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Spoken language, both perception and production, is thought to be facilitated by an ensemble of predictive mechanisms. We obtain intracranial recordings in 37 patients using depth probes implanted along the anteroposterior extent of the supratemporal plane during rhythm listening, speech perception, and speech production. These reveal two predictive mechanisms in early auditory cortex with distinct anatomical and functional characteristics. The first, localized to bilateral Heschl’s gyri and indexed by low-frequency phase, predicts the timing of acoustic events. The second, localized to planum temporale only in language-dominant cortex and indexed by high-gamma power, shows a transient response to acoustic stimuli that is uniquely suppressed during speech production. Chronometric stimulation of Heschl’s gyrus selectively disrupts speech perception, while stimulation of planum temporale selectively disrupts speech production. This work illuminates the fundamental acoustic infrastructure—both architecture and function—for spoken language, grounding cognitive models of speech perception and production in human neurobiology. The human brain fluently parses continuous speech during perception and production. Using direct brain recordings coupled with stimulation, the authors identify separable substrates underlying two distinct predictive mechanisms of “when” in Heschl’s gyrus and “what” in planum temporale.

Background: Long-chain fatty acids (LCFAs) cross the plasma membrane via a protein-mediated mechanism involving one or more LCFA-binding proteins. Among these, FAT/CD36 has been identified as key LCFA transporter in the heart and skeletal muscle, where it is regulated acutely and chronically by insulin. In skeletal muscle, FAT/CD36 expression and/or subcellular distribution is altered in obesity and type 2 diabetes. There is limited information as to whether the expression of this protein is also altered in subcutaneous and/or visceral adipose tissue depots in human obesity or type 2 diabetes. Objectives: To compare (a) the expression of FAT/CD36 in subcutaneous and visceral adipose tissue depots in lean, overweight, and obese individuals and in type 2 diabetics, (b) to determine whether the protein expression of FAT/CD36 in these depots is associated with the severity of insulin resistance (type 2 diabetes>obese>overweight/lean) and (c) whether FAT/CD36 protein expression in these adipose tissue depots is associated with alterations in circulating substrates and hormones. Subjects: Subjects who were undergoing abdominal surgery and who were lean ( n =10; three men, seven women), overweight ( n =10; three men, seven women) or obese ( n =7; one man, six women), or who had been diagnosed with type 2 diabetes ( n =5; one man, four women) participated in this study. Measurements: Subcutaneous and visceral adipose tissue samples, as well as blood samples, were obtained from the subjects while under general anesthesia. Adipose tissue samples were analyzed for FAT/CD36 using Western blotting. Serum samples were analyzed for glucose, insulin, FFA and leptin. BMI was also calculated. Results: Subcutaneous adipose tissue FAT/CD36 expression was upregulated by +58, +76 and +150% in overweight, obese and type 2 diabetics, respectively. Relative to subcutaneous adipose tissue, visceral adipose tissue FAT/CD36 expression was upregulated in lean (+52%) and overweight subjects (+30%). In contrast, in obese subjects and type 2 diabetics, no difference in FAT/CD36 protein expression was observed between their subcutaneous and visceral adipose tissue depots ( P >0.05). The subcutaneous adipose tissue FAT/CD36 expression ( R =0.85) and the visceral adipose tissue FAT/CD36 expression ( R =0.77) were associated with alteration in BMI and circulating glucose and insulin. Conclusions: Subcutaneous adipose tissue FAT/CD36 expression is upregulated in obesity and type 2 diabetes. As FAT/CD36 expression is not different in lean, overweight and obese subjects, and was only increased in type 2 diabetics, it appears that visceral adipose tissue FAT/CD36 may respond in a less dynamic manner to metabolic disturbances than subcutaneous adipose tissue FAT/CD36.

Light chain (AL) amyloidosis is the result of a clonal plasma cell disorder which causes organ damage by deposition of misfolded light chains. Kidney is a common site of amyloid deposition. Proteinuria, usually in nephrotic range and unexplained renal insufficiency are the main manifestations of renal injury. We report a unique case of renal involvement by AL amyloidosis masquerading as metabolic bone disease. 38 year old male patient presented with progressively increasing diffuse bony pains, low backache and proximal weakness of both lower limbs since two years. On investigation, he was detected to have hypophosphatemic osteomalacia due to renal phosphate loss which was fibroblast growth factor 23 (FGF23)- independent. He also had nephrotic range low molecular weight proteinuria. Renal biopsy to ascertain the aetiology revealed deposition of amyloid fibrils in the glomerular mesangium on electron microscopy. Its characterization by immunofluorescence (IF) was consistent with immunoglobulin light chain (AL) amyloidosis. In the absence of a demonstrable plasma cell clone on bone marrow biopsy, we made a diagnosis of monoclonal gammopathy of renal significance (MGRS). He was treated with chemotherapy following which there was symptomatic improvement and reduction in phosphaturia. This case describes a unique presentation of renal injury due to AL amyloidosis masquerading as hypophosphatemic osteomalacia. The aim of this report is to highlight that hypophosphatemia in adults is usually acquired and treatment of underlying etiology results in cure, unlike in children where genetic counseling and phosphate replacement is the mainstay of treatment.

A recent workshop brought together global leaders in diabetes to assess existing approaches to disease heterogeneity and to identify research gaps, with a goal of achieving precision diabetology for all patients globally.

NRC publication: Yes

The prophetic warning by the Nobel Laureate Joshua Lederberg[1] that “the microbe that felled one child in a distant continent can reach yours today and seed a global pandemic tomorrow” has once again proved its relevance with the emergence of coronavirus disease 2019 (COVID-19) as the latest pandemic that is affecting human health and economy across the world. Both World Trade Organization (WTO) and Organization for Economic Cooperation and Development (OECD) have indicated COVID-19 pandemic as the biggest threat to global economy since the financial crisis of 2008-2009. Post-script: Within a week of submitting this manuscript for publication the situation both in respect to health and economy, has rapidly deteriorated globally. [...]as per latest information (WHO coronavirus disease 2019 (COVID-19) Situation Report - 59) the infection has spread to 147 countries, involving over 0.2 million individuals and resulting in over 8,000 deaths.

Occasionally there may be other congenital anomalies of the central nervous system associated with the encephalocoele. [...]one of our patients had a congenital dermal sinus 3 to 4 cm. above an occipital encephalocoele. The herniating mass lies deep to the nasal bone, making its appearance at the junction of the nasal bone and the nasal cartilage. [...]both frontal poles are seen herniating through the defect.