insulin aspart (alone/in combination) in routine clinical practice. This sub-analysis evaluated the safety and effectiveness of switching from basal insulin with either insulin glargine (GLA group) or insulin neutral protamine Hagedorn (NEU group) to biphasic insulin aspart 30. RESULTS: A total of 2,818 participants received biphasic insulin aspart 30 (1,395 in the GLA group and 1,423 in the NEU group). After 24 weeks of treatment, there were significant reductions in the proportion of patients with at least one hypoglycemia event: total [baseline vs. 24 weeks: 15.5% vs. 9.7% (p < 0.001) and 12.3% vs. 9.9% (p < 0.05), in NEU and GLA groups, respectively], major [2.5% vs. 0.08% (p < 0.001) and 1.2% vs. 0.08% (p < 0.001), in NEU and GLA groups, respectively] and nocturnal hypoglycemia [7.2% vs. 3.5% (p < 0.001) and 5.4% vs. 3.9% (p < 0.05), in NEU and GLA groups, respectively]. After 24 weeks of biphasic insulin aspart 30 there were statistically significant improvements from baseline in glycated hemoglobin, fasting plasma glucose, and post-prandial plasma glucose levels (p < 0.001) and in health-related quality of life (p < 0.001) in both groups. CONCLUSIONS: Biphasic insulin aspart 30 may benefit patients with poor glycemic control on basal insulin regimens who are seeking to change treatment.